Term
| What supports the trachea laterally & ventrally? |
|
Definition
| 20 U shaped catilaginous ribs |
|
|
Term
|
Definition
| half in the neck, half in the thorax |
|
|
Term
| What is the trachea attached to cranially? |
|
Definition
|
|
Term
| What is the trachea attached to distally? |
|
Definition
| diaphragm (via surface forces) |
|
|
Term
| What happens to the tracheal bifurcation in inspiration? |
|
Definition
| decend by 1 vertebral level |
|
|
Term
| What happens to the thoracic portion of the trachea in rapid deep inspiration? |
|
Definition
| trachea is markedly narrowed |
|
|
Term
| How does the trachea terminate? |
|
Definition
| bifurcating into the R & L primary bronchi |
|
|
Term
|
Definition
| the crest formed at the point of birfurcation of the trachea |
|
|
Term
| When is the carina esp. important? |
|
Definition
surgery
biopsy needs to be done prior to surgical resection bc if invaded by a tumor it is impossible to so a R or L lung resection |
|
|
Term
| Do the bronchioles have cartilage? |
|
Definition
|
|
Term
| What occurs in the non-resp. areas of the bronchioles? |
|
Definition
|
|
Term
| What occurs in the resp. areas of the bronchioles? |
|
Definition
|
|
Term
|
Definition
terminal bronchiole
resp. bronchioles
alveolar ducts
alveolar sacs
alveoli
(resp. bronchiole) |
|
|
Term
| What are the 4 common cell types in the large airways? |
|
Definition
1) ciliated
2) undifferentiated columnar
3) secretory
4) basal |
|
|
Term
| What are the 4 common cell types in the small airways? |
|
Definition
1) ciliated
2) undifferentiated columnar
3) clara
4) basal |
|
|
Term
| What are the 2 common cell types in the alveoli? |
|
Definition
1) Type I pneumocytes
2) Type II pneumocytes |
|
|
Term
| What lines the healthy normal trachea? |
|
Definition
| columnar ciliated epi. mixed with goblet cells with basal cells at the base of the epi. parallel to the BM 9basement membrane) |
|
|
Term
| What determines the differentiation of the basal cells of the tracheal epi? |
|
Definition
| not understood, but they are extremely sensitive to irritants that impinge on the mucosa |
|
|
Term
| Where does each cilium originate? |
|
Definition
| in a basal body beneath the cell surface |
|
|
Term
| What is contained in each cilium? |
|
Definition
a pair of separate central filaments & a peripheral ring of 9 paird, but closed bound filaments (~ to microtubules)
peripheral filaments end in th basal body, but the central ones don't |
|
|
Term
|
Definition
| in a whip-like cyclical fashion |
|
|
Term
| What are the 2 parts of the cilia beating cycle? |
|
Definition
1) rapid forward stroke
2) slower recovery stroke |
|
|
Term
|
Definition
| move a superimposed carpet of mucus (mucus blanket) along with a variable number of trapped particles & cells up towards the larynx |
|
|
Term
|
Definition
|
|
Term
| What can slow down the rate of cilia? |
|
Definition
| noxious agents s.a. sulphur dioxide, cigarette smoking, exposure to cold, & EtOH intoxication |
|
|
Term
| What are the 3 types of columnar cells in tracheo-bronchial epi? |
|
Definition
1) ciliated
2) goblet
3) brush cells |
|
|
Term
|
Definition
|
|
Term
| What are the 2 types of basal cells in tracheo-bronchial epi? |
|
Definition
1) stem cell (multipotent)
2) Kulchitsky (neuroendocrine) |
|
|
Term
| What shape are Clara cells? |
|
Definition
|
|
Term
|
Definition
| secretory cells in bronchioles |
|
|
Term
| Where are the goblet cells in tracheal epi? |
|
Definition
| singly or in groups b/w the ciliated epi. |
|
|
Term
| What is contained in large amounts in goblet cells? |
|
Definition
| sulphated MPS (mucopolysaccharide) |
|
|
Term
How frequent do goblet cells occur in large airways?
more distal airways? |
|
Definition
large: 1/30
distal: 1/100s |
|
|
Term
| What controls goblet cell secretion? |
|
Definition
| direct stimulation (s.a. trapped matter) |
|
|
Term
| What controls gland secretion in resp. epi? |
|
Definition
|
|
Term
| When is there a marked increase in the proportion of goblet cells to the other cells in the tracheobronchial mucosa? |
|
Definition
| in cases of chronic irritation |
|
|
Term
| Why is an increase in goblet cells bad for the tracheobronchial epi? |
|
Definition
| increased goblet cells is at the expense of ciliated cells ∴ more mucus with less cilia to remove the secretions |
|
|
Term
| Where normally are goblet cells (&bronchial neoplasms) found in increased numbers in tracheo-bronchial epi? |
|
Definition
| branching of larger airways |
|
|
Term
| Why is there a predilection for bronchial neoplasms at large airway branches? |
|
Definition
1) increased mucus cells?
2) temporary stasis of mucus carrying carcinogenic material carried by cilia |
|
|
Term
| What are contained in the Kulchitsky cells? |
|
Definition
|
|
Term
| Where is a "carcinoid tumor" commonly found? |
|
Definition
|
|
Term
| What is created by a carcinoid tumor? |
|
Definition
|
|
Term
| What tumors can the Kulchitsky cells on resp. epi make? |
|
Definition
1) a similar tumor to the carcinoid tumor
2) small cell carcinoma (oat tumors) |
|
|
Term
| What secretes the mucus on the surface of the ciliated epi of the resp. tract? |
|
Definition
| bronchial glands & goblet cell secretions |
|
|
Term
|
Definition
| surface of mucus on resp. epi. |
|
|
Term
|
Definition
| layer below the gel layer (doesn't stain with mucin stain) |
|
|
Term
| Why is the sol layer necessary? |
|
Definition
| cilia do not beat in a viscous mucus, so they must be bathed in fluid of considerably lower viscosity |
|
|
Term
| What is usually contained in bronchial glands? |
|
Definition
| mucus secreting & serous cells |
|
|
Term
| What are the bronchial glands called in cross sections? |
|
Definition
|
|
Term
| Where do the mucus secreting cells of the bronchial glands open into? |
|
Definition
| lie centrally & open into a wide lumen |
|
|
Term
| Where do the serous secreting cells of bronchial glands open into? |
|
Definition
|
|
Term
| What are contained in the bronchial gland mucus secreting cells? |
|
Definition
| sulfated MPS & sialomucin |
|
|
Term
| What is contained in the serous cells of bronchial glands? |
|
Definition
| MPS & very little sialomucin |
|
|
Term
| When do bronchial glands undergo hypertrophy & hyperplasia (& chemical changes of the mucus)? |
|
Definition
| with various noxious agent exposure |
|
|
Term
| When are bronchial glands scarce? |
|
Definition
|
|
Term
| When are the bronchial glands well established? |
|
Definition
| 5th or 6th month after birth |
|
|
Term
Function
mucus in the bronchial tree |
|
Definition
| prevents contamination & infection |
|
|
Term
| What controls the secretion of the bronchial glands? |
|
Definition
nerve control (vagus)
stimulation => secretion
cutting/atropine => secretion prevention |
|
|
Term
| Where does normal secretion of mucus arise from in resp. epi? |
|
Definition
| goblet cells of epi. & bronchial glands |
|
|
Term
| Where are bronchial glands found? |
|
Definition
| submucosal layer of bronchi |
|
|
Term
| What is the structure of the bronchial glands? |
|
Definition
simple mixed tubo-alveolar (-acinar)
w/ short funnel-shaped ciliated duct OR non-ciliated collecting duct |
|
|
Term
| What innervates the bronchial glands? |
|
Definition
|
|
Term
| What does the trachea divide into at it's termination? |
|
Definition
|
|
Term
| Which main bronchus has a greater diameter? |
|
Definition
|
|
Term
| Is the combined cross section of the R & L main bronchi larger or smaller than the trachea? |
|
Definition
| larger (tho each are separately smaller) |
|
|
Term
| Why do foreign objects often lodge in the R main bronchus over the L? |
|
Definition
1) it's larger
2) it deviates less from the directionality of the trachea |
|
|
Term
| When does aspiration pneumonia occur? |
|
Definition
| When people are laying down & aspirated material ends up in the post. segment of the R upper lobe |
|
|
Term
| Which pneumonia is considered aspiration pneumonia (& ∴ most commonly seen in the RUL)? |
|
Definition
|
|
Term
| What does each main bronchus supply? |
|
Definition
| an appropriate number or lobar bronch => divides into segmental branches remarkedly constant in their number * distribution with the lobe |
|
|
Term
| What deliniates a segment of lobe aerated by a segmental bromchus from adjoining segments? |
|
Definition
| more or less complete planes of CT |
|
|
Term
| When is segmental anatomy of the lung important? |
|
Definition
1) pulmonary disease may be limited to a particular segment of a lobe
2) radiology
3) bronchoscopy
4) pulmonary surgery |
|
|
Term
| How many bronchopulmonary segments are there? |
|
Definition
10 in the R lung
9 in the L lung |
|
|
Term
| What are the 3 segments of the R superior lobe? |
|
Definition
1) apical
2) anterior
3) posterior |
|
|
Term
| What are the 2 segments of the middle lobe of the R lung? |
|
Definition
|
|
Term
| What are the 5 segments of the R lower lobe of the lung? |
|
Definition
1) superior
2) anterior basal
3) lateral basal
4) posterior basal
5) medial basal |
|
|
Term
| What are the 2 segments of the L superior portion of the upper lobe? |
|
Definition
1) apical posterior
2) anterior |
|
|
Term
| What are the 2 segments of the inferior division of the L upper lobe (lingula)? |
|
Definition
|
|
Term
| What are the 5 segments of the L lower lobe? |
|
Definition
same as R lower lobe:
1) superior
2) anterior basal
3) lateral basal
4) posterior basal
5) medial basal |
|
|
Term
| How many generations of bronchial branching is there? |
|
Definition
varies among different locations of the lung
(posterior basal segments - 25 divisions) |
|
|
Term
| What is the most peripheral airway to contain cartilage? |
|
Definition
|
|
Term
| What are the 3 types of bronchi (by size since the bronchial wall varies)? |
|
Definition
|
|
Term
| Where are large bronchi found? |
|
Definition
| main & lower lobe bronchi |
|
|
Term
| What structure do large bronchi resemble? |
|
Definition
|
|
Term
| Where are medium bronchi found? |
|
Definition
| upper, middle lobe bronchi & segmental bronchi |
|
|
Term
| How are medium bronchi distinguished from large bronchi? |
|
Definition
| medium bronchi have more glands |
|
|
Term
| How are small bronchi distinguished? |
|
Definition
| fewer glands & have a rich venous plexus b/w the muscularis & cartilage |
|
|
Term
| What happens to bronchi do with each resp. cycle? |
|
Definition
lengeth & shorten
may widen or narrow under certain circumstances |
|
|
Term
| How are bronchioles differentiated from bronchi? |
|
Definition
1) diameter of 1 mm or less
2) no cartilage
3) continuous cuboidal epi lining of ciliated & non-ciliated vells (except in the resp. bronchioles) |
|
|
Term
| What do bronchioles have the highest proportion of compaired to all the airways? |
|
Definition
| highest proportion of smooth muscle in their walls relative to the lumen diameter |
|
|
Term
| Where do bronchioles of the first oder arise from? |
|
Definition
| tip of the terminal bronchus |
|
|
Term
| What cells lines the bronchiole divisions? |
|
Definition
| cuboidal epi (3-4 divisions) |
|
|
Term
| What are the 3 cuboidal cell types that line the bronchioles? |
|
Definition
1) Clara cells (non-ciliated secretory)
2) ciliated cells
3) almost no mucus cells |
|
|
Term
| What is the most distal part of the conducting airway? |
|
Definition
|
|
Term
| What cells line the terminal bronchiole? |
|
Definition
|
|
Term
| What happens to the ciliated cells in the terminal bronchiole as the resp. bronchioles are approached? |
|
Definition
|
|
Term
| Are there goblet cells in the terminal bronchiole? |
|
Definition
| no, but there's clara cells |
|
|
Term
|
Definition
secretory
stem cell for epi. renewal in sm. bronchioles |
|
|
Term
| What do the terminal bronchioles give rise to? |
|
Definition
| additional generations of bronchioles (resp. bronchioles) |
|
|
Term
| How are the generations of respiratory bronchioles differing from their predecessors? |
|
Definition
| presence along their walls of an occational alveolus |
|
|
Term
| Is there gas exchange in the terminal bronchiole? |
|
Definition
|
|
Term
| What lines the resp. bronchioles? |
|
Definition
|
|
Term
| How many divisions are there of resp. bronchioles? |
|
Definition
|
|
Term
| What do terminal bronchioles open into? |
|
Definition
|
|
Term
|
Definition
vary in size & shape
1-2cm at the base, height varies more so |
|
|
Term
| Is there fibrous septa in the human lobules like in pigs? |
|
Definition
| yes, but are insufficient |
|
|
Term
| Where do the fibrous septa of the lobules extend? |
|
Definition
| 2-3 cm into the parenchyma from the pleural space |
|
|
Term
|
Definition
| occasional outpouchings of alveoli from the wall within the lobule |
|
|
Term
| What can the epi. surface of the resp. bronchiole be likend to? |
|
Definition
| large funnel with the resp. bronchiole being the narrow, short end in which the funnel contents must pass en route to the mucociliary escalator up above |
|
|
Term
| Why is resp. bronchioles more susceptible to damage than other areas? |
|
Definition
| recieves a larger dose of irritant than more distal alveoli |
|
|
Term
| Where are initial/primary inflammatory changes caused by toxic gases s.a. ozone & phosgene or liquids s.a. kerosene are found? |
|
Definition
|
|
Term
| Where does "broncho-pneumonia" occur? |
|
Definition
| from the center of the lobule i.e. its a lobular pneumonia |
|
|
Term
| How does lobular pneuomonia contrast with lobar pneumonia? |
|
Definition
| lobar: infection spreads uniformly from level of alveoli, not restricted to the center of the lobule |
|
|
Term
| What happens when the center of the lobule becomes destroyed? |
|
Definition
|
|
Term
| What happens with the last of the series of resp. bronchioles? |
|
Definition
| bifurcate to become albeolar ducts |
|
|
Term
| How are resp. bronchioles and alveolar ducts distinguished? |
|
Definition
| alveoli of alveolar ducts follow closely upon one another that their openings are only separated by the narrow framework of their entrance ring |
|
|
Term
| What maintains the ovoid to circular contours of each alveolar entrance? |
|
Definition
| frameworkd consisting of elastic, collagenous, & smooth muscle fibers |
|
|
Term
| What do alveolar ducts terminate into? |
|
Definition
|
|
Term
| What do the alveolar sacs bear? |
|
Definition
|
|
Term
| How many alveoli are in the adult lung? |
|
Definition
|
|
Term
| What is the total gas exchange surface? |
|
Definition
|
|
Term
| What is the difference b/w the epithelium covering the surface of alveolar sacs & alveoli? |
|
Definition
| they're essentially identical |
|
|
Term
| What are the 2 cell types covering the alveolar sacs & alveoli? |
|
Definition
1) type I epithelial cells
2) type II epithelial cells |
|
|
Term
| What cell types covers most of the surface of the alveoli (by virtue of extended & attenuated peripheral cytoplasm)? |
|
Definition
|
|
Term
Function
Type I eithelial cell |
|
Definition
1) gas diffusion
2) pinocytotic uptake of various foreign proteins (part of alveolar clearing mech) |
|
|
Term
| What is the attenuated portion of the type I epithelial cell part of? |
|
Definition
|
|
Term
| What is responsible for keeping alveoli from being overwhelmed by extravasated serum? |
|
Definition
| alveolar epi (NOT capillary endothelium nor the CT) |
|
|
Term
| How common are type II epithelial cells in each alveolus? |
|
Definition
| 3-8/alveolus (alveolar epi NOT covered by type I cells) |
|
|
Term
Function
Type II epithelial cells |
|
Definition
1) produce surfactant, dipalmitoyl lecithin (with participation of lysosomal enzymes) => osmiophilic lamellar inclusions to control alveolar stability
2) stem cell for alveolar epi. |
|
|
Term
Function
peroxisomes in type II epi cells |
|
Definition
| protection against oxygen toxicity |
|
|
Term
| What disease occurs with premature lungs deficient in type II cells? |
|
Definition
| RDS (resp. distress syndrome) |
|
|
Term
| Where are alveolar macs derived from? |
|
Definition
bone marrow => blood monocytes
(there are also partially differentiated interstitial macs ready immediately upon request) |
|
|
Term
Function
pulmonary surfactant |
|
Definition
1) high tension @ high lung volumes (elastic recoil)
2) low tension @ low lung volumes (prevents alveolar collapse) |
|
|
Term
| Where is the pulmonary surfactant located? |
|
Definition
| air-fluid interface of the alveolar surface |
|
|
Term
| Where is the alveolar lining layer? |
|
Definition
| b/w the alveolar air & alveolar epi cells |
|
|
Term
| What is contained in the surface of the alveoli with the air? |
|
Definition
| multiple layers of pulmonary surfactant (to be smooth) |
|
|
Term
| What is contained in the space b/w the surface film & alveolar epithelial cell (hypophase)? |
|
Definition
|
|
Term
| What are the 4 components of the air-blood barrier? |
|
Definition
1) alveolar lining layer (surfactant)
2) type I epi cells
3) Tissue elements of the intestitial space(BM, CT)
4) endothelial cells
(total thickness, 200-400 nm) |
|
|
Term
| What can partially offset when the airway is occluded? |
|
Definition
|
|
Term
| What are the 2 principal mechanisms of collateral ventilation? |
|
Definition
1) pores of Kohn on the alveolar septa (connection b/w 2 adjoining alveoli for gas movement)
2) Lambert's sinus/canal (broncho-alveolar communication) |
|
|
Term
| Are the pores of Kohn seen in newborns? |
|
Definition
|
|
Term
| When are the pores of Kohn larger than normal? |
|
Definition
|
|
Term
| What does Lambert's sinus communicate b/w? |
|
Definition
| terminal bronchioles & some neighboring alveolar ducts |
|
|
Term
| Why does the human lung favor collateral ventilation? |
|
Definition
| lobular septa are not well developed |
|
|
Term
| What segments of the lung tend to have well developed fibrous septa? |
|
Definition
| apices of both upper lobes & lingula of the left upper lobe |
|
|
Term
Is there collateral ventilation in the apices of both upper lobes of the lung & the lingula of the left upper lobe?
What does this mean? |
|
Definition
| it's poor ∴ they are the most common sites to reveal some form of lung damage in otherwise normal lung |
|
|
Term
| What constitutes the major resp. tract defense apparatus? |
|
Definition
| pulmonary alveolar macs + ciliated epi cells |
|
|
Term
| What do macs possess that allow it the capability to digest ingested matter (as a phagocyte)? |
|
Definition
|
|
Term
| What is contained in alveolar macs? |
|
Definition
1) lysosomes
2) ferritin
3) assorted alveolar debris
4) multilaminar inclusion bodies of type II epi cells |
|
|
Term
| How are the alveolar mac organelles? |
|
Definition
1) well developed Golgi
2) varying amounts of ER (dependent on demand for lysosomal enzyme formation)
3) polysomes separate from the membrane of ER => most of the synthesized proteins are retained by cells (not exported) |
|
|
Term
| What is the thin core within the alveolar wall? |
|
Definition
|
|
Term
| What is contained in the alveolar interstitium? |
|
Definition
| occasionally: fibroblasts, collagen & elastic fibers |
|
|
Term
| What is found on either side of the alveolar interstitium? |
|
Definition
|
|
Term
| Why must the flow of lymph in the alveolar wall traverse the interstitial space? |
|
Definition
| interstitium doesn't have lymphatic channels |
|
|
Term
| Where are the lymphatic vessels first seen in the lung? |
|
Definition
| within the CT surrounding the bronchiole => from there on lymphatic vessels traverse peribronchial CT space into draining lymph nodes at the hilus |
|
|
Term
| What are the 2 networkds of pulmonary lymphatics? |
|
Definition
1) pleural (superficial)
2) peribronchovascular (deep) |
|
|
Term
| Where is the pleural lymphatics of the lung composed of? |
|
Definition
| broad lymphatic channe;s, roughly outlining lung lobules & form a polyhedral network on the pleural surface |
|
|
Term
| When is communication b/w the deep (parenchymatous) & superficial lymphatics of the lung common? |
|
Definition
| in young (nonexistant in adults) |
|
|
Term
| How is pleural lymph drained into the hilus? |
|
Definition
|
|
Term
| Why are the pulmonary lymphatics so permeable? |
|
Definition
1) fenestrated endothelium
2) discontinuous BM |
|
|
Term
| Where do both the deep & superficial lymphatics drain? |
|
Definition
| hilar & intrapulmonary nodes (both do both) |
|
|
Term
Is pulmonary vasculature high or low flow?
high or low resistance? |
|
Definition
high flow
low resistance
(able to handle entire R ventricular output...only organ to recieve entire cardiac output) |
|
|
Term
| What supplies the lung with blood? |
|
Definition
1) pulmonary a. & branches (lung parenchyma)
2) bronchial a. - aortic origin (airways) |
|
|
Term
Function
broncho-pulmonary anastamoses |
|
Definition
| premits collateral circulation during altered perfusion states |
|
|
Term
def
resistive work done by resp. system |
|
Definition
| work to move air thru the "pipes" of the system |
|
|
Term
def
elastic work done by resp. system |
|
Definition
| work done to stretch the lungs & thoracic structures |
|
|
Term
def
inertial work done by resp. system |
|
Definition
work to change the direction or rate of airflow
(generally this contributes little to total resp. work @ normal breathing frequency - so it can be ignored) |
|
|
Term
| Who normally does the elastic work to strech the lungs & thoracic cage with respiration? |
|
Definition
|
|
Term
| What resp. muscles do the elastic work for inspiration? |
|
Definition
quiet breathing: diaphragm
exercise: diaphragm + accessory muscles |
|
|
Term
| What resp. muscles do the elastic work for exhalation? |
|
Definition
quiet breathing: passive
forced exhalation: abdominal muscles assist |
|
|
Term
| How does the diaphragm work in inspiration? |
|
Definition
| when it contracts & shortens, it moves downward & creates negative pressure within the chest so that air moves in from the outside |
|
|
Term
| How is exhalation passive? |
|
Definition
| the elastic elements in the resp. system which were stretched return to their resting position |
|
|
Term
| What is used to describe elastic work loads in the same way resistance is used to describe resistibe work loads? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
the inverse of compliance
(i.e. E = 1/C = ΔP/ΔV) |
|
|
Term
| If the lung were alone on the table, what would the pressure be inside the alveoli? |
|
Definition
|
|
Term
| What type of pressure needs to be applied to the airway to fill the lung? |
|
Definition
|
|
Term
| Formula
Pressure inside alveoli (Palv) |
|
Definition
| Palv = Ppl - Pao
(Ppl is the pressure surrounding the alveoli in the pleural space
Pao is the presure applied inside the alveoli from the airways) |
|
|
Term
| Is Ppl positive or negative during inspiration? |
|
Definition
|
|
Term
| Is Palv positive or negative? |
|
Definition
| Could be either depending how you write the equation (with Ppl or Pao first) |
|
|
Term
| What determines lung volume? |
|
Definition
|
|
Term
def
slope of the pressure volume curve |
|
Definition
|
|
Term
| By convention, what is compliance measured at? |
|
Definition
| FRC (functional residual capacity) |
|
|
Term
| What does it mean if the lung has high compliance? |
|
Definition
it's "floppy" s.a. with a disease like emphysema
(i.e it doesn't take much pressure to change the volume) |
|
|
Term
| What does it mean if the lung has low compliance? |
|
Definition
it's "stiff" s.a. with fibrotic or scarring lung diseases
(i.e. it takes a large pressure to inflate) |
|
|
Term
| What are the 3 components of elastic forces of the resp. system? |
|
Definition
1) surfactant
2) lung elastic elements
3) chest wall |
|
|
Term
Function
surfactant in elastic force |
|
Definition
1) creates hysteresis
2) stabilizes the lung
3) contributes to elastic recoil |
|
|
Term
Function
lung elastic elements in elastic force |
|
Definition
1) recruitment of alveoli => hysteresis & recoil
2) collapses to min. volume |
|
|
Term
Function
chest wall in elastic force |
|
Definition
1) tends to move outward
2) interacts with the lung via the pleural space fluid bilayer |
|
|
Term
| If the lung is comparable to a balloon, what is the chest wall comparable to? |
|
Definition
|
|
Term
| How does the chest wall act like a spring? |
|
Definition
1) can be compressed shorter
2) can be stretched longer
3) resting position is b/w the 2 extremes |
|
|
Term
def
elastic pressure of the chest wall |
|
Definition
| pressure inside vs. pressure outside
Pelcw = Ppl - PB |
|
|
Term
| Is the pressure-volume (elastic) behavior of the chest wall linear or exponential? |
|
Definition
|
|
Term
| What happens to the lung if there is no chest wall? |
|
Definition
| lung collapses to a min. volume (lower than RV) |
|
|
Term
| What happens to the chest wall at low lung volume? |
|
Definition
|
|
Term
| What happens to the chest wall as lung volumes approach TLC? |
|
Definition
|
|
Term
| What determines FRC (functional residual capacity)? |
|
Definition
| lung-chest wall interaction |
|
|
Term
|
Definition
| blanace point b/w lung's tendency to collapse to min. volume & chest wall's tendency to move outward to resting volume
(i.e. when PelL = Pelcw) |
|
|
Term
|
Definition
| on the PV curve, the curves for inspiration & expiration are not the same |
|
|
Term
| Is a lung filled with air or saline going to be more compliant? |
|
Definition
|
|
Term
| Why is the air filled lung less compliant than the saline filled lung? |
|
Definition
the lung filled with air has created an air-liquid interface where surface tension is created when the lung tries to decrease it's free energy by decreasing the area of the interface
the lung filled with liquid created a liquid-liquid interface that decreases or abolishes surface tension |
|
|
Term
|
Definition
| contractile force parallel to the liquid surface which pulls molecules to the interior of the liquid |
|
|
Term
|
Definition
P = (2T/r)
(T = surface tension
r = radius of alveolus) |
|
|
Term
| What is implies by La Place's formula? |
|
Definition
| if surface tension is fixed, as the radius of the alveoli decrease, increased pressure is needed to keep the alveoli open |
|
|
Term
| What happens to smaller vs. larger alveoli since all alveoli "see" the same airway pressure? |
|
Definition
small ones collapse as larger ones get bigger
(NOT stable) |
|
|
Term
| How does surfactant alter surface tension? |
|
Definition
makes it so T is no longer fixed, ∴ as r decreases, T decreases & smaller alveoli need less pressure to stay open
(more stable) |
|
|
Term
| Besides surfactant, what other mech. does the lung have to help with stability? |
|
Definition
| interdependence of alveolar "net" i.e. collapse of one unit will increase stress on other units, keeping remaining open lung units stable |
|
|
Term
| What 2 factors affect airflow? |
|
Definition
1) pressure difference
2) resistance to flow |
|
|
Term
| How does pressure affect flow directly? |
|
Definition
the more pressure, the more flow
(pressure difference also is directly related to airflow) |
|
|
Term
def
pressure difference for expiratory flow |
|
Definition
| alveolar pressure - atm pressure |
|
|
Term
def
pressure difference during inspiration |
|
Definition
| atm pressure - negative intrathoracic pressure (created by resp. muscles) |
|
|
Term
| How is airflow inversely related to resistance? |
|
Definition
| increased resistance, decreased airflow |
|
|
Term
|
Definition
Flow = ΔP/R
(∴ R = ΔP/Flow) |
|
|
Term
Effect
obstructive lung diseases (s.a. asthma) |
|
Definition
|
|
Term
| When are resistances said to be in series? |
|
Definition
| if they share a common flow |
|
|
Term
| What does it mean if resistance is in series? |
|
Definition
the resistances in series add directly to total resistance
(2 + 2 = 4) |
|
|
Term
| What is the flow of resistance series in the resp. system? |
|
Definition
| Nose => nasopharynx => oropharynx => larynx => trachea => carina |
|
|
Term
| What happens to the flow in the resp. system after the carina? |
|
Definition
| flow is divided as the airways branch |
|
|
Term
| When are resistances said to be in parallel? |
|
Definition
|
|
Term
| What does it mean if resistance is in parallel? |
|
Definition
| the resistances add as reciprocals
(1/Rtot = 1/R1 + 1/R2) |
|
|
Term
| How much of total resp. system resistance is due to series resistance? |
|
Definition
|
|
Term
| How much of total resp. system resistance is due to parallel resistances? |
|
Definition
|
|
Term
| What increases total resistance more rapidly; resistance in series or parallel? |
|
Definition
series
(if in parallel increases, little effect on total resistance) |
|
|
Term
| Where does congestion have large effects on resp. system total resistance? |
|
Definition
| nasal congestion/tracheal leison |
|
|
Term
| Why are small airway diseases difficult to detect early in the disease (when therapy might make a difference)? |
|
Definition
| little change to resistance so difficult for patient to notice |
|
|
Term
| How much frictional resistance is there from the lung & chest wall tissues? |
|
Definition
|
|
Term
| How much of the resp. resistance is due to airflow? |
|
Definition
|
|
Term
| What 6 factors affect resp. resistance? |
|
Definition
1) Flow pattern
2) Convective acceleration
3) Lung volume
4) sm. muscle tone
5) radial traction
6) pleural pressure |
|
|
Term
| What are the 2 types of airflow pattern? |
|
Definition
1) laminar (smooth)
2) turbulent (chaotic) |
|
|
Term
| What 3 factors affect pressure of laminar moving gas? |
|
Definition
| 1) length of tube (direct)
2) diameter of tube (greatest effect, inverse 1/r4)
3) speed/viscosity of gas moving (direct) |
|
|
Term
| Where is laminar airflow likely to occur? |
|
Definition
|
|
Term
| What 3 factors affect pressure of turbulent moving gas? |
|
Definition
| 1) gas density (direct)
2) length of tube (direct)
3) radius of tube (inversely, greatest effect 1/r19/4) |
|
|
Term
| What is the most important factor for both laminar & turbulent airflow in regards to pressure? |
|
Definition
|
|
Term
| What is used to predict whether flow will be laminar or turbulent? |
|
Definition
| Reynold's number (>2000 turbulent) |
|
|
Term
| Does turbulent or laminar flow require expending more energy (a greater pressure drop)? |
|
Definition
|
|
Term
| What has to happen to velocity of flow to maintain the same volume of flow when going from a larger to smaller cross sectional area (alveoli to trachea)? |
|
Definition
|
|
Term
| What happens to pressure due to the convective acceleration from alveoli to the trachea? |
|
Definition
| loss of pressure (even under conditions of no friction) |
|
|
Term
def
convective acceleration |
|
Definition
| potential energy is converted to kinetic energy |
|
|
Term
|
Definition
resistance is proportional to both flow
resistance is inversely related to the cross sectional area of the tube |
|
|
Term
| When is the Bernouilli Effect important? |
|
Definition
| gas flow thru the lungs during exhalation |
|
|
Term
| Is energy expended in a pressure drop or increase? |
|
Definition
|
|
Term
|
Definition
| produced by diseases which increase airway resistance |
|
|
Term
| What are the 2 major categories of pulmonary disease |
|
Definition
1) obstructive process
2) restrictive process |
|
|
Term
|
Definition
| involves elastic problems |
|
|
Term
| What happens to gas viscosity & density under usual conditions? |
|
Definition
|
|
Term
| What varies with lung volume? |
|
Definition
|
|
Term
| What are the major determinants of airway resistance? |
|
Definition
| factors that alter airway area/diameter/readius |
|
|
Term
| What 3 mucosal factors affect airway resistance? |
|
Definition
1) secretions
2) inflammation
3) environmental irritants |
|
|
Term
| What 3 factors affect smooth muscle tone? |
|
Definition
| 1) CO2
2) bronchoconstrictors
3) bronchodilators |
|
|
Term
| Is lung volume directly or inversely related to resistance? |
|
Definition
|
|
Term
| How do you create a linear relationship b/w volume & reistance? |
|
Definition
|
|
Term
| What 2 factors extrinsic to the airway affect airway resistance? |
|
Definition
1) lung volume
2) radial traction on airways |
|
|
Term
| What happens to flow rate when pressure is increased in the lungs? |
|
Definition
|
|
Term
def
equal pressure point/choke point/point of flow limitation |
|
Definition
| a point in which further increase in pressure will NOT cause an increase in flow (becomes independent of effort) |
|
|
Term
| Is the initial 25% effort dependent or independent in the pressure airflow curve? |
|
Definition
|
|
Term
| Is the driving pressure for expiratory flow positive or negative pressue? |
|
Definition
|
|
Term
| Where is the positive pressure generated for the driving pressure for expiratory flow? |
|
Definition
| in the pleural space around the alveoli |
|
|
Term
| What are the 2 theories of why flow becomes limited? |
|
Definition
1) equal pressure point theory
2) wave speed theory |
|
|
Term
def
equal pressure point theory |
|
Definition
pressure inside the airway is highest in the alveolus & gradually falls along the airway to 0 @ the airway opening (mouth).
Pressure outside the airway (positive pleural pressure) will @ some point along the airway be higher than pressure inside the airway & it will collapse |
|
|
Term
|
Definition
the physical characteristics of the tube & the substance flowing in the tube create a "speed limit" for flow
the point at which this limit is reached is called the choke point |
|
|
Term
| What 6 clinical factors increase airway resistance? |
|
Definition
1) secretions
2) mucosal edema
3) bronchoconstriction
4) loss of radial traction forces on airways
5) low lung volume
6) high pleural pressures @ low lung volumes |
|
|
Term
| What 4 clinical factors decrease airway resistance? |
|
Definition
| 1) anti-inflammatory agents
2) bronchodilators
3) higher lung volumes
4) PCO2 |
|
|
Term
| What is done to overcome resistance? |
|
Definition
|
|
Term
| What does higher resistance mean for work or flow? |
|
Definition
|
|
Term
| What does increasing pressure do to air flow? |
|
Definition
| increase air flow until flow limitation of the airway is reached |
|
|
Term
| What is the major factor that can increase or decrease resistance? |
|
Definition
|
|
Term
| Can measuring airway resistance help detect early small airway disease? |
|
Definition
| no, the parallel part of the lung's airways is where early disease would occur and increase in resistances there add reciprocally so there can be a lot of disease before it's reflected in total resistance of the system |
|
|
Term
| What happens to the flow volume curves of patients with airway disease? |
|
Definition
| concavity in the middle portion of the curve which is quantitated by the FEF 25-75% |
|
|
Term
| Does the flow volume curve work for finding early small airway disease? |
|
Definition
| no (it works for late disease) |
|
|
Term
| What happens in a diseased person on the compliance curve vs. breathing prequency? |
|
Definition
| appears as if compliance decreases since the diseased person can't move air as quickly, they move less volume |
|
|
Term
| Is frequency dependence of compliance a way to find early small airway disease? |
|
Definition
|
|
Term
| In the wave speed theory, when is there no flow limitation? |
|
Definition
| when airflow is low speed, large area (peripheral airways) |
|
|
Term
| What happens to pressure as airspeed increases in the wave speed theory? |
|
Definition
|
|
Term
| What happens to the cross sectional area in the wave speed theory of a compliant tube as airspeed increases & pressure decreases? |
|
Definition
|
|
Term
| What are the 2 types of work in breathing? |
|
Definition
|
|
Term
| What elastic work is there in breathing? |
|
Definition
stretch lungs & chest wall
(muscles contribute dynamically) |
|
|
Term
| What resistive work is there in breathing? |
|
Definition
|
|
Term
| What time constants are there in resistive-elastic interaction? |
|
Definition
| the time it takes to empty or fill an alveolus |
|
|
Term
Formula
resistive-elastic interaction (time constant) |
|
Definition
| R*C = time constant (= seconds) |
|
|
Term
| When will lung units empty faster? |
|
Definition
| stiffer (lower C) &/or have lower R |
|
|
Term
| When will lung units empty slower? |
|
Definition
| floppy (high C) &/or high R |
|
|
Term
| What is Ppl equal to at peak inspiration when flow = 0 (transiently)? |
|
Definition
|
|
Term
| Compliance will remain the same if measured at peak inspiration up to what breathing frequency? |
|
Definition
|
|
Term
| Whwn might lung units not fully empty or sill as the time per breath is shortened? |
|
Definition
| in disease states where there are regions of varying R or C, lung units with slower time constants will not fully empty/fill with increased breath frequency |
|
|
Term
| What happens to the apparent measure compliance dureing fast breathing (dynamic compliance) compared to static conditions in disease state? |
|
Definition
|
|
Term
| Is the size of alveoli static? |
|
Definition
| no, it varied in different regions of the lung |
|
|
Term
| Per breath, can smaller or larger alveoli take in more volume? |
|
Definition
|
|
Term
| What 3 experiments has demonstrated the distribution of differences in ventilation in different lung regions? |
|
Definition
1) radiolabelled gas inhalation
2) frozen dogs
3) nitrogen washout curve |
|
|
Term
| How is the nitrogen washout curve (closing volume measurement) measured? |
|
Definition
| patient inhales one breath of 100% oxygen from RV to TLC, then slowly exhales while expired volume & nitrogen concentration are monitored |
|
|
Term
| How many phases are there in closing volume measurement? |
|
Definition
|
|
Term
def
Phase I
Closing volume measurement |
|
Definition
| 100% oxygen from conducting airways (aka anatomic dead space) is exhales, nitrogen is zero |
|
|
Term
def
Phase II
Closing volume measurement |
|
Definition
| rapid increase in nitrogen as lung units begin emptying |
|
|
Term
def
Phase III
Closing volume measurement |
|
Definition
(plateau phase)
all lung units emptying |
|
|
Term
def
Phase IV
Closing volume measurement |
|
Definition
at volumes near RV, the lower zones cease contributing gas to the expired volume.
The upper zones, which recieved the nitrogen containing air from the conducting airways at the start of inhalation of 100% oxygen empty their air with higher nitrogen concentration |
|
|
Term
def
closing volume
Closing volume measurement |
|
Definition
| the point where the upslope occure from phase III to phase IV |
|
|
Term
| Why is the point of the upslope called the closing volume? |
|
Definition
| lower zones are closed & not contributing to the expired gas |
|
|
Term
| Where is the closing volume in disease state compared to non-diseased states? |
|
Definition
nearer & nearer to FRV instead of near RV
(tried as a test to detect early lung disease, but not effective) |
|
|
Term
| Are all alveoli structurally similar? |
|
Definition
|
|
Term
| What pressure do all alveoli "see"? |
|
Definition
| inside pressure (all the same) |
|
|
Term
| Since all alveoli see the same pressure from the airway side, what has to happen with the pressure outside (Ppl)? |
|
Definition
| must vary in a systematic way |
|
|
Term
| Why can direct measurement with a needle of pleural pressure only be measured at one point? |
|
Definition
|
|
Term
| What is the indirect method for measuring pleural pressure? |
|
Definition
|
|
Term
| Where is pleural pressure most negative? |
|
Definition
|
|
Term
| Where is pleural pressure lease negative (sometimes positive)? |
|
Definition
|
|
Term
| Where is Palv larger; at the apex or lung base? |
|
Definition
|
|
Term
| Where are alveoli larger at FRC? |
|
Definition
|
|
Term
| Where is perfusion greatest in the lung? |
|
Definition
|
|
Term
| Where is the largest ΔV seen in the lung when a breath is taken? |
|
Definition
|
|
Term
| When are all alveoli fully inflated? |
|
Definition
|
|
Term
Where are apical alveoli on the PV curve at RV?
basal alveoli? |
|
Definition
apical: steep portion
basal: flat part of the s shaped curve |
|
|
Term
| When will a breath taken in go into the basal regions? |
|
Definition
| initially apical, but basal too once pressure applied allows basal regions to reach the steep portion of the curve |
|
|
Term
| What must each alveoli experience to have different alveolar volumes? |
|
Definition
| different transpulmonary pressures |
|
|
Term
| Since each alveoli must experience different transpulmonary pressures to have different alveolar volumes and all alveoli have the same "inside" Pao, what pressure must vary? |
|
Definition
|
|
Term
| Does the lower lung regions ventilate (change volume) more or less than the upper lung regions? |
|
Definition
|
|
Term
| What is the ratio of ventilation:perfusion in the lower portions of the lung? |
|
Definition
| 1:1 (match = good for gas exchange) |
|
|
Term
| What allows for determination of restrictive (elastic) problems? |
|
Definition
| measurement of lung volumes |
|
|
Term
| What is the most commonly performed pulmonary function study? |
|
Definition
|
|
Term
| Can spirometry help determine obstructive/restrictive lung diseases? |
|
Definition
defines degree of obstructive (resistive)
may show characteristics of restrictive |
|
|
Term
|
Definition
| measurement of airflows & exhaled volumes vs time |
|
|
Term
| What are 4 mechanisms of obstruction? |
|
Definition
1) mucosal factors (secretions, edema, inflam.)
2) sm. muscle constriction
3) loss of elastic support forces (radial traction) for airways
4) dynamic collapse of airways (with pleural pressure) |
|
|
Term
| What are the steps for a spirometry test? |
|
Definition
1) inhale maximally
2) exhale forcefully while recording ehaled volumes, air flow rates & time |
|
|
Term
| What 2 curves can be plotted from a spirometry test? |
|
Definition
|
|
Term
def
FVC (forced vital capacity) |
|
Definition
|
|
Term
|
Definition
TLC - V @ 1 sec exhaled
(usually ~75% FVC) |
|
|
Term
| Normally, how long does it take to reach 100% of FVC? |
|
Definition
|
|
Term
| What is determined from the V vs T curve in spirometry? |
|
Definition
| 1) TLC
2) FEV
3) FEV1
4) RV? |
|
|
Term
| What is the area enveloped by the curve in the flow vs. V curve? |
|
Definition
| maximum performance & "can't" be exceeded, no matter how much effort is expended |
|
|
Term
| What happens to FVC in an obstructive pattern of dysfunction? |
|
Definition
| should be normal, but can be decreased if there is dynamic collapse of the airways |
|
|
Term
| What happens to FEV1 in obstructive pattern of dysfunction? |
|
Definition
|
|
Term
| *What is the hallmark of an obstructive pattern of dysfunction (i.e. defines an obstructive process)? |
|
Definition
|
|
Term
| What happens to RV in an obstructive pattern of dysfunction? |
|
Definition
|
|
Term
| What are examples of obstructive disease processes? |
|
Definition
1) COPD (emphysema & chronic bronchitis)
2) asthma |
|
|
Term
| What happens to FVC in restrictive pattern of dysfunction? |
|
Definition
| decreased (lungs are smaller ∴ less volume to exhale) |
|
|
Term
| What happens to FVC1 in restrictive pattern of dysfunction? |
|
Definition
| decreased bc all lung volumes are reduced |
|
|
Term
| What happens to the ratio of FEV1/FvC in restrictive pattern of dysfunction? |
|
Definition
|
|
Term
| *What defines a restrictive process of dysfunction? |
|
Definition
|
|
Term
| What are examples of disease processes seen with restrictive patterns of dysfunction? |
|
Definition
1) parenchymal inflam.
2) fibrosis
3) alveolar filling (pneumonia)
4) chest wall deformity
5) neuromuscular conditions
6) poor effort |
|
|
Term
Obstructive Restrictive
FVC
FEV1
FEV1/FVC **
RV
TLC ** |
|
Definition
Obstructive Restrictive
FVC N or [image] [image]
FEV1 [image] N or [image]
FEV1/FVC [image]** N or [image]
RV [image]
TLC [image]** |
|
|
Term
|
Definition
|
|
Term
| What value FEV1 is considered mild obstruction? |
|
Definition
|
|
Term
| What value FEV1 is considered moderate obstruction? |
|
Definition
|
|
Term
| What value FEV1 is considered severe obstruction? |
|
Definition
|
|
Term
| What value FEV1 is considered very severe obstruction? |
|
Definition
|
|
Term
|
Definition
a) normal
b) intrathoracic obstruction (any obstructive disease)
c) poor effort or restrictive process
d) fixed obstruction of upper airway
e) strange: possible vocal cord weakness, such that only inspiration is affected |
|
|
Term
| Why are lung volumes termed "static volume measurements"? |
|
Definition
| all are measures under conditions of no air flow |
|
|
Term
|
Definition
| air remaining in lung at end of a forced expiratory (as low as you can go) |
|
|
Term
|
Definition
the volume of air moved during a normal quiet breath.
(extremely variable, tho end point is stable - FRC) |
|
|
Term
def
ERV (expiratory reserve volume) |
|
Definition
the volume of air which can be expelled at the end of a normal tidal breath
(requires muscular effort) |
|
|
Term
def
IRV (inspiratory reserve volume) |
|
Definition
| the volume of air which can be inhaled after inhaling a normal breath |
|
|
Term
*Formula
FRC (functional residual capacity) |
|
Definition
|
|
Term
|
Definition
| the gas remaining in the lung at the end of a normal tidal breath |
|
|
Term
|
Definition
| the balance of forces b/w the lung (tending to collapse) & the chest wall (tending to move outward) |
|
|
Term
def
IC (inspiratory capacity) |
|
Definition
| the maximal volume inhaled from a normal end-expiratory (or FRC) |
|
|
Term
|
Definition
| maximal volume of air which can be inhaled or exhaled |
|
|
Term
|
Definition
|
|
Term
|
Definition
| amount of air in the lungs at the end of a maximal inhalation |
|
|
Term
|
Definition
|
|
Term
| What are the 3 methods to measuing lung volumes? |
|
Definition
1) open circuit nitrogen washout
2) closed circuit helium dilution
3) body plethysmograph |
|
|
Term
| What are the properties that make helium good for detecting lung volumes? |
|
Definition
| helium is inert, insoluble & not usually part of exhaled gas |
|
|
Term
| How does the closed circuit helium dilution work? |
|
Definition
| 1) begin with a closed measurement system of known volume & known concentration of He
2) patient breathes in & out of this closed system for 10 min & the final [He] is recorded. The gas in the lungs will dilute the original He mixture
3) Calculate lung volume with a variant for Boyle's Law (CV = C2V2)
with C & C1 are the initial final concentrations. V is the original volume of the system. Solve for V2 = lung volume + test system V |
|
|
Term
| What are the disadvantages to closed circuit helium dilution? |
|
Definition
| tends to underestimate lung volumes, esp. for areas of low ventilation |
|
|
Term
| How does the body plethysmograph work? |
|
Definition
| 1) subject is placed in a box of known constant volume
2) resp. efforts will cause increases & decreases in box pressure
3) using Boyle's law (PV = P2V2), you obtain FRC |
|
|
Term
| What is the most accurate way to measure the gas in the thorax? |
|
Definition
|
|
Term
| What are 2 causes of increased TLC? |
|
Definition
1) Obstructive Lung Diseases
2) Acromegaly |
|
|
Term
|
Definition
| size of lung parenchymal is increased |
|
|
Term
| What are the effects of emphysema? |
|
Definition
| decreased lung elastic recoil |
|
|
Term
| What are the effects of asthma? |
|
Definition
| increased chest wall recoil, increased FRC |
|
|
Term
| What are the effects of chronic obstruction? |
|
Definition
|
|
Term
| What causes decreased TLC (i.e. by def. restrictive lung disease)? |
|
Definition
1) Lung disease
2) deformities of the rib cage or thoracic spine (reduced volume of the thoracic cage)
3) resp. muscles (reduction in max. inspiratory & expiratory effort) |
|
|
Term
| What are 2 examples of restrictive lung disease? |
|
Definition
1) fibrosis or scarring
2) fluid or exudate in alveoli |
|
|
Term
| What are the effects of fibrosis or scarring of the lung? |
|
Definition
| decreased distensibility or stiff lungs |
|
|
Term
| What are the effects of fluid or exudate in alveoli? |
|
Definition
|
|
Term
| What can cause deformities of the rib cage (∴ reduced volume of the thoracic cage)? |
|
Definition
1) Kyphosis or scoliosis
2) pectus excavatum or pectus carinum
3) morbid obesity
4) ascites
5) pregnancy
6) congenital deformities of the chest |
|
|
Term
| What can cause the resp. muscles to cause decreased TLC (∴ reduction in maximal inspiratory & expiratory effort)? |
|
Definition
1) neuromuscular disease
2) cannot fully inspire to TLC (so TLC is decreased)
3) usually cannot fully exhale, so RV is increased
4) weakness |
|
|
Term
| What will a happen normally after a single breath of CO? |
|
Definition
enter lungs, cross to the blood & be strongly bound to Hb
If there are no abnormalities with airflow, alveoli, vessels, cardiac output, RBCs, or Hb, all CO will be taken up & away & none will be present in exhaled gas |
|
|
Term
| If there ARE abnormalities with airflow, alveoli, vessels, cardiac output, RBCs, or Hb, what will happen when CO is inspired in a test for diffusing capacity for CO? |
|
Definition
| less than 100% of the CO breath will enter the body ∴ there will be presence of CO in exhales gas producing a lower measurement value for the DLCO |
|
|
Term
| What will the diffusing capacity for CO indicate if the spirometry & lung volumes indicate a restrictive process? |
|
Definition
| 1) low value for DLCO = parenchymal disease
2) normal DLCO = chest wall disease? |
|
|
Term
| What will the diffusing capacity for CO indicate if the spirometry & lung volumes indicate a obstructive process? |
|
Definition
| 1) low DLCO suggests chronic bronchitis, but lowest values suggest emphysema
2) normal DLCO suggests asthma |
|
|
Term
| Patterns of Dysfunction
Obstructive pattern
FVC?
FEV1?
FEV1/FVC?
RV? |
|
Definition
| FVC: normal, but can be reduced if there is dynamic collapse of airways
FEV1: decreased
FEV1/FVC: decreased** (defines obstructive process)
RV: increased |
|
|
Term
| Patterns of Dysfunction
Restrictive pattern
FVC?
FEV1?
FEV1/FVC?
TLC? |
|
Definition
| FVC: decreased (lungs are smaller - less volume to exhale)
FEV1: decreased
FEV1/FVC: normal to increased
TLC: decreased** (low TLC defines restrictive process) |
|
|
Term
| What values should you use to diagnose obstruction or to suggest a restriction? |
|
Definition
|
|
Term
| What value should be used to diagnose a restrictive process? |
|
Definition
|
|
Term
| What values are needed to subdivide restrictive processes? |
|
Definition
| 1) elevated RV => neuromuscular disease
2) using diffusing capacity of CO (DLCO - transfer factor):
a) lung parenchyma if values low
b) chest wall if values normal |
|
|
Term
A 37 yo female compains of SOB & cough. She has dyspnea w/ exercise, particularly in cold weather. The cough is productive of whitish sputum w/ occasional mucus "chunks."
PE shows hyperresonance of the thorax to percussion & diffuse wheezing on expiration on auscultation.
PFTs:
FVC low
FEV1 low
FEV1/FVC low
RV high
TLC normal
RV/TLC high
Is this an obstructive or restrictive process? |
|
Definition
| Obstructive (most likely asthma) |
|
|
Term
| If there is an increase in PFT spirometry reading post-bronchodilator, what does that tell you? |
|
Definition
| suggests reversible airway obstruction |
|
|
Term
67 yo male complains of progressive dyspnea on exertion over the past 4 years. He has been a heavy smoker for many years.
PE shows thin man who appears SOB. Breath sounds are decreased bilaterally & scattered exiratory wheezes are heard.
PFTs:
FVC low
FEV1 low
FEV1/FVC low
RV high
TLC high
RV/TLC high
Is this an obstructive or restrictive process? |
|
Definition
| obstructive (most likely COPD) |
|
|
Term
| If there is hardly an increase in PFT spirometry reading post-bronchodilator, what does that tell you? |
|
Definition
| irreversible obstructive process |
|
|
Term
50 yo female is evaluated for 5 months of progressive dyspnea on exertion, associated with dry cough.
PE reveals bilateral basilar inspiratory crackles (rales).
PFTs:
FVC low
FEV1 low
FEV1/FVC high
RV low
TLC low
RV/TLC low
Is this a obstructive or restrictive process? |
|
Definition
|
|
Term
| What are the features that distinguish a restrictive process from an obstructive process? |
|
Definition
R: decreased TLC, decreased RV, elevated FEV1/FVC
O: normal/increased TLC, increased RV, decreased FEV1/FVC |
|
|
Term
| What is arterial blood gas important to the diagnosis & management of? |
|
Definition
| many acute & chronic medical disorders, esp. pulmonary disorders |
|
|
Term
| How must numerical values for blood gases always be interpreted? |
|
Definition
| in relation to the clinical Hx of the patient (by themselves have little merit) |
|
|
Term
| What are the 3 major components of the arterial blood gas? |
|
Definition
1) oxygen
2) carbon dioxide
3) pH |
|
|
Term
| What does oxygen blood arterial gas level tell us? |
|
Definition
| efficiency of oxygenation of blood as it passes thru the lung capillaries |
|
|
Term
| What does carbon dioxide blood arterial gas level tell us? |
|
Definition
| efficiency of the resp. system to remove carbon dioxide (measurement of ventilation) |
|
|
Term
| What does pH blood arterial gas level tell us? |
|
Definition
| with CO2 indicated the acid-base status of the patient |
|
|
Term
| What are the 2 forms that oxygen is carried in the blood? |
|
Definition
| 1) dissolved O2
2) Hb-bound O2 |
|
|
Term
| How is dissolved O2 measured? |
|
Definition
| by PaO2 (arterial oxygen tension) |
|
|
Term
| How is Hb-bound O2 measured? |
|
Definition
| by SaO2 (arterial oxygen saturation) |
|
|
Term
| Which form of O2 is an indicator of the efficiency of oxygenation of blood as it passes thru the lung capillaries? |
|
Definition
|
|
Term
|
Definition
| amount of Hb saturated with oxygen |
|
|
Term
| Formula
Oxygen content (CaO2) |
|
Definition
| CaO2 = (1.39*Hb*SaO2) + (0.003*PaO2) |
|
|
Term
| Does PaO2 or SaO2 make a bigger contribution to total oxygen content? |
|
Definition
|
|
Term
| What is the normal value of CaO2? |
|
Definition
|
|
Term
Formula
alveolar gas equation |
|
Definition
|
|
Term
|
Definition
| partial pressure of O2 in the alveolus |
|
|
Term
|
Definition
| inspired partial pressure of oxygen |
|
|
Term
def
R in the alveolar-gas equation |
|
Definition
respiratory quotient
(0.8 under normal dietary conditions) |
|
|
Term
|
Definition
| PIO2 = (FIO2)*(PB - Pwater) |
|
|
Term
|
Definition
| fraction of oxygen in the inspired air |
|
|
Term
|
Definition
|
|
Term
|
Definition
| partial pressure of H2O in inspired air |
|
|
Term
| Since at sea level, FIO2 = .21, PB = 760 mmHg, & Pwater = 47 mmHg, what is PIO2 normally at sea level? |
|
Definition
|
|
Term
| Since normal PIO2 = 150 mmHg, PaCO2 = 40 mmHg, & R = 0.8, what is PAO2 at room air, under normal dietary conditions, with a normal breathin pattern? |
|
Definition
|
|
Term
| Is the PaO2 = PAO2 under normal conditions?
Why or why not? |
|
Definition
| no b/c of the normal ventilation-perfusion relationships, the presence of physiologic shunts, and the shape of the oxyhemoglobin curve |
|
|
Term
| What occurs since PaO2 is not equal to PAO2? |
|
Definition
| there is a gradient b/w the alveolar & arterial partial pressures of oxygen |
|
|
Term
Formula
alveolar-arterial gradient |
|
Definition
| A-aO2 gradient = PAO2 - PaO2 |
|
|
Term
| What is the alveolar-arterial gradient in a 20 year old under normal physiologic conditions?
What does this imply about the PaO2? |
|
Definition
| a-aO2: 10 mmHg
=> PaO2: 90 mmHg |
|
|
Term
| Per decade of life, how much does the alveolar-arterial gradient increase per decade of life due to changes in normal physiology?
What does this imply about PaO2? |
|
Definition
| A-aO2: +2.5 mmHg
PaO2: -2.5mmHg/decade |
|
|
Term
| What does an increased A-aO2 gradient imply? |
|
Definition
| primary parenchymal lung disease |
|
|
Term
| What does the oxyhemoglobin dissociation curve describe the relationship b/w? |
|
Definition
|
|
Term
| What causes the sigmoidal shape of the oxyhemoglobin dissociation curve? |
|
Definition
| configurational changes in the Hb => uptake of oxygen enhances the uptake of more oxygen until the Hb is saturated |
|
|
Term
| What is the significance of the plateau phase of the oxyhemoglobin dissociation curve? |
|
Definition
| Hb is nearly/fully saturated ∴ further increase in PaO2 doesn't appreciably increase SaO2 or the total oxygen content of arterial blood (CaO2) |
|
|
Term
| What is the significance of the steep middle phase of the oxyhemoglobin dissociation curve? |
|
Definition
| there will be large changes in saturation for small changes in PaO2 |
|
|
Term
| Where do the steep portion of the oxyhemoglobin curve exist in the body? |
|
Definition
| in the peripheral tissues ∴ allowing for increased release of oxygen where it is most needed |
|
|
Term
| What does the overall non-linear relationship b/w PaO2 & SaO2 provide? |
|
Definition
| a reserve of oxygen in the blood |
|
|
Term
| For what value of PaO2 is SaO2 50% (i.e. P50)? |
|
Definition
|
|
Term
| What is the P50 used for in the oxyhemoglobin dissociation curve? |
|
Definition
| as an indicator of the position of the dissociation curve |
|
|
Term
| For what value of PaO2 is SaO2 75%? |
|
Definition
|
|
Term
| What does the SaO2 75% tell us? |
|
Definition
| the partial pressure/saturation of oxygen in mixed venous blood |
|
|
Term
| For what values of PaO2 & SaO2 do patients qualify for home oxygen? |
|
Definition
| PaO2 = 55 mmHg
SaO2 = 88% |
|
|
Term
| For what values of PaO2 & SaO2 is at the beginning of the plateau phase & ∴ indicates smaller changes in CaO2?
(also considered the low end of normal) |
|
Definition
| PaO2 = 60 mmHg
SaO2 = 90% |
|
|
Term
| What value of PaO2 is reached when SaO2 is 97% (Hb nearly saturated)? |
|
Definition
|
|
Term
| What happens if there is a right shift to the oxyhemoglobin dissociation curve? |
|
Definition
| affinity of Hb for O2 is decreased & the ability for Hb to release O2 is enhanced |
|
|
Term
| When would a right shift of the oxyhemoglobin dissociation curve be normal? |
|
Definition
| to deliver increased oxygen to tissues during periods of oxygen deficit |
|
|
Term
| What 4 factors can shift the oxyhemoglobin curve to the right? |
|
Definition
| 1) increase PaCO2 (Bohr effect)
2) decreased pH
3) increased body T
4) increased 2,3-DPG |
|
|
Term
| Why do hemoglobinopathies show a right shift of the oxyhemoglobin dissociation curve? |
|
Definition
1) secondary to genetic mutation
2) possibly secondary to an increase in 2,3-DPG |
|
|
Term
| What happens if there is a left shift to the oxyhemoglobin dissociation curve? |
|
Definition
| affinity of Hb for O2 is increased and the ability of Hb to release O2 is lowered |
|
|
Term
| What 4 factors can cause a left shift of the oxyhemoglobin dissociation curve? |
|
Definition
| 1) decreased PaCO2 (Bohr effect)
2) increased pH
3) ddecreased body T
4) decreased 2,3-DPG |
|
|
Term
| What alternative hemoglobins tend to have a left shift in the oxyhemoglobin dissociation curve? |
|
Definition
1) fetal hemoglobin
2) carboxyhemoglobin (CO binding to Hb)
3) methemoglobin (oxidation of iron from ferrous to ferric state - congenital or oxidant drugs) |
|
|
Term
| What plays a critical role in maintaining the relatively narrow range of pH in which cellular and extracellular physiologic processes operate most efficiently? |
|
Definition
|
|
Term
| What is the major biologic buffer system? |
|
Definition
|
|
Term
| What other biological buffer systems are there besides CO2-bicarb system? |
|
Definition
1) intracellular proteins
2) Hb
3) plasma proteins |
|
|
Term
| Where is the bicarb anion (HCO3-) found? |
|
Definition
| in most body fluids (constitutes a large reservoir of buffer) |
|
|
Term
Equation
Bicarb as a buffer |
|
Definition
| H+ + HCO3- ↔ H2CO3 ↔ H2O + CO2 |
|
|
Term
| What enzyme catalyzes the reaction:
H2CO3 ↔ H2O + CO2 ? |
|
Definition
|
|
Term
| What equation is used to describe properties of an acid-base? |
|
Definition
| Henderson-Hasselbalch Equation |
|
|
Term
Formula
Henderson-Hasselbalch Equation |
|
Definition
| KA = ([H+][HCO3-])/[H2CO3] |
|
|
Term
| What is the logarithmic form of the Henderson-Hasselbalch equation? |
|
Definition
| log KA = log [H+]+ log ([HCO3-]/[H2CO3]) |
|
|
Term
| How is pH determined by the Henderson-Hasselbalch equation? |
|
Definition
| pH = pKA + log ([HCO3-]/[H2CO3]) |
|
|
Term
| Does the equilibrium b/w CO2 & H2CO3 favor CO2 or H2CO3? |
|
Definition
|
|
Term
| Since CO2 is proportional to it's solubility coefficient, how can we rearrange Henderson-Hasselbalch for pH? |
|
Definition
| pH = pKA + log {[HCO3-]/(0.03*PaCO2)} |
|
|
Term
| What are pH, pKA, & log {[HCO3-]/(0.03*PaCO2)} under normal conditions? |
|
Definition
| pH = 7.4
pKA = 6.1
log {[HCO3-]/(0.03*PaCO2)} = 1.3 |
|
|
Term
| What changes occur to cause metabolic alkalosis? |
|
Definition
| increased [HCO3-] => increased pH |
|
|
Term
| What changes occur to cause metabolic acidosis? |
|
Definition
| decreased [HCO3-] => decreased pH |
|
|
Term
| What changes occur to cause resp. acidosis? |
|
Definition
| increased PaCO2 => decreased pH |
|
|
Term
| What changes occur to cause resp. alkalosis? |
|
Definition
| decreased PaCO2 => increased pH |
|
|
Term
| What are the 3 forms CO2 is transported in the blood? |
|
Definition
| 1) dissolved CO2
2) bicarb anion
3) carbamino compounds |
|
|
Term
| How much of blood CO2 is dissolved? |
|
Definition
|
|
Term
| How is dissolved CO2 measured? |
|
Definition
|
|
Term
| How much of arterial CO2 is in the form of bicarb anion? |
|
Definition
|
|
Term
| Where is reaction of CO2 & H2O slow?
fast? |
|
Definition
|
|
Term
| Why is the rxn of CO2 & H2O fast in RBCs? |
|
Definition
|
|
Term
| Why is there a chloride shift in the RBCs due to the bicarb reactions? |
|
Definition
| as HCO3- accumulates in the RBC, it diffuses across the cell membrane into the plasma, but H+ is impermeable, so it remains in the cell.
To preserve electrical neutrality, Cl- shifts into RBCs |
|
|
Term
| How is H+ buffered in the blood? |
|
Definition
|
|
Term
| Where is H+ buffered by Hb enhanced? |
|
Definition
| in tissues with loe O2 content & Hb is deoxygenated |
|
|
Term
| How are carbamino compunds formed? |
|
Definition
| by the reaction of CO2 with the terminal amino groups of blood proteins |
|
|
Term
| What is the major CO2 binding protein? |
|
Definition
|
|
Term
| How much of arterial CO2 is in carbamino compounds? |
|
Definition
|
|
Term
| What is the relationship b/w CO2 & HB in the carbon dioxide hemoglobin dissociation curve at physiological concentrations of CO2? |
|
Definition
|
|
Term
|
Definition
| carbon dioxide Hb dissociation curve is shifted to the:
1) left if Hb is deoxygenated (enhancing affinity of Hb for CO2)
2) right if Hb is oxygenated (decreased affinity of Hb for CO2) |
|
|
Term
| What are the 4 primary acid-base disorders? |
|
Definition
1) resp. acidosis
2) resp. alkalosis
3) metabolic acidosis
4) metabolic alkalosis |
|
|
Term
|
Definition
| primary increase in PaCO2 => decrease pH |
|
|
Term
|
Definition
| primary decrease in PaCO2 => increased pH |
|
|
Term
|
Definition
| primary increase in acid or decrease in base => decreased HCO3- => decreased pH |
|
|
Term
|
Definition
| primary increase in base or decrease in acid => increased HCO3- => decreased pH |
|
|
Term
| Why is it necessary for the body to compensate for changes in PaCO2 or HCO3- to adjust the pH back to normal? |
|
Definition
| the pH must be kept within a narrow range for physiologic processes |
|
|
Term
| Is compensation for a pH change ever complete in the body? |
|
Definition
| no (pH or PaCO2 don't get back to normal) |
|
|
Term
Effects
metabolic acidosis |
|
Definition
| acid added to the system => bicarb & H+ combine => increased CO2 formation => increased ventilation => decreased PaCO2 => increased pH |
|
|
Term
Effect
Metabolic alkalosis |
|
Definition
| base added to system => formation of H+ => decreased CO2 => decreased ventilation => increased PaCO2 => decreased pH |
|
|
Term
| How do the kidneys compensate for chronic change in the PaCO2? |
|
Definition
| adjusting the renal reabsorption of bicarb anion |
|
|
Term
|
Definition
| increased PaCO2 => increased bicarb anion absorption (increased acid secretion) |
|
|
Term
|
Definition
| decreaed PaCO2 => decreased bicard anion absorption (decreased acid excretion) |
|
|
Term
| What is normal PaO2 breathing room air for a 20 year old? |
|
Definition
|
|
Term
| How much does PaO2 decrease by per decade? |
|
Definition
|
|
Term
| Formula
PaO2 age correction |
|
Definition
|
|
Term
| What is the normal pH range? |
|
Definition
|
|
Term
| What is the normal PaCO2 range? |
|
Definition
|
|
Term
| What is the normal bicarb anion range? |
|
Definition
|
|
Term
| What is the standard abbreviation for blood gases? |
|
Definition
| pH/PaCO2/PaO2/bicarb/SaO2
(i.e. 7.40/40/100/24/100%) |
|
|
Term
| How much will pH increase or decrease per ±10 mmHg change of PaCO2 acutely? |
|
Definition
|
|
Term
| How much will pH increase or decrease per ±10 mmHg change of PaCO2 chronicly? |
|
Definition
|
|
Term
| With chronic acidosis, how much with bicarb increase per 10 mmHg increase of PaCO2? |
|
Definition
|
|
Term
| With chronic alkalosis, how much with bicarb decrease per 10 mmHg decrease of PaCO2? |
|
Definition
|
|
Term
|
Definition
| difference b/w unmeasured cations & unmeasured anions in the serum |
|
|
Term
| What are included as unmeasured cations? |
|
Definition
|
|
Term
| What are included as unmeasured anions? |
|
Definition
| 1) PO4
2) SO4
3) organic acids |
|
|
Term
|
Definition
| AG = [Na+] - [Cl-] - [HCO3-] |
|
|
Term
Why are the assumptions that
1) there is a gap b/w anions & cations
2) anion gap represents the unmeasured anions
incorrect? |
|
Definition
1) concentrations of cations & anions in the serum must always be equal
2) concentration of unmeasured anions in 23 (not 12) meq/L |
|
|
Term
| What is the normal range for anion gap? |
|
Definition
|
|
Term
| What is the anion gap important for? |
|
Definition
| differential Dx of metabolic acidosis |
|
|
Term
| What does an increased anion gap indicate? |
|
Definition
| increase in unmeasured anions in the blood |
|
|
Term
| What does a normal anion gap (with metabolic acidosis) imply? |
|
Definition
| loss of base (or inhestion of a pure acid) |
|
|
Term
| What can increase the anion gap? |
|
Definition
1) decreased unmeasured cations (hypokalemia, hypomagnesemia, hypocalcemia)
2) increased unmeasured anions |
|
|
Term
| What endogenous acids increase the anion gap? |
|
Definition
| 1) inorganic: PO4-3, SO4-3
2) organic: ketoacids, lactic acid |
|
|
Term
| What exogenous acids can increase the anion gap? |
|
Definition
| drug or toxin s.a. MeOH, poylethylene glycol, salicylate acid |
|
|
Term
| Clinically, what can cause acute resp. acidosis? |
|
Definition
1) drug OD
2) stroke
3) asthma
4) COPD
5) neuromuscular syndromes s.a. Guillain-Barre |
|
|
Term
| Clinically, what can cause chronic resp. acidosis? |
|
Definition
1) obesity-hypoventilation syndrome
2) COPD
3) Kyphoscoliosis
4) Neuromuscular syndromes s.a. ALS, myasthenia gravis |
|
|
Term
| Clinically, what can cause resp. alkalosis? |
|
Definition
1) hypoxemia of any cause
2) cortical influences (anxiety, pain, fever)
3) disorders of the airway (asthma/COPD) or lung tissue (pulmonary edema, pneumonia)
4) drugs (salicylates)
5) pregnancy |
|
|
Term
| What are the 2 groups of clinical metabolic acidosis? |
|
Definition
1) w/ anion gap
2) w/o anion gap |
|
|
Term
| Clinically what can cause metabolic acidosis w/ anion gap? |
|
Definition
1) ketoacidosis (diabetic or alcoholic)
2) lactic acidosis
3) intoxicants (MeOH, ethylene glycol, salicylates)
4) renal failure |
|
|
Term
| Clinically what can cause metabolic acidosis w/o anion gap? |
|
Definition
1) GI bicarb loss (diarrhea)
2) diuretics (acetazolamide)
3) ingestion of HCl
4) renal tubular acidosis
5) early renal failure |
|
|
Term
| What are the 2 groups of clinical metabolic alkalosis? |
|
Definition
| 1) chloride responsive (urine Cl- <10 mEq/L)
2) chloride unresponsive (urine Cl- >20 mEq/L) |
|
|
Term
| Clinically, what can cause metabolic alkalosis that's chloride responsive? |
|
Definition
| 1) volume depletion
2) GI H+ loss (vomiting)
3) diuretics (furosemide)
4) ingestion of alkali |
|
|
Term
| Clinically, what can cause metabolic alkalosis that's chloride unresponsive? |
|
Definition
1) mineralcorticoid excess (primary aldosteronism)
2) glucocorticoid excess (Cushing's syndrome) |
|
|
Term
|
Definition
|
|
Term
| What is the number one death from indectious disease? |
|
Definition
|
|
Term
|
Definition
| inflammation of the gas exchanging areas of the lungs/lower RT |
|
|
Term
| What are the 4 normal host defenses to pneumonia? |
|
Definition
1) mechanical
2) reflexes
3) mucociliary transport
4) Immune cells |
|
|
Term
| What mechanical host defense is there against pneumonia? |
|
Definition
1) curved anatomic shape of the upper airway
2) vibrissae (nose hair) - filters |
|
|
Term
| What reflexive host defense is there against pneumonia? |
|
Definition
| coughing & sneezing to expel material |
|
|
Term
| What is the mucociliary host defense against pneumonia? |
|
Definition
| unidirectional beating of airway cilia to move the blanket of mucus upward to allow trapped material to be swallowed or expectorated |
|
|
Term
| What immune cells of the host defense is there against pneumonia? |
|
Definition
1) alveolar macs (phagocytosis & chemotaxin release)
2) T cells (cell mediated)
3) B cells (Ab) |
|
|
Term
| What 7 factors can alter host defenses to pneumonia? |
|
Definition
1) age
2) debilitation, malnutrition
3) depressed level of consciousness
4) airway abnormalities
5) problems with mucociliary function
6) co-morbid illnesses
7) immunosuppression |
|
|
Term
| For what ages are there altered host defenses? |
|
Definition
young (immature immune system)
old (depressed immune function to debilitation, disease) |
|
|
Term
| What are examples of depressed levels of consciousness that could alter host defenses? |
|
Definition
1) neurologic illness/injury
2) seizures
3) drug OD
4) anesthesia
etc. |
|
|
Term
| What airway abnormalities can alter host defenses? |
|
Definition
1) trauma
2) inhalant injury
3) obstruction |
|
|
Term
| What problems with mucociliary function can arise that could alter host defenses? |
|
Definition
1) abnormal mucus (CF)
2) poor ciliary function: inhibition of ciliary motion (smoking, COPD, drugs, EtOH, anesthesia, viral inf., etc.) or immotile/dysfunctional cilia syndromes |
|
|
Term
| What co-morbid diseases can alter host defenses against pneumonia? |
|
Definition
1) cancer (depressed immunity, obstruction, debilitation)
2) CHF
3) diabetes (altered upper airway flora, decreased cell function)
4) viral inf. (mucociliary function. depressed PMN function)
5) alcoholism (debility, malnutrition, depressed consciousness, poor ciliary function) |
|
|
Term
| How can immunosuppression be primary? |
|
Definition
| congenital defect in any system component |
|
|
Term
| How can immunosuppression be secondary? |
|
Definition
1) neutropenia (drug induced, irradiation, malignancy)
2) defective PMNs (malignancies, uremia, burns, diabetes, steroids)
3) depressed T cells (AIDS, steroids, uremia, cancers, chemotherapy)
4) depressed B cells (splenectomy, sickle cell, malignancies, irradiation, chemo, malnutrition) |
|
|
Term
What are the 4 modes of transmission of pneumonia?
What's the most common? |
|
Definition
1) aspiration of oropharyngeal orgs(**most common)
2) inhalation of airborne orgs
3) hematogeneous spread
4) lymphatic spread
(in order of most common to least common) |
|
|
Term
| What is the most common org to cause bacterial pneumonia? |
|
Definition
|
|
Term
| Where is pneumococcus found? |
|
Definition
|
|
Term
| Where do anaerobes live in the oropharynx? |
|
Definition
|
|
Term
| When might there be altered upper airway flora? |
|
Definition
1) colonization with pathogens (G-) after coming to hospital/nursing home
2) people using needles (IV drugs abusers, diabetics, dialysis patients) |
|
|
Term
| What predisposes someone to aspiration pneumonia? |
|
Definition
1) altered state of consciousness
2) neuromuscular illness
etc. |
|
|
Term
| What common airborne orgs can be inhaled to cause pneumonia? |
|
Definition
1) mycoplasma
2) TB
3) legionella
4) fungi |
|
|
Term
| What is important in determining if a person will acquire pneumonia from airborne orgs? |
|
Definition
1) size of innoculum
2) state of hose defenses |
|
|
Term
| Who is at a predisposition to acquire pneumonia via a hematogenous spread? |
|
Definition
| IV drug users, infected IV lines, etc |
|
|
Term
| What are the 3 ways pneumonia can be classified? |
|
Definition
1) by org (bacterial, fungal, etc)
2) by host factors
3) by radiographic appearance |
|
|
Term
| *What is the importance of classifying pneumonia by host factors? |
|
Definition
| suggests potential orgs so Abx may be started ealy while lab studies are pending |
|
|
Term
| What are the 3 categories of host factors to classify pneumonia? |
|
Definition
1) CA (community acquired)
2) nosicomial
3) immunocompromised/immunosuppressed patients |
|
|
Term
| Who is at risk for CA pneumonia? |
|
Definition
1) normal population
2) nursing home, skid row, etc. |
|
|
Term
|
Definition
| acquired due to hospital environment |
|
|
Term
| Where do nosocomial orgs colonize? |
|
Definition
|
|
Term
| What type of nosocomial pneumonia are you worried about for a patient on medications or under anesthesia? |
|
Definition
|
|
Term
| What makes a patient susceptible to nosocomial pneumonia? |
|
Definition
1) medications, anesthesia (=> aspiration pneumonia)
2) invasive devices
3) lack of hand washing
4) contaminated resp. equipment |
|
|
Term
| What can cause immunocompromised pneumonia? |
|
Definition
1) underlying disease (AIDS, cancer)
2) therapy (chemo, radiation, steroids, immunosuppressive drugs) |
|
|
Term
| What orgs are the immunocompromised at risk for acquiring pneumonia? |
|
Definition
1) unusual orgs s.a. fungi, atypical TB, protozoans (pneumocystis)
2) common bacteria |
|
|
Term
| How can a the radiographic appearance classify pneumonia? |
|
Definition
the x-ray appearance may be distinctive & help determine the potential org causing a pneumonia
(it's a rough guide, not diagnostic) |
|
|
Term
| What 5 pneumonias have a distinctive radiographic appearance? |
|
Definition
1) lobar pneumonia
2) bronchopneumonia
3) interstitial pneumonia
4) cavitary leisons
5) pleural effusions |
|
|
Term
| What occurs in lobar pneumonia & what is seen on the radiograph? |
|
Definition
1) consolidation (alveolar fillinf process)
2) homogenous white area following anatomic segments (lobes)
3) air bronchogram (air filled airway outlined b consolidated lung) |
|
|
Term
| What org classically causes lobar pneumonia? |
|
Definition
|
|
Term
| What 6 things can help with the Dx of bacterial pneumonia? |
|
Definition
1) clinical presentation
2) patient Hx
3) PE
4) chest x-ray (CXR)
5) sputum sample
6) other means s.a. cultures from blood or pleural fluid, serology, skin testing, invasive Dx s.a. bronchoscopy or surgical biopsy |
|
|
Term
| What is the classic clinical presentation of bacterial pneumonia? |
|
Definition
1) actuely ill
2) febrile
3) shaking chills at onset
4) cough with sputum production
5) may have chest pain/tightness/dyspnea |
|
|
Term
| What of the patient Hx can help Dx bacterial pneumonia? |
|
Definition
1) onset/rapidity of course
2) CA? Nosocomial? Immunocompromised?
3) risk for aspiration
4) patient contacts
5) travel/occupational/environmental exposures |
|
|
Term
What on PE can help Dx bacterial pneumonia?
Lobar pattern?
Patchy/interstitial pattern?
effusion? |
|
Definition
vital signs (fever, tachycardia, tachypnea)
Lobar: percussion dullness, bronchial breath sounds, increased tactile/vocal fremitus
Patchy/Interstitial: rales/crackles
Effusion: percussion dullness, decreased transmission of sounds & fremitus |
|
|
Term
| What things are we looking for when examining the sputum of a patient with bacterial pneumonia? |
|
Definition
1) color/consistency
2) Gram stain
3) culture |
|
|
Term
| What org are we concerned about if the sputum is rusty colored? |
|
Definition
|
|
Term
| What org are we concerned about if the sputum is like "currant jelly"? |
|
Definition
|
|
Term
| What org are we concerned about if the sputum is creamy yellow colored? |
|
Definition
|
|
Term
| What org are we concerned about if the sputum has a foul odor? |
|
Definition
|
|
Term
| What immune cell should be in high abundance in the sputum of a patient with bacterial pneumonia? |
|
Definition
PMNs
(PMN:epi cells ~ 5:1) |
|
|
Term
| What is ideal when using a gram stain for bacterial pneumonia Dx? |
|
Definition
| ID single or one prominent org |
|
|
Term
| What 4 pneumonia causing orgs are NOT seen on gram stain? |
|
Definition
1) mycoplasma
2) legionella
3) TB
4) viruses |
|
|
Term
| Why is sputum culture not always helpful in pneumonia Dx? |
|
Definition
1) difficult to sort out contaminant from pathogens
2) org may not grow on "routine" media |
|
|
Term
| What are the 4 gourps used to categorize petients by age, co-morbidities, & pneumonia severity? |
|
Definition
1) outpatient pneumonia, no co-morbidity, age <60y
2) outpatient pneumonia, co-morbidity AND/OR age >60y
3) hospitalized with CAP
4) severe pneumonia, hospitalized, ICU |
|
|
Term
| *What is the number one org to cause pneumonia in ALL 4 groups of patients (by age, co-morbidity, and severity)? |
|
Definition
|
|
Term
| What is the most common bacterial cause of pneumonia? |
|
Definition
|
|
Term
| Where is pneumococca pneumonia commonly found? |
|
Definition
| normal flora of oropharynx |
|
|
Term
| What is the classic clinical picutre of a person with pneumococcal pneumonia? |
|
Definition
1) acute onset of shaking chill
2) upper RTI may have preceeded
3) fever, dyspnea, pleuritic chest pain
4) cough, rusty sputum
5) often SOB
6) increased WBC
7) signs of consolidation on exam
8) CXR: lobar consolidation
9) G+ lancet shaped, intracellular, diplococci |
|
|
Term
|
Definition
3G ceph + macrolide
(vaccine available for prophylaxis) |
|
|
Term
| What are 5 signs of poor prognosis for penumococcal pneumonia? |
|
Definition
1) bacteremia
2) hematogenois spread (meningitis, endocarditis, arthritis)
3) more than 1 lobe involved
4) type 3 serotype (most virulent)
5) very young/old |
|
|
Term
| What are the advantages of the pneumococcal vaccine? |
|
Definition
1) against 24+ common serotypes
2) effective for high risk patients
3) can last up to 10+ years
4) can check for Ab response |
|
|
Term
| What org causes "atypical/walking pneumonia"? |
|
Definition
|
|
Term
| Who are commonly affected by mycoplasma pneumonia? |
|
Definition
| young, otherwise heathy people |
|
|
Term
| When are outbreaks of mycoplasma pneumonia common? |
|
Definition
|
|
Term
| How is mycoplasma pneumonia spread? |
|
Definition
| inhalation of infected aerosol |
|
|
Term
| What is the classic clinical presentation for mycoplasma pneumonia? |
|
Definition
1) insidious onset
2) fever, headache, chills, malaise, systemic manifestations
3) non productive cough
4) mild WBC increase
5) bullous myringitis
6) rarely: signs of consolidation
7) patchy rales/crackles
8) CXR: bronchopneumonia
9) no gram stain & doesn't grow on routine media (3 layered membrane with no cell wall)
10) 33-75% have cold agglutinins |
|
|
Term
| How is mycoplasma pneumonia diagnosed? |
|
Definition
|
|
Term
| Is mycoplasma pneumonia more mild or severe compared to pneumococcal pneumonia? |
|
Definition
| more mild (may recover spontaneously) |
|
|
Term
|
Definition
| macrolide or tetracycline |
|
|
Term
| How can legionella present as an epidemic, sporadically, & as a nosocomial inf? |
|
Definition
| lives in contaminated water supply or air conditioning |
|
|
Term
| What are the risk factors for legionella? |
|
Definition
1) immunosuppression
2) smoking
3) COPD
4) advanced age
5) male
6) cardiac disease |
|
|
Term
| What is the classic clinical presentation of a patient with legionella pneumonia? |
|
Definition
1) high fever, recurrent chills, cough
2) GI involvement (diarrhea) common
3) "relative bradycardia" for degree of fever
4) hyponatremia, hypophosphatemia
5) may have fulminant systemic course
6) CXR: varied patterns
7) DFA or sliver stain (will not Gram stain)
8) cultured on selective media
9) serology |
|
|
Term
|
Definition
|
|
Term
| Who is at risk for h. flu pneumonia? |
|
Definition
COPD
alcoholics
debilitated
sickle cell
healthy adults |
|
|
Term
| What will sputum with h. flu look like (shape/G stain)? |
|
Definition
G-
intracellular coccobacilli |
|
|
Term
| What is the classic clinical presentation for h. flu pneumonia? |
|
Definition
1) low grade fever
2) dyspnea
3) PRODUCTIVE cough (lots of sputum)
4) pleuritis |
|
|
Term
|
Definition
cephalosporins
sulfa drugs
ampicillin |
|
|
Term
| Who is at risk for klebsiella pneumonia? |
|
Definition
1) alcoholics
2) diabetics
3) debilitated
4) nosocomial
5) underlying disease |
|
|
Term
| What is the classic clinical presentation of klebsiella pneumonia? |
|
Definition
1) CXR: bulging fissure
2) lobar pneumonia
3) abrupt onset, high fever
4) sputum with plump G- rod |
|
|
Term
|
Definition
| cephalosporin or aminoglyoside |
|
|
Term
| Are "other" G- pneumonias more commonly CA or HA? |
|
Definition
|
|
Term
| Who are are risk for "other" G- pneumonias? |
|
Definition
1) alcoholics
2) diabetics
3) debilitated
4) immunocompromised |
|
|
Term
| Which "other" G- pneumonia is particularly nosocomial? |
|
Definition
|
|
Term
| Why do "other" G- pneumonias have a high mortality? |
|
Definition
necrotizing (destructive) infections
often Abx resistant |
|
|
Term
| Who are at risk for CA staph aureus pneumonia? |
|
Definition
1) IV drug users
2) those who have it as normal flora in nasopharynx
3) elderly after the flu |
|
|
Term
| Who are at risk for HA staph aureus pneumonia? |
|
Definition
|
|
Term
| What does sputum with staph aureus look like (Gram/shape)? |
|
Definition
|
|
Term
| What complications are often seen with staph aureus pneumonia? |
|
Definition
1) multiple cavitary leisons
2) destruction
3) pleural complications |
|
|
Term
| How do anaerobic orgs cause pneumonia? |
|
Definition
|
|
Term
| What factors predispose aspiration? |
|
Definition
1) alcoholism
2) impaired level of consciousness (drugs, seizures, CNS insult)
3) dysphagia
4) neuromuscular disease
5) poor oral hygeine, dental carries (increased orgs present) |
|
|
Term
| What anaerobes tend to cause aspiration pneumonia? |
|
Definition
mixed oral flora
(fusobacterium, bacteroides, peptosteptococcus, etc) |
|
|
Term
| What is the spectrum of diseases that can be incurred from anaerobic aspiration? |
|
Definition
1) pneumonitis
2) lung abscess
3) necrotizing pneumonia
4) empyema |
|
|
Term
| What is the classic clinical presentation of aspiration pneumonia? |
|
Definition
1) FOUL smelling sputum
2) subacute/chronic course
3) Hx suggests aspiration
4) poor dental hygeine (no teeth = no anaerobes)
5) sweats, malaise, weight loss, leukocytosis |
|
|
Term
| What is seen clinically with aspiration lung abscess? |
|
Definition
1) CXR: cavity with air-fluid level
2) 12 days b/w aspiration & necrosis/liquefaction of tissue
3) 1/3 extend to pleural space (empyema) |
|
|
Term
| What is seen in aspiration necrotizing pneumonia? |
|
Definition
1) multiple small cavities
2) very ill - high fever, leukocytosis |
|
|
Term
|
Definition
| inf. of the pleural space |
|
|
Term
|
Definition
1) penicillin or clindamycin (long course)
2) drainage (chest clapping, cough, postural drainage, chest tube) - usually not using bronchoscopy |
|
|
Term
| What are 4 CA fungal pneumonias? |
|
Definition
1) coccidioidomycosis
2) histoplasmosis
3) blastomycosis
4) aspergillus |
|
|
Term
| What is the only funal inf. for which there is a helpful skin test & serology? |
|
Definition
|
|
Term
| Where is coccidioidomycosis endemic? |
|
Definition
| SW US, northern border zone of MExico, San Joaquin Valley area of Cali |
|
|
Term
| What is the life cycle of coccidioidomycosis? |
|
Definition
1) germinates in the soil as an arthrospore
2) spores are the infectious form (digging, construction, high winds can introduce innoculum)
3) tissue form of org is the spherule (contains endospores) |
|
|
Term
| What is the interpretation of the coccidioidin skin test? |
|
Definition
- to +: new infection
+ to -: severe or disseminated disease |
|
|
Term
| When will a positive coccidioidin skin test occur? |
|
Definition
|
|
Term
| What IgM serologic test there is for coccidioidomycosis? |
|
Definition
| Tube percipitin or latex partivle agglutination |
|
|
Term
| When will the IgM serologic test be positive for coccidioidomycosis? |
|
Definition
|
|
Term
| What IgG serologic test is there for coccidioidomycosis? |
|
Definition
|
|
Term
| When will IgG serologic test for coccidioidomycosis be positive? |
|
Definition
8 weeks after inf
(results are diagnostic & prognostic) |
|
|
Term
| How are IgG serologic tests for coccidioidomycosis diagnostic & prognostic? |
|
Definition
diagnostic: + = infected
prognostic: high titer = high chance of disseminated disease |
|
|
Term
| Why is timing of tests for coccidioidomycosis important? |
|
Definition
| window of diagnosis can be missed |
|
|
Term
| Why is it dangerous to culture coccidioidomycosis? |
|
Definition
| airborne arthrospores are infectious |
|
|
Term
| How much of patients infected with coccidioidomycosis are asymptomatic? |
|
Definition
|
|
Term
|
Definition
1) primarily asymptomatic
2) acute (2-3 mo. post exposure): low grade fever, productive cough, chest pai, headaches, malaise, joint aches, other consititutional Sx
3) persistant/chronic (>8 weeks) - not common
4) disseminated disease: can affect any organ system - skin is most common - worst in meningitis |
|
|
Term
| Who is most commonly affected by "Valley Fever" (specific subtype of coccidioidomycosis)? |
|
Definition
|
|
Term
|
Definition
| skin leisons (particularly erythema nodosum) |
|
|
Term
| Is coccidioidomycosis pneumonia more or less severe than bacterial pneumonia? |
|
Definition
| less severe, most recover w/o Tx in about 8 weeks |
|
|
Term
| What are the 3 risk factors for dissemination of coccidioidomycosis pneumonia? |
|
Definition
1) age: >50y or <5y
2) immunosuppression
3) "race": african americans, native americans, mexicans, filipinos have higher risk than caucasians, oriental |
|
|
Term
Tx
acute coccidioidomycosis pneumonia |
|
Definition
| none needed, most resolves within 8 weeks |
|
|
Term
Tx
chronic coccidioidomycosis pneumonia |
|
Definition
|
|
Term
Tx
disseminated coccidioidomycosis |
|
Definition
fatal w/o Tx
IV anti-fungals |
|
|
Term
| When should disseminated coccidioidomycosis be suspected? |
|
Definition
if illness lasts >8 weeks
skin test turns from + to - |
|
|
Term
| Where is histoplasmosis found? |
|
Definition
| worldwide, but endemic in the US is centered around Mississippi, Ohio, Missouri, & Tennessee River Valleys |
|
|
Term
| What is the life cycle of histoplasmosis? |
|
Definition
1) infectious spore (microconidia) is in soil
2) dusty conditions increase airborne spores
3) fowl & bat excrement increase growth of fungus
4) tissue form is characterized by narrow necked budding yeast |
|
|
Term
| Why isn't there a good serologic or skin test for histoplasmosis? |
|
Definition
skin test:
1) too many people test + ∴ not useful for Dx
2) can cause + serologic tests
seologic:
can detect Ab by immunodiffusion, so can be helpful diagnostically, but not prognostically |
|
|
Term
| Can histoplasmosis be grown in culture? |
|
Definition
|
|
Term
| How is histoplasmosis identified? |
|
Definition
|
|
Term
|
Definition
majority: asymptomatic (prolonged "cold")
CXR: may show calcifications from olf inf.
nonspecific malaise, headache, fever, nonproductive cough, pain on swallowing |
|
|
Term
| Who is at risk for chronic histoplasmosis? |
|
Definition
| patients with severe COPD |
|
|
Term
| Who is at risk for disseminated histoplasmosis (very rare)? |
|
Definition
| decreased cell mediated immunity |
|
|
Term
|
Definition
| none needed, most recover w/o Tx |
|
|
Term
|
Definition
| may need antifungal therapy |
|
|
Term
Tx
disseminated histoplasmosis |
|
Definition
fatal if untreated
high dose IV antifungals |
|
|
Term
| Where can histoplasmosis disseminate to? |
|
Definition
lung
bone marrow
lymph nodes
GI
oropharynx (ulcerations) |
|
|
Term
| Where is blastomycosis endemic? |
|
Definition
unknown - maybe similar to histoplasmosis
outbreaks reported in S US & in regions surrounding the Great Lakes |
|
|
Term
| What is the life cycle of blastomycosis? |
|
Definition
1) dumbbell shaped spores become airborne from soil
2) reproduce in tissue as broad necked budding yeast |
|
|
Term
| Why is there no useful skin/serologic test for blastomycosis? |
|
Definition
skin: more likely to indicate histo.
serologic: high titer may suggest illness in someone in whom the inf. was not suspected |
|
|
Term
| How do you diagnose blastomycosis? |
|
Definition
| culture is definitive (org is fast growing & easy to culture) |
|
|
Term
|
Definition
majority: asymptomatic
acute: abrupt onset, high fever, productive cough
chronic: same as acute
disseminated: lung, ulcerated skin leisons, destructive bony leisons. Males - prostatitis, epididymitis |
|
|
Term
|
Definition
| none needed, most recover in about 4 weeks |
|
|
Term
|
Definition
|
|
Term
Tx
disseminated blastomycosis |
|
Definition
|
|
Term
| Where is aspergillus found? |
|
Definition
|
|
Term
| What does the type of disease produced by aspergillus depend on? |
|
Definition
|
|
Term
| When is skin testing valuble for aspergillus? |
|
Definition
| acute forms (an immediate hypersensitivity rxn) |
|
|
Term
| When can serologic Ab to aspergillus can be seen in infection? |
|
Definition
IgE Ab
IgG Ab
in patients with acute manifestations or with fungus balls |
|
|
Term
| What are the 4 clinical patterns of aspergillus inf.? |
|
Definition
1) hypersensitivity pneumonitis/extrinsic allergic alveolitis
2) allergic bronchopulmonary aspergillosis
3) aspergilloma (fungus ball(
4) invasive aspergillosis |
|
|
Term
| Who is at risk for hypersensitivity pneumonitis? |
|
Definition
|
|
Term
| What is hypersensitivity pneumonitis aka? |
|
Definition
|
|
Term
Sx
hypersensitivity pneumonitis/extrinsic allergic alveolitis due to aspergillus |
|
Definition
| cough, dyspnea, fever & chills w/in 4-6 hrs of exposure to spores |
|
|
Term
Tx
hypersensitivity pneumonitis/extrinsic allergic alveolitis due to aspergillus |
|
Definition
|
|
Term
| Who only is at an increased risk for allergic bronchopulmonary aspergillosis (ABPA)? |
|
Definition
| patients w/ longstanding asthma |
|
|
Term
|
Definition
| manifests as worsening of episode airflow obstruction, eosinophilia, + skin test, + serology, elevated serum IgE, migratory CXR infiltrates (V or Y shaped), brown mucus plugs coughed up |
|
|
Term
|
Definition
|
|
Term
| What causes aspergilloma? |
|
Definition
| colonization of a pre-exisiting cavity (old TB, etc) |
|
|
Term
Sx
aspergilloma (fungus ball) |
|
Definition
| can cause bleeding due to erosion => potentially life threatening hemoptysis |
|
|
Term
|
Definition
| may need to be removed surgically |
|
|
Term
| Who only is at risk for invasive aspergillosis? |
|
Definition
| immunocompromised (esp. those with hematologic malignancies) |
|
|
Term
| How is invasive aspergillosis diagnosed? |
|
Definition
culture
(serologic tests not valuable here) |
|
|
Term
|
Definition
1+ IV antifungal
(very high mortality despite therapy) |
|
|
Term
|
Definition
| rapidly progressive diffuse lung disease |
|
|
Term
| What % of all pneumonias are nosocomial? |
|
Definition
|
|
Term
| Why are nosocomial pneumonias bad? |
|
Definition
1) high cost
2) high morbidity/mortality |
|
|
Term
| What is the mechanism of nosocomial pneumonia inf? |
|
Definition
1) patients have @ least 1 risk factor to decrease normal host defense
2) altered upper airway flora (colonization with G- bacteria & others - all likely Tx resistant)
3) aspiration of pathogens => pneumonia |
|
|
Term
| What orgs are often responsible for nosocomial pneumonia? |
|
Definition
1) G- (60%) s.a. E. coli, klebsiella/enterobacter, PSA, serratia, proteus
2) Staph aureus (10%)
3) legionella
4) others |
|
|
Term
| What are the goals when dealing with nosocomial pneumonia? |
|
Definition
1) prevention
2) recognition of patient's at high risk
3) prompt recognition & Tx of inf. |
|
|
Term
|
Definition
|
|
Term
| How can a person becomes immunocompromised? |
|
Definition
1) disease induced
2) therapy induced |
|
|
Term
| What % of all pneumonia orgs in the immunocompromised are "routine" G+ & G- bacteria? |
|
Definition
| up to 75% (tho occur with atypical presentations) |
|
|
Term
| What is used in the immunocompromised to prevent "routine" org infection? |
|
Definition
|
|
Term
|
Definition
| orgs which are not pathogenic in a normal hose, but can cause disease in immunocompromised patients |
|
|
Term
| What orgs tend to cause opportunistic inf? |
|
Definition
1) fungi
2) viruses
3) protozoans |
|
|
Term
| What are 3 common fungal opportunistic orgs? |
|
Definition
1) aspergillus (esp. hemtologic malignancies)
2) candida
3) dissemination of normally self-limited inf (histo., coccidiodo, blasto) |
|
|
Term
| Who in the immunocompromised community is most susceptible to opportunistic viral inf? |
|
Definition
|
|
Term
| What is the most common opportunistic viral inf? |
|
Definition
|
|
Term
| What is the source of opportunistic CMV inf? |
|
Definition
1) donor blood/organ
2) reactivation of dormant inf in host/recipiant |
|
|
Term
|
Definition
| fever & interstitial pneumonia |
|
|
Term
| How is opportunistic CMV diagnosed? |
|
Definition
viral inclusions in cells
cultures
monoclonal Abs |
|
|
Term
|
Definition
supportive care
immune replacement
antivirals |
|
|
Term
| What protozoa is often opportunistic? |
|
Definition
|
|
Term
Sx
pneumocystis carinii in HIV patients |
|
Definition
| slowly progressive inf. w/ fever, cough, dyspnea, progressive CXR infiltrates, & decreasing oxygenation |
|
|
Term
Sx
pneumocystis carinii in children with leukemia |
|
Definition
| fulminant downhill course |
|
|
Term
| How is pneumocystis carinii diagnosed? |
|
Definition
| demonstrate the org in secretions or tissue |
|
|
Term
|
Definition
DOC: trimethoprim-sulfa
pentamidine by IV or aerosol in those who don't tolerate T-S |
|
|
Term
| Are CAPs normally bacterial, viral, fungal, or protozoan? |
|
Definition
|
|
Term
| *What characterizes obstructive lung disease? |
|
Definition
| decreased rate of forced expiratory air volume |
|
|
Term
| What causes decreased rate of forced expiratory air volume in obstructive lung disease? |
|
Definition
1) increased airflow resistance
OR
2) decreased outflow pressure |
|
|
Term
|
Definition
| COPD characterized by permanently enlarged air spaces distal to the terminal bronchioles with destruction of their walls, but w/o fibrosis |
|
|
Term
| What is the pathogenesis of emphysema? |
|
Definition
| increased pulmonary proteolysis &/or decreased antiproteolysis => destruction of elastic tissue in the airspace walls |
|
|
Term
| What are the 2 major causes of emphysema? |
|
Definition
| 1) cigarette smoke
2) hereditary impaired secretion of abnormal α1antitrypsin |
|
|
Term
| How does cigarette smoke cause emphysema? |
|
Definition
| => increased chemotaxis & activation of PMNs & macs in the alveoli => increased release of elastase, other proteases & oxygen free radicals => increased elastolytic activity & oxidation of α1antitrysin => decreased α1antitrypsin function |
|
|
Term
| How does hereditary impaired hepatic secretion of abnormal α1antitrypsin cause emphysema? |
|
Definition
| => chronic liver disease & decreased α1antitrypsin => increased pulmonary proteolytic activity of circulating WBCs (esp. neutrophilic elastase)
(exacerbated by smoking) |
|
|
Term
|
Definition
| circulating glycoprotein & major protease inhibitor |
|
|
Term
| What are the 5 morphologic subtypes of emphysema? |
|
Definition
1) *centrilobular (centriacinar)
2) panlobular (panacinar)
3) paraseptal (distal acinar)
4) irregular
5) interstitial |
|
|
Term
| *What is centrilobular emphysema usually associated with? |
|
Definition
| cigarette smoking & anthracosis |
|
|
Term
*What part of the lung is predominately involed in centriacinar emphysema?
Why? |
|
Definition
| resp. bronchioles due to their higher concentration of inhaled irritants |
|
|
Term
*Where is centrilobular emphysema more severe?
Why? |
|
Definition
| in the upper lung fields due to less vascular perfusion & ∴ lower amounts of circulating α1antitrypsin |
|
|
Term
| What can centriloblar emphysema progress to? |
|
Definition
|
|
Term
| When is panlobular emphysema seen? |
|
Definition
| 1) α1antitrypsin deficiency
2) end-stage centrilobular emphysema |
|
|
Term
| What part of the lung is distroyed in panacinar emphysema? |
|
Definition
| uniform distruction of the pulmonary lobule |
|
|
Term
Where is panlobular emphysema more severe?
Why? |
|
Definition
| lower lobes due to greater vascular perfusion & ∴ higher numbers of circulating neutrophils (when secondary to α1antitrypsin deficiency) |
|
|
Term
| Where is paraseptal emphysema found in the lung? |
|
Definition
more severe destruction of the alveolar ducts & distal alveoli in the pulmonary lobule adjacent to areas of pulmonary fibrosis
(ususally a somewhat localized event) |
|
|
Term
| Where is distal acinar emphysema often localized to? |
|
Definition
| subpleural areas of the upper lobes |
|
|
Term
| What can paraseptal emphysema spontaneously induce? |
|
Definition
|
|
Term
| What is irregular emphysema associated with? |
|
Definition
|
|
Term
def
interstitial emphysema |
|
Definition
| dissection of air into CT w/in the lungs, mediastinum or subq tissue |
|
|
Term
| What does an emphysema lung look like grossly? |
|
Definition
| expanded, hyperinflated lungs with enlarged airspaces (occasionally blebs/bullae) & a remaining thin, lacy network of supporting tissue |
|
|
Term
| What does an emphysema lung look like microscopically? |
|
Definition
| large, irregular air spaces with a decreased number of attenuated fragmented alveolar septa |
|
|
Term
|
Definition
1) worsening dyspnea with minimal, nonproductive cough (unless complicated by chronic bronchitis)
2) tachypnea w/ prolinged expiratory phase & use of accessory muscles of resp. (=> near-normal atertial Hb saturation => "pink puffers")
3) weight loss due to increased work of breathing
4) CXR shows overinflated lungs & an increased anteroposterior diameter ("barrel chest") |
|
|
Term
| What does chronic bronchitis often co-exist with? |
|
Definition
|
|
Term
|
Definition
| presence of a persistent productive cough w/o a discernible cause for @ least 3 mo. in at least 2 consecutive years |
|
|
Term
| What are the 2 major causes of chronic bronchitis? |
|
Definition
1) chronic inhalation of air pollutants (esp. cigarette smoke - 90% cases are smokers)
exacerbated by
2) recurrent RTIs |
|
|
Term
| What is the pathogenesis of chronic bronchitis? |
|
Definition
| chronic exposure to toxic inhalents => increased mucus production, ineffective inflam., & epithelial squamous metaplasia of variably-sized airways => chronic airflow obstruction & predisposition to pulmonary inf. |
|
|
Term
| What causes increased mucus secretion in chronic bronchitis? |
|
Definition
| hyperplasia of goblet cells & subepithelial mucus-secreting glands |
|
|
Term
|
Definition
| ratio of the tickness of the mucous glands to that of the airway wall |
|
|
Term
| *What happens to the Reid index in chronic bronchitis? |
|
Definition
|
|
Term
What happens to the smooth muscle in chronic bronchitis?
Why? |
|
Definition
| increased smooth muscle due to hyperactive airways |
|
|
Term
| What is the inflammatory infiltrate associated with in chronic bronchitis? |
|
Definition
|
|
Term
| What happens to the epithelial lining of the bronchus/bronchioles in chronic bronchitis? |
|
Definition
| focal epithelial squamous metaplasia & dysplasia |
|
|
Term
|
Definition
1) chronic cough with sputum production
2) eventual dyspnea & cyanosis (hypoxia & hypercapnea) => cor pulmonale due to pulmonary HTN => peripheral edema
(cyanosis + edema = "blue bloater")
3) increased pulmonary inf. |
|
|
Term
| Is asthma incidence increasing or decreasing? |
|
Definition
|
|
Term
|
Definition
| chronic pulmonary disease characterized by intermittent episodes of mostly reversible airflow obstruction associated with hyperreactive airways (bronchospasm) following exposure to a variety of agents |
|
|
Term
|
Definition
| most severe subtype of asthma characterized by a prolonged interval of continual symptoms unresponsive to therapy & which may lead to life-threatening ventilatory dysfunction |
|
|
Term
| What is the pathogenesis of asthma? |
|
Definition
| diverse stimuli in susceptible host => release of inflam. mediators => incerased vascular perm (edema), neural & cytokine-induced bronchoconstriction, mucus hypersecretion, & chemotaxis of additional inflam. cells (amplify the process) |
|
|
Term
| What are the 8 major inciting factors (intrinsic & extrinsic) of asthma? |
|
Definition
1) *inhalation of airborne allergens
2) airway colonization with Aspergillus
3) occupational exposures
4) environmental air pollutants
5) viral RTI
6) various drugs
7) exercise & cold
8) emotional stress |
|
|
Term
| *What is induced in an asthmatic when they inhale airborne allergens? |
|
Definition
| type I hypersensitivity response |
|
|
Term
| What happens when an asthmatic is re-exposed to a previously sensitized inhaled allergen in a type I hypersensitivity rxn? |
|
Definition
| Ag-induced cross-linking of IgE on mucosal & submucosal mast cells in the airways => mast cell degranulation & release of chemical mediators => acute & late phase response |
|
|
Term
| What occurs in the acute phase response of a type I hypersensitivity reaction of an asthmatic? |
|
Definition
1) bronchoconstriction
2) increased vascular perm
3) increased mucus secretion |
|
|
Term
| What occurs in the late phase response of a type I hypersensitivity reaction of an asthmatic? |
|
Definition
| prolongation & augmentation of the disease process by an influx of WBCs (esp. eosinophils) into affected airways |
|
|
Term
| How can airway colonization os aspergillus org incite asthma? |
|
Definition
|
|
Term
| How can occupational exposures (s.a. wood, dust, chemicals, etc.) incite asthma? |
|
Definition
| => hypersensitivity rxn OR direct toxic effects on the airways |
|
|
Term
| How can viral RTIs incite asthma? |
|
Definition
|
|
Term
| How can exercise & cold incite asthma? |
|
Definition
| possibly due to increased vacular perfusion & release of inflam. mediators w/ rewarming & rehydration of the airways after exercise or cold exposure |
|
|
Term
| How can emotional stress incite asthma? |
|
Definition
|
|
Term
| What does an asthmatic lung look like grossly? |
|
Definition
| distended, overaerated lungs w/ multiple airways obstructed by viscid mucus plugs |
|
|
Term
| What does an asthmatic lung look like microscopically? |
|
Definition
1) goblet cell metaplasia
2) subepithelial mucus gland hyperplasia
3) luminal mucus plugs
4) sub-BM fibrosis
5) edematous submucosa
6) sm. muscle cell hyperplasia & hypertrophy |
|
|
Term
| What is contained in the luminal mucus plugs in asthma? |
|
Definition
| Curshmann spirals, eosinophils & Charcot-Leyden crystals |
|
|
Term
|
Definition
| mucoid swirls of epithelial cells |
|
|
Term
def
Charcot-Leyden crystals |
|
Definition
| needle-like structures formed from extruded, coalesced granules of eosinophils |
|
|
Term
| What is the edematous submucosa containing in an asthmatic lung? |
|
Definition
| mixed inflam. cell infiltrate containing numerous eosinophils |
|
|
Term
| What causes sm. muscle cell hyperplasia & hypertrophy in an asthmatic lung? |
|
Definition
| chronic bronchoconstriction |
|
|
Term
|
Definition
| paroxysms of wheezing, tachypnea, dyspnea, & coughing alternating w/ asymptomatic periods or superimposed on a background of chronic airway obstruction |
|
|
Term
|
Definition
| permanent airway dilation due to recurrent inf. w/ necrosis |
|
|
Term
| What is the pathogenesis of bronchiectasis? |
|
Definition
| airway occlusion w/ associated distal resorptive atelectasis &/or decreased ciliary function => recurrent pulmonary inf. => inflam. & necrosis of airways => continual loss of their structural support => eventual permanent airway dilation |
|
|
Term
| What does bronchiectasis look like grossly? |
|
Definition
| markedly dilated peripheral airways extending out to the pleura, esp. within the lower lobes |
|
|
Term
| What does bronchiectasis look like microscopically? |
|
Definition
| a mixed inflam. cell infiltrate within the involved airways, associated with ulceration, necrosis & scarring |
|
|
Term
|
Definition
| chronic, intermittent cough productive of purulent sputum, fever, & eventual resp. insufficiency |
|
|
Term
|
Definition
| collapse of previously inflated lung tissue (usually reversible) |
|
|
Term
def
atelectasis neonatorum |
|
Definition
| incomplete expansion of the lungs at birth |
|
|
Term
| What are the 4 parts of the patogenesis of acquired atelectasis? |
|
Definition
1) obstructive (resorptive)
2) compression
3) contraction
4) patchy |
|
|
Term
| What effect does complete airway obstruction have in atelectasis? |
|
Definition
| => resorption of trapped O2 => alveolar collapse
∴ mediastinal shift toward atelectatic lung |
|
|
Term
| What causes complete airway obstruction in atelectasis? |
|
Definition
1) increased bronchial secretion or exudate (asthma, COPD, bronchiectasis)
2) foreign body aspiration |
|
|
Term
| What compression occurs in atelectasis? |
|
Definition
pulmonary compression
∴ mediastinal shift away from the atelectatic lung |
|
|
Term
| What causes pulmonary compression in atelectasis? |
|
Definition
1) accumulations w/in pleural cavity (*pleural effusion, hemothorax, pneumothorax)
2) diaphragmatic elevation (peritonitis, subdiaphragmatic abscess, critically ill post-op patients) => basal atelectasis |
|
|
Term
| What causes contraction in atelectasis? |
|
Definition
|
|
Term
| What causes patchy lung in atelectasis? |
|
Definition
| loss of pulmonary surfactant |
|
|
Term
| What is the major complication of atelectasis? |
|
Definition
|
|
Term
def
obstructive lung diseases |
|
Definition
| airflow limitation due to either narrowing or obstruction of intrathoracic airways |
|
|
Term
| What are the 2 categories ob obstructive lung disease? |
|
Definition
1) acute & reversible
2) chronic & irreversible |
|
|
Term
def
acute/reversible obstructive disease |
|
Definition
| obstruction is episodic w/ return to normal pulmonary function b/w exacerbations |
|
|
Term
def
chronic/irreversible obstructive lung disease |
|
Definition
obstruction is chronic w/o periods of normal pulmonary function
it's often punctuated by acute exacerbations |
|
|
Term
|
Definition
clinical syndrome characterized by:
1) reversible airway obstruction
2) airway inflammation
3) increased airway responsiveness to a variety of stimuli |
|
|
Term
| What are the 5 risk factors for asthma? |
|
Definition
1) gender (young: m>f, middle-age: f>m)
2) race (aa>c)
3) socioeconomic status (lower>higher)
4) young maternal age & prematurity
5) cigarette smoking (esp. maternal cigarette smoking) |
|
|
Term
| Is it acute or chronic inflam. that pays a central role in the pathogenesis of airway hyperreactivity & airflow obstruction? |
|
Definition
|
|
Term
| What in the immune system is central to the asthmatic hypersensitivity? |
|
Definition
|
|
Term
| How is IgE central to the asthmatic hypersensitivity response? |
|
Definition
1) allergic inflam. is triggered by by cross-linking of allergen & IgE on effector cells => degranualtion & release of mediators
2) IgE levels have been associated with developing both nonspecific airway hyperresponsiveness & asthma |
|
|
Term
| What are the 4 key cells to airway inflammation in asthma? |
|
Definition
| 1) mast cells
2) eosinophils
3) macs
4) TH2 lymphocytes |
|
|
Term
| What products of mast cells assist in asthmatic airway inflam.? |
|
Definition
1) leukotrienes
2) prostaglandins
3) histamine
4) PAF |
|
|
Term
| What products of eosinophils assist in asthmatic airway inflam.? |
|
Definition
1) major basic protein
2) eosinophil cationic protein |
|
|
Term
| What products of macs assist in asthmatic airway inflam.? |
|
Definition
1) cytokines
2) lipid mediators
3) reactive oxygen species
4) PAF
(also act as APCs) |
|
|
Term
| What products of TH2 lymphocytes assist in asthmatic airway inflam.? |
|
Definition
| various cytokines inc. IL-4, IL-5, GM-CSF |
|
|
Term
| What happens to the epithelium do to inflammation? |
|
Definition
|
|
Term
| What does epithelial injury as a result from cellular inflam. result in? |
|
Definition
1) release of additional epi. cells derived from mediators that promote further inflam. or modulate airway sm. muscle tone
2) increased permeability to Ags, irritants, & inflam. mediators |
|
|
Term
| What innervates airway sm. muscle? |
|
Definition
1) PS
2) SS
3) non-adrenergic, non-cholinergic (NANC) neural pathways |
|
|
Term
| What is the effect of PS innervation on the airway sm. muscle? |
|
Definition
1) maintains bronchial sm. muscle tone
2) cholinergic stimulation (via vagus) => airway narrowing |
|
|
Term
| What is the effect of SS innervation on the airway sm. muscle? |
|
Definition
adrenergic stimulation relaxes airway sm. muscle
(minor role in humans) |
|
|
Term
|
Definition
| local neural pathways that mediate sm. muscle tone |
|
|
Term
| What inhibitory neurotransmitters are included in NANC? |
|
Definition
| NO & VIP (vasoactive intestinal peptide) |
|
|
Term
| What excitatory neurotransmitters are included by NANC? |
|
Definition
| substance P and neurokinins A & B |
|
|
Term
| What does nerve injury secondary to inflam. result in due to NANC? |
|
Definition
| increased excitatory neuropeptide release => bronchoconstriction, increased vascular perm., & mucus hypersecretion (=> increased local inflam. & edema) |
|
|
Term
def
allergen inhalation challenge |
|
Definition
| an allergic asthmatic challenged with an inhaled allergen to which s/he is sensitive will have a biphasic decline in resp. function (early & late response) |
|
|
Term
def
early asthmatic response |
|
Definition
1) occurs w/in minutes
2) resolves by 2 hrs
3) mast cell & its mediators are response |
|
|
Term
| What can block the early asthmatic response? |
|
Definition
| β agonists & cromolyn sodium |
|
|
Term
def
late asthmatic response |
|
Definition
(seen in half of patients)
1) occurs w/in 6-8 hrs
2) may last 24 hrs
3) mediated by remaining inflam. cells
4) associated with bronchial hyperreactivity |
|
|
Term
| What prevents the late asthmatic response? |
|
Definition
| cromolyn sodium & corticosteroids |
|
|
Term
| What are the 2 effects of inflammation in asthma? |
|
Definition
1) bronchial hyperreactivity
2) airflow obstruction |
|
|
Term
| What is the bronchial hyperreactivity in asthma to? |
|
Definition
a variety of nonspecific stimuli
(tho not specific to asthma) |
|
|
Term
| How does airway inflam. lead to airway obstruction in asthma? |
|
Definition
1) airway sm. muscle activation (bronchospasm)
2) vascular congestion & bronchial edema
3) accumulation of airway secretions, mucus casts, cellular debris |
|
|
Term
| What van be used clinically to Dx asthma? |
|
Definition
| methecholine or histamine |
|
|
Term
| What does an asthmatic PFT look like b/w attacks? |
|
Definition
|
|
Term
| What happens to asthmatic PFTs during attacks? |
|
Definition
| 1) decreased FEV1
2) decreased FVC
3) decreased FEV1/FVC ratio
4) increased lung volumes s.a. RV & FRC (due to air trapping => hyperinflation) |
|
|
Term
| What causes increased work of breathing in asthma? |
|
Definition
1) increased airway resistance
2) hyperinflation => flattened diaphragm => increase work b/c muscle fibers of flattened diaphragm are no longer operating at optimal point
3) hyperinflation => increased compliance => more pressure needed to change lung volume |
|
|
Term
| What happens to gas exhange during asthmatic attacks? |
|
Definition
| ventilation-perfusion mismatching => hypoxemia & increased dead space |
|
|
Term
|
Definition
1) sudden onset dyspnea, cough, wheezing
2) chest tightness, feeling of suffocation
3) Sx-free period
4) family Hx of allergies/asthma
5) possibly able to ID triggers to attacks |
|
|
Term
| What is seen on PE of an asthmatic? |
|
Definition
b/w attacks: may be normal or wheeze with a forced exiration
during attack:
1) mild: wheezes, prolonged expiratory time
2) moderate: appears in distress, wheezes, tachypnea, tachycardia, diaphoresis, use of accessory resp. muscles
3) severe: chest quiet (not moving any air), fatigue/somnolence, cyanosis |
|
|
Term
| What 4 tests can be done to test for asthma? |
|
Definition
1) PFTs
2) PEFR (peak expiratory flow rate)
3) CXR
4) arterial blood gases |
|
|
Term
| What is seen on PFTs when testing for asthma? |
|
Definition
| b/w attacks: normal - can do methacholine challenge test to induce bronchospasm
during attacks: obstructive pattern - FEV1 should increase with a bronchodilator (usually β-agonist) |
|
|
Term
|
Definition
| measurement of expiratory flow during maximal exhalation |
|
|
Term
| What is PEFR usually used for? |
|
Definition
| track day to day changes in patient's functioning & asthma severity |
|
|
Term
| What is seen on the CXR of an asthmatic? |
|
Definition
| usually normal, but may show hyperinflation |
|
|
Term
| What changes are seen in arterial blood gases in an asthmatic? |
|
Definition
| 1) mild: resp. alkalosis (decreaed PCO2)
2) moderate: mild hypoxemia, PCO2 can be normal or decreased
3) severe: severe hypoxemia & resp. acidosis (increased PCO2) |
|
|
Term
| What are the 4 classification of asthma based on severity? |
|
Definition
1) intermittent
2) mild
3) moderate
4) severe |
|
|
Term
| When is the classification of asthma most important? |
|
Definition
| patients not previously diagnosed & not on chronic medications (used to guide initial clinical decision for Tx) |
|
|
Term
| What are the 2 components of the asthma classification? |
|
Definition
1) impairment (frequency & intensity of Sx & functional limitations)
2) risk (likelihood of asthma exacerbations or progressive decline in lung function) |
|
|
Term
| What is asthma Tx directed toward? |
|
Definition
| underlying inflammation since Tx of inflam. will treat the bronchospasm (Tx of the bronchospasm will NOT treat the inflam.) |
|
|
Term
| Besides medication, what is also an inportant part of asthma Tx? |
|
Definition
1) patient education
2) patient self-monitoring of disease
3) environmental control
4) Tx of gastroesophageal reflux disease & nasal/sinus congestion/post-nasal drip |
|
|
Term
| What anti-inflammatory agents are used in the Tx of asthma? |
|
Definition
1) corticosteroids (mainstay b/c broad action): inhaled for chronic outpatient, oral/IV for exacerbation
2) leukotriene antagonists (interfer with LT cascade, tho role unclear)
3) anti-IgE Ab (binds IgE to prevent initiation of inflam. cascade): poorly controlled in asthmatics |
|
|
Term
| What bronchodilators are used in the Tx of asthma? |
|
Definition
| 1) β2 selective agonist (most widely used): generally given as inhaler
2) anticholinergics (second line)
3) methylxanthines (unclear mech): only used in severe asthmatics |
|
|
Term
| What are the 2 goals of asthma therapy? |
|
Definition
1) reduced impairment
2) reduce risk |
|
|
Term
| What are the goals to reduce impairment of asthma? |
|
Definition
| 1) prevent Sx
2) infrequent use of short-acting β2 agonist (no more than 2x/week)
3) maintain normal pulmonary function & activity levels
4) meet patient/family satisfaction/needs |
|
|
Term
| What are the goals to reduce the risk of asthma? |
|
Definition
1) prevent acute exacerbations
2) minimize ED/hospital visits
3) prevent progressive decline in lung function (esp. children)
4) minimize adverse medication effects |
|
|
Term
| When will a bronchodilator aline be recommended for asthma Tx? |
|
Definition
|
|
Term
| Besides most the most mild asthma, what does Tx include? |
|
Definition
| escalating doses of inhaled corticosteroids w/ or w/o long-acting bronchodilators & occasional oral corticosteroids |
|
|
Term
| After initial Tx, what is further management of asthma based on? |
|
Definition
how well the Sx are controlled
if not well controlled: intensify
if well controlled: consider stepping down therapy |
|
|
Term
|
Definition
| group of disorders characterized by chronic cough, dyspnea on exertion, & chronic, irreversible obstructive airway disease |
|
|
Term
| What are the 2 clinical disorders included under COPD? |
|
Definition
1) chronic bronchitis
2) emphysema |
|
|
Term
|
Definition
| cough with sputum for 3+ months/year for 2+ consecutive years |
|
|
Term
| What is chronic bronchitis characterized by? |
|
Definition
1) hypertorphy & hyperplasia of airway mucus glands
2) accumulation of mucus in small airways
3) narrowing & inflam. of small airways |
|
|
Term
| What characterizes emphysema? |
|
Definition
enlargement of airspaces distal to the terminal bronchioles accompanied by destruction of the alveolar walls
(anatomic diagnosis) |
|
|
Term
| What are the 6 risk factors for COPD? |
|
Definition
1) smoking (not all smokers develop COPD, and second hand smoke can play a role too)
2) gender (m>f)
3) occupation (dust, gas, fumes)
4) soscionomic status (lower>higher)
5) asthma
6) biomass fuels (important in developing nations) |
|
|
Term
| What effect does tobacco smoke have on lung function? |
|
Definition
1) accelerated deterioration of ventilatory function is common
2) lung function (in susceptible smokers) declines 5x faster than normal |
|
|
Term
| What % of chronic, heavy smokers develop COPD? |
|
Definition
|
|
Term
| What is the role of genetics in COPD? |
|
Definition
1) genes on chromosome 2q are important for presence/degree of airflow obstruction
2) increased/decreased risk with certain polymorphisms |
|
|
Term
def
protease-antiprotease hypothesis
(on COPD pathogenesis) |
|
Definition
| destruction of the lung parenchyma occurs bc the balance b/w lung proteases & antiproteases tips in favor of proteases (toward lung tissue breakdown) |
|
|
Term
| How does smoking play a role in the prostease-antiprotease hypothesis of COPD pathogenesis? |
|
Definition
| smoking tips the balance by recruiting neutrophils & macs => release proteases (inc. neutrophil elastase, serine & cysteine proteinases, cathepsins, & MMPs) |
|
|
Term
| What autosomal recessive disease results in emphysema in up to 95% of patients? |
|
Definition
|
|
Term
|
Definition
| secretory glycoprotein synthesized in heptocytes |
|
|
Term
| Where is the α1antitrypsin gene found? |
|
Definition
|
|
Term
|
Definition
| inhibit many proteolytic enzymes (protecting the lung from emphysema) |
|
|
Term
| With α1antitrypsin deficiency, when will signs/Sx of emphysema appear? |
|
Definition
| 3rd/4th decade (hastened by smoking) |
|
|
Term
| What part of the lung is affected by emphysema in those with α1antitrypsin deficiency? |
|
Definition
| lower lobes (unlike in smokers, where the upper lobe is affected) |
|
|
Term
| What liver complication is seen in 1-3% of patients with α1antitrypsin deficiency? |
|
Definition
|
|
Term
| When should α1antitrypsin deficiency be considered? |
|
Definition
1) emphysema of all non-smokers
2) premature onset of moderate/severe COPD
3) bronchiectasis w/o clear risk factors
4) postive family Hx |
|
|
Term
| What are the α1antitrypsin phenotypes? |
|
Definition
| Normal: PIMM
heterozygote: PIMZ
homozygote: PIZZ (prevalence 1:3000) |
|
|
Term
| What is the role of inflam. on the pathogenesis of COPD? |
|
Definition
1) there is significant inflam. in bronchioles & lung parenchyma
2) macs, T cells, & PMNs predominate
3) eosinophils absent, except during exacerbations or if concomitant with asthma
4) inflam. mediators less well-defined |
|
|
Term
| What is the role of oxidative stress in the pathogenesis of COPD? |
|
Definition
| several markers of oxidative stress are elevated in COPD => avtivation of the transcription of nuclear factor κB or by damaging antiproteases |
|
|
Term
| What is the role of amplification in the pathogenesis of COPD? |
|
Definition
| increased inflam. cells are seen in both current & ex- smokers w/o COPD ∴ patients who develop COPD show amplification of the inflam. mech. underlying the disease |
|
|
Term
| What controls gene expression? |
|
Definition
| histones that open up the chromatin structure => allows transcription |
|
|
Term
| What regulates expression of inflam. genes? |
|
Definition
increased acetylation of histone 4
reversed by histone deacetylases => suppression of gene expression |
|
|
Term
| What role do histones have in COPD pathogenesis? |
|
Definition
1) increased histone acetylation of inflam. genes s.a. IL-8
2) reduced HDAC (histone deacetylases) - esp. HDAC 2 |
|
|
Term
| What drug is not effective in COPD due to the histone involvement? |
|
Definition
glucocorticoid steroids since they act by coupling HDAC 2 to inflam. genes => inflam. suppression
∴ with less HDAC 2 present in COPD, the steroids are less effective |
|
|
Term
| What causes airflow obstruction in COPD? |
|
Definition
1) loss of elastic recoil (esp. in emphysema)
2) excess secretions/mucus plugs (esp. in chronic bronchitis)
3) sm. muscle contraction, bronchial wall edema, & airway inflam. |
|
|
Term
| What alterations in PFTs are seen in COPD? |
|
Definition
| 1) decrased FEV1
2) decreased FEV1/FVC ratio
3) FVC can be N or decreaed
4) decreased expiratory flow rates
5) increased lung volumes (s.a. RV) => hyperinflation
6) increased compliance (esp. in emphysema)
7) increased airway resistance (esp. in chronic bronchitis)
8) decreased DLCO |
|
|
Term
| What alterations in ventilation-perfusion are seen with COPD? |
|
Definition
1) disruption of the relationship b/w ventilation & perfusion is common
2) areas of low V/Q ratios => hypoxemia
3) areas of high V/Q ratios => increased dead space => hypercapnia |
|
|
Term
| What causes increased work of breathing in COPD? |
|
Definition
| increased resistance & hyperinflation (same as asthmatics) |
|
|
Term
| What are the 5 key Sx for considering a COPD diagnosis? |
|
Definition
1) chronic cough
2) chronic sputum production
3) dyspnea (insideous, progressive, persistent)
4) repeated episodes of acute bronchitis
5) Hx of exposure to risk factors |
|
|
Term
| What are other possible Sx of COPD? |
|
Definition
1) wheezing
2) chest tightness
3) frequent RTIs (esp. chronic bronchitis)
4) Sx of cor pulmonale seen in late |
|
|
Term
|
Definition
relatively acute onset of one of the following:
1) increase in SOB
2) new increased cough
3) change in sputum quality |
|
|
Term
| What are COPD exacerbations generally related to? |
|
Definition
| bacterial or viral inf. of the airways |
|
|
Term
| What does it mean if a COPD patient has frequent exacerbations? |
|
Definition
1) more severe disease
2) clinical phenotype |
|
|
Term
| When is an increase in mortality seen due to COPD exacerbations? |
|
Definition
| patients requiring hospitalization for exacerbation |
|
|
Term
| What are the systemic manifestations of COPD? |
|
Definition
1) Weight loss (loss of sk. muscle, esp. in limbs)
2) sk. muscle dysfuntion
3) osteoporosis
4) increased CVD morbidity & mortality |
|
|
Term
| What is weight loss in COPD related to? |
|
Definition
increased TNFα
increased metabolism |
|
|
Term
| How often is weight loss seen in COPD? |
|
Definition
half of patients with severe disease
10-15% of patients with mild/moderate disease |
|
|
Term
| Is weight loss directly or inversely related to survival? |
|
Definition
|
|
Term
| What is the sk. muscle dysfunction in COPD secondary to? |
|
Definition
| immobility, hypoxia, & increased metabolism |
|
|
Term
| What COPD Sx is exacerbated by sk. muscle dysfunction? |
|
Definition
|
|
Term
| What is osteoporosis seen with COPD inversely correlated with? |
|
Definition
|
|
Term
| What is seen on the PE of a patient with COPD? |
|
Definition
1) wheezing (esp. on forced exiration)
2) prolongation of expiratory phase
3) if hyperinflated => increased anteroposterior diameter of the chest & hyperresonant lung fields
4) if late course => signs of cor pulmonale |
|
|
Term
|
Definition
peripheral edema
jugular venous distention |
|
|
Term
| What 3 tests are done to eveluate COPD? |
|
Definition
1) PFTs
2) CXR
3) arterial blood gases |
|
|
Term
| What is seen on the CXR of a patietn with COPD? |
|
Definition
emphysema: hyperinflation w/ sm. cardiac silhouette
chronic bronchitis: congestion, scattered infiltrates, possibly enlarged heart & prominent pulmonary vessels |
|
|
Term
| When should arterial blood gases be performed on COPD patients? |
|
Definition
| 1) outpatients with FEV1 <40%
2) clinical signs of resp. failure
3) clinical signs of R heart failure
4) during exacerbation |
|
|
Term
| What should the values for PCO2 be expected to be in a patient with COPD? |
|
Definition
| 1) b/w exacerbations can be normal, low or high
if high: compenstated resp. acidosis - patients known as "chronic CO2 retainers"
2) during exacerbations can be low, normal, or high - what's most important is how much it's changed from baseline |
|
|
Term
| What should the values for PO2 be expected to be in a patient with COPD? |
|
Definition
| hypoxemia is common in late COPD |
|
|
Term
| What are the 5 classifications of COPD? |
|
Definition
| 1) at risk (chronic Sx, normal spirometry)
2) mild (FEV1 normal)
3) moderate (FEV1 b/w 50-80%)
4) severe (FEV1 b/w 30-50%)
5) very severe (FEV1 <30%) |
|
|
Term
|
Definition
| patient with chronic bronchitis |
|
|
Term
|
Definition
|
|
Term
| Why is it sometimes hard to tell the difference b/w a pateitns with emphysema & chronic bronchitis? |
|
Definition
| most patietns have features of both |
|
|
Term
| What is the "typical" patient with emphysema? |
|
Definition
| old
tall, thin
cor pulmonale late in course
mild hypoxemia
hypercapnia late in course
increased lung compliance
decreased DLCO
severe airway obstruction
normal hematocrit |
|
|
Term
| What is the "typical" patient with chronic bronchitis? |
|
Definition
| young
stocky, obese
cor pulmonale early in course
prominent hypoxemia
hypercapnia early in course
normal lung compliance
normal DLCO
moderate airway obstruction
increased hematocrit |
|
|
Term
| What is the goal of Tx for COPD? |
|
Definition
palliative since lung function can't be restored to normal
QUIT SMOKING |
|
|
Term
|
Definition
1) prevention & early Tx of inf.
2) oxygen
3) nutritional support
4) medication
5) lung volume reduction surgery |
|
|
Term
| How is prophylaxis & early Tx of infections maintained in patients with COPD? |
|
Definition
1) pneumococcus vaccine
2) yearly flu vaccine
3) pulmonary hygeine (cough/deep breathing exercises, postural drainage)
4) empiric Abx w/ increased resp. Sx (esp. in patients w/ chronic bronchitis) |
|
|
Term
| Why is oxygen part of the Tx plan for COPD? |
|
Definition
| use of oxygen 24hr/day in patietns with hypoxemia => increased survival |
|
|
Term
| When is nutritional support important with patients with COPD? |
|
Definition
1) underweight
2) losing weight & BMI is b/w 21-25 |
|
|
Term
| What medications are used in COPD Tx? |
|
Definition
1) bronchodilators
2) corticosteroids |
|
|
Term
Function
bronchodilators in COPD |
|
Definition
| relieving dyspnea (tho no evidence of spirometry improvement) |
|
|
Term
| What bronchodilators are used in COPD? |
|
Definition
| 1) long acting anticholinergics or β agonits (DOC)
2) Ipratropium bromide (anticholinergic) or albuterol (β2 agonist) for quick relief
3) theophylline (methylxanthine) => decreased SOB & increased muscle function (patients with severe disease) |
|
|
Term
| What corticosteroids are used in patients with COPD? |
|
Definition
1) systemic steroids during exacerbation
2) inhaled steroids => decreased exacerbations with severe/very severe COPD |
|
|
Term
| What medication is on an only as needed basis for patients with mild COPD? |
|
Definition
| short-acting bronchodilator |
|
|
Term
| What is added as regular Tx to the medication regimen for moderate COPD? |
|
Definition
| 1+ long-acting bronchodilators |
|
|
Term
| What is added to the medication regimen when a person have severe COPD? |
|
Definition
| inhaled glucocorticosteroids if repeated exacerbations |
|
|
Term
| What is added to the medication regimen of a very severe COPD patient? |
|
Definition
long term oxygen if chronic resp. failure
consider surgery |
|
|
Term
def
lung volume reduction surgery |
|
Definition
| resection of the most severely affected areas of the lung => reamining lung to function more normally |
|
|
Term
Effects
lung volume reduction surgery |
|
Definition
decreased dyspnea
increased exercise capacity
improved gas exchange
survival benefit in only a subset of patients |
|
|
Term
|
Definition
| condition characterized by chronic, irreversible dilation & distortion of bronchi caused by inflam. distruction of the bronchial walls |
|
|
Term
| Is bronchiectasis a discrete disease entity? |
|
Definition
| no, its a clinical syndrome that is the possible end result of several disease processes |
|
|
Term
| What is the cause of bronchiectasis? |
|
Definition
1) necrotizing ing. in the tracheobronchial walls & surrounding parenchyma
2) impaired tracheobronchial clearance
3) impaired pulmonary function |
|
|
Term
| How does necrotizing inf. of trachrobronchial walla & surrounding parenchyma lead to bronchiectasis? |
|
Definition
1) inflam. destruction of cartilage, muscle & elastic tissue
2) diseased bronchi can't resist pressure changes associated with frequent coughing b/c of recurrent inf. => distortion & dilation |
|
|
Term
| How does impaired tranchobronchial clearance help cause bronchiectasis? |
|
Definition
1) particle clearance impaired due to loss of normal ciliated epi. & altered mucus blanket (mucus is most mucoid & viscid)
2) secretions prequently pool in the larger, distorted airways => more sm. airway occlusion |
|
|
Term
| What does the severity of pulmonary function impairment in bronchiectasis depend on? |
|
Definition
|
|
Term
| What do the PFTs look like in bronchiectasis? |
|
Definition
| changes consistent with airway obstruction |
|
|
Term
| What are the 5 etiologies of bronchiectasis? |
|
Definition
1) inf. (s.a. pertussis, necrotizing pneumonia, viral pneumonias, TB)
2) immotile cilia syndrome
3) hypogammaglobulinemia
4) CF
5) allergic bronchopulmonary aspergillosis |
|
|
Term
| What is the most common syndrome of nonfunctional cilia? |
|
Definition
|
|
Term
Effect
nonfunctional cilia |
|
Definition
| impaired mucociliary clearance |
|
|
Term
|
Definition
autosomal recessive disorder => lost of dynein arm
often with situs inversus |
|
|
Term
| Why do hypogammaglobulinemias lead to bronchiectasis? |
|
Definition
| syndromes associated with decreased circulating gamma globulins => increaed frequency of inf. with pyogenic bacteria |
|
|
Term
|
Definition
| autosomal recessive disease of endocrine & exocrine glands characterized by unusually viscid mucus secretions |
|
|
Term
| How do the viscid secretions of CF lead to bronchiectasis? |
|
Definition
viscid secretions =>
1) extensive peripheral small airway obstruction & air trapping
2) impaired clearance of bacterial => recurrent inf. => chronic inf. (esp. with staph aureus & PSA) |
|
|
Term
def
allergic bronchopulmonary aspergillosis |
|
Definition
| a form of asthma in which immunologic rxns to aspergillus sp. play an important pathogenic role. |
|
|
Term
| How do the immunologic rxns associated with allergic bronchopulmonary aspergillosis lead to bronchiectasis? |
|
Definition
| => bronchial inflam. & mucoid impaction |
|
|
Term
Sx
allergic bronchopulmonary aspergillosis |
|
Definition
| episodic wheezing in association w/ febrile episodes, expectoration of mucus plugs, peripheral blood eosinophilia, & intermittent pulmonary infiltrations |
|
|
Term
|
Definition
1) persistent or recurrent cough in association with large volume production of purulent, often foul smelling sputum
2) hemoptysis
3) dyspnea
4) wheezing |
|
|
Term
| What should be seen on PE of a patient with bronchiectasis? |
|
Definition
1) wheezing
2) rhonchi
3) crackles |
|
|
Term
| What 4 tests can be done to help Dx bronchiectasis? |
|
Definition
1) PFTs
2) CXR
3) Chest CT
4) aterial blood gases |
|
|
Term
| What will be seen on PFTs of a patient with bronchiectasis? |
|
Definition
|
|
Term
| Is CXR a reliable way to Dx bronchiectasis? |
|
Definition
|
|
Term
| What can been seen on a CXR suggestive of bronchiectasis? |
|
Definition
increased bronchovascular markings
cystic air spaces |
|
|
Term
| What is seen in a chest CT of patient with bronchiectasis? |
|
Definition
| dilated bronchi w/o normal tapering toward periphery |
|
|
Term
| What are the expected results of arterial blood gases of a patient with bronchiectasis? |
|
Definition
| low PO2
normal or low PCO2 |
|
|
Term
|
Definition
1) eliminate identifiable underlying problem
2) improve clearance of tracheobronchial secertions
3) control inf. (vaccines, Abx)
4) reversal of airflow obstruction |
|
|
Term
| How are the identifiable underlying problems eliminated in bronchiectasis? |
|
Definition
|
|
Term
| How is clearance of tracheobronchial secretions improved in bronchiectasis? |
|
Definition
|
|
Term
| How is airflow obstruction reversed in bronchiectasis? |
|
Definition
|
|
Term
| What are the Tx strategies for asthma & COPD? |
|
Definition
| control the underlying condition & provide symptomatic relief |
|
|
Term
| Why are aerosol agents used whenever possible in the Tx of COPD & asthma? |
|
Definition
1) high concentration of drug in lungs with low systemic effects
2) PK parameters are based on lung function response
3) minimal drug interactions if delivered by inhalation vs systemic |
|
|
Term
| What are the main types of medical therapies used in the Tx of asthma & COPD? |
|
Definition
1) bronchodilators & anti-inflam. agents
2) quick relief & long acting |
|
|
Term
| What 7 drug classes are used in the Tx of asthma? |
|
Definition
2) corticosteroids
3) mast cell stabilizers
4) anticholinergics
5) methylxanthines
6) immunomodulators
7) leukotriene modifiers |
|
|
Term
| What 7 drug classes are used in the Tx of COPD? |
|
Definition
| 1) β agonists
2) corticosteroids
3) anticholinergics
4) methylxanthines
5) oxygen
6) α1antitrypsin
7) phosphodiesterase 4 inhibitors |
|
|
Term
| What are the 3 types of non-selective bronchodilators? |
|
Definition
| 1) α receptor stimulation
2) β1 receptor stimulation
3) β2 receptor stimulation |
|
|
Term
|
Definition
1) vasoconstriction
2) vasopressor
=> decongestion in the upper airways (nasal) |
|
|
Term
|
Definition
1) increased myocardial conductivity
2) increased HR
3) increased contractile force |
|
|
Term
|
Definition
1) relaxation of bronchial smooth muscle
2) inhibition of inflam. mediator release
3) stimulation of mucociliary clearance |
|
|
Term
| What receptors do epinephrine non-selectively stimulate? |
|
Definition
|
|
Term
| What receptors do ephedrine non-selectively stimulate? |
|
Definition
|
|
Term
| What receptors do isoproterenol non-selectively stimulate? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| CAD or HTN => can induce myocardial stress & MI |
|
|
Term
| When might a non-selective α, β agonist be used in the Tx of asthma or COPD? |
|
Definition
not in COPD
occassionally in severe asthma exacerbation |
|
|
Term
|
Definition
| bind β2 receptor => increased AC => increased CAMP => decreased bronchocontriction (smooth muscle relaxation) |
|
|
Term
| What are the 3 short acting (quick relief) β2 agonists used in Tx of asthma & COPD? |
|
Definition
1) albuterol
2) levalbuterol
3) pirbuterol
(βe Prepared for Al to Leave) |
|
|
Term
| Onset/duration
quick relief β2 agonists |
|
Definition
onset: 3-5 min
duration: 4-6 hr |
|
|
Term
|
Definition
tachycardia
tremor
hypokalemia |
|
|
Term
| How does albuterol exist? |
|
Definition
| as a racemic mixture b/w R & S enantiomers |
|
|
Term
| For albuterol, are both the R & the S enantiomers of the reacemic mixture equally as effective? |
|
Definition
no, the therapeutic activity lies primarily with the R enantiomer
(S enantiomer may have deleterious effects) |
|
|
Term
| How does levalbterol compare to albuterol? |
|
Definition
| levalbuterol is the isometric formulation & is as effective as the racemic formulation of albuterol, but only needs 1/2 dose to get comparable bronchodilation & sustemic SE |
|
|
Term
| What are the 5 ling-acting β2 agonists used in COPD & asthma? |
|
Definition
1) Salmeterol
2) Formoterol
3) Aformotrol
4) albuterol SR
5) Indacaterol
(βe somewhat ready [SR] For Al to Stay After Indicated) |
|
|
Term
|
Definition
onset: 30-45 min
duration: 12 hr |
|
|
Term
Onset/duration
formeterol & arformotrol |
|
Definition
onset: 5-15 min
duration: 12 hr |
|
|
Term
onset/duration
albuterol SR |
|
Definition
onset: 15 min
duration 8-12 hr |
|
|
Term
onset/duration
indacaterol |
|
Definition
onset: 15 min
duration: 24 hr |
|
|
Term
| What 2 long acting β2 agonists are also used in combination products? |
|
Definition
1) salmeterol
2) formoterol |
|
|
Term
| In 2011 indacaterol was approved for use in what disease? |
|
Definition
|
|
Term
| SE
long acting β2 agonists |
|
Definition
tachycardia
tremor
hypokalemia
prolinged QT (in OD) |
|
|
Term
| What makes the long-acting β2 agonists last longer than the short acting ones? |
|
Definition
|
|
Term
| Why does salmeterol have a longer time before onset than the other long-acting β2 agonists? |
|
Definition
|
|
Term
| Why does formoterol have a shorter onset than salmeterol? |
|
Definition
|
|
Term
| Is there a difference in efficacy of salmeterol & formoterol? |
|
Definition
|
|
Term
| Is there tachyphylaxis (tolerance) associated with chronic β2 agonist use? |
|
Definition
| conflicting data: probably, but only with certain polymorphisms of the receptor |
|
|
Term
| What is the black box warning on β2 agonists in asthmatic patients? |
|
Definition
1) don't use as a monotherapy
2) only use with patients who are not controlled on a low or medium dose corticosteroid
3) increased risk of asthma-related deaths |
|
|
Term
|
Definition
inhibit muscarinic cholinergic receptors & reduce vagal tone of the airway
may cause drying of pulmonary secretions
(on smooth muscle muscarinic receptors are responsible for sm. muscle contraction & inhibition of relaxation) |
|
|
Term
| What is the short acting anticholinergic used in COPD & asthma? |
|
Definition
ipratropium
(I PRAY i can breathe shortly) |
|
|
Term
onset/duration
ipratropium |
|
Definition
onset: 10-15 min
duration: 4-8 hr |
|
|
Term
|
Definition
dry mouth
blurred vision (if sprayed in eyes) |
|
|
Term
| Does ipratropium come in a combo product? |
|
Definition
|
|
Term
|
Definition
| allergy to soy lecithin or peanuts (contains ouls of lecitin) |
|
|
Term
| What is the long acting anticholinergic used in COPD & asthma? |
|
Definition
|
|
Term
|
Definition
onset: 30 min
duration: 24+ hrs |
|
|
Term
|
Definition
|
|
Term
| Is tiotropium part od a combo product? |
|
Definition
|
|
Term
| What receptors does tiotropium block? |
|
Definition
|
|
Term
| For which muscarinic receptors does tiotropium exert it's long lasting effects? |
|
Definition
| M1 & M3 (rapidly dissocaites from M2) |
|
|
Term
| What are the 3 antileukotriene agents used in asthma? |
|
Definition
1) Monteleukast
2) Zafirlukast
3) Zileuton |
|
|
Term
| What are the 2 leukotriene receptor antagonists used in asthma? |
|
Definition
1) Montelukast
2) Zafirlukast |
|
|
Term
|
Definition
| selectively & competetively inhibit Cys LT1 receptor |
|
|
Term
Onset/duration
montelukast |
|
Definition
onset: 3-4 hrs
duration: 24 hrs |
|
|
Term
Onset/duration
zafirlukast |
|
Definition
onset: 30 min
duration: 12 hrs |
|
|
Term
|
Definition
montelukast: none
zafirlukast: reversible hepatitis & rare irreversible hepatitis |
|
|
Term
| What is the 5-lipooxygenase inhibitor used in asthma? |
|
Definition
Zileuton
(when you have COPD, you have have Zilch LOX) |
|
|
Term
MOA
5-lipoxygenase inhibitor |
|
Definition
| inhibts production of LTs from arachidonic acid, LTB4 & cysteinyl LTs |
|
|
Term
|
Definition
onset: 30 min
duration: 12 hr |
|
|
Term
|
Definition
| elevated LFTs & reversible hepatitis |
|
|
Term
| What is the effect of antileukotriene agents? |
|
Definition
decreased allergy
decreased bronchocontriction
decreased mucus production |
|
|
Term
| When are antileukotriene agents used in the asthma regimen? |
|
Definition
| chronic ONLY since maximal efficacy develops progressively & may take several days |
|
|
Term
| How often in monteleukast dosed? |
|
Definition
|
|
Term
| Is monteleukast indicated in children? |
|
Definition
|
|
Term
| How often is zafirlukast dosed? |
|
Definition
|
|
Term
| When during the day should zafirlukast be taken in order to obtain maximum benefit? |
|
Definition
| 1 hr before or 2 hours after meal |
|
|
Term
| Is zafirlukast indicated in children? |
|
Definition
|
|
Term
| When is dose reduction of zafirlukast needed? |
|
Definition
| with hepatic insufficency since metabolized extensively in the liver |
|
|
Term
| Which liver enzymes metabolize zafirlukast? |
|
Definition
|
|
Term
| How often is zileuton dosed? |
|
Definition
| 2 times daily (a lot higher dose than zafirlukast) & w/o regard to meals |
|
|
Term
| Is zileuton indicated in children? |
|
Definition
|
|
Term
| What tests must be done prior to zileuton administration? |
|
Definition
|
|
Term
| Is zileuton bound to proteins? |
|
Definition
|
|
Term
| How is zileuton metabolized? |
|
Definition
hepatic metabolism
phase I: CYP1A2, CYP2C9, CYP3A4
phase II: glucuronidation |
|
|
Term
|
Definition
mutliple sites of action:
1) inhibits leukocyte recruitment to airways
2) induce anti-inflam. protein lipocortin
3) decrease inflam. by stabilization of lysosomes & PMNs
4) upregulation of anti-inflam. genes
5) decrease stability of selected mRNAs => altered gene transcription after interaction with glucocorticoid receptor |
|
|
Term
|
Definition
1) inhibits phospholipase A2
2) decreased production of PGs & LTs |
|
|
Term
Effect
stabilization of lysosomes & neutrophils |
|
Definition
| prevents degranulation & resulting inflam. response |
|
|
Term
| What are the 6 inhaled corticosteroids used in COPD & asthma? |
|
Definition
1) Beclomethasone
2) Triamcinolone
3) Budnesonide
4) Mometasone
5) Flunisolide
6) Fluticasone |
|
|
Term
SE
inhaled corticosteroids |
|
Definition
1) cough
2) dyspnea
3) oral thrush
4) high doses: postential for adrenal suppression, osteoporosis, skin thinning
5) low/med dose: decrease growth velosity in children (may be transient) |
|
|
Term
| Which 3 inhaled corticosteroids come in a combo product? |
|
Definition
1) budesonide
2) fluticasone
3) mometasone |
|
|
Term
Onset/duration
inhaled corticosteroids |
|
Definition
onset: variable, but can day from days to 2 weeks
duration: asthma stability usually persists for several days after discontinuation |
|
|
Term
| Is there any difference b/w efficacy & SE profile of inhaled corticosteroids? |
|
Definition
|
|
Term
| What is the difference b/w the different inhaled corticosteroids? |
|
Definition
| amount of drug aerosolized per inhaler activation ∴ the # of puffs per day per dose is different per drug |
|
|
Term
| How many puffs would a patient need for high dose trimcinolone? |
|
Definition
|
|
Term
| How many puffs would a patient need for high dose fluticasone? |
|
Definition
|
|
Term
| What are the 3 oral corticosteroids used in asthma & COPD? |
|
Definition
1) methylprednisolone
2) prednisolone
3) prednisone |
|
|
Term
| What is prednisone activated to in vivo? |
|
Definition
|
|
Term
SE
short term PO corticosteroids |
|
Definition
1) reversible abnormality in glucose metabolism
2) increaed appetite
3) fluid retention
4) wt. gain
5) mood alteration
6) HTN
7) peptic ulcer
8) rare: aseptic necrosis |
|
|
Term
SE
long term PO corticosteroids |
|
Definition
1) immune suppression
2) osteoporosis
3) HTN
4) Cushing's disease
5) growth suppression
6) cataracts
7) adrenal suppression |
|
|
Term
| What are the 3 methylxanthines used in COPD & asthma? |
|
Definition
1) theobromine
2) theophylline
3) caffiene
4) aminophylline
(Theo & Amy eXit the Cafe) |
|
|
Term
|
Definition
1) non-selective inhibtion of phosphodiesterase => increase in cAMP => smooth muscle relaxtion
2) direct & indirect effect on intracellular calcium
3) mild anti-inflam. activity |
|
|
Term
Onset/duration
theophylline & aminophylline |
|
Definition
onset: 1 hr
duration: variable |
|
|
Term
SE
theophylline & aminophylline
usual dose |
|
Definition
1) insomnia
2) GERD
3) GI upset
4) hyperactivity in children
5) difficulty urinating if BPH |
|
|
Term
SE
throphylline & aminophylline
dose related toxicity |
|
Definition
1) tachycardia
2) N/V
3) SVT
4) CNS stimulation
5) seizures
6) hyperglycemia
7) hypokalemia |
|
|
Term
| How is 90% of methylxanthines metabolized? |
|
Definition
liver
CYPA2, CYP2E1, CYP3A3 |
|
|
Term
| Why must theophylline be monitored closely? |
|
Definition
|
|
Term
What is the goal level of theophylline?
What is the toxic level of theophylline? |
|
Definition
goal: 5-15 mcg/mL
toxic: >20 mcg/mL |
|
|
Term
| How equivalent is aminophylline to theophylline? |
|
Definition
| 0.8 of eqipotent throphylline dose |
|
|
Term
| What should be taken into consideration of each patient prior to a theophylline regimen? |
|
Definition
| caffeine ingestion & smoking status |
|
|
Term
|
Definition
anti-inflam agent & mast cell stablizer:
blocks release of mediators of hypersensitivity rxns from mast cells, eosinophils, neutrophils, macs, monocytes, histamine, & platelets |
|
|
Term
| Do mast cell stablizers exert any bronchodilating, antihistaminic or corticosteroid effects? |
|
Definition
|
|
Term
| What drug is a mast cell stabilizer used in asthma? |
|
Definition
|
|
Term
|
Definition
onset: 1+ weeks for max benefit (∴ not for an acute attack)
duration: 3-4 weeks after multiple doses |
|
|
Term
|
Definition
1) cough
2) irritation
3) bad taste |
|
|
Term
|
Definition
1) inhibt binding of IgE to high-affinity IgE receptor on surface of mast cells & basophils
2) reduction of surface-bound IgE => limits degree of release of mediators of allergic response |
|
|
Term
| What immunomodulator is used in asthma? |
|
Definition
| omalizumab (monoclonal Ab) |
|
|
Term
| What additional MOA does omalizumab have? |
|
Definition
| reduce number of high-affinity IgE receptors on basophils in atopic patients |
|
|
Term
|
Definition
onset: 1-2 hr (steady state in 2 weeks)
duration: 2-4 weeks |
|
|
Term
|
Definition
1) pain/brusing @ injection site
2) anaphylaxis in 0.2% of patients
3) malignant neoplasms in .5% of patients (vs. 0.2% on placebo) |
|
|
Term
|
Definition
| replacement therapy with α1Pl plasma protein & the principal inhibitor of neutrophil elastase => adequate antineutrophil elastase activity & protection in the lungs of individuals with α1antitrypsin deficiency |
|
|
Term
| What α1antitrypsin drug is used in patients with COPD? |
|
Definition
|
|
Term
| Onset/duration
α1 proteinase inhibitor |
|
Definition
onset: 1-2 hr
duration 2-4 weeks |
|
|
Term
| SE
α1 proteinase inhibitor |
|
Definition
1) increased LFTs
2) headache
3) somnolence |
|
|
Term
MOA
phosphodiesterase 4 inhibitor |
|
Definition
| selective inhibitor of phosphodiesterase 4 (PDE4) => accumulation of cAMP within inflam. & structural cells in the pathogenesis of COPD |
|
|
Term
| What anti-inflam. effects are seen with a PDE1 inhibitor? |
|
Definition
1) suppression of cytokine release
2) inhibitor of lung infiltration by neutrophils & other leukocytes
(also pulmonary remodeling & mucociliary malfunction becomes better) |
|
|
Term
| What PDE4 inhibitor is used in COPD? |
|
Definition
roflumilast
(Peepee makes you ROFL) |
|
|
Term
Onset/duration
roflumilast |
|
Definition
onset: 1 hr
duration: 17-30 hrs |
|
|
Term
|
Definition
1) diarrhea
2) wt. loss
3) insomnia
4) anxiety
5) depression |
|
|
Term
| What are the 4 drug names of the combinations used for Tx in asthma/COPD? |
|
Definition
1) combivent
2) advair
3) symbicort
4) dulera
(Combos Are Super Duper) |
|
|
Term
| What combo drugs are used in both COPD & asthma? |
|
Definition
|
|
Term
What combo drug is ONLY used in COPD?
asthma? |
|
Definition
COPD: combivent
asthma: dulera |
|
|
Term
| What is the only combo drug used for quick relief (∴ the rest are used for control)? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
Which of the following is the MOA for cromolyn?
A) blocks the release of mediators of hypersensitivity rxns from mast cells, eosinophils, neutrophils, macs, monocytes, histamine, & platelets
B) non-selective inhibition of PDE4 => increase cAMP => smooth muscle relaxtion
C) agonism of the beta receptors => increased AC => increased cAMP => smooth muscle relaxtion
D) inhibits binding of IgE to high affinity IgE receptor on the surface of mast cells & basophils, limiting the degree of release of mediators of allergic response |
|
Definition
|
|
Term
Which of the following dsease state interactions would NOT be responsible for increasing theophylline levels, potentially causing toxicity?
A) decompensated CHF
B) ciprofloxacin
C) rifampin
D) cimetidine |
|
Definition
|
|
Term
|
Definition
| mycobacterium tuberculosis |
|
|
Term
|
Definition
|
|
Term
MTb
motility?
shape?
Gram?
Acid-fast?
ana/aerobic?
Growth/metabolism? |
|
Definition
non-motile
non-sporulating
bacillus
weak G+
strong AF
obligate aerobe
slow growth & metabolism |
|
|
Term
| Why is the size of MTb important? |
|
Definition
| optimal size for reaching lung |
|
|
Term
|
Definition
|
|
Term
| Why is MTb a long-lived org in the human body (∴ can cause disease years after initial inf. & why Tx needs to be so long)? |
|
Definition
|
|
Term
|
Definition
| No, what causes the clinical aspects of the disease is the host's response to the org. |
|
|
Term
| What forms the basis of the diagnostic TB skin test? |
|
Definition
| the immunologic host rxn elicited by MTb |
|
|
Term
def
NTM (nontuberculosis mycobacteria) |
|
Definition
group of orgs w/in mycobacterium genus that share some characteristics w/ MTb, but:
1) differ in significant ways
2) can be confused w/ MTb |
|
|
Term
| Can TB ever be left untreated? |
|
Definition
| no, always a pathogen, always requires Tx |
|
|
Term
| When NTM is found, is Tx always required? |
|
Definition
| not always, it doesn't always manifest as disease |
|
|
Term
| How can NTM confuse contamination & disease? |
|
Definition
| it can sometimes contamine water & clinical specimen |
|
|
Term
| How can NTM cause confusion b/w colonization & disease? |
|
Definition
| can sometimes colonize airways w/o causing disease |
|
|
Term
| What tests for TB can NTM confuse interpretation of? |
|
Definition
1) acid fast stains (are AF+)
2) TB skin tests (cause cross-rxn w/ TB Ags)
3) histology (cause granulomas that are noncaseating) |
|
|
Term
| Since NTM can colonize the airways w/o causing disease, when should it be a suspected pathogen as opposed to a colonizer? |
|
Definition
1) multiple + specimen
2) biosy
3) lr # of orgs
w/o another explanation for Sx |
|
|
Term
| Is MTb always a pathogen? |
|
Definition
|
|
Term
| What disease can NTM produce in the lungs? |
|
Definition
1) a disease that resembles TB
2) nodules
3) bronchiectasis |
|
|
Term
| When are some NTB found more frequently in people's lungs? |
|
Definition
| if they have a co-morbid lung disease (COPD, CF, etc) |
|
|
Term
| What NTM should be considered with lymphadenitis? |
|
Definition
|
|
Term
| What NTM should be considered with cutaneous disease? |
|
Definition
1) m. marinum
2) m. ulcerans |
|
|
Term
| What is implied when a patient's blood cultures are positive for NTB? |
|
Definition
|
|
Term
| What NTB often disseminated in HIV patients? |
|
Definition
| MAC (mycobacterium avium/intracellulare complex) |
|
|
Term
| What is the most common mycobacterial infection in AIDS? |
|
Definition
|
|
Term
| What are m. avium & m. intracellulare? |
|
Definition
|
|
Term
| With what CD4 count do MACs tend to occur in AIDS patients? |
|
Definition
| <50 (usually disseminated) |
|
|
Term
| When can MAC cause pulmonary disease? |
|
Definition
1) normal hosts
2) those w/ underlying disease |
|
|
Term
| Can MAC just be a colonizer? |
|
Definition
|
|
Term
| What are the 6 possible NTM pathogens? |
|
Definition
1) MAC
2) m. kansasii
3) m. abscessus
4) m. fortuitum
5) m. xenopi
6) m. chelone
(MAC Fortuitously was in Kasas playing Cello & X-caped the Abscess NighTMare) |
|
|
Term
| Can all NTM pathogens be colonizers? |
|
Definition
|
|
Term
| What disease can all NTM pathogens cause? |
|
Definition
|
|
Term
| In which patients is m. abscessus more likely to cause pulmonary disease? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Why is it important that MTb orgs be less than 10 microns in size? |
|
Definition
| larger particles impact on upper airway & are removed by mucus blanket & swallowed or coughed out |
|
|
Term
|
Definition
| water & soil source (contamination - NOT PERSON-PERSON) |
|
|
Term
| What does MTb transmission depend on? |
|
Definition
1) # of droplet nuclei
2) # of orgs in droplet nuclei
3) duration of exposure |
|
|
Term
| How is transmission of TB prevented? |
|
Definition
1) ventilation (over 20 air changes per hour)
2) UV light (decrease viable orgs)
3) chemotherapy (infectivity can be prevented after 1-2 weeks of therapy)
4) masks (HEPA for contacts, regular ones for infected) |
|
|
Term
| What fraction of people in contact with a person with TB will be infected? |
|
Definition
|
|
Term
| Of the 1/3 infected with MTb, what % actually develop the disease? |
|
Definition
|
|
Term
| What % of those that develop TB, how many develop TB early (2 years) compared to those that develop it late? |
|
Definition
|
|
Term
| What happens to after inhalation & proliferation of MTb? |
|
Definition
1) spread to lymph nodes
2) spread hematogeneously
3) asymptomatic primary TB
4) cell-mediated immunity
5) + TB skin test or IGRA (3-8 weeks post exposure) - Delayed type hypersensitivity |
|
|
Term
| Though 85-90% of patients infected with MTb will never become infected, are they still capable from this infection to develop TB years later? |
|
Definition
| yes, once a person is infected, the bacilli remain in the body - capable of one day multiplying & causing disease ∴ life-long risk |
|
|
Term
|
Definition
| a person who has no Sx or signs of TB, but has a + TB skin test or IGRA |
|
|
Term
| What happens to MTb in primary TB (initial inf.)? |
|
Definition
1) droplet nuclei containing bacilli impact on alveoli or bronchioles
2) bacilli are engulfed by macs
3) bacilli proliferate IN macs
4) macs die & release bacilli
5) cytokines, chemokines attract other immune-effector cells
6) cycle is repeated
7) bacilli spread to regional lymph nodes
8) bacilli spread hematogenously to other organs |
|
|
Term
| What is the host response after infection & multiplication of MTb in macs? |
|
Definition
1) APCs process & present TB Ag to T cells
2) T cells proliferate & produce mediators
3) Activated T cells release IFNγ
4) blood lymphocytes & monocytes infiltrate area & enhance immune response |
|
|
Term
| What is the host response 3-8 weeks after an MTb inf? |
|
Definition
1) cell-mediated (relative)
2) delayed hypersensitivity rxn (TB skin test, IFNγ assay) |
|
|
Term
|
Definition
| usually asymptomatic or mild flu-like Sx |
|
|
Term
| How can primary Tb be Dx? |
|
Definition
| during contact investigations |
|
|
Term
| Who is most commonly diagnosed with primary TB? |
|
Definition
|
|
Term
| What happens in the lung after primary TB inf? |
|
Definition
1) healing occurs
2) bacilli remain intracellular & dormant
3) TB doesn't occur in 85-90% of inf.
4) relative immunity to re-inf. |
|
|
Term
| How do the initial sites of the primary disease heal? |
|
Definition
| in lung & lymps nodes, granulomas may fibrosis & frequently become calcified (appear on xrays) |
|
|
Term
| What are the 3 possible forms of early TB disease? |
|
Definition
1) progressibe primary
2) miliary
3) pleural effusions |
|
|
Term
|
Definition
| disseminated sm. nodules composed of granulomas |
|
|
Term
| What are 2 types of late TB disease? |
|
Definition
1) classic cavitary lung disease
2) extra-pulmonary disease |
|
|
Term
| How does extra-pulmonary TB occur? |
|
Definition
| activation of TB bacilli that lodged in extra-pulmonary areas during early hematogenous spread during initial inf. |
|
|
Term
| What is the pathology of TB? |
|
Definition
1) inflam./exudative leison
2) productive leisons (granulomas)
3) caseous necrosis
4) sclerosis & calcification
5) liquifaction, cavitation |
|
|
Term
| Do NTM inf. also cause granulomas? |
|
Definition
|
|
Term
| What can cause granulomas? |
|
Definition
1) MTb
2) NTM
3) other inf.
4) other diseases (i.e sarcoidosis) |
|
|
Term
|
Definition
1) cough
2) wt. loss
3) night sweats
4) chills
5) hemoptysis
6) malaise
7) fevers
8) chest pain |
|
|
Term
|
Definition
1) Sx
2) CXR
3) skin test
4) IFNγ test
5) AF stain on sputum
6) nucleic amplification tests
7) culture
8) histologic exam of tissue
9) clinical Dx (Sx, no org. ID, but good response to therapy) |
|
|
Term
| What does the nucleic amplification test tell us? |
|
Definition
| if the org is a MTb complex or not MTb complex |
|
|
Term
|
Definition
| tuberculoprotein that is antigenic |
|
|
Term
|
Definition
purified protein derivative
(standardized to be biologically equivalent to 5 tuberculin units of a standard) |
|
|
Term
def
mantoux method of TB skin test |
|
Definition
| intracutaneous injection of 5 TU PPD |
|
|
Term
| When is induration of TB skin test measured (results)? |
|
Definition
|
|
Term
| What is a positive TB test? |
|
Definition
|
|
Term
| Why can MTb be IDed thru an acid fast stain? |
|
Definition
| water soluble dyes are taken up thru the wall of the bacillus & can't be eliminated b an acid wash |
|
|
Term
| Why are the advantages of a AF test for TB? |
|
Definition
1) fast
2) provides an estimate of # of bacilli & infectiousness |
|
|
Term
| Why are the disadvantages of a AF test for TB? |
|
Definition
| 1) 105 AFB per mL to detect (can give false -)
2) other orgs s.a. NTM can give a + AF test (false +)
3) they can't rule out nor rule in TB |
|
|
Term
| Can AF stains differentiate b/w MTb & NTM? |
|
Definition
|
|
Term
| When should a sputum test be done to test for TB? |
|
Definition
|
|
Term
| What is tested for in the MTb complex when testing the sputum? |
|
Definition
1) MTb
2) m. bovis
3) m. africanum
4) m. microti
5) m. canetti |
|
|
Term
| What is the difinitive diagnostic test for TB? |
|
Definition
|
|
Term
| Is the culture more or less sensitive than the stains for TB? |
|
Definition
|
|
Term
| How long does it take to culture MTb? |
|
Definition
3-6 weeks w/ standard methods
1-2 weeks w/ modern methods |
|
|
Term
| Can the culture differentiate b/w MTb & NTM? |
|
Definition
| yes (& precisely which NTM as well) |
|
|
Term
| How can the cultures help determine which Abx to use? |
|
Definition
| Abx susceptibility testing |
|
|
Term
| What tests should be ordered right away when TB is suspected? |
|
Definition
|
|
Term
| What tests should be ordered right away when bacterial pneumonia is suspected? |
|
Definition
|
|
Term
| What is the turn around time for an AFB? |
|
Definition
|
|
Term
| What is the turn around time for a nucleic acid amplification assay? |
|
Definition
|
|
Term
| What is the turn around for a growth detection is broth? |
|
Definition
|
|
Term
| What is the turn around for TB ID in DNA or broth? |
|
Definition
|
|
Term
| What is the turn around for Abx susceptibility test for primary TB drugs? |
|
Definition
|
|
Term
| What is the turn around for Abx susceptibility testing for secondary TB drugs? |
|
Definition
|
|
Term
| What can be done to test for resistance mutations of TB (but not FDA approved)? |
|
Definition
|
|
Term
| What are the advantages/disadvantages of a nucleic acid amplification assay for TB? |
|
Definition
ad: rapid, helps differentiate b/w MTb & NTM
dis: can be false -, esp. after false - AFB |
|
|
Term
| In culture how can NTM differ from MTb? |
|
Definition
1) rates of growth (some are faster growing)
2) some NTM cultures can be pigmented |
|
|
Term
| What are the 5 first line TB drugs? |
|
Definition
1) isoniazid
2) rifampin
3) pyrazinamide
4) ethambutol
5) rifapentine |
|
|
Term
| What are the 5 seond line TB drugs? |
|
Definition
1) streptomycin
2) capreomycin
3) cycloserine
4) p-aminosalicylic acid
5) ethionamide |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Is the drug therapy for NTM the same as TB? |
|
Definition
|
|
Term
| What can cause primary TB drug resistance? |
|
Definition
| patient received Abx <1 month prior to TB |
|
|
Term
| How can drug resistance arise among those with previously treated TB? |
|
Definition
1) acquired/secondary resistance
2) reinfection (second TB source while on Abx) |
|
|
Term
def
MDR TB (multi drug resistant) |
|
Definition
| @ LEAST resistant to INH & RIF |
|
|
Term
| Which cases of TB have a very high mortality rate? |
|
Definition
| XDR TB (extensively drug resistant) |
|
|
Term
|
Definition
MDR TB also resistant to:
1) ANY flurorquinolone
2) ANY of the following injectibles: amikacin, capreomycin, kanamycin |
|
|
Term
| Where does drug resistance originate from? |
|
Definition
1) genetic mutations (single nucleotide substitutions, no horizontal gene transfer)
2) selective pressure => secondary or acquired resistance (inappropriate Tx)
3) transmission to contact => primary resistance |
|
|
Term
| What is the paradox of drug resistant orgs? |
|
Definition
| development of resistance requires availability of drugs |
|
|
Term
| What 2 gene mutations account for 85% of all INH drug resistance? |
|
Definition
|
|
Term
| What gene mutation accounts for >95% of all RIF drug resistance? |
|
Definition
|
|
Term
| Why can MTb drugs only develop resistance to 1 drug while in infected host? |
|
Definition
| there are not enough orgs for any one to develop resistance to to Abx (spontaneous mutations occur at >108 divisions) |
|
|
Term
| When is drug resistance more common? |
|
Definition
| large, rapidly dividing populations of org |
|
|
Term
| What are the 5 principles of MTb Tx? |
|
Definition
1) prevent resistance
2) prevent relapse
3) assure compliance
4) consider drug toxicities & DDIs
5) conversion of sputum, sterilization |
|
|
Term
| How is drug resistance in MTb prevented? |
|
Definition
1) never use a single Abx therapy
2) never add a single Abx to a failing regimen |
|
|
Term
| When should TB drug resistance be suspected? |
|
Definition
1) previously treated patient who is non-compliant
2) poor clinical response to therapy
3) positive cultures after 4 months of therapy
4) contact with person w/ resistant disease
5) emigration from high incidence region ( >1/2 MDR cases are foreign born) |
|
|
Term
| How is TB relapse prevented? |
|
Definition
|
|
Term
| What does duration of TB TX depend on? |
|
Definition
1) specific drugs used (6 mo. if RIF & PZA)
2) presence of drug resistance
3) persistance of + cultures after initiation phase & either caviatary disease or HIV (add 3 mo. Tx)
4) # doses taken within a given time frame |
|
|
Term
| How many drugs are recommended in the Tx of MTb? |
|
Definition
| 4, with different options for dosing intervals in continuation phase |
|
|
Term
| What is the 4 drug regimen in the initial phase of TB Tx (2 months)? |
|
Definition
1) INH
2) RIF
3) PZA
4) EMB
(RIPE) |
|
|
Term
| How long is the continuation phase of TB Tx (after initial phase 2 months)? |
|
Definition
| 4 months (or 7 if +sputum culture after initial phase in patients with caviatr disease or HIV) |
|
|
Term
| When might adjustments to Abx in TB Tx be changed? |
|
Definition
| once Abx susceptibility known |
|
|
Term
| How can we assure compliance of Tb Tx? |
|
Definition
1) DOT (direct observed therapy)
2) intermittent dosing (2-3x/week) |
|
|
Term
| How is sputum in TB converted, sterilization? |
|
Definition
| first line medications (esp. INH, RIF, & PZA) |
|
|
Term
|
Definition
| TB inf, no evidence of disease, skin test or INFγ +, presumes persistence of orgs, life-long risk of TB disease |
|
|
Term
| How indicative is a positive skin TB test of eventual disease? |
|
Definition
| more than 90% of people with active TB arise from those who've had a +TB test |
|
|
Term
| How is the risk of TB disease reduced in those with latent TB inf. (LTBI)? |
|
Definition
Tx w/
isoniazid for 9 mo.
or
rifampin for 4 mo.
(both drugs weekly for 12 weeks has recently been found to be effective as well) |
|
|
Term
|
Definition
|
|
Term
| Why is targeted TB skin testing recommended as opposed to testing everyone? |
|
Definition
| it's costly & inefficient |
|
|
Term
| Who should be tested for TB vis skin test? |
|
Definition
| those @ high risk of exposure or high risk of developing disease after inf. |
|
|
Term
| Who should be treated for TB? |
|
Definition
| anyone with positive TB test (tho must rule out active inf.) |
|
|
Term
| Who is at risk for exposure/inf.? |
|
Definition
1) close contacts of person known/suspected w/ active TB (+ skin test is 5mm)
2) foreign-born persons from areas where TB is common
3) persons who visit TB-prvalent countries
4) residents/employees of high-risk settings
5) heath care workers w/ high risk clients
6) children & adolescents exposed to adults w/ increased risk
7) populations @ high risk (medically underserved, low income, alcoholics, drug users, mentally ill, homeless) |
|
|
Term
| Who is at risk for progression to disease after inf.? |
|
Definition
1) Immune suppressed (+ skin test is 5mm)
2) stable CXR consistent w/ old healed TB (+ skin test is 5mm)
3) children <4y
4) silicosis, DM, ESRD, underweight low dose corticosteroids, head & neck cancer |
|
|
Term
| What complicated TB skin test results? |
|
Definition
|
|
Term
| How can people never inf. with MTb have a positive skin test? |
|
Definition
1) BCG vaccination
2) NTM exposure |
|
|
Term
|
Definition
| avirulent strain of M. bovis used |
|
|
Term
| Why does efficacy, immunogenicity, & reactogensicity vary in those who've obtained the BCG vaccine? |
|
Definition
|
|
Term
| Does skin test results always remain postivie with BCG vaccine? |
|
Definition
| no, wanes over time, also gets smaller over time |
|
|
Term
| Does a positive skin test of someone with BCG vaccine influence targeted skin testing & Tx of LTBI? |
|
Definition
|
|
Term
| Does the + skin test from a NTM tend be larger or smaller than a + skin test with MTb? |
|
Definition
|
|
Term
| What 7 things can produce a false - skin TB test? |
|
Definition
1) anergy
2) immune suppression
3) debility, old age
4) age <6 mo.
5) overwhelming TB
6) live virus vaccination |
|
|
Term
| Why is determining the size reaction to call + in a TB skin test a balancing act? |
|
Definition
| do not want to consider a false + to be positive nor a false - to be negative |
|
|
Term
| When should the lowest threshold for a + skin TB test be used? |
|
Definition
| individuals with the most risk for developing disease |
|
|
Term
| When should the highest threshold be used in a + skin TB test? |
|
Definition
| individuals least likely to be inf. w/ TB or to develop disease |
|
|
Term
| When should a 5 mm threshold be used as a + TB skin test (lowest threshold)? |
|
Definition
1) close contacts of an infectious person (high risk for recent inf.)
2) HIV
3) previous untreated TB &/or CXR evidence of stable old TB
4) immune suppression |
|
|
Term
| For what high risk individuals should 10mm be considered a + skin TB test? |
|
Definition
1) skin test conversion (increase) in 2 years
2) recent immigrants from endemic regions
3) children <4y
4) residents/employees high risk settings
5) children/adolescents in cantact w/ high risk individuals
6) mycobacteriology lab personnel |
|
|
Term
| For what moderate risk individuals should 10mm be considered a + skin TB test? |
|
Definition
1) IV drug users
2) medical risk factors (silicosis, gastrectomy, jejunoileal bypass, chronic malabsorption, malnutrition, end stage renal disease, DM, head & neck cancer, low dose corticosteroids) |
|
|
Term
| When should 15mm be considered a + skin TB test? |
|
Definition
persons w/ no known risk factors
(targeted skin testing not recommended for this group) |
|
|
Term
|
Definition
| test for IFNγ release from exposure of sesitized lymphocyte to selected MTb Ags |
|
|
Term
def
quantiferon-TB gold in-tube test |
|
Definition
| ELISA assay measures the release of IFNγ in whole blood by sensitized lymphocytes when stimulated by Ag (Ag used are not shart by most NTM or BCG strains - except m. kansasii, szugai, marinum) |
|
|
Term
| What 3 Ag are tested for in the QFT-TB gold test? |
|
Definition
1) ESAT-6
2) CFP-10
3) TB7.7(p4): present in m. kansasii, szulgai, marinum |
|
|
Term
| hod used in QFT-TB gold test? |
|
Definition
1) heparanized whole blood
2) mixed w/ the 3 Ags, incubated
3) ELISA for measuring INFγ |
|
|
Term
| What is used as a positive control for QFT-TB gold test? |
|
Definition
| mitogen phytohemaglutinin |
|
|
Term
| How are the results of QFT-TB gold test interpreted? |
|
Definition
+: ≥ 0.35 IU/mL
-: <0.35 IU/mL
indeterminate (invalid): + control has an inadequate response or - control has too high a response |
|
|
Term
| What is used in the T-spot test? |
|
Definition
| peripheral blood mononuclear cells (PBMCs) that are incubated w/ controls & 2 separate mixtures of peptides |
|
|
Term
| What mixtures of peptides are used in the T-spot test? |
|
Definition
1) entire aa sequence of ESAT6
2) entire aa sequence of CFP10 |
|
|
Term
| What is used to detect # of cells that secrete IFNγ in T-spot? |
|
Definition
|
|
Term
| How are the results of T-spot interpreted? |
|
Definition
+: ≥ 8 spots
-: ≤ 4 spots
indeterminate: 5,6,7 spots, if + control has inadequate response or - control has too high a response |
|
|
Term
| Are IGRAs used w/ or instead of skin tests to diagnose TB & LBTI? |
|
Definition
|
|
Term
| When are IGRAs preferred over skin tests in TB diagnosis? |
|
Definition
1) persons vaccinated w/ BCG
2) persons unlikely to return for skin test reading |
|
|
Term
| How does IGRA compare to TB skin test? |
|
Definition
IGRA:
1) in vivo, severe rxn
2) 2 visits, results 2-3 days
3) cross-racting Ags
4) trained injectors/interpreters
5) boosting
6) need for intact immune system
7) no controls
skin test:
1) in vitro
2) single visit, results 1 day
3) specific
4) lab: cost, quality
5) no boosting
6) need for intact immune system
7) controls for anergy & test performence |
|
|
Term
| What is the most common mycobacterium isolated from individuals w/ HIV? |
|
Definition
|
|
Term
|
Definition
disseminated disease:
high fevers, + blood cultures
(occurs when CD4 count is <50) |
|
|
Term
| Does TB often occur prior to or after other opportunistic diseases in HIV patients? |
|
Definition
|
|
Term
| Does the diagnosis of TB occur prior to or after diagnosis of HIV? |
|
Definition
| preceeds or coincides ∴ anyone who tests positive for TB should be HIV tested |
|
|
Term
|
Definition
1) primary TB often diagnosed
2) infiltrates in any lung zone w/ lymphadenopathy
3) extrapulmonary disease more common - often occurs WITH lung disease
4) lymphatic & hemtatogenous disease common (blood cultures +) |
|
|
Term
| Why is TB Tx in patients w/ HIV complicated? |
|
Definition
complex drug interaction b/w rifamycins & anti-retroviral medications
(tho Tx of TB faciliates Tx of HIV & vice versa) |
|
|
Term
| What are the goals of therapy in Tx of TB? |
|
Definition
1) kill MTb bacilli rapidly
2) minimize resistance
3) sterilize host tissues |
|
|
Term
| What are the 2 phases of TB Tx? |
|
Definition
1) initial
2) continuation |
|
|
Term
| What are the 7 first line Abx Tx options for TB? |
|
Definition
1) Rifampin
2) Isoniazid
3) Pyrazinamide
4) Ethanmbutol
5) Rifabutin
6) Rifapentene
7) streptomycin (if susceptibility confirmed) |
|
|
Term
| What are the 5 second line TB Tx Abx? |
|
Definition
1) AMGs (amikacin, kanamycin, capreomycin)
2) FQs (levofloxacin, moxifloxacin)
3) ethionamide
4) cycloserine
5) PAS (p-aminosalicylic acid) |
|
|
Term
| How many drugs are needed in the drug regimen for TB Tx? |
|
Definition
|
|
Term
| Which first line drug do many people have isolates with a high propotion resistance? |
|
Definition
|
|
Term
| Why is a 4 drug regimen required for maximal efficacy of TB Tx? |
|
Definition
1) minimize development of resistance
2) some colonies are already resistance to isoniazid
3) if monothereapy, drug resistance will develop |
|
|
Term
| What 4 drugs are often given in the initial phase of TB Tx? |
|
Definition
RIPE
1) Rifampin
2) Isoniazid
3) Pyrazinamide
4) ethambutol |
|
|
Term
| How long is the intial phase of TB Tx? |
|
Definition
|
|
Term
| How long is the continuation phase of TB Tx? |
|
Definition
|
|
Term
| How many drugs are needed in the continuation phase of TB Tx? |
|
Definition
|
|
Term
| What 2 drugs are often given as the 2 drug regimen of the continuation phase of TB Tx? |
|
Definition
1) rifampin (or a dirivative)
2) isoniazid |
|
|
Term
| When is a 7 mo. continuation phase used over a 4 mo? |
|
Definition
1) cavitary pulmonary TB whose sputum culture at 2 mo. Tx is positive
2) initial phase did not contain pyrazinamide (liver disease, possibly pregnancy)
3) patients recieving once weekly isoniazid & rifapentene whose sputum culture is positive after intital phase |
|
|
Term
| What are the 2 options of continuation phase dosing? |
|
Definition
1) once weekly
2) 2-3x/weekly with DOT (direct observed therapy) |
|
|
Term
MOA
rifampin & dirivatives s.a. rifabutin & rifapentine |
|
Definition
binding to the β subunit of the bacterial DNA dependent RNA polymerase => inhibition of RNA synthesis
(specific for bacterial enzyme) |
|
|
Term
|
Definition
1) discoloration of secretions
2) hepatotoxicity (hyperbilirubinemia rises in alkaline phosphatase - additive effect w/ other TB drugs) |
|
|
Term
|
Definition
potent CYP450 INDUCER
notable: HIV protease inhibitors, calcineurin inhibitors, oral contraceptives, warfarin |
|
|
Term
| Why were the rifampin derivatives created? |
|
Definition
to decrease DDIs
rifampin > rifapentene > rifabutin |
|
|
Term
| Why would someone be given rifapentene over rifabutin if there are less DDIs with rifabutin? |
|
Definition
| rifapentene has a once weekly option |
|
|
Term
|
Definition
|
|
Term
|
Definition
prodrug => activated by mycobacterium cells
inhibits mycolic acids (components of mycobacterial cell wall) |
|
|
Term
|
Definition
| n-acetyltransferase (∴ slow acetylaters will have decreased metabolism) |
|
|
Term
|
Definition
1) hepatitis (most common)
- 10-20% develop asymptomatic rises in LFTs
- clinically significant in <1%
- most common 4-8 weeks during therapy
2) peripheral neuropathy (dose related) |
|
|
Term
Tx
INH induced peripheral neuropathy |
|
Definition
| pyridoxine supplementation |
|
|
Term
|
Definition
additive hepatotoxicity
increased phenytoin levels |
|
|
Term
|
Definition
|
|
Term
|
Definition
| unknown, but requires activation via pyrazinamdase into active form pyrazinoic acid |
|
|
Term
|
Definition
1) N/V (most common)
2) hepatotoxicity (dose dependent)
3) elevation of serum uric acid (acute gout only if pre-exisiting condition)
4) non-gouty polyarthralgias
5) potential teratogenicity |
|
|
Term
| How are the non-gouty arthralgias precipitated by PZA controlled? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| inhibit arabinosyl transferase => decreased formation of cell wall components |
|
|
Term
|
Definition
| Retrobullar optic neuritis (dose dependent, usually reversible) |
|
|
Term
Sx
Retrobullar optic neuritis |
|
Definition
bilaterally blurry vision
impairment of visual acuity
red-green color vision |
|
|
Term
| When can EMB be discontinued from the TB Tx regimen? |
|
Definition
| if/when drug susceptibility results are known |
|
|
Term
| What drug category is stereptomycin in? |
|
Definition
|
|
Term
MOA
streptomycin (& other AMGs) |
|
Definition
| 30S ribosomal subunit protein synthesis inhibition |
|
|
Term
| Why has streptomycin fallen out of favor for first line TB Tx? |
|
Definition
| high resistance rates (∴ only first line if susceptibility confirmed) |
|
|
Term
|
Definition
| 1) nephrotoxicity (2) ototoxicity (3) vestibular toxicity (>other AMGs) |
|
|
Term
| What FQs are commonly used in TB Tx? |
|
Definition
| levofloxacin & moxifloxacin |
|
|
Term
| Are FQs first line TB Tx? |
|
Definition
|
|
Term
MOA
levofloxacin & moxifloxacin (& other FQs) |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| 50S ribosomal subunit protein synthesis inhibitor |
|
|
Term
|
Definition
| dose/duration dependent thrombocytopenia |
|
|
Term
|
Definition
|
|
Term
|
Definition
same as other AMGs
stronger associated ototoxicity |
|
|
Term
| Why would kanamycin or amikacin be used instead of streptomycin for TB Tx? |
|
Definition
| may retain activity in streptomycin resistant strains, but will need to test for susceptibility |
|
|
Term
|
Definition
peptide protein synthesis inhibitor
same as other AMGs (often lumped in as an AMG) |
|
|
Term
|
Definition
|
|
Term
| What is ethionamide structurally related to? |
|
Definition
|
|
Term
|
Definition
| inhibits mycolic acid synthesis |
|
|
Term
|
Definition
~ to INH:
1) hepatotoxicity
2) neuropathies
3) GI (high, often leads to non-adherence) |
|
|
Term
| What is cycloserine the structural analog to? |
|
Definition
|
|
Term
|
Definition
| inhibits alanine racemase => inhibition of cell wall synthesis |
|
|
Term
| What limits the clinical utility of cycloserine? |
|
Definition
|
|
Term
|
Definition
1) CNS (headache, tremors, psychosis, convulsions)
2) peripheral neuropathy |
|
|
Term
| What can prevent some of the neurological effects associated with cycloserine? |
|
Definition
|
|
Term
Abbreviation
aminosalicylic acid |
|
Definition
|
|
Term
| What is PAS structurally similar to? |
|
Definition
|
|
Term
|
Definition
| inhibits folate synthesis |
|
|
Term
|
Definition
1) GI intolerance
2) hypersensitivity |
|
|
Term
| What are the common SE of TB Tx? |
|
Definition
1) GI
2) rash
3) hepatotoxicity |
|
|
Term
| When is GI upset common in the Tx of TB? |
|
Definition
|
|
Term
| If GI upset occurs with TB Tx, why is it essential to check LFTs? |
|
Definition
to r/o hepatotoxicity, which has GI upset as a presenting sign
(if LFTs <3x the upper limit of normal, then liver dysfunction is not the cause) |
|
|
Term
| What can help alleviate the GI upset associated w/ TB Tx? |
|
Definition
| administration of drugs w/ food |
|
|
Term
Tx
mild rash seen w/ TB Tx |
|
Definition
| antihistamines for symptomatic relief |
|
|
Term
Tx
severe rash associated w/ TB Tx |
|
Definition
1) stop all meds
2) once rash clears, re-administer meds one by one @ 2-3 day intervals |
|
|
Term
Tx
increased LFTs, but asymptomatic while on TB Tx |
|
Definition
| increase frequency of monitoring (does NOT necessarily mean stop medication) |
|
|
Term
Tx
While on TB Tx, AST increases >5x ULN (upper limit of normal) w/ no Sx
OR
AST increases to >3x ULN w/ Sx |
|
Definition
1) therapy should be discontinued
2) perform workup for alternative causes
3) When AST becomes <2X ULN, retintroduce meds one by one @ 1 week intervals |
|
|
Term
| What is suggestive of a rifampin toxicity? |
|
Definition
| increased bilirubin & alkaline phosphatase |
|
|
Term
| What is the preferred management strategy of TB Tx in the US? |
|
Definition
|
|
Term
|
Definition
| observe patient as they swallow medication |
|
|
Term
| What are the advantages to DOT? |
|
Definition
1) ensure adherence
2) can catch SE early |
|
|
Term
| What drug regimen should be given to all patients with a high clinical suspician for active TB? |
|
Definition
|
|
Term
| If after intial phase of therapy (@ 2 months), a TB patient has no cavitation on CXR & negative smear on AFB, what drug regimen should be given? |
|
Definition
inh/rif (or a derivative)
end Tx @ 6 mo. |
|
|
Term
| If after intial phase of therapy (@ 2 months), a TB patient has cavitation on CXR OR postive smear on AFB, what drug regimen should be given? |
|
Definition
inh/rif
can stop regimen @ 6 mo. if @ 4 mo. check there is no cavitation on CXR OR negative smear on AFB
can stop regimen @ 9 mo. if @ 4 mo. AFB is positive & CXR reveals caviatation |
|
|
Term
Patients on which of the following medications will need close monitoring of visual acuity?
A) rifampin
B) INH
C) PZA
D) Ethambutol |
|
Definition
|
|
Term
When a patient is on this DNA gyrase inhibitor, he will have to be counceled on separating his tablets from any multivitamins.
A) streptomycin
B) moxifloxacin
C) INH
D) PZA |
|
Definition
|
|
Term
Which of the following is routinely avoided in patients on HIV protease inhibitors?
A) rifampin
B) INH
C) PZA
D) Ethambutol |
|
Definition
|
|
Term
| What are the 3 stages of normal lung development? |
|
Definition
1) pseudoglandular
2) canalicular
3) alveolar/viable |
|
|
Term
| What is developing in the pasudoglandular stage of lung development? |
|
Definition
|
|
Term
| What gives rise to the lung bud @ about 4 weeks development? |
|
Definition
|
|
Term
| What happens to the lung bud after formation? |
|
Definition
| branching into the mass of mesenchyme |
|
|
Term
| When can lung lobes be distinguished? |
|
Definition
|
|
Term
| When is branching of the airways complete? |
|
Definition
|
|
Term
| When are mucus glands first seen in the lungs? |
|
Definition
week 8
growth proceeds proximally to distally until week 25 |
|
|
Term
| When are goblet cells first seen in the lungs? |
|
Definition
week 13
growth proceeds proximally to distally thru week 32 |
|
|
Term
| When do serous glands first sppear? |
|
Definition
|
|
Term
| When are cilia first seen in the lungs? |
|
Definition
large airways: 10 weeks
peripheral airways: 13-14 weeks |
|
|
Term
| Of the vasculature seen in the lungs, what arises first? |
|
Definition
| pulmonary veins => pulmonary arteries => bronchial arteries |
|
|
Term
| When are the pulmonary veins first seen? |
|
Definition
|
|
Term
| When are the pulmonary arteries first seen? |
|
Definition
|
|
Term
| When are the bronchial arteries first seen? |
|
Definition
|
|
Term
| When does the canalicular stage of lung development begin? |
|
Definition
| ~ week 16 w/ the completion of major bronchial & vascular development |
|
|
Term
| What 3 things develop in the canalicular period of lung development? |
|
Definition
1) resp. bronchioles
2) capillaries - surround terminal airways & grow from periphery in to out
3) **formation of alveolar duct & air sacs lines w/ precursor Type I & II alveolar cells |
|
|
Term
| When is the alveolar/viable stage of lung development? |
|
Definition
|
|
Term
| What is forming in the alveolar/viable stage of lung development? |
|
Definition
|
|
Term
| Why is it called the viable stage of lung development? |
|
Definition
| potential gas exchange surfaces gradually increase as cuboidal cells lining alveolar sacs gradually thin out & become closely associated w/ capillaries |
|
|
Term
| When are alveolar type II cells seen (i.e. surfactant producing cells)? |
|
Definition
| in the alveolar stage of lung development |
|
|
Term
|
Definition
| lipid product that lines the alveoli and decreased surface tension |
|
|
Term
|
Definition
| prevents collapse of alveoli on exhalation |
|
|
Term
| What does lack of surfactant in premature infants contribute to? |
|
Definition
|
|
Term
| How can lung maturity be assessed prenatally? |
|
Definition
determining the ratio of the phospholipids lecithin & sphingomyelin.
Lecithin INCREASES w/ maturity & sphingomyelin remains stable ∴ lecithin:sphingomyeline ratio INCREASES w/ maturity as well |
|
|
Term
| What 6 agents accelerate the maturation of the lungs? |
|
Definition
1) cortisone
2) stress
3) thyroxine
4) prolactin
5) theophylline
6) sympathomimetics |
|
|
Term
| What 3 agents decrease the rate of maturation of the lungs? |
|
Definition
1) insulin
2) metapyrone (steroid antagonist)
3) barbituates |
|
|
Term
| When does surfactant production begin? |
|
Definition
| w/ the onset of the alveolar stage of lung development ~ week 26-28 |
|
|
Term
| Why is the 3rd trimester so important in lung development? |
|
Definition
1) increased surfactant
2) development of resp. control systems (chemoreceptors, etc) |
|
|
Term
| How does vaginal birth help the infant take his/her first breath of air? |
|
Definition
| expels amniotic fluid from lungs & creates negative intrathoracic pressure for the first breath of air |
|
|
Term
| Why do alveoli remain open? |
|
Definition
| surfactant, which reduces surface tension that would otherwise force the alveoli to collapse |
|
|
Term
| Are alveoli mature at birth? |
|
Definition
| very few are true alveoli |
|
|
Term
| When does alveolar maturation complete? |
|
Definition
age 20
8-10 y: intentense proliferation
10-20 y: hypertrophy of alveoli |
|
|
Term
| When will congenital & airway malformation occur? |
|
Definition
| prenatal injury early in pregnancy when air branching & lung lobar structures are defined |
|
|
Term
| What are 5 possible congenital pulmonary & airway malformations? |
|
Definition
1) tracheo-esophageal fistula
2) absence of lung or lobe
3) accessory or extra lobes
4) cysts
5) sequestrations |
|
|
Term
| When does the insult occur that results in a tracheo-esophageal fistula? |
|
Definition
|
|
Term
def
tracheo-esophageal fistula |
|
Definition
| failure of separation of the esophageal & lung buds from the foregut => abnormal connection b/w the trachea & the esophagus |
|
|
Term
| What are the clinical problems seen with a tracheo-esophageal fistula? |
|
Definition
1) neonatal feeding difficulties
2) coughing w/ feeding - coughing up milk/formula
3) aspiration of feedings into airways (pneumonia) |
|
|
Term
| When does the insult occur that causes absence of a lung or lobe? |
|
Definition
|
|
Term
| What leads to the absence of a lung/lobe? |
|
Definition
| failure of airway budding into mesenchyme |
|
|
Term
|
Definition
| generally asymptomatic but can have reduced resp. reserves w/ trauma, surgery, or inf. |
|
|
Term
| What causes accessory or extra lobes of the lung? |
|
Definition
| variant of airway branching (not uncommon) |
|
|
Term
| What are 2 common accessory lung lobes? |
|
Definition
1) azygous lobe (R upper lung)
2) cardiac lobe (R lower lung) |
|
|
Term
Sx
accessory/extra lung lobes |
|
Definition
|
|
Term
| When does the insult occur to induce the formation of pulmonary cysts? |
|
Definition
|
|
Term
|
Definition
| abnormal detachment of lung tissue from primative airway buds |
|
|
Term
| How are pulmonary cysts connected to the bronchial tree? |
|
Definition
|
|
Term
|
Definition
1) poor clearance of mucus => infections
2) CXR shows persistent asp/infiltrate/pneumonia |
|
|
Term
| What supplies blood to the pulmonary cysts? |
|
Definition
|
|
Term
|
Definition
| early on, may not cause a problem, but with repeated or persistent inf, may need surgical removal |
|
|
Term
| When does the insult occur to cause pulmonary sequestration? |
|
Definition
|
|
Term
def
pulmonary sequestration |
|
Definition
| ectopic lung tissue w/ NO connection to the tracheobronchial tree |
|
|
Term
| What is the blood supply to any pulmonary sequestrations? |
|
Definition
|
|
Term
Sx
pulmonary sequestrations |
|
Definition
|
|
Term
| Why is surgical removal of pulmonary sequestrations more difficult than pulmonary cysts? |
|
Definition
|
|
Term
| Why was RDS (resp. distress syndrome) formally known as hyaline membrane disease? |
|
Definition
| due to the pathological finding of exudates of fibrinogen-containing material adherent to alveolar walls & terminal airways |
|
|
Term
|
Definition
| impaired/delayed surfactant synthesis => low lung compliance, atelectasis (collapse) & increased work of breathing => hypoxia => resp. acidosis => pulmonary HTN => cap. endothelial damage/leak => epi. necrosis |
|
|
Term
|
Definition
premature birth of weeks 26-30 weeks
slight male predominance
more frequent w/ diabetic mothers, asphyxia to infant, mother w/ bleeding
less common w/ intrauterine stress, maternal toxemia, heroin addicted mothers |
|
|
Term
| Why doesn't RDS occur in very premature infants (<24 weeks)? |
|
Definition
| no alveolar surface for gas exchange |
|
|
Term
|
Definition
1) birth: cyanosis
2) tachypnea, grunting, nasal flaring, chest wall retractions
3) worsening oxygenation & resp. acidosis over 24 hrs |
|
|
Term
|
Definition
1) supplemental oxygen
2) mechanical ventilation until: the infant's lungs mature & positive pressure keeps lungs open
3) other medical support (fluids, Abx, etc)
4) surfactant replacement (introduced intratracheally w/ generally good results) |
|
|
Term
| What complications can arise in RDS? |
|
Definition
| 1) lung injury due to high FIO2 (due to oxygen)
2) retrolental fibroplasias (blindness due to oxygen)
3) barotrauma w/ mechanical ventilation
4) chronic lung disease (fibrosis, pilmonary HTN) |
|
|
Term
| How is retrolental fibroplasias due to oxygen from RDS prevented? |
|
Definition
|
|
Term
|
Definition
1) prenatal care
2) corticosteroids - given 24 hrs before delivery to enhance/accelerate lung maturation |
|
|
Term
|
Definition
| sudden death of an infant or young child unexpected by Hx & unexplained by post-mortem evaluation |
|
|
Term
| What is the hypothesis for what causes SIDS? |
|
Definition
| brain stem development abnormalities or maturation delay => problems or neuroregulation & cardiac controls |
|
|
Term
| What pathological Sx are seen upon autopsy of a SIDS baby? |
|
Definition
1) pulmonary edema
2) petechiae
3) signs of chronic asphyxia
4) variety of brainstem abnormalities |
|
|
Term
| What are the theories of SIDS? |
|
Definition
| 1) poorly developed or abnormal brain stem controls of resp. => decreased chemoreceptor responses to CO2
2) poor control & decreased receptor input from upper airways => apneas
3) problem w/ sleep arousals |
|
|
Term
| What will be observes upon autopsy of a SIDS infant? |
|
Definition
| signs of chronic asphyxia & sublte brain leisons |
|
|
Term
| What are the maternal risk factors for SIDS? |
|
Definition
1) intrauterine hypoxia
2) fetal growth retardation
3) UTI
4) smoking
5) anemia
6) cocaine, heroin use
7) nutritional deficiency
8) less prenatal care
9) lower socioeconmonic status
10) young maternal age
11) increased placental weight
12) short inter-pregnancy interval
13) increasing parity |
|
|
Term
| What are the genetic risk factors of SIDS? |
|
Definition
blood type B
(not strongly familial - usually infanticide) |
|
|
Term
| What are the neonatal risk factors for SIDS? |
|
Definition
1) growth failure
2) asphyxia
3) prematurity |
|
|
Term
| What is the peak age for SIDS? |
|
Definition
| 2-4 mo. (rare after 6 mo.) |
|
|
Term
| What are the post-natal risk factors for SIDS? |
|
Definition
1) males >> females
2) bottle fed
3) heat stress
4) co-sleeping
5) recent febrile illness
6) smoke exposure
7) soft sleeping surface
8) swaddling
9) prone body position |
|
|
Term
| What do the risk factors for SIDS indicate? |
|
Definition
| high stress environment for parents & infants & a higher risk for child abuse |
|
|
Term
| Why has there been a dramatic decrease in SIDS deaths since 1992? |
|
Definition
1) supine sleeping position
2) recommended: no soft sleeping surfaces, no sleeping w/ parents, watch room temp. |
|
|
Term
| What further recommendations are currently in place to decrease SIDS risk? |
|
Definition
1) no pillows/soft matresses
2) no bumper pads
3) breast feeding
4) baby in parent's room (NOT bed) |
|
|
Term
| Is there currently any way to make the diagnosis of SIDS pre-mortem? |
|
Definition
|
|
Term
| Do infant apnea monitors help prevent SIDS? |
|
Definition
|
|
Term
| What seems to be the best means for prevention of SIDS? |
|
Definition
| family counseling & intervention in high risk situations |
|
|
Term
|
Definition
| inherited disorder involving the exocrine glands |
|
|
Term
| When do Sx of CF ususally appear? |
|
Definition
| during infancy or childhood (occasionally deferred until adolescece/adulthood) |
|
|
Term
|
Definition
| single gene mutation for the gene encoding CFTR protein |
|
|
Term
|
Definition
| cAMP regulated chloride channel |
|
|
Term
| What race is generally affected by CF? |
|
Definition
|
|
Term
|
Definition
GI:
meconium ileus, appendicitis, pancreatic insufficiency, cirrhosis
Resp:
recurrent inf., obstructive lung disease, bronchiectasis, fibrosis, resp. failure, hemoptysis
Reproductive tract:
male infertility |
|
|
Term
|
Definition
1) Hx (inc. family Hx)
2) PE
3) CXR
4) sweat chloride
5) genetic testing
6) pancreatic evaluation
7) PFTs |
|
|
Term
|
Definition
GI:
pancreatic enzymes, fat aoluble vitamins
Resp:
bronchodilators, postural drainage chest physiotherapy, Abx as needed
genetic counseling |
|
|
Term
| Why did death occur early in CF in the past? |
|
Definition
| progressive resp. insufficiency & malnutrition |
|
|
Term
| What is the life expectancy of a patient w/ CF? |
|
Definition
|
|
Term
| When were abnormalities of cilia able to be detected and correlated to clinical problems? |
|
Definition
|
|
Term
| What is the structure of normal cilia? |
|
Definition
1) outer tubule doublets (A & B tubules)
2) paur of central tubules
3) dynein arms from A microtubules to coordinate ciliary motion
4) nexin links b/a outer tubules
5) radial spokes connecting outer central tubules |
|
|
Term
| What are the 3 types of immotile cilia syndromes? |
|
Definition
I: classic kartagener's syndrome (lack of dynein arms)
II: defect of the radial spokes
III: transposition of the A & B outer microtubules |
|
|
Term
Sx
immotile cicial syndromes |
|
Definition
1) impaired/absent ciliary motion
2) recurrent/chronic inf. of upper & lower airways: sinusitis, nasal polyps, otitis media, bronchitis, bronchiectasis, pneumonia
3) immotile sperm flagella |
|
|
Term
Special Sx
Kartagener's Syndrome |
|
Definition
| situs inversus & dextrocardia |
|
|
Term
| Is lifespan shortened w/ immotile cilia syndromes? |
|
Definition
| w/ proper care, not appreciably |
|
|
Term
| When should you suspect someone has a immotile cilia syndrome? |
|
Definition
| any child or young adult w/ chronic or recurrent upper or lower RTIs, nasal polyps |
|
|
Term
Dx
immotile cilia syndrome |
|
Definition
perform CXR:
if dectrocardia, diagnose Kartagener's & confirm by evaluating motility of resp. cilia or sperm
if CXR NOT diagnostic:
consider anatomic obstruction, CF, immune deficiency, asthma
If none of the diagnoses can be made, suspect immotile cilia syndrome & check ciliary motion by LM & consider EM |
|
|
Term
| What are the organs that are affected by CF? |
|
Definition
1) primary: lung/sinuses & pancreas
2) others: sweat glands, intestines, liver, male GU |
|
|
Term
| What is the inheritance pattern of CF? |
|
Definition
| autosomal recessive ∴ carriers are asymptomatic |
|
|
Term
|
Definition
|
|
Term
| Of the 1800 mutations found at the CF gene, are all disease causing? |
|
Definition
|
|
Term
| Can mutations in CF gene only cause CF? |
|
Definition
| no, can cause other diseases |
|
|
Term
|
Definition
| variation present in at least 1% of the general posulations & may be associated w/ no disease at all |
|
|
Term
| Can disease cauing mutations be unique to an individual (i.e. only in that one person)? |
|
Definition
|
|
Term
| What is the most common mutation present in CF? |
|
Definition
| delta F508 (88% carrying at least 1 delta F508 mutation, and almost 1/2 being homozygous) |
|
|
Term
| What is the CF carrier frequency for caucasians? |
|
Definition
1/29
(less common in other racial groups) |
|
|
Term
|
Definition
| deletion (Δ) of 3 nucelotides in DNA => loss of aa phenylalanine @ position 508 |
|
|
Term
| What % of worlswide CF is in the US? |
|
Definition
|
|
Term
| Before 1950, what was the average life expectancy of a person w/ CF? |
|
Definition
|
|
Term
| What is the current life expectancy of a patient w/ CF? |
|
Definition
|
|
Term
| What does the CF gene code for? |
|
Definition
| CFTR protein (CF transmembrane regulator) |
|
|
Term
| Where does CFTR function? |
|
Definition
plasma membrane of epithelial cells lining the:
1) lung (inc. mucus producing submucosal glands)
2) pancreas
3) intestines
4) gallbaldder/liver
5) kidney tubule
6) salivary sweat glands
7) epididymis |
|
|
Term
|
Definition
1) cAMP dependent chloride conductance channel
2) regulator of other channels & transporters
3) regulates salt & water transport in plasma membranes |
|
|
Term
| What is the hypothesized structure of CFTR? |
|
Definition
1) 1480 aa
2) number of discrete globular & transmembrane domains |
|
|
Term
| What does activation of CFTR rely on? |
|
Definition
| phosphorylation (esp. thru kinase A) |
|
|
Term
| What governs CFTR channel activity? |
|
Definition
| 2 nucleotide binding domains that regulate channel gating |
|
|
Term
| What anchors the caroxyl terminal of CFTR? |
|
Definition
| PDZ type binding interaction w/ cytoskeleton |
|
|
Term
| Why is CFTR kept in close approximation to certain important proteins? |
|
Definition
proteins influence CFTR functions inc:
1) conductance
2) regulation of other channels
3) signal transduction
4) localization @ apical plasma membrane |
|
|
Term
| What is contained in each of the membrane-spaning domains of CFTR? |
|
Definition
| 6 membrane spanning alpha helixes, portions of which form the chloride conductance pore |
|
|
Term
| Where is the site of protein kinase A phosphorylation on CFTR? |
|
Definition
|
|
Term
| Where does the common ΔF508 mutation of CFTR occur? |
|
Definition
| on the surface of nucelotide-binding domain 1 (which remember regulates channel opening & closing) |
|
|
Term
| What abnormalities can be seen if there is a mutation in the CF gene? |
|
Definition
one or more of the following:
1) quantity of CFTR
2) processing of CFTR
3) trafficking of CFTR
4) function of CFTR
5) rate of turnover of CFTR |
|
|
Term
| What are the 6 classes of CFTR mutations? |
|
Definition
I: defective protein production
II: defective protein processing & trafficking
III: defective cAMP regulation of CFTR
IV: defective conductive pathway
V: abnormally spliced CFTR
VI: accelerated turnover of CFTR |
|
|
Term
| What defect is seen w/ ΔF508 mutation? |
|
Definition
| Class II: defective protein processing & ttrafficking |
|
|
Term
| What causes Class I: defective CFTR protein production? |
|
Definition
| CFTR is not produced b/c of a premature stop signal in the CFTR DNA (nonsense mutation) |
|
|
Term
Effect
ΔF508 mutation of CFTR |
|
Definition
| deletion of phenylalanine @ position 508 in 1st nucelotide binding fold of CFTR => improper folding of polypeptide => abnormal interaction w/ chaperone proterins in the ER & degradation of CFTR in ER => CFTR fails to arrive @ apical membrane |
|
|
Term
|
Definition
| protein fails to arrive at final destination |
|
|
Term
| What defects can be seen in Class II: defective CFTR protein processing & trafficking? |
|
Definition
1) folding
2) degradation & maturation thru ER
3) export from ER for further trafficking & maturation in Golgi
4) trafficking to cell durface
5) stabilization & recycling back to plasma membrane
6) functioning @ cell surface |
|
|
Term
Effect
Class III: defective cAMP regulation of CFTR chloride channel (resistance to mediators) |
|
Definition
reduced chloride transport
(aka a gating abnormality) |
|
|
Term
Effect
Class V: abnormally spliced CFTR |
|
Definition
| complete or partial reduction of normal CFTR protein (not a change in the functional characteristics of the channel) |
|
|
Term
| Where does Class VI: accelerated turnover of CFTR occur? |
|
Definition
|
|
Term
| What does airway defense depend on? |
|
Definition
| mechanical clearance of mucus from airway surfaces |
|
|
Term
| What does mechanical clearance of mucus from airway surfaces depend on? |
|
Definition
1) ion transport systems in airway epi.
2) secreted products (mucins) that for mucus layer
3) ciliary beating |
|
|
Term
| What are the 3 ion transport systems located in the apical airway epithelium? |
|
Definition
|
|
Term
|
Definition
| epithelial sodium channel |
|
|
Term
|
Definition
| control rate of transepithelial Na+ & volume absorption |
|
|
Term
|
Definition
| cAMP chloride conductance channel |
|
|
Term
|
Definition
| 1) confers the tonic (basal) Cl- conductance to airway epithelium
2) regulates other channels (down regulates Na+ channel & regulates CaCC) |
|
|
Term
|
Definition
| Ca2+ activated Cl- channel |
|
|
Term
|
Definition
|
|
Term
| What are the consequences of mutant CFTR on the airway environment? |
|
Definition
1) abnormal ion transport
2) decreased secretion of chloride
3) increased sodium reabsorption
4) relative impermeability to chloride
5)**decreased hydration of airway surface fluid (aka pericilliary liquid)
6) abnormal mucus that is thick & viscous
7) abnormal ciliary function |
|
|
Term
| How does the decreased hydration of airway surface fluid (aka pericilliary liquid) occur in CF? |
|
Definition
| initially volume of fluid is low, but bc the mucus continues to be produced, the end result is a gel |
|
|
Term
| Why is the mucus in CF patients thick & viscous? |
|
Definition
| CFTR is expressed in the cells of the submucosal glands as well as in the epithelial cells of the airway |
|
|
Term
| What occurs in the CF airway in regards to ions and their effects? |
|
Definition
1) hyperabsorption of sodium thru ENaC
2) low secretion of chloride via CFTR
3) relative impermeability to chloride
4) dehydration & abnormal properties of airway surface liquid
5) impairment of mucociliary clearance |
|
|
Term
| Does the lumen of a CF airway have a greater + or - charge? |
|
Definition
|
|
Term
| Why is the - lumen potential of CF airway useful? |
|
Definition
| forms the basis of of a diagnostic & research test (nasal potential difference) |
|
|
Term
| In normal airways, is sodium chloride absorbed or secreted from the airways? |
|
Definition
|
|
Term
|
Definition
| a measurement of the transepithelial potential difference |
|
|
Term
| Why is the lumen of normal airways negative? |
|
Definition
| relative impermeability of chloride compared to sodium |
|
|
Term
| What does it mean that the transepithelial potential difference is markedly hyperpolarized in CF? |
|
Definition
|
|
Term
| What are the 2 models to propose why the transepithelial potential difference is markedly hyperpolarized in CF? |
|
Definition
1) high salt model
2) low volume model |
|
|
Term
|
Definition
situation resembles sweat duct:
absence of CFTR => inability to reabsorb chloride ion from airway-surface liquid.
Since there is continued activity of sodium ion reabsorption, the airway surface negativity is increased
=> overall decreased reabsorption of NaCl |
|
|
Term
|
Definition
both sodium & chloride are hyperabsorbed:
airways of patients w/ CF are slightly less permeable to chloride ions than to sodium ions => increased transepithelial potential difference
=> predicts depletion of volume of airway-surface liquid |
|
|
Term
| What directly links the physiologic consequences of mutant CFTR to lung disease? |
|
Definition
| Direct link is still missing |
|
|
Term
| What indirectly links the physiologic consequences of mutant CFTR to lung disease? |
|
Definition
| 1) excess Na+ absorption & decreased Cl- secretion & continued mucus production => dehydrated surface liquid
2) abnormal airway mucus
3) abnormal mucociliary clearance
4) airway obstruction occurs
5) promotion of bacterial inf. (biofilms that protect bacteria, mucoid PSA) & may become chronic/impossible to eradicate
6) immune response => inflam.
=> lung destruction => bronchiectasis |
|
|
Term
| What produces an osmotic pressure in the lungs? |
|
Definition
|
|
Term
| What happens if osmotic pressure is greater in mucins than PCL? |
|
Definition
| water is drawn out of PCL to mucus & PCL collapses |
|
|
Term
| What is the classic CF phenotype (85-90% of CF patients)? |
|
Definition
1) chronic sino-pulmonary disease/inf., airway obstruction, bronchiectasis
2) GI & nutritional abnormalities
3) male infertility (obstructive uropathy)
4) salt loss syndromes |
|
|
Term
| Why is there a wide spectrum of CF phenotypes within a genotype? |
|
Definition
| Modifier genes (TGFβ1 => severe disease) |
|
|
Term
| How do genotypes differ in CF? |
|
Definition
1) some have less pancreatic insufficiency
2) less effect of genotype on lung disease, tho there is a mild lung disease
3) "non-classic CF"
4) non CF disorders - depend on quantity of function CFTR (pancreatitis, sinusitis, male infertility) |
|
|
Term
|
Definition
1) abnormal airway mucus
2) bacterial inf.
3) dyspnea
4) chronic inflam.
5) bronchiectasis, airway obstruction
6) digital clubbing
7) allergic bronchopulmonary aspergillosis
8) hemoptysis
9) pneumothorax
10) resp. failure or cor pulmonale |
|
|
Term
| What orgs. tend to inf. CF lungs? |
|
Definition
1) s. aureus
2) h. flu
3) PSA (mucoid & not)
4) burkholderia capacia
5) stenotrophomonas maltiphilia
6) alcaligenes xylosoxidans
7) aspergillus sp.
8) NTM (MAC & abscesses in particular) |
|
|
Term
| What type on inf. is seen in CF lung? |
|
Definition
1) new
2) persistent
3) transient
4) colonization |
|
|
Term
|
Definition
1) rare
2) resistant to Abx
3) can be associated w/ fetal sepsis syndrome in relatively healthy CF patients
4) transmission can occur b/w patients ∴ patients separated from those uninfected |
|
|
Term
|
Definition
1) airway clearance techniques
2) prevent persistent PSA inf by eradicating at first appearance
3) Tx acute pulmonary exacerbations
4) decrease bacterial load
5) Drugs
6) Lung transplant |
|
|
Term
Tx
CF
airway clearance techniques |
|
Definition
1) percussion & postural drainage
2) active cycle of breathing techniques
3) PEP (positive expiratory pressure)
4) autogenic drainage
5) oscillating flutter, acapella device
6) high frequency chest compression |
|
|
Term
| What drugs are used in the Tx of CF? |
|
Definition
1) Abx
2) Agents to change viscosity of mucus
3) Anti-inflam. agents
4) Azythromycin |
|
|
Term
| When are Abx used for CF patients? |
|
Definition
1) chronic suppressive
2) for exacerbations |
|
|
Term
Function
Azythromycin in CF |
|
Definition
not as a usual Abx:
1) improved lung function
2) decreases exacerbations
3) possible anti-inflam.?
4) possible effect on biofilm of PSA?
mech. unknown |
|
|
Term
| What nasal/sinus abnormalities are seen in CF patients? |
|
Definition
1) abnormal development (36% no prontal sinus or abnormally small)
2) CFTR associated ion transport abnormalities in nasal mucosa |
|
|
Term
| What are the CFTR associated ion transport abnormalities in nasal mucosa useful for? |
|
Definition
1) Dx of CF
2) determining efficacy in research protocols |
|
|
Term
|
Definition
1) radiologic evidence of pansinusitis
2) daily Sx less common
3) opacification on radiographs (doesn't confirm Sx are due to CF related sinusitis)
4) nasal polyps (~25% will have sympotomatic polyposis w/ high recurrence rate) |
|
|
Term
| What is the normal function of the pancreas? |
|
Definition
1) endocrine (insulin, glucagon, others)
2) exocrine (digestive enzymes, water & bicarb secretion) |
|
|
Term
|
Definition
1) exocrine pancreatic insifficiency (~85% of CF patients)
2) chloride & bicard secretion reduced (abnormal CFTR) => reduced ductal fluid secretion & protein precipitation in ducts
3) dilated ducts & loss of acinar cells |
|
|
Term
|
Definition
abnormal:
1) mucus
2) pH
3) bacterial overgrowth
4) motility
5) mixing |
|
|
Term
| What are the clinical manifestations of CF panceatic/GI disease? |
|
Definition
1) stool fat losses >7% of fat intake
2) steatorrhea, poor wt. gain
3) malabsorption of fat soluble vit.
4) gastritis, esophagitis, GE reflux (lack of bicarb)
5) meconium ileus in newborns, rectal prolapse, DIOS (inspissated intestinal contents in terminal ileum, cecum, colon)
6) CF related biliary cirrhosis
7) microgallbaladder
8) fibrosing colonopathy
9) colon cancer
10) megacolon, intussusception, volvulus
11) pseudomembranous colitis
12) DM
13) acute recurrent pancreatitis |
|
|
Term
Tx
CF pancreatic/GI disease |
|
Definition
1) pancreatic enzyme relacement therapy
2) suppression of gastric acid (to help enzymes work better & treat reflux)
3) osmotic agents for DIOS (distal intestinal obstructive syndrome)
4) motility promotors
5) nutritional support |
|
|
Term
| What nutritional support is needed in CF pancreatic/GI disease? |
|
Definition
1) high cal, high fat diet
2) food supplements (vit ADEK)
3) nocturnal tube feeding |
|
|
Term
| Why is nutritional support so important for CF patients? |
|
Definition
1) aggressive nutritional support is associated w/ better pulmonary function
2) CF patients have higher than normal resting energy expenditure
3) CF patients remain underweight, tho progress has been made |
|
|
Term
Tx
CF related biliary cirrhosis |
|
Definition
|
|
Term
| Why are CF patients susceptible to DM? |
|
Definition
| reduction of beta cell mass in pancreatic islets cause insulin deficiency |
|
|
Term
| What other complications can aise throughout the bosy in CF patients? |
|
Definition
1) osteroporosis
2) male infertility
3) heat exhaustion
4) increased renal clearance of drugs
5) hypertrophic pulmonary osteroarthropathy
6) episodis arthropathy (asymmetric, nonerosive, pupuric, skin leisons, fever) |
|
|
Term
| What test is performed to check for male infertility in CF patients? |
|
Definition
| semen analysis for azoospermia (absence of sperm) |
|
|
Term
| What causes male infertility in CF patients? |
|
Definition
CF obstructive azoospermia
where:
spermatogenesis is normal, but sperm cannot travel thru ducts b/c
1) duct system is absent or abnormal
2) congenital bilateral absence of vas deferens |
|
|
Term
|
Definition
1) sweat chloride measurement
2) genetic testing
3) nasal potential difference
(newborn screening is done) |
|
|
Term
def
sweat chloride measurement |
|
Definition
| using the pilocarpine iontophoresis method where ≥ 60 is abnormal |
|
|
Term
| What genetic testing is done to Dx CF? |
|
Definition
carrier testing, tho routine diagnostic tests don't test for most mutations
(there are tests that analyze the entire CF gene) |
|
|
Term
| Why isn't the nasal potential difference used often in Dx of CF? |
|
Definition
1) complicated
2) limited availability |
|
|
Term
| What made a physician suspicious of CF in the past? |
|
Definition
family Hx or Sx
(now there's newborn screening) |
|
|
Term
| What is needed for the diagnosis of CF? |
|
Definition
1) 2 known CF causing mutations
or
2) 2 sweat chloride levels ≥ 60 + any of the following:
+ Family Hx, + newborn screening test, thypical Sx/findings |
|
|
Term
What can cause intermediate sweat chloride values?
(30-59 in infants ≤ 6 mo; 40-59 in infants ≥ 6 mo) |
|
Definition
1) CF
2) non-classic CF
3) CFTR related disorders |
|
|
Term
| How do sweat ducts in patients w/ CF differ from those w/o disease? |
|
Definition
| differ in the ability to reabsorb chloride before emergence of sweat on the skin surface since a major pathyway for Cl= absorption is thru CFTR in the luminal plasma membranes of cells lining the duct |
|
|
Term
| What does diminised chloride reabsorption in the setting of continued sodium uptake lead to in sweat ducts? |
|
Definition
| elevated transepithelial potential difference across the wall of the sweat duct => lumen becoming more negatively charged b/c of failure to reabsorb chloride |
|
|
Term
| What is the result of an elevated transepithelial potential difference across the wall of the sweat duct & the negative lumen in a CF patient? |
|
Definition
| total sodium chloride flux is markedly decreased => increased salt content |
|
|
Term
| Why are sleep disorders important to diagnose as associated w/? |
|
Definition
1) impaired QOL
2) increased motor vehicle accidents
3) CV morbidity
4) increased health care costs |
|
|
Term
| Are sleep disorders over or under diagnosed? |
|
Definition
|
|
Term
| Why are sleep disorders under diagnosed? |
|
Definition
1) paucity of sleep education in medical curriculum
2) patient underreporting of sleep Sx |
|
|
Term
|
Definition
| gradual sensory perception shut down by the brain |
|
|
Term
|
Definition
| active brainstem, thalamic, subcortical, & cortical processes |
|
|
Term
| Is sleep an active or passive process? |
|
Definition
|
|
Term
| How does sleep need accumulate? |
|
Definition
|
|
Term
| What is the only way sleep need can be met? |
|
Definition
|
|
Term
| If someone sleeps more, do they end up needing less sleep? |
|
Definition
|
|
Term
| What can oppose the homeostatic drive to sleep & allow for consolidated wake? |
|
Definition
| biological clock (which is "on" ~ 16 hr/day) |
|
|
Term
| What happens when the biological clock is turned "off"? |
|
Definition
| allows for consolidated sleep (~8 hours) |
|
|
Term
| What is the homeostatic sleep drive proportional to? |
|
Definition
| amount of previous wake & sleep debt (sleep debt builds throughout the day) |
|
|
Term
Effects
alerting effects of biological clock |
|
Definition
1) oppose homeostatic drive to sleep
2) allow for consolidated wake during the day
(there is a mid-day dip of alterting activity) |
|
|
Term
| What are the 4 determinants of sleep? |
|
Definition
1) homeostatic sleep drive
2) biological clock
3) social/external factors
4) intrinsic illness |
|
|
Term
| What social/external factors are determinants of sleep? |
|
Definition
1) sleeping environment (noise, light, safety)
2) emotion (fear, anxiety, stress, elation, sadness)
3) effects of others (co-sleepers, infants/children)
4) drugs/medication |
|
|
Term
| What intrinsic illnesses are determinants of sleep? |
|
Definition
1) psychiatric (depression)
2) neurologic (dementia)
3) medical (pain, asthma, GERD, heart failure, pregnancy) |
|
|
Term
| What are the 2 types of sleep one gets each night? |
|
Definition
|
|
Term
| What are the characteristics of NREM? |
|
Definition
| 1) decreased metabolic rate w/ reduced minute ventilation, reduced tidal volume, no change in frequency, increased PaCO2
2) decreased HR (PS predominance) & BP
3) normal thermoregulation
4) decreased metabolic rate |
|
|
Term
| What are the 3 stages of NREM? |
|
Definition
|
|
Term
|
Definition
transition b/w wakefulness & sleep
(often perceive that you're still awake) |
|
|
Term
|
Definition
| true sleep in that thoughts are now short & fragmented |
|
|
Term
|
Definition
| slow wave sleep w/ little to no mentation |
|
|
Term
| What are the characteristics of REM? |
|
Definition
1) dreaming
2) REM
3) muscle atonia (except diaphragm)
4) instability of cardiopulmonary system: minute ventilation, HR, & BP remain below wake values but fluctuate widely in relation to REM
5) poikilothermic state
6) penile erection |
|
|
Term
|
Definition
|
|
Term
| What are the first 2 stages of sleep seen during the night? |
|
Definition
|
|
Term
| What are the 2 stages that predominate during the night? |
|
Definition
|
|
Term
| When does N3 predominate? |
|
Definition
| early part of night (amount decreases w/ age) |
|
|
Term
| When does REM first appear after sleep onset? |
|
Definition
| ~90-110 min after (1st one short, and increase w/ each cycle) |
|
|
Term
| How is sleep in childhood characterized? |
|
Definition
1) longer total sleep time
2) increased slow wave sleep
3) increased REM sleep |
|
|
Term
| How is sleep in the elderly characterized? |
|
Definition
1) decreased sleep efficiency
2) daytime napping
3) decreased slow wave sleep |
|
|
Term
|
Definition
| number of hours a person needs to feel alert/awake throughout the day (normally 7-8 hrs) |
|
|
Term
|
Definition
1) unstable/unreliable alterness & vigilance
2) cognitive slowing & time pressure increases errors
3) preformance declines w/ increasing rapidity
4) growing neglect of activities judged to be nonessential (loss of situlational awareness)
5) loss of perceptive abilities
6) involuntary sleep attacks begin to occur
7) risks of accidents & crashes increase |
|
|
Term
|
Definition
| daily activities & habits that are consistent w/ &/or promote the maintenance of good quality of sleep & full daytime alertness |
|
|
Term
| What are the parts of good sleep hygiene? |
|
Definition
1) develop regular sleep habits
2) slow down & unwind before bedtime
3) bedroom should be dark, cool, & quiet
4) daily exercise, best performed late afternoon
5) light snack before bedtime |
|
|
Term
| What are bad sleep habits? |
|
Definition
1) napping during the day
2) forcing self to sleep
3) taking problems to bed
4) strenuous mental/physical activities before bed
5) use of caffeine, EtOH or tobacco just before bed
6) reading, eating, or watching TV in bed |
|
|
Term
| What are the components of a good regular sleeo schedule? |
|
Definition
1) sleep as much as needed to feel refreshed/alter the next day
2) don't spend more time in bed than needed
3) keep a regular bedtime & wake (to strengthen circadian rhythm) |
|
|
Term
|
Definition
| difficulty initiating or maintaining sleep NOT secondary to other medica/psychiatric disorders |
|
|
Term
| What are some examples of insomnias? |
|
Definition
1) adjustment sleep disorder
2) psychophysiologic insomnia
3) limit-setting sleep disorder
4) sleep-onset association disorder
5) paradoxical insomnia
6) idiopathic insomnia
7) inadequate sleep hygeine |
|
|
Term
def
sleep-related breathing problems |
|
Definition
| abnormal breathing at night |
|
|
Term
| What are some examples of sleep-related breathing disorders? |
|
Definition
1) obstructive sleep apnea (adult or pediatric)
2) central sleep apnea (primary central sleep apnea, secondary to Cheyne Stokes breathing pattern) |
|
|
Term
def
hypersomnias not related to a breathing disorder |
|
Definition
| excessive daytime sleepiness w/o evidence of a breathing disorder |
|
|
Term
| What are some examples of hypersomnias not related to a breathing disorder? |
|
Definition
1) narcolepsy (w/ or w/o cataplexy)
2) insufficient sleep syndrome
3) iodiopathic hypersomnia w/ long or short sleep pattern
4) behaviorally induced insufficient sleep time |
|
|
Term
def
circadian rhythm disorders |
|
Definition
| misalignment b/w the patient's sleep pattern & that which is desired or regarded as the societal norm |
|
|
Term
| What are some examples of circadian rhythm disorders? |
|
Definition
1) shift work sleep disorder
2) time zone change syndrome
3) delayed sleep phase syndrome
4) advanced sleep phase syndrome
5) irregular sleep-wake type
6) free-running type |
|
|
Term
|
Definition
| clinical disorders that are undesirable phenomena that occur predominately during sleep |
|
|
Term
| Who are parasomnias more likely to affect? |
|
Definition
| bed partner than the patient |
|
|
Term
| Are parasomnias often more prominent in childhood or adulthood? |
|
Definition
|
|
Term
| What are some examples of parasomnias? |
|
Definition
1) arousal disorders (sleep walking, night terrors, confusional arousals)
2) associated w/ REM sleep (nightmares, sleep paralysis, REM behavior disorder)
3) other (sleep enuresis, sleep related dissociative disorders, sleep related groaning, exploding head syndrome, sleep related hallucinations, sleep related eating disorder) |
|
|
Term
def
sleep related movement disorders |
|
Definition
| abnormal movements during sleep |
|
|
Term
| What are some examples of sleep-related movement disorders? |
|
Definition
1) resless leg syndrome
2) bruxism
3) periodic limb movement disorder
4) sleep related leg cramps
5) sleep related rhythmic movement disorder |
|
|
Term
| Where does screening for sleep disorders being? |
|
Definition
|
|
Term
| What 4 screening questions for scleep disorders should all patients be asked during the ROS? |
|
Definition
1) how many of hours to sleep do you get a night?
2) do you have trouble falling asleep or staying asleep during the night?
3) are you excessively sleepy during the day?
4) do you snore? |
|
|
Term
|
Definition
| overnight study during which multiple body functions are monitored simultaneously |
|
|
Term
| What body functions are monitored in a polysomnography? |
|
Definition
1) EEG
2) EOGs (electrooculograms)
3) EMGs
4) ECG
5) airflow @ nose &/or mouth
6) resp. movements
7) pulse oximetry |
|
|
Term
Function
EEG
in polysomnography |
|
Definition
monitor brain electrical activity
stage sleep |
|
|
Term
Function
EOGs
in polysomnography |
|
Definition
monitor eye movements
stage sleep |
|
|
Term
Function
EMGs
in polysomnography |
|
Definition
1) chin: sleep staging
2) anterior tibialis: diagnosis of movement disorders |
|
|
Term
Function
ECG
in polysomnography |
|
Definition
| diagnose arrythmias during sleep |
|
|
Term
Function
airflow @ nose &/or mouth
in polysomnography |
|
Definition
| diagnose hypopneas/apneas |
|
|
Term
Function
resp. movements
in polysomnography |
|
Definition
| differentiation of apneas into subtypes |
|
|
Term
Function
pulse oximetry
in polysomnography |
|
Definition
| measure oxygen saturation during sleep |
|
|
Term
|
Definition
| persistent difficulty in initiating or maintaining sleep |
|
|
Term
| Is insomnia a symptom or a disorder? |
|
Definition
|
|
Term
| What are the 3 types of insomnia? |
|
Definition
1) transient
2) short-term
3) chronic |
|
|
Term
|
Definition
(adjustment sleep disorder)
insomnia lasting usually <1 week |
|
|
Term
| What normally precipitaes transient insomnia? |
|
Definition
| anxiety/emotion produing life event |
|
|
Term
|
Definition
| insomnia lasting up to several weeks |
|
|
Term
| What can precipitate short-term insomnia? |
|
Definition
| temporary stressful experiences or inability or adjust sleep-wake cycle to new needs |
|
|
Term
|
Definition
| insomnia lasting months to years |
|
|
Term
| What can precipitate chronic insomnia? |
|
Definition
|
|
Term
| Who is most likely affected by insomnia? |
|
Definition
|
|
Term
| What are the common causes of insomnia? |
|
Definition
1) inadequate sleep hygiene
2) disruptive or irregular sleep-wake cycles
3) extended use of sleep medication or other sleep disruptive drugs
4) excessive EtOH intake
5) medical causes |
|
|
Term
| What are common medical causes of insomnia? |
|
Definition
1) onstructive sleep apnea
2) restless leg syndrome/periodic leg movement disorder
3) circadian rhythm disorders
4) chronic pain
5) GE reflux
6) psychiatric illness, esp. mood & anxitey disorders |
|
|
Term
|
Definition
1) nocturnal: delayed sleep onset, early morning awakening, multiple prolonged awakenings, insufficient sleep time
2) daytime: being unrefreshed in mornin &/or throughout day, feeling fatigued or sleeping during the day w/ inability to nap, poor concentration, poor attentiveness, & poor memory |
|
|
Term
| What is the importance of daytime complaints of insomnia? |
|
Definition
| necessary for insomnia to be a disorder rather than a complaint |
|
|
Term
| What are the consequences od insomnia? |
|
Definition
1) impairments in daytime function
2) poor school/job performance
3) impairments in interpersonal relationships
4) impaired driving skills
5) self medication |
|
|
Term
| What is insomnia ususally the result oof interaction b/w? |
|
Definition
| interaction of biological, physicial, psychological & environmental factors |
|
|
Term
def
hyperarousal theory of insomnia |
|
Definition
1) insomniacs have a generalized disorder of hyperarousability
2) poor sleep is the nighttime manifestation of this disorder & not necessarily the cause of the daytime dysfunction
(normals thrown into induced insomnia resemble sleep deprivation and more resemble insomniacs if given caffeine) |
|
|
Term
| Do insomniacs have higher or lower rates of depression/anxiety compared to normals? |
|
Definition
|
|
Term
| Do insomniacs score higher or lower on scales of arousal than normals? |
|
Definition
|
|
Term
| Do insomniacs have higher or lower night to night variability in their sleep compared to normals? |
|
Definition
|
|
Term
| Do insomniacs have more or less EEG activity at sleep onset than normals? |
|
Definition
|
|
Term
| Do insomniacs have an increased or decreased metabolic rate compared to normals? |
|
Definition
|
|
Term
def
cognitive theory of insomnia |
|
Definition
1) patients prone to rumination
2) increased problem solving leading to sleeplessness
3) once insomnia become chronic, they worry about sleep all day
4) individual beliefs/attitudes moderate propensity to worry |
|
|
Term
def
behavioral theory of insomnia
stimulus control model |
|
Definition
| normal cues associated w/ sleep become associated with wakefulness has predisposing factos and are percieved as reasonable & successful |
|
|
Term
def
behavioral theory of insomnia
chronic insomnia |
|
Definition
1) all insomniacs have predisposing factors
2) insomnia begins w/ a precipitaing factor
3) insomnia becomes chronic w/ onset of perpetuating factors and conditioned arousals which are the target of cognitive behavioral therapy |
|
|
Term
| What are the 4 components that contribute to insomnia? |
|
Definition
1) physiological factors
2) psychological factors
3) behavioral factors
4) cognitive factors |
|
|
Term
| What phsyiologic factors contribute to insomnia? |
|
Definition
| 1) heightened autonomic arousal
2) increased metabolic rate/TB
3) HPA dysregulation
4) immune dysfunction |
|
|
Term
| What psychological factors contribute to insomnia? |
|
Definition
1) anxiety
2) dysphoria
3) somatized tension
4) hypersensitivity
5) over-responsiveness to stress |
|
|
Term
| What behavioral factors contribute to insomnia? |
|
Definition
1) poor sleep hygiene
2) condistioned arousals |
|
|
Term
| What cognitive factors contribute to insomnia? |
|
Definition
1) excessive cognitive activity
2) excessive problem solving |
|
|
Term
| What is the most common promary insomnia? |
|
Definition
| psycophysiological insomnia |
|
|
Term
| What are the key characteristics of psychophysiologic insomnia? |
|
Definition
1) disorder of somatized tension & learned sleep-preventing associations
2) stimuli surrounding bedtime become conditioned triggers to arousal
3) patient makes great efforts to fall asleep unaware of the effect of this effort on causing arousal
4) sleepy until betime routine starts
5) frequent racing thoughts once in bed
6) tried to force self asleep/feels tense in bed
7) worries about getting to sleep all day
8) sleeps better on couch or away from home |
|
|
Term
def
excessive daytime sleepiness |
|
Definition
| sleepiness at times other than normal mid-afternoon sleepiness or during situations in which alertness is warranted is abnormal. (sleepy NOT fatigued, laving in energy or depressed) |
|
|
Term
def
physiological sleep tendency |
|
Definition
| tendency for sleep to occur in absence of alerting factors |
|
|
Term
def
manifest sleep tendency |
|
Definition
| changes moment to monent depending on host factors s.a. light, noise, motivation, recumbency |
|
|
Term
| Does reduction of impinging stimuli unmask or cause physiological sleep tendency? |
|
Definition
|
|
Term
| What are the determinants of physiological sleepiness? |
|
Definition
1) quantity of sleep
2) quality of sleep
3) circadian rhythms
4) drugs
5) CNS |
|
|
Term
def
truly alert individual |
|
Definition
| does not feel or appear to be sleepy when placed in a low stimulus environment |
|
|
Term
| What are drugs are common determinants of physiological sleepiness? |
|
Definition
1) antihistamines
2) bonzos & other sedative-hypnotics
3) antidepressants
4) neuroleptics
5) anticonvulsants
6) narcotics |
|
|
Term
| What are the consequences of excessive daytime sleepiness (EDS)? |
|
Definition
| problems in vigilance, cognitive function, memory/concentration, mood => problems in school/job performance, social relationships/family life, driving skills |
|
|
Term
|
Definition
1) insufficient sleep
2) social/external factors
3) fregmented sleep
4) circadiam rhythm disruption
5) medication
6) primary sleep disorders |
|
|
Term
def
multiple sleep latency test (MSLT) |
|
Definition
| objective test of sleepiness that measures the tendency to fall asleep while lying a quiet, dark bedroom @ 4 times during the day - removes alterting factors & thus enables the underlying (physiologic) sleep tendency to be measured |
|
|
Term
| What is normal daytime sleep latency? |
|
Definition
| >15 min in well rested adults (should be no REM in a 20 min nap) |
|
|
Term
| What is pathologic sleep latency? |
|
Definition
|
|
Term
| What is the MSLT most useful for? |
|
Definition
| diagnosing narcolepsy (narcoleptics have at least 2 naps w/ REM sleep) |
|
|
Term
def
epworth sleepiness scale (ess) |
|
Definition
| a simple questionnaire designed to meaure the general level of excessive daytime sleepiness or sleep propensity in adults (quantifies subjective sleepiness). |
|
|
Term
|
Definition
| measure EDS that persists from week to week or longer in a given subject, independent of changes in time and from day to day, similar to MSLT |
|
|
Term
|
Definition
measures the chance of dozing off in 8 situations that most asults have found themselves in during the last month s.a. sitting and reading, watching TV, sitting, inactive in a public place, as a passenger in a car for an hour w/o a break, lying down to rest in the afternoon, sitting and talking w/ someone, sitting quietly after lunch, in car while stopped in traffic for a few minutes
(scores less than 10 considered normal, the higher the score indicates a greater propensity to fall asleep on MSLT, but doesn't correlate w/ falling asleep faster) |
|
|
Term
| What is the ESS score useful for? |
|
Definition
| tracking patient's EDS Sx (score decreases w/ Tx) |
|
|
Term
| What is on the differential Dx list for EDS? |
|
Definition
1) behaviorally induced insufficient sleep
2) obstructive sleep apnea
3) narcolepsy
4) resless lef syndrome/periodic leg movement disorder
5) disorders of the sleep-wake cycle: shift work, sleep phase delay syndrome, jet lag
6) drugs: antihistamines, narcotics, anti-seizure medications, neuroleptics, sedative-hypnotics |
|
|
Term
| What is the ventilatory response during sleep? |
|
Definition
| ventilatory response to both CO2 & O2 decrease during NREM & REM |
|
|
Term
|
Definition
| PaCO2 level below which a subject will become apneic during NREM sleep |
|
|
Term
| Is the apneic threshold phenomenon seen during wakefulness & REM? |
|
Definition
not suring wakefulness
rearely during REM |
|
|
Term
| What does a higher apneic threshold indicate? |
|
Definition
| greater propensity to sleep-disordered breathing |
|
|
Term
| Do men or women have higher apneic thresholds? |
|
Definition
|
|
Term
| Do patients w/ sleep apnea patients have a higher or lower apneic threshold than normal subjects? |
|
Definition
|
|
Term
| What is the ventilatory pattern in N1 sleep? |
|
Definition
| can be irregular w/ periodic breathing |
|
|
Term
| What is the ventilatory pattern in N2 sleep? |
|
Definition
|
|
Term
| What is the ventilatory pattern in REM sleep? |
|
Definition
| irregular breathing in association w/ REM |
|
|
Term
| What happens to tidal volume, minute ventilation, & breathing frequency during sleep? |
|
Definition
1) tidal volume decreases
2) minute ventilation decrease
3) no change in breathing frequency |
|
|
Term
| What happens to metabolic rate & PaCO2 during sleep? |
|
Definition
| metabolic rate decreased
PaCO2 increase |
|
|
Term
| What is the effect of sleep on the upper airway? |
|
Definition
1) dilator activity decreases (esp in REM)
2) decreased upper airway dilator response to negative pressure
3) decreased upper airway caliber => increased upper airway resistance, increased compliance & collapsibility |
|
|
Term
| What does the loss of wakefulness drive to breath cause? |
|
Definition
1) failure to compensate for loads
2) decreased pump muscle activity
3) decreased upper airway dilator activity |
|
|
Term
| What does increased upper airway resistance (due to decreased upper airway dilator acitivity, failure to compensate for loads, & decreased pump muscle activity cause? |
|
Definition
| decreased tidal volume => increased PaCO2 |
|
|
Term
| What characterizes obstructive sleep apnea? |
|
Definition
| recurrent episodes of upper airway collapse & obstruction during sleep |
|
|
Term
| What are the episodes of obstruction in obstructive sleep apnea associated w/? |
|
Definition
| recurrent oxyhemoglobin desaturations & arousals from sleep |
|
|
Term
def
obstructive sleep apnea syndrome (OSAS) |
|
Definition
| obstructive sleep apnea associated w/ daytime sequelae |
|
|
Term
| How is obstructive sleep apnea diagnosed? |
|
Definition
|
|
Term
| What can identify apneas & hypoapneas in polysomnography? |
|
Definition
| combining airflow & resp. movements |
|
|
Term
|
Definition
| complete cessation of airflow for 10 seconds |
|
|
Term
|
Definition
| persistent ventilatory effort seen |
|
|
Term
|
Definition
|
|
Term
|
Definition
| 20-50% reduction in airflow associated w/ either an arousal or 2-4% drop in oxygen saturation |
|
|
Term
def
apnea-hypoapnea index (AHI) |
|
Definition
| the total number of apneas & hypoapneas divided by the total sleep time for a whole night |
|
|
Term
|
Definition
|
|
Term
| How does AHI determine the severity of obstructive sleep apnea? |
|
Definition
1) mild: 5-15
2) moderate: 16-30
3) severe: >30 |
|
|
Term
| Is obstructive sleep apnea genetic? |
|
Definition
| there is evidence of a familial tendency (independent of familial obesity) |
|
|
Term
| Who tends to be affects be obstructed sleep apnea? |
|
Definition
|
|
Term
| What conditions are often associated w/ obstructive sleep apnea? |
|
Definition
1) obesity
2) adenotonsillar hyperplasia (esp. children & young adults)
3) hypothyroidism
4) craniofacial skeletal abnormalities (retrognathia, micrognathia) |
|
|
Term
| What craniofacial structure differences are seen in a patient w/ obstructive sleep apnea? |
|
Definition
1) smaller airway dimentions
2) mandibular retrognathia
3) decreased posterior airspace
4) inferiorly placed hyoid bone
5) increased soft palate length/dimentions |
|
|
Term
| What can change the surrounding pressure in obstructive sleep apnea? |
|
Definition
1) tongue
2) tonsils
3) pharyngeal fat |
|
|
Term
| How is the upper airway anatomy different in a patient w/ obstructive sleep apnea? |
|
Definition
1) upper airway is smaller
2) volume of the tongue, lateral pharyngeal walls, & total soft tissue are larger
3) increased soft palate length & inferiorly placed hyoid bone
4) structures that surround the upper airway s.a. the tonsils are enlarged |
|
|
Term
| What happens to the central control of breathing in a person w/ obstructive sleep apnea? |
|
Definition
| abnormal control of breathing during sleep => increased propensity to develop central apnea (increased apneic threshold) |
|
|
Term
| What is the pathophysiological process of central apnea/hypopnea? |
|
Definition
| hyperventilation => hypocapnea => central apnea/hypopnea (due to predisposing factors) |
|
|
Term
| How does central apnea/hypopnea initial continual central apnea/hypopnea? |
|
Definition
| => pharyngeal narrowing/occlusion & hypoxia
pharyngeal narrowing/occlusion (caused by predisposing factors) => mucosal adhesion => apnea prolongation => increased PaCO2 & hypoxia
hypoxia & increased PaCO2 => arousal => hyperventilation |
|
|
Term
| What are the consequences of obstructive sleep apnea? |
|
Definition
1) EDS
2) CV morbidity
3) mortalilty |
|
|
Term
| What CV morbidities are consequences of obstructive sleep apnea? |
|
Definition
1) HTN
2) metabolic syndrome (esp. insulin resistance)
3) heart disease (L ventricular hypertrophy & diastolyic dysfunction)
4) cerebrobascular disease (stroke)
5) pulmonary HTN & R sided heart failure (uncommon unless evidence of lung disease &/or daytime hypoxemia) |
|
|
Term
Sx
obstructive sleep apnea |
|
Definition
1) while asleep: snoring (habitual, loud, irregular, bothersome to bed partner/others in house), gasping/snorting, witnessed apneas, sudden/jerky body movements, resless sleep
2) while awake: wake up feeling non-refreshed, morning headache, morning dry/sore throat, EDS, personality change, problems with memory/concentration |
|
|
Term
| When should patients be screened for obstructive sleep apnea, HTN, DM, & hyperchloesteremia? |
|
Definition
|
|
Term
Tx
mild obstructive sleep apnea |
|
Definition
conservative measures s.a.
1) weight loss (min. 10-15% drop in body weight)
2) EtOH avoidance 4-6 hrs prior to bed
3) sleeping on side (worse on back)
4) Tx of sinus Sx |
|
|
Term
Tx
obstructive sleep apnea |
|
Definition
1) conservatice measures
2) CPAP
3) dental devices
4) surgery |
|
|
Term
| How does CPAP (continuous positive airway pressure) work? |
|
Definition
| splinting the upper airway, preventing the soft tissues from collapsing |
|
|
Term
| Is CPAP effective at treating obstructive sleep apnea? |
|
Definition
| shown to improve daytime sleepiness, mood, cognitive performance, QOL, modify inflam./metabolic abnormalities associated w/ metabolic syndrome |
|
|
Term
| What is the problem w/ CPAP Tx for obstructive sleep apnea? |
|
Definition
| compliance (esp. long term) |
|
|
Term
| How do dental devices work in obstructive sleep apnea? |
|
Definition
| moving tongue/mandible forward (w/ better compliance than CPAP) |
|
|
Term
| When is surgical Tx the option for obstructive sleep apnea? |
|
Definition
1) always in patients w/ a correctible abnormality
2) otherwise, considered second or third option b/c of overall success rates |
|
|
Term
| What 2 questions should be in the ROS for ALL patients (not just obese patients) to screen for sleep apnea? |
|
Definition
1) Do you snore?
2) are you sleepy during the day? |
|
|
Term
| What are the characteristics of narcolepsy? |
|
Definition
1) irresistible episodes of sleep of short duration
2) inappropriate intrusion of REM sleep into a person's waking hours |
|
|
Term
| Are men or women more affected by narcolepsy? |
|
Definition
|
|
Term
| What is the usual age of onset of narcolepsy? |
|
Definition
|
|
Term
| What is the pathophysiology of narcolepsy? |
|
Definition
| specific HLA hapolotypes (tho minimal evidence that it's auto-immune) |
|
|
Term
| What neurons are associated to be lost in narcolepsy? |
|
Definition
| hypocretin neurons in hypothalamus |
|
|
Term
Function
hypocretin neurons in hypothalamus |
|
Definition
| control/coordinate other wake centers in the brain |
|
|
Term
|
Definition
1) EDS (sleep attacks irresistible & unwanted, usually followed by a refractory period)
2) cataplexy
3) sleep paralysis
4) hypnagogic hallucinations
5) automatic behavior
6) disturbed nocturnal sleep w/ frequent awakenings |
|
|
Term
|
Definition
| sudden brief loss of muscle control (mild or severe) usually precipitated by strong emotions s.a. laughter, surprise, anger |
|
|
Term
|
Definition
| feeling totally paralyzed even tho awake |
|
|
Term
def
hypnagogic hallucinations |
|
Definition
| extrememly vivid dreams while going to sleep |
|
|
Term
|
Definition
| wake up & realize were actively doing something s.a. driving, writing, cooking |
|
|
Term
| What 2 tests are done to diagnose narcolepsy? |
|
Definition
1) polysomnography
2) multiple sleep latency exam
(make sure to do a careful history) |
|
|
Term
| What does it mean that cataplexy is pathognomonic of narcolepsy? |
|
Definition
| it's a destinctive characteristic of it (seen in 80%) |
|
|
Term
| What is characteristically seen on a polysomnography of a narcoleptic? |
|
Definition
| decreased latency to REM (< 60 min) w/ frequent awakenings for no apparent reason |
|
|
Term
| What are the results of the multiple sleep latency exam characteristically seen in narcoleptics? |
|
Definition
| mean sleep latency < 5 min w/ 2 or more REM periods w/in 10 min of sleep onset |
|
|
Term
Tx
EDS associated w/ narcolepsy |
|
Definition
| stimulants s.a. modafinil, armodafinil, methylpenidate, & dextroamphetamine |
|
|
Term
Tx
cataplexy associated w/ narcolepsy |
|
Definition
tricyclic antidepressants s.a. protryptyline, imipramine
OR
SSRIs s.a. flyoxetine or sertraline
sodium oxybate
(agents that decrease REM sleep) |
|
|
Term
Tx
behavioral Tx of narcoleptic |
|
Definition
avoidance of triggers
short scheduled naps
optimize nocturnal sleep hygeine
education of patient/family/employer |
|
|
Term
| What is the prognosis of narcolepsy? |
|
Definition
it's a life-long disease
long-term, it's associated w/ emotional, psychological, social & financial consequences |
|
|
Term
| How does restless leg syndrome often present itself? |
|
Definition
| as insomnia (usually), but also EDS |
|
|
Term
| Who is more likely to be affected by restless leg syndrome? |
|
Definition
|
|
Term
| What are the characteristic features of restless leg syndrome? |
|
Definition
1) urge to move, usually due to uncomfortable senstations (esp. in leg)
2) motor resltessness expressed as activity (walking) that can relieve the urge to move
3) worsening Sx by relaxation; improved if legs move
4) day to day variablity but generally wose in evening/early night |
|
|
Term
| Is resltess leg syndrome genetic? |
|
Definition
| yes (~50% have some familial Hx => earlier onset) |
|
|
Term
|
Definition
1) +Family Hx
2) presence of periodic limb movements during sleep
3) response to dopaminergic therapy |
|
|
Term
| What conditions are associated with resltess leg syndrome? |
|
Definition
1) iron deficiency (esp. ferritin <50)
2) renal insufficiency
3) pregnancy
4) Parkinson's disease |
|
|
Term
|
Definition
1) DA agonist (ropirinole, pramipexole, levodopa)
2) opiates (oxycodone, propoxyphene)
3) anticonvulsants (gabapentin encarbil) |
|
|
Term
| What is seen pathologicially in pulmonary edema of the newborn? |
|
Definition
| alveolar spaces are filled w/ granular, eosinophilic material |
|
|
Term
| Where might a thromboembolus be seen? |
|
Definition
| in an artery & may propagate into arterial branches |
|
|
Term
| What is seen pathologicially in a pulmonary infarct? |
|
Definition
| pyramid shaped w/ base at pleural surface & hemorrhagic |
|
|
Term
| How is the pulmonary infarct characterized microscopically? |
|
Definition
| by diffuse hemorrhage, apparently obliterating remnants of necrotic alveolar septae |
|
|
Term
| What happens to an embolus over time? |
|
Definition
| may disappear thru fibrolytic mechs or organize |
|
|
Term
| What can form if an embolus organizes? |
|
Definition
| can form an eccentric fibrous intimal plaque or completely fill the arterial lumen & become renalalized |
|
|
Term
| How can hypoxic pulmonary parenchymal disease cause pulmonary HTN? |
|
Definition
| obliteration of portions of the pulmonary circulation by multiple emboli or by heart disease and be called secondary |
|
|
Term
| When is pulmonary HTN primary? |
|
Definition
| if it occurs in the lungs w/ normal parenchyma, perfused by a normal heart |
|
|
Term
| What does the chronic elevation of pulmonary arterial pressure cause? |
|
Definition
1) changes in systemic vessels subject to HTN
2) arterial lumen compromised by arterial thickening
3) result of cellular proliferation & fibrosis of the intima & hyoerplasia of the medial sm. muscle |
|
|
Term
| What leison is unique to pulmonary HTN? |
|
Definition
| angiomatoid body or plexiform leison |
|
|
Term
def
angiomatoid body or plexiform leison |
|
Definition
| large thin walled vessels w/ internal septae arise as branches of severely sclerotic muscular pulmonary arteries (indicative of pulmonary HTN of a severe degree) |
|
|
Term
| What leads to hypertrophy of the R ventricle? |
|
Definition
|
|
Term
| What happens to the thickness of the R ventricle in hypertrophy of the R ventricle? |
|
Definition
| ~ same size as the L ventricle |
|
|
Term
| When will RDS (resp. distress syndrome) develop? |
|
Definition
| neonates born before the maturation of their surfactant system |
|
|
Term
| What is the key morphologic finding in the lungs of infants w/ RDS? |
|
Definition
widespread atelectasis (collapse of alveoli)
(also seen is epithelial necrosis, mixing of necrotic debris w/ blood proteins => eiosinophilic hyaline membranes which line the alveolar ducts) |
|
|
Term
def
centrilobular emphysema |
|
Definition
terminal bronchiole is surrounded by large abnormal air spaces created by destruction of the alveolar septae.
Alveolar air spaces in periphery of the lobules are of normal size |
|
|
Term
| Where is centrilobular emphysema most severe? |
|
Definition
|
|
Term
|
Definition
alveolar wall destruction occurs throughout the lobule so that all the alveoli (from resp. bronchiole to those at lobule periphery) are enlarged
(leisons are throughout the lung, unlike centrilobular which are at the upper lobe, and tend to be more severe at the base of the lung) |
|
|
Term
| How is chronic bronchitis diagnosed? |
|
Definition
| clinically on the basis of chronic cough & sputum production |
|
|
Term
| What is the morphologic change in chronic bronchitis that leads to increased production of sputum? |
|
Definition
|
|
Term
| How is mucous gland hyperplasia measured? |
|
Definition
| Reid index (rario of C/W) |
|
|
Term
| Are inflammatory changes in chronic bronchitis more or less significant than the gland changes? |
|
Definition
|
|
Term
|
Definition
| the walla of the small noncartilagenous airways (bronchioles) are thickened by chronic inflam. & fibrosis => obstruction to air flow (tho not percieved by patient unless widespread) |
|
|
Term
| What plays a role in emphysema, mucous gland hyperplasia, & small airway disease? |
|
Definition
| smoking (∴ all 3 generally occur in the same patient) |
|
|
Term
|
Definition
| disease characterized by recurrent episodes of reversible airway obstruction dur to contraction of bronchial sm. muscle & inflam. infiltrates |
|
|
Term
| When can mucus plugging occur with asthma? |
|
Definition
| in severe cases (& can be fatal since they fill the branching bronchi) |
|
|
Term
| What is contained in mucus plus of asthmatics microscopically? |
|
Definition
| eosinophils & macs embedded in mucus |
|
|
Term
| What epithelial changes are seen microscopically in asthma? |
|
Definition
| increased goblet cells & very thick BM |
|
|
Term
| What doess the purulent material in lobar pneumonia contain? |
|
Definition
| in bacterial pneumonia, alveoli fill with blood derived fluid, neurtrophils, bacteria => necrotic debris (components of purulent exudate) |
|
|
Term
|
Definition
| alveoli are primarily infected & fill w/ acute inflam. exudate (bronchus unaffected) |
|
|
Term
| When can the pleural cavity become involed in the pneumonia? |
|
Definition
| if the pneumonic alveoli butt up against the pleural surface |
|
|
Term
| What results from the pleural cavity becoming involved with the pneumonia if the causative agents are contained by the visceral pleura? |
|
Definition
|
|
Term
|
Definition
| inf. of the pleural cavity |
|
|
Term
|
Definition
| if the causative org. of pneumonia is not contained by the viseral pleura => pluearal cavity becomes infected & pus can be found on the pleural surface |
|
|
Term
| Where does the primary inf. occur in bronchopenumonia? |
|
Definition
| small bronchi & bronchioles & spread to adjacent alveoli |
|
|
Term
| Why are the alveoli involed in bronchopneumonia more pale the surrounding parenchyma? |
|
Definition
| they are filled w/ inflam. exudate |
|
|
Term
| What type of process is bronchopneumonia usually? |
|
Definition
|
|
Term
|
Definition
| destructive alterations in bronchial walls so that the bronchi become ectatic (dilated) |
|
|
Term
|
Definition
| bronchi w/ cartilage in their walls surrounded by dense fibrous tissue (instead of alveoli) |
|
|
Term
| What distinctive changes are seen w/ viral pneumonia? |
|
Definition
| alveolar epithelial destruction accompanied by exudation of blood plasma |
|
|
Term
| What does the exuded blood plasma in viral pneumonia form? |
|
Definition
pink, granular edema fluid that fill many alveoli => form hyaline membranes
(response is minimal except around bronchi) |
|
|
Term
| What characteristic cytopathic changes in epithelial cells can viral pneumonia cause? |
|
Definition
| giant cells with eosinophilic intranuclear & cytoplasmic inclusions |
|
|
Term
| Are pulmonary fungal infections invasive or non-invasive? |
|
Definition
|
|
Term
| What fungus has the propensity to grow into a fungus ball contained w/in a pre-existing cavitary leison? |
|
Definition
|
|
Term
| What does aspergillus look like microscopically? |
|
Definition
|
|
Term
| When are pulmonary invasive fungal inf. more likely to be seen? |
|
Definition
|
|
Term
| What does mucor look like microscopically? |
|
Definition
| branched, non-septae hyphae |
|
|
Term
| Where is coccidioidomycosis immitis endemic to? |
|
Definition
|
|
Term
|
Definition
result of prolonged, pregressive inflam. destruction in a region of the lung, almost invariably associated w/ total destruction of the corresponding airway
(can be bacterial or fungal) |
|
|
Term
| What host cells are the early responders to bacterial inf? |
|
Definition
|
|
Term
| What are the predominant inflam. cell in pulmonary TB? |
|
Definition
|
|
Term
| What do the macs form in pulmonary TB in response to tuberculi bacillus? |
|
Definition
|
|
Term
| What surrounds the periphery of a granuloma? |
|
Definition
|
|
Term
|
Definition
| cytoplasmic fusion of macs |
|
|
Term
| What causes the caseous necrosis typical of TB? |
|
Definition
| centrally located macs die & release intracellular enzymes => act on debris from destruction of host tissue & invading bacilli |
|
|
Term
| What tends to rim around the outer lymphocyte rim of a granuloma? |
|
Definition
|
|
Term
| What stain is used to ID tuberble bacillus? |
|
Definition
|
|
Term
|
Definition
| peripheral pulmonary granulomatous leison w/ a similar leison in the hilar lymph nodes |
|
|
Term
| What is secondary (actice) TB often the result of? |
|
Definition
| reactivation of a primary inf |
|
|
Term
| Where are reactivation TB inf. most often seen? |
|
Definition
| near the apex of the lung |
|
|
Term
| How does miliary TB form? |
|
Definition
spread of bacilli from large fibrocaseous, cavitating focus in the apex => many small miliary tubercles throughout the parenchyma (due to seeding of the org thru the blood)
usually involves many organs |
|
|
Term
|
Definition
| multisystem disease of unknown cause & can cause enlargement of hilar lymph nodes & disease w/in the pulmonary parenchyma |
|
|
Term
| What is seen microscopically at the hilar lymph nodes in sarcoidosis? |
|
Definition
| numerous, small, non-caseating epithelioid granulomas |
|
|
Term
|
Definition
| one of the various cytoplasmic inclusions that are in the giant cells of the granulomas in sarcoidosis |
|
|
Term
| Where, besides the hilar lymph nodes, are granulomas seen in sarcoidosis? |
|
Definition
| pulmonary parenchyma (=> resolution w/o residue or severe, disabling pulmonary fibrosis) |
|
|
Term
| What does the inhalation of certain inorganic dusts lead to? |
|
Definition
| deposition of fibrous tissue in the lung |
|
|
Term
|
Definition
| inhaled silia particles are inhaled & then ingested by macs & are released upon the death of the macs (since indigestible) & are re-ingested by other macs |
|
|
Term
| What causes the collagen deposition is silicosis? |
|
Definition
| response to cytokine & products released by dying macs |
|
|
Term
| What is typically formed by the collagen deposition in silicosis? |
|
Definition
| acellular concentric fibrous nodules |
|
|
Term
|
Definition
| fibrous material which, upon entering the lung, is ingested by macs |
|
|
Term
| What do the macs deposit around the asbestos fiber after ingestion? |
|
Definition
| layers of an iron-protein material |
|
|
Term
| What is released when a mac that ingested asbestos dies? |
|
Definition
| iron coated, beaded asbestos body |
|
|
Term
| What is induced by asbestos in the lung (by unclear mech)? |
|
Definition
1) fibrosis (asbestosis)
2) tumors s.a. pleural mesothelioma & bronchogenic carcinomas |
|
|
Term
| What are the asbestos tumors composed of? |
|
Definition
| varying proportions of transformed epithelial-like & stromal components, derived from neoplastic transformation of pleural mesothelial cells |
|
|
Term
| What does lung w/ pulmonary alveolar proteinosis resemble? |
|
Definition
| pneumonia, but the alveoli don't contain inflam. exudate |
|
|
Term
| What are the alveoli in pulmonary alveolar proteinosis filled with? |
|
Definition
| dense, eosinophilic material containing protein & many lipids of the pulmonary alveolar surfactant (not surface active) |
|
|
Term
| What is the origin of pulmonary alveolar proteinosis? |
|
Definition
|
|
Term
Tx
pulmonary alveolar proteinosis |
|
Definition
| periodic broncho-alveolar lavage (BAL) |
|
|
Term
| What can cause honeycomb lung (diffuse interstitial fibrosis)? |
|
Definition
| variety of processes, some of unknown etiology |
|
|
Term
def
honeycomb lung (diffuse intersitial fibrosis) |
|
Definition
| distal air spaces are enlarged & bordered by thick fibrous septae |
|
|
Term
| What is the effect of UIP (usual interstitial pneumonia)? |
|
Definition
|
|
Term
| What happens in interstitial lung disease as the process progresses & the septal infiltrates regress? |
|
Definition
| leaves in their wake an abnormal amount of interstitial fibrous tissue |
|
|
Term
| What condition is related to intersitital lung disease caused by UIP? |
|
Definition
| DIP (desquamative intersitial pneumonia) |
|
|
Term
| Hoe does DIP differ from UIP? |
|
Definition
| DIP causes interstitial inflam. to a lesser degree than UIP & concentrated in lymphoid nodules (center). |
|
|
Term
| What is the striking feature of DIP? |
|
Definition
| intra-alveolar accumulation of densely packed cells that have been found by electron microscopy to be mainly macs & a few type II epithelial cells |
|
|
Term
|
Definition
| tumor arising in bronchis invading the surrounding lung & adjacent lymph node |
|
|
Term
| Historically, what type of lung carcinoma is typically seen? |
|
Definition
| keratinizing squamous cell carcinoma |
|
|
Term
| Why are various changes (s.a. endogenous lipioid pneumonia) seen in the lung peripheral to the lung carcinoma? |
|
Definition
| the tumor often obstructs the bronchus in which it arises |
|
|
Term
| What is seen microscopically in endogenous lipoid pneumonia? |
|
Definition
| intra-alveolar macs are large & foamy since they have ingested lipid material that would have otherwise been cleared thru the obstructed bronchus |
|
|
Term
| When does lipoid pneumonia occur? |
|
Definition
| when massive lipid accumulation occurs (or release from lipid cells) & they coalesce into large droplets => fibrosis |
|
|
Term
| What lung carcinoma is often seen in the lung's periphery? |
|
Definition
|
|
Term
def
BAC (bronchio-alveolar cell carcinomas) |
|
Definition
| a form of adenocarcinoma that is derived from the epithelial cells of the bronchioles &/or alveoli |
|
|
Term
| What does BAC often resemble? |
|
Definition
|
|
Term
| What is seen microscopically in BAC? |
|
Definition
| columnar tumor cells grow along pre-existing alveolar septae, which epithelium the tumor replaces |
|
|
Term
| What suggests a more agressive lung carcinoma & ∴ a poorer prognosis? |
|
Definition
|
|
Term
def
small cell (oat cell) carcinoma |
|
Definition
| tumors derviced from putative neuroectodermal, endocrine-like cells in the bronchial mucosa & often produce bizzare paraneoplastic endocrine syndromes |
|
|
Term
|
Definition
| many, multinucleated tumor giant cells |
|
|
Term
|
Definition
| a mechanism by which lung carcinoma may spread |
|
|
Term
|
Definition
| centrally located, locally agressibe tumors of bronchi |
|
|
Term
| Are bronchial adenomas more or less likely to metastasize |
|
Definition
|
|
Term
|
Definition
| type of bronchial adenoma composed of uniform nests of cells w/ a distinct cytological appearance |
|
|
Term
|
Definition
| entirely benign (usually peripheral) lung tumor w/ cartilaginous surfaces & crossed by deep clefts (tends to fall out of the area containing it) |
|
|
Term
| What do lung hamartomas look like microscopically? |
|
Definition
composed mostly of cartilage that is crossed by epithelium (bronchial, bronchiole, & alveolar) lined channels.
B/w epi. & catrilage is found fibrous tissue w/ or w/o foci of fat cells, sm. muscle cells, or lymphocytes |
|
|
Term
| Is inerstitial lung disease (ILD) a(n)chronic or acute condition? |
|
Definition
| chronic (w/ acute exacerbations) |
|
|
Term
| What pathology is seen in ILD? |
|
Definition
| variable degrees of inflam., infiltration, & fibrosis of the alveolar-capillary units & adjacent interstitium (& vasculature & small airways) |
|
|
Term
| How much of the lung is affected by ILD? |
|
Definition
| diffusely throughout the lung, but not necessarily w/ uniform distribution |
|
|
Term
|
Definition
| structural & functional derangements of the gas exchanging units & interstitium => abnormal gas exchange (hypoxemia) & abnormal lung mechanics (typically sm. non-compliant lungs) |
|
|
Term
| When should ILD be suspected? |
|
Definition
1) Sx: cough & dyspnea
2) CXR: diffuse changes (not necessarily uniform)
2) PE: crackles |
|
|
Term
|
Definition
| diverse etiologies (tho NOT infectious or neoplastic) |
|
|
Term
| What 3 conditions mimic ILD? |
|
Definition
1) neoplasms (s.a. lymphangitic spread of cancer, bronchioalveolar carcinoma, lymphoproliferative disorders)
2) infections (s.a. PCP, CMV, fungi, viruses)
3) pulmonary edema |
|
|
Term
| What are some causes of ILD? |
|
Definition
1) pneumoconiosis (inorganic substances)
2) toxins (oxides of nitrogen)
3) drugs
4) radiation
5) oxygen
6) hypersensitivity (farmer's lung - organic substances)
7) idiopathic interstitial pneumonias
8) sarcoidosis |
|
|
Term
|
Definition
| fibrotic lung disease associated w/ collagen vascular disease |
|
|
Term
| What are 7 other fibrotic lung diseases associated w/ collagent vascular disease? |
|
Definition
1) RA
2) scleroderma
3) mixed CT disease
4) SLE
5) Sjogren's Syndrome
6) polymyositis/dermatomyositis
7)vasculitis |
|
|
Term
| Can you have ILD w/ RA, scleroderma, mixed CT disease, SLE, Sjogren's Syndrome, polymyositis/dermatomyositis, or vasculitis? |
|
Definition
|
|
Term
| What are 6 miscellaneous conditions w/ unknoen cause? |
|
Definition
1) histocytosis X
2) lymphangioleiomyomatosis
3) idiopathic hemosiderosis
4) chronic eosinophilic pneumonia
5) pulmonary alveolar proteinosis
6) amyloidosis |
|
|
Term
| What are 5 lung diseases that are inherited? |
|
Definition
1) tuberous sclerosis
2) neurofibromatosis
3) hermansky-pudlak syndrome
4) metabolic stroage disorders
5) hypocalcuric hypercalcemia |
|
|
Term
| Why is the differential diagnosis of ILD suspected? |
|
Definition
Sx & abnormal CXR => long list on dd
you'll need to think beyond pneumonia & CHF |
|
|
Term
| What are 7 patterns of idiopathic interstitial pneumonias? |
|
Definition
1) NSIP (nonspecific interstitial pneumonia)
2) UIP (usual interstitial pneumonia)
3) DIP (desquamative interstitial pneumonia)
4) RB (resp. bronchiolitis)
5) DAD (diffuse alveolar damage)
6) OP (organizing pneumonia)
7) LIP (lymphoid interstitial pneumonia)
(Note: these are histopathoilogic patterns, NOT diseases) |
|
|
Term
| What are the 7 entities of idiopathic interstitial pneumonia defined by? |
|
Definition
1) Clinical criteria (natural Hx, response to therapy)
2) radiologic criteria (high resolution CT appearance)
3) pathologic criteria (histopathology)
∴ diagnosis depends on interaction b/w clinicians, radiologists, & pathologists |
|
|
Term
| Of the 7 patterns of idiopathic interstitial pneumonias, which 3 are smoking related? |
|
Definition
|
|
Term
| Of the 7 patterns of idiopathic interstitial pneumonias, which 3 are corticosteroid responsive? |
|
Definition
|
|
Term
| What is the diagnosis when UIP is seen? |
|
Definition
| IPF (interstitial pulmonary fibrosis) |
|
|
Term
| What is the diagnosis when NSIP is seen? |
|
Definition
|
|
Term
| What is the diagnosis when OP is seen? |
|
Definition
| cryptogenic organizing pneumonia |
|
|
Term
| What is the diagnosis when DAD (or acute alveolar damage) is seen? |
|
Definition
| acute interstitial pneumonia |
|
|
Term
| What is the diagnosis when RB is seen? |
|
Definition
|
|
Term
| What is the diagnosis when DIP is seen? |
|
Definition
|
|
Term
| What is the diagnosis when LIP is seen? |
|
Definition
|
|
Term
| What is the most common idiopathic interstitial pneumonia? |
|
Definition
|
|
Term
|
Definition
| distinctive type of chronic, progressive, fatal fibrosing interstitial pneumonia |
|
|
Term
| What is IPF often hard to distinguish b/w? |
|
Definition
|
|
Term
| Is IPF limited to the lungs? |
|
Definition
|
|
Term
| What histological pattern is associated w/ IPF? |
|
Definition
|
|
Term
| Who is most likely affected by IPF? |
|
Definition
|
|
Term
| What are the risk factors for IPF? |
|
Definition
1) +family Hx
2) smoking
3) ?environment, ?GE reflux, ?infectious agents |
|
|
Term
| What is the inheritance pattern of IPF? |
|
Definition
| autosomal dominant w/ variable penetrance |
|
|
Term
| What gene has been implicated in familial IPF? |
|
Definition
|
|
Term
| What do the mututations in IPF affect? |
|
Definition
1) surfactant protein C
2) TERT
3) TERC
(TERT & TERC have to do w/ telomerases => shortening of DNA & poor regeneration of DNA => dysfunctional cells & cell death) |
|
|
Term
|
Definition
| 1) progressive dyspnea on exertion
2) paroxysmal cough, ususally non-productive
3) abnormal breath sounds on chest ascultation (crackles)
4) tachypnea
5) clubbing (up to 50%)
6) abnormal CXR or HRCT (high res. CT)
7) restrictive pulmonary physiology w. decreased LVs & DLCO & wide p(A-a)O2 |
|
|
Term
| What is the UIP pathology seen w/ IPF? |
|
Definition
1) variation w/in the lung - "temporal heterogeneity" (NSIP is homogeneous)
2) subpleural distribution
3) fibrosis
4) honeycombing (air spaces surrounded by thickened collagenous septa)
5) discrete areas of proliferation of fibroblasts & myofibroblasts
6) hyperplastic Type 2 pneumocytes
7) minimal inflam.
8) traction bronchiectasis |
|
|
Term
| How does the histopathology of NSIP differ from IPF? |
|
Definition
| more uniform distribution |
|
|
Term
| What is seen in radiology for NSIP? |
|
Definition
| more ground glass opacities |
|
|
Term
| What are the 2 types of NSIP? |
|
Definition
|
|
Term
| What leads to a better prognosis for NSIP? |
|
Definition
1) more responsive to corticosteroids = better prognosis
2) cellular type has better prognosis than fibrotic type |
|
|
Term
| What are the IPF PFT results? |
|
Definition
| 1) Restrictive process w/ impaired gas exchange (reduced FEV1 & FVC, normal FEV1/FVC ratio, reduced TLC
2) reduced DLCO ∴ parenchymal
3) reduced compliance
4) increased exercise P(A-a)O2 difference |
|
|
Term
| Do normal resting PFTs exclude IPF? |
|
Definition
| no (can have normal FVC, FEV1/FVC ratio, & TLC) |
|
|
Term
| What happens in IPF on a 6 minute walk test? |
|
Definition
| oxygen desaturation (faster transit time of RBCs in caps & for oxygen to diffuse into caps) |
|
|
Term
| What is seen on the CXR of a patient w/ IPF? |
|
Definition
1) small lungs
2) peripheral densities
3) honeycombing |
|
|
Term
| Is the CXR sensitive for IPF? |
|
Definition
|
|
Term
| Why is HRCT a good diagnostic tool for ILDs & bronchiectasis? |
|
Definition
| see structures at level of lobule & ∴ see the location & shape of abnormalities |
|
|
Term
| What vessel runs w/ the bronchiole in the middle of the lobule? |
|
Definition
|
|
Term
| Where do tyhe pulmonary veins & lymphatics run? |
|
Definition
| in septum that separates one lobule from the other |
|
|
Term
| What is seen in HRCT in a patient w/ IPF? |
|
Definition
1) irregular reticular (net-like) structures
2) sub-pleural, posterior, lower lobe location
3) sub-pleural honeycombing
4) traction bronchiectasis
5) mildly enlarged lymph nodes |
|
|
Term
| What are the hypotheses for the pathogenesis of IPF? |
|
Definition
1) inflam.
2) "multiple hit" hypothesis
3) abnormal vascular remodeling |
|
|
Term
| Why is inflammation not a good hypothesis for IPF? |
|
Definition
1) poor response to immunosuppresive agents
2) measures of inflam. don't correlate w/ severity of outcome |
|
|
Term
def
"multiple hit" hypothesis of IPF |
|
Definition
| fibrosis results from epi. injury & abnormal wound healing |
|
|
Term
def
abnormal vascular remodeling hypothesis of IPF |
|
Definition
|
|
Term
| What is requireded for the diagnosis of IPF? |
|
Definition
1) R/O other causes of ILD (s.a. exposures, CT disorders, etc)
2) HRCT typical UIP pattern
3) surgical biopsy w/ uncertainty
4) multi-disciplinary approach (to increase accuracy of Dx) |
|
|
Term
|
Definition
|
|
Term
|
Definition
1) poor w/ progressive lung disease
2) periods of acute deterioration
3) median survival ~3 yrs after Dx
(5 yr survival 20-40%) |
|
|
Term
|
Definition
| specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause, occuring primarily in older adults, limited to the lungs, and associated w/ the histopathologic &/or radiologic pattern of UIP and is fatal |
|
|
Term
| What is the usual course of IPF? |
|
Definition
gradual worsening of lung function over years w/ a minority of patients remaining stable or declining rapidly
(some patients may experience episodes of acute resp. worsening despite previous stability) |
|
|
Term
| How is disease progression of IPF manifested? |
|
Definition
| increasing resp. Sx, worsening PFTs, progressibe fibrosis on HRCT, acute resp. decline, or death |
|
|
Term
| What sub-clinical or overt co-morbid conditions can patients w/ IPF have? |
|
Definition
1) pulmonary HTN
2) GE reflux
3) obstructive sleep apnea
4) obesity
5) emphysema
=> unclear impact on the outcome of IPF |
|
|
Term
|
Definition
| multisystem disease of unknown etiology |
|
|
Term
| Who is most commonly affected by sarcoidosis? |
|
Definition
age <40
females
Swedes, Danes, blacks |
|
|
Term
| What is the hypothesis of the pathophysiology of sarcoidosis? |
|
Definition
| genetically susceptible host + inciting environmental factor => accumulation of activated T (CD4) cells & macs @ sites of ongoing inflam. => release of IFNγ, IL-2, & other cytokines |
|
|
Term
| What pathology occurs in the lung in sarcoidosis? |
|
Definition
1) granuloma formation
2) healing OR fibrosis |
|
|
Term
| Is a resitrictive or an obstructive process going to be seen on PFTs w/ sarcoidosis? |
|
Definition
| either, but w/ abnormal diffusion capacity |
|
|
Term
| What is going to bee seen on the CXR of a patient w/ sarcoidosis? |
|
Definition
| lymph nodes + infiltrates |
|
|
Term
| What are the sites of disease in sarcoidosis? |
|
Definition
1) lung
2) lymph nodes
3) skin
4) heart
5) GI
6) eyes
7) nervous system
8) paranasal sinuses
9) kidneys
10) bone marrow
11) bone & joint
12) parotid glands |
|
|
Term
| What lymph nodes are affected in sarcoidosis? |
|
Definition
1) hilar
2) mediastinal
3) peripheral |
|
|
Term
| What skin changes are seen in sarcoidosis? |
|
Definition
1) papules
2) macules
3) pigment change
4) subq nodules
5) keloids |
|
|
Term
| What abnormalities can occur in the heart of apaitent w/ sarcoidosis? |
|
Definition
1) conduction defects
2) sudden death |
|
|
Term
| What GI organs are commonly affected in sarcoidosis? |
|
Definition
|
|
Term
| What commonly occurs in the eyes of patients w/ sarcoidosis? |
|
Definition
| uveitis => glaucoma & blindness |
|
|
Term
| What occurs in the nervous system of patients w/ sarcoidosis? |
|
Definition
1) base of skull: facial palsies & pituitary leisons
2) space occupying masses |
|
|
Term
| What occurs in the kidneys of patients w/ sarcoidosis? |
|
Definition
1) stones
2) 25 hydroxyvitamin D is 1 hydroxylated by activated macs => elevated levels of 1,25 di-hydroxyvitamin D => hypercalcuria & hypercalcemia |
|
|
Term
| What effects are seen due to bone marrow involement in sarcoidosis? |
|
Definition
|
|
Term
| What are the PFTs for a patient w/ sarcoidosis? |
|
Definition
| 1) restrictive process (can be obstructive or mixed obstructive/restrictive)
2) low DLCO ∴ parenchymal
(if mixed, low FEV1/FVC & low TLC) |
|
|
Term
|
Definition
1) compatible clinical picture
2) granulomas on biopsy (bronchoscopy has high yield)
3) exclusion of other entities (s.a. infectious TB, fungi, NTM, occulational diseases, or neoplasm) |
|
|
Term
| Which disease is sometimes hard to distinguish sarcoidosis b/w? |
|
Definition
| TB (sometimes the 2 co-exist) |
|
|
Term
|
Definition
1) 60% w/ spontaneous remissions
2) 10-30% chronic or progressive
3) death is 1-5% due to resp. failure |
|
|
Term
|
Definition
only for serious Sx or organ involvement => corticosteroids
(no clear effect on mortality tho) |
|
|
Term
| What expands the alveolar sacs upon inspiration? |
|
Definition
| air via stretching the alveolar septa |
|
|
Term
| How thick are the alveolar septa normally? |
|
Definition
| extremely thin, composed only of a single layer of flattened pneumocytes, a cap, & a sm. amount of CT (mainly elastic fibers) |
|
|
Term
| What happens to the interstitium in interstitial lung disease (ILD)? |
|
Definition
| destroys alveoli & add cells & fibrous tissue => reduced echange surface, thicker & stiffer septa => restriction & stretching => harder to breathe |
|
|
Term
| Why is classification of ILD necessary? |
|
Definition
| to help guide Tx, predict prognosis, & may allow for worker's compensation in occupational related disease |
|
|
Term
|
Definition
| combination of morphological & clinical features, inc. possible exposures to known etiologic factors, co-morbid conditions, imaging features, and biopsy |
|
|
Term
| What can a lung biopsy of an ILD tell us? |
|
Definition
interstitial injury pattern based on:
1) type & location of cells
2) degree of distribution of fibrosis & changes in other lung structures |
|
|
Term
| Fow which ILD is bronchoscopic biopsy useful? |
|
Definition
|
|
Term
| What type of biopsy (other than for sarcoidosis) is the preferred method for ILD Dx/Classification? |
|
Definition
wedge biopsies since most ILDs affect peripheral lung
(tho radiologic findingas are also critical to ensure accurate classification) |
|
|
Term
| What are the 2 borad categories of ILD? |
|
Definition
1) those of known cause
2) those of unknown cause |
|
|
Term
| What are the 3 known causes of ILD? |
|
Definition
1) inhalents (inorganic dusts/pneumoconiosis, organic dusts - hypersensitivity pneumonitis, gases)
2) drugs/toxins (chemotherapeutics, Abx, toxins)
3) infections (viruses, bacteria, fungi) |
|
|
Term
| What are the 6 types of ILD w/ unknown cause? |
|
Definition
1) idopathic interstitial pneumonias (aka idiopathic pulmonary fibrosis)
2) CT disease associated w/ ILD
3) sarcoidosis
4) eosinophilic granuloma
5) eosinophilic pneumonia
6) pulmonary hemorrhage syndromes |
|
|
Term
| What are the 7 patterns seen w/ idiopathic interstitial pneumonias? |
|
Definition
1) UIP (usual interstitial pneumonitis)
2) DIP (desquamative interstitial pneumonitis)
3) OP (organizing pneumonia)
4) RBILD (respiratory bronchiolitis-associated ILD)
5) NSIP (nonspecific interstitial pneumonia)
6) LIP (lymphocytic interstitial pneumonia)
7) DAD (diffuse alveolar damage) |
|
|
Term
| What is the only ILD w/ an acute presentation? |
|
Definition
|
|
Term
| What pathological processes occur in ILD? |
|
Definition
1) interstitial chronic inflam.
2) cyst formation
3) interstitial fibrosis
=> honeycomb lung = end stage result of tisse damage (scarred lung w/ dilated air spaces created from destroyed lung & fibrous scars) |
|
|
Term
| What is the most common ILD? |
|
Definition
|
|
Term
| When is UIP most commonly seen? |
|
Definition
|
|
Term
| What is the median survival of UIP? |
|
Definition
|
|
Term
| What happens progressively in UIP? |
|
Definition
|
|
Term
| What is the pathology od UIP IPF? |
|
Definition
1) patchy distribution - heterogeneity of tissue damage (areas of marked fibrosis & areas of less w/ more inflam.)
2) bibasilar & sb-pleural accentuation
3) "fibroblastic foci"
4) often progresses to end stage honeycomb lung |
|
|
Term
| Does UIP have a better or worse prognosis than most ILDs? |
|
Definition
|
|
Term
| What is the pathogenesis of UIP IPF? |
|
Definition
| unknown agent triggers lymphocyte/cytokine mediated inflam. reaction => proteases, growth, VEGFs, TGFβ, procoagulant factors, PGs => proliferation of fibroblasts & formation of myofibroblasts, transformation of pneumocytes into myofibroblasts => fibrosis, vascular proliferation |
|
|
Term
| Is a UIP lung larger or smaller than normal lungs? |
|
Definition
|
|
Term
| Why does lungs w/ UIP have :hobnailed" pleura? |
|
Definition
| retraction by underlying fibrous scarring |
|
|
Term
| What metaplasia occurs in UIP? |
|
Definition
| intersitial fibrosis & replacement of alveolar epi w bronchiolar epi |
|
|
Term
|
Definition
| looser, "younger" CT (indicate ongoing lung injury) |
|
|
Term
| What inhalant looks similar to UIP upon autopsy? |
|
Definition
|
|
Term
| Why are lung pathology, Hx, radiology, and lab findings important in determining ILD type? |
|
Definition
| many diseases can produce similar lung pathology |
|
|
Term
|
Definition
| dissolve the lung in bleach & look for numberous fibers coated w/ iron |
|
|
Term
| Is DIP a more common or more rare ILD? |
|
Definition
|
|
Term
| Is DIP linked to smoking? |
|
Definition
|
|
Term
| Does DIP respond to steroids? |
|
Definition
|
|
Term
| What is the mean age of diagnosis of DIP? |
|
Definition
|
|
Term
| Does DIP generally ahve good or poor prognosis? |
|
Definition
|
|
Term
| What is the pathologenesis of DIP similar to? |
|
Definition
| UIP (but linked to smoking) |
|
|
Term
| What is the pathology of DIP? |
|
Definition
1) large # alveolar macs
2) interstitial lymphocytes
3) mild interstitial fibrosis
4) progresses to honeycomb lung (less common than UIP) |
|
|
Term
| IS DIP patchy like UIP or more uniform lung involvment? |
|
Definition
| more uniform w/ interstitial thickening due to fibrosis + inflam. & airspaces filling w/ macs |
|
|
Term
|
Definition
| alveolar macs look like epi cells thought to be desquamating |
|
|
Term
| What is the second most common ILD? |
|
Definition
|
|
Term
| Who is more likely to get NSIP? |
|
Definition
50s
women (slightly more common than men) |
|
|
Term
| What is the median survival of NSIP? |
|
Definition
|
|
Term
What are the 2 typs of NSIP?
Which one has a worse prognosis? |
|
Definition
1) cellular
2) fibrotic - worse prognosis |
|
|
Term
|
Definition
| an IP that doesn't fit any of the other defined histopathological categories |
|
|
Term
| Does the tissue damage, inflam. & fibrosis in NSIP tend to be patchy or uniform? |
|
Definition
|
|
Term
| Of UIP, DIP, NSIP, which has the most subpleural accentuation? |
|
Definition
|
|
Term
| Of UIP, DIP, NSIP, which leads to honeycomb lung? |
|
Definition
|
|
Term
| Of UIP, DIP, NSIP, which has a more uniform pathological procress & tissue damage? |
|
Definition
|
|
Term
| Of UIP, DIP, NSIP, which has the best/worst prognosis? |
|
Definition
UIP = worst
DIP = best
NSIP = good for cellular form, intermediate for fibrosing form |
|
|
Term
| What are some other names of hypersensitivity pneumonitis? |
|
Definition
1) farmer's lung (exposure to mold in hay)
2) pigeon breeder's (exposure to protein particles in pigeon droppings)
3) sauna taker's (exposure to mold in wet containers)
4) mushroom worker's disease (exposure to moldy compost)
5) bagassosis (exposure to moldy sugar cane) |
|
|
Term
| What causes hypersensitivity pneumonitis? |
|
Definition
|
|
Term
| Why is it especially important not to miss the diagnosis of hypersensitivity pneumonitis? |
|
Definition
| reducing exposure to inciting agent = key in Tx |
|
|
Term
| Is hypersensitivity pneumonitis an acute event or a chronic ILD? |
|
Definition
|
|
Term
| What is the pathology of hypersensitivity pneumonitis? |
|
Definition
1) interstitial lymphocytes
2) mild interstitial fibrosis
3) intersitial granulomas (~67%)
4) often peribronchiolar inflam.
5) can produce sm. airway obstruction
6) rarely progresses to honeycomb lung |
|
|
Term
|
Definition
bronchiolitis obliteran-organizing pneuonia
where granulation tissue plugs in alveoli &/or bronchi w/ nonspecific pattern of OP & heterogeneous etiological factors |
|
|
Term
| What is the pathogenesis of hypersensitivity pneumonitis? |
|
Definition
| sensitization to inhaled organic allergens => long latency => + co-morbid conditions s.a. smoking/infections + genetic predisposition => type III & type IV reactions (immune complex & cell mediated) |
|
|
Term
| Where is interstitial chronic inflam. accentuated in hypersensitivity pneumonitis (HP)? |
|
Definition
|
|
Term
| Is there any honeycomb change in HP? |
|
Definition
| no, but there is mild fibrosis |
|
|
Term
| What is the interstitial infiltrate comprised of in HP? |
|
Definition
| mainly of lymphocytes & sm number of macs & eosinophils |
|
|
Term
|
Definition
| tissue injury pattern in a number of lung diseases w/ patchy plugs of loose fibrous tissue fill bronchioles, alveolar ducts, & alveoli => mized restrictive/obstructive pattern on PFT |
|
|
Term
| What are seen in HP due to the combination of type II & type IV reactions? |
|
Definition
1) allergens
2) Ag-Aby complex or direct activation of complement by alternate pathway
3) alveolitis
4) activation of alveolar macs
5) cytokines, GFs
6) type IV, cell mediated immunity
7) granuloma formation
8) fibrosis |
|
|
Term
| What is the problem in the diagnosis of ILD? |
|
Definition
1) complexity of diseases
2) overlap of syndromes
3) inter-observer variability among pathologists in the classification of ILD |
|
|
Term
| What is the approach to diagnosis of ILD? |
|
Definition
1) interdiscciplinary approach = necessary
2) R/O exposure to toxic agents (inc. chemo & radiation)
3) R/O infectious etiology (via cultures)
4) R/O co-morbid conditions w/ pulmonary manifestations
5) Wedge biopsy (not bronchoscopic biopsy)
6) CT/radiologic picture
7) histological pattern vs. disease |
|
|
Term
| What is the key to an effective approach to the diagnosis of ILD? |
|
Definition
multidisciplinary approach w/ HRCT (big picture)
(so crucial infact, that biopsy may not be needed) |
|
|
Term
| What is pathology more important for in the Dx of ILD? |
|
Definition
| ruling out other entities, rather than making a definitive Dx |
|
|
Term
| What has diminished the inter-observer variablity in the Dx of ILD type? |
|
Definition
|
|
Term
| What 6 criteria can definitively R/O UIP? |
|
Definition
1) hyaline membrane formation
2) OP
3) granuloma
4) marked interstitial inflam. cell infiltrate away from honeycombing
5) prominant airway centered changes
6) other features suggestive of another Dx |
|
|
Term
| What is the etiology of sarcoidosis? |
|
Definition
|
|
Term
|
Definition
| common systemic disease most often involving the lungs & mediastinal lymph nodes that may progress to end stage lung (honeycomb) |
|
|
Term
| What leads to the Dx of sarcoidosis? |
|
Definition
1) incidental CXR finding
2) Sx presented relating to any of the multiple organ systems involved |
|
|
Term
| What pathology is seen in sarcoidosis? |
|
Definition
1) non-necrotizing granulomata
2) diffuse interstitial granulomas & fibrosis
3) perilymphangitic pattern & regional nodes commonly involved
4) focal necrosis may be present => extensive necrosis in fungal & AFB inf. |
|
|
Term
| What must be ruled out prior to a sarcoidosis Dx? |
|
Definition
| infection via cultures & stains |
|
|
Term
| What type of biopsy is used to Dx sarcoidosis? |
|
Definition
|
|
Term
| Can diagnosis of sarcoidosis be made just on the pathological findings? |
|
Definition
|
|
Term
| What is the pathogenesis of sarcoidosis? |
|
Definition
| unknown factor => activation of T cells (esp CD4) & APCs => cytokine production => recruitment & activation of macs => formation of granuloma => tissue damage & fibrosis |
|
|
Term
def
lymphangitis distribution |
|
Definition
| around vessels & bronchioles |
|
|
Term
| What does it mean that the granulomas in sarcoidosis are "well formed"? |
|
Definition
| they are tight clusters of macs & giant cells w/ a rim of lymphocytes & there is no necrosis |
|
|
Term
|
Definition
| diseases involving proliferation & tissue infiltration by Langerhans cells |
|
|
Term
|
Definition
| part of the widespread system of dendritic cells (APCs of monocytic-macrophagic lineage) |
|
|
Term
| What are the 3 presentations of histocytoses X? |
|
Definition
1) eosinophilic granuloma
2) hand-schuller-christian disease
3) letterer-siwe disease |
|
|
Term
| Of the 3 histocytoses X presentations, which is the most common? |
|
Definition
| eosinophilic granuloma (60-80%) |
|
|
Term
| Who is affected by histocytosis X eosinophilic granulomas? |
|
Definition
|
|
Term
| Of the 3 presentations of histocytoses X, which presentation has the best prognosis? |
|
Definition
| eosinophilic granuloma (affects lung only) |
|
|
Term
| Who is affected by histocytosis hand-schuller-christian disease? |
|
Definition
|
|
Term
| What part of the body is affected by histocytosis X hand-schuller-christian disease? |
|
Definition
| lung & bone (may be systemic) |
|
|
Term
| Of the 3 presentations of histocytoses X, which has the worst prognosis? |
|
Definition
| letterer-siwe (multisystem involvement w/ 70% mortality) |
|
|
Term
| Who is affected by histocytosis X letterer-siwe disease? |
|
Definition
|
|
Term
def
eosinophilic granuloma |
|
Definition
| rare pulmonary disease that occurs primarily in young adults |
|
|
Term
| Is there an association b/w langerhans cell histocytosis & eosinophilic granuloma? |
|
Definition
| yes, strong association (up to 95% of thos eaffected are smokers & Sx improve w/ cessation) |
|
|
Term
| What is the pathology of eosinophilic granulomas? |
|
Definition
1) eosinophils, neutrophils, & lymphocytes w/ focal leisons around smaller pronchioles producing stellate leisons
2) granulomatous infiltration of alveolar septa & bronchial walls by langerhans cells => nodules
3) can result in progressive lung distruction & cystic change |
|
|
Term
| Why is eosinophilic granuloma a misnomer? |
|
Definition
| eosinophils are not always present |
|
|
Term
| Where in the lung do eosinophil granulomas favor? |
|
Definition
|
|
Term
|
Definition
| large polygonal (epitheloid) cells w/ ample cytoplasm & folds in nuclear membrane |
|
|
Term
| What inclusions are often seen in langerhans cell? |
|
Definition
| Birbeck granules (typical racket shaped inclusions) |
|
|
Term
| What immunohistochemistry stain is positive for langerhans cells? |
|
Definition
|
|
Term
| What is the pathogenesis of eosinophilic granules? |
|
Definition
| cigarette smoke + environmental & genetic factors => activation of immune response => activation of inflam. mediators facilitating fibrosis => proliferation of macs & langerhans cells |
|
|
Term
| What happens to pulmonary mechanics w/ age (muscle strength, chest wall, eleastic recoil)? |
|
Definition
1) decreased resp. muscle strength
2) stiffening of chest wall
3) loss of lung elastic recoil |
|
|
Term
| What are the resp. muscles that lose strength w/ age? |
|
Definition
1) diapragm
2) accessory muscles
3) intercostal muscles |
|
|
Term
| What does effect does a decline in resp. muscle strength have? |
|
Definition
| lower max. inspiratory & expiratory pressure |
|
|
Term
| What causes resp. muscel strength decline? |
|
Definition
| changes in neural & muscle compnents of the motor unit |
|
|
Term
| What causes the chest wall stiffening seen in aging? |
|
Definition
| calcification or rib cage articulations that are detectible after age 20y |
|
|
Term
| What causes loss of elastic recoil w/ age? |
|
Definition
| change in location & orientation of elastic fibers (NOT from loss in elastic fiber # nor loss in elastic fiber size) |
|
|
Term
| What is the effect os loss of lung elastic recoil w/ age? |
|
Definition
| increased lung tisue compliance |
|
|
Term
| What happens to lung volumes (TLC, RV, & closing volume) w/ age? |
|
Definition
TLC remains the same
RV & closing volume increase |
|
|
Term
| Where is the increase in closing volume more prominent? |
|
Definition
|
|
Term
| What causes the increased closing volume w/ age? |
|
Definition
| loss of orientation of elastic fibers allows closure of small airways to begin earlier in expiration => amount of air in the lung @ the time the airways being to close (closing volume) is higher since this occurs earlier in expiration |
|
|
Term
| What happens to loung flow rates (FVC, FEV1, FEF) w/ age? |
|
Definition
| All decrease, w/ greatest decrease in FEF by 25-75% |
|
|
Term
| What happens to gas exchange (ventilation/perfusion mismatch, alveolar diffusion capacity, PaO2) w/ age? |
|
Definition
| 1) increased ventialtion/perfusion mismatch
2) decreased alveolar dissusion capacity
3) (1+2=>) reduced PaO2 by 3 mmHg/decade |
|
|
Term
| Why is there diminished alveolar diffusion capacity w/ age? |
|
Definition
1) reduced alveolar cap surface area
2) recuded lung size |
|
|
Term
| What causes the increased ventilation/perfusion mismatch w/ age? |
|
Definition
1) Ventilation &, to a greater extent, flow are increased from apex to base in the upright lung
2) V/Q is >1 in apex, <1 in base, but averages to 1 in young
3) earlier closure of the small airways (esp. in bases w/ aging), increased ventilation to the upper regions w/o decreasing flow to the lower regions => enhances mismatch |
|
|
Term
| What happens to pulmonary defense mechanisms (clearance, humoral immunity, cellular immunity) w/ age? |
|
Definition
decreased clearance
altered humoral & cellular immunity |
|
|
Term
| How is clearance decreased w/ age? |
|
Definition
1) decreased laryngeal & cough reflex
2) decreased mucociliary clearance rates |
|
|
Term
| Due to the decreased/altered pulmonary defence mechanisms, what prophylaxis is needed in the geriatric community? |
|
Definition
1) vaccines (pnumococcal & influenza)
2) counseling (smoking & exercise) |
|
|
Term
| Why is there increased vulnerability to disease w/ increasing age? |
|
Definition
1) decreased pulmonary reserve
2) similar burden of disease may produce greater morbidity
3) prolonged environmental exposure |
|
|
Term
| What delays diagnosis in the elderly? |
|
Definition
| altered/nonspecific presentation of disease & aging changes may mimic disease, so you need to separate out true Sx |
|
|
Term
| What is the main risk factor for 85-90% of all lung cancers? |
|
Definition
|
|
Term
| What carcinogens are in cigarettes? |
|
Definition
"tar" - residue after eliminating nicotine & water (NOT nictoine)
s.a.
1) aromatic hydrocarbons
2) radioactive elements (nickel)
3) free radicals |
|
|
Term
| What effect does seconda hand smoke have? |
|
Definition
1) causes 15% of lung cancer in non-smokers (& possibly COPD)
2) causes decreases in lung function, more asthma, ear infection, etc. |
|
|
Term
| Besides lung cancer, what other cancers are at an increased risk due to smoking? |
|
Definition
1) larynx
2) oral cavity
3) esophagus
4) pancreas
5) bladder
6) cervix |
|
|
Term
| What factors (besides smoking) can contribute to lung cancer? |
|
Definition
1) asbestos
2) ionizing radiation
3) nickel
4) arsenic
5) methyl ethers
6) vinyl chloride
7) coal tars, coke ovens
8) mustard gas
(NOTE: any of this + smoking = greater risk & ususally synergestic) |
|
|
Term
| What is the second most common cause of lung cancer? |
|
Definition
|
|
Term
|
Definition
| inert radioactive gas that ubiquitous in the atmosphere |
|
|
Term
| What does radon decay into? |
|
Definition
|
|
Term
| How can radon induce cancer? |
|
Definition
| α particles damage tissue and induce cancer |
|
|
Term
| Where are there increased concentrations of radon? |
|
Definition
| in dwellings near underground sources of uranium |
|
|
Term
| How many americans smoke? |
|
Definition
| <30% (50 million) => 400,000 deaths/year |
|
|
Term
| What is the most common cause of cancer death in men & women? |
|
Definition
|
|
Term
| What helps w/ smoking cessasion? |
|
Definition
1) higher education
2) repeated suggestion by health professional
3) nicotine replacement
4) other medication |
|
|
Term
| What are the 2 types of lung cancer? |
|
Definition
1) small cell ("oat cell")
2) non-small cell |
|
|
Term
| What are the 4 types of non-small cell lung cancers? |
|
Definition
1) squamous
2) adenocarcinoma
3) BACA (bronchoalveolar cell carcinoma)
4) large cell carcinoma |
|
|
Term
| Is small cell or non-small cell cancers more common? |
|
Definition
|
|
Term
Small Cell/Oat Cell Lung Cancer
location?
growth/doubling time/size?
cavitation?
spread?
response to therapy?
autopsy data?
frequency? |
|
Definition
location: center
growth/doubling time/size: fast/30d/initally sm., but grows lg.
cavitation: not usually
spread: local + most distal spread of lung cancer
response to therapy: good initially, but doesn't last
autopsy data: 4-9% w/in the chest
frequency: 20% |
|
|
Term
| What is the hallmark of small cell/oat cell lung cancer? |
|
Definition
| distal spread (metastases) |
|
|
Term
Squamous Cell Lung Cancer
location?
growth/doubling time/size?
cavitation?
spread?
response to therapy?
autopsy data?
frequency? |
|
Definition
location: central
growth/doubling time/size: "medium"/100d/large
cavitation: high tendency
spread: locally to hilum - has least distant spread
response to therapy: poor
autopsy data: 40-50% have disease in chest
frequency: 30% (declining) |
|
|
Term
Adenocarcinoma of the Lung
location?
growth/doubling time/size?
cavitation?
spread?
response to therapy?
autopsy data?
frequency? |
|
Definition
location: peripheral
growth/doubling time/size: slow-medium/100-180d/sm-med.
cavitation: usually not
spread: pleural & chest wall, distant spread small cell>adenocarcinoma>squamous
response to therapy: poor
autopsy data: 18% w/in chest wall
frequency: ~40% |
|
|
Term
|
Definition
| slow growing adenocarcinoma of the lung |
|
|
Term
| Who are usually affected by BACA? |
|
Definition
| elderly, and can occur in non-smokers |
|
|
Term
| What is BACA often mistakenly diagnosed as? |
|
Definition
| pneumonia ∴ failure of Abx therapy can be a clue to diagnosis |
|
|
Term
| When is large cell carcinoma the diagnosis? |
|
Definition
1) very undifferentiated cells
2) often present as a large mass w/ hemorrhage & necrosis in leison
3) multiple sample w/in the leison done to look for more differentiated elements (diagnosis of exclusion)
4) frequency: 10% |
|
|
Term
| What of the non-small cell lung cancers has the worst prognosis? |
|
Definition
|
|
Term
|
Definition
1) long pre-clinical phase that is asymptomatic
2) CXR: mass/nodule, atelectasis, infiltrate, cavity, mediastinal or hilar enlargement due to adenopathy, pleural thickening, pleural effusion, elevated diaphargm
3) Clinical phase (symptomatic): cough, change in sputum, hemoptysis, chest pain, dyspnea, fever, weight loss, dysphagia, pancoast syndrome, hoarseness, superior vena cava syndrome, arrythmias, metastases Sx, paraneoplastic syndromes |
|
|
Term
| What causes Pancoast syndrome? |
|
Definition
| local growth of an apical lung tumor => invasion of leura, chest wall, destroys bone & involves brachial plexus |
|
|
Term
|
Definition
1) shoulder & back pain
2) pain, weakness, & atrophy of arm
3) ipsilateral horner's syndrome (pstosis, miosis, loss of sweating) |
|
|
Term
| What nerve damaged can cause hoarse voice? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
edema
venous dilation of face, neck, arms
headache
dizziness |
|
|
Term
| What causes arrythmias in lung cancer? |
|
Definition
|
|
Term
| What possible Sx can arise due to metastases? |
|
Definition
1) CNS
2) liver
3) bone
4) adrenal glands
5) abdominal lymph nodes
6) kidneys |
|
|
Term
| What 4 paraneoplastic syndromes can occur due to lung cancer? |
|
Definition
1) endocrinopathies
2) neuromuscular
3) dermatologic
4) hypertrophic pulmonary osteoarthropathy |
|
|
Term
| Which 2 paraneoplastic syndromes are most common w/ small cell lung cancer? |
|
Definition
1) endocrinopathies
2) neuromuscular |
|
|
Term
| What is the precursor cell of small cell lung cancer? |
|
Definition
|
|
Term
| Why are endocrinopathies more common w/ small cell lung cancer? |
|
Definition
| Kulchitsky cells demonstrate APUD (amine precursor uptake & decarboxylation) |
|
|
Term
|
Definition
| tumors produce biologically active substances s.a. ACTH, ASH, ADH, others |
|
|
Term
| Which endocrinopathy is most common w/ squamous lung cancer? |
|
Definition
|
|
Term
| What are some neuromuscular paraneoplastic syndromes seen w/ lung cancer? |
|
Definition
1) polyneuropathies
2) myopathies
3) subacute corticocerebellar degeneration
4) myasthenic syndrome |
|
|
Term
| What dermatologic paraneoplastic syndromes are seen w/ lung cancer? |
|
Definition
1) dermatomyosis
2) acanthosis nigricans |
|
|
Term
| What is seen w/ hypertrophic pulmomary osteoarthopathy? |
|
Definition
|
|
Term
| How is lung cancer diagnosed? |
|
Definition
1) sputum cytology
2) bronchoscopy
3) transthoracic needle aspiration
4) thoracotomy
5) pleural tap & biopsy
6) tissue or fluid from a metastatic site |
|
|
Term
| Why is sputum cytology used less frequently in diagnosis of lung cancer? |
|
Definition
1) difficult to collect
2) false - & + |
|
|
Term
Function
bronchoscopy in tumor Dx |
|
Definition
1) visualize tumor site
2) cytologic & histologic specimens |
|
|
Term
| How does transthoracic needle aspiration work for lung cancer Dx? |
|
Definition
| usually CT guided & yields good cytology |
|
|
Term
| What are the 5 Tx options for lung cancer? |
|
Definition
1) surgery
2) radiation
3) chemo
4) other palliative Tx
5) supportive care |
|
|
Term
| When is surgery used for lung cancer Tx? |
|
Definition
1) non-small cell patients w/ low staging (almost never for small cell)
2) can be curative or may be used as an adjunct or palliative measure |
|
|
Term
| Is radiation therapy curative for lung cancer? |
|
Definition
|
|
Term
| What's the purpose of radiation therapy in lung cancer if not curative? |
|
Definition
1) local control (external mean, endobronchial)
2) pallation |
|
|
Term
| When is chemotherapy used in the Tx of lung cancer? |
|
Definition
1) small cell - low curative rate
2) experimental in non-small cell
3) distant disease control |
|
|
Term
| What other palliative Tx options are there for lung cancer? |
|
Definition
1) bronchial stents
2) laser therapy
3) cryotherapy |
|
|
Term
| What are the 3 current possible future Tx options for lung cancer? |
|
Definition
1) genetic markers to predict risk
2) modulation of tumor growth regulators
3) manipulation of intracellular signals |
|
|
Term
| What 3 factos are involved in the choice of therapy for lung cancer? |
|
Definition
1) histology
2) physiologic status
3) stage of disease |
|
|
Term
| What is the major histological determinant of lung cancer therapy? |
|
Definition
| small cell vs non-small cell |
|
|
Term
Why can't surgery be curative in small cell lung cancer?
What is the possible curative Tx option? |
|
Definition
surgery isn't an option since most likely there is metastatic spread
It may respond to chemotherapy |
|
|
Term
| What are the 4 physiologic status properties evaluated before Tx for lung cancer is decided? |
|
Definition
1) operability (will patient tolerate surgery & have adequate pulmoary function post-op?)
2) overall status (adequate to tolerate chemo, risk:benefit ratio?)
3) survivorship (will it improve w/ Tx?)
4) QOL |
|
|
Term
| What is used to determine a patient's operability? |
|
Definition
1) PFTs
2) others: exercise tests, ABGs, V/Q studies |
|
|
Term
|
Definition
| local extent/distal spread |
|
|
Term
| What is the rationale for staging cancer? |
|
Definition
1) determine resectability & extent of disease
2) determination of prognosis
3) uniformity when comparing treatments & responses in studies |
|
|
Term
| What are the 2 types of methods for staging cancer? |
|
Definition
1) non-invasive
2) invasive |
|
|
Term
| What are the non-invasive ways to stage cancer? |
|
Definition
1) H & P
2) routine blood work
3) other radiologic studies based on signs & Sx |
|
|
Term
| What are the 5 invasive methods to staging lung cancer? |
|
Definition
1) bronchoscopy (to evaluate airways, distance of tumor from carina, biopsy)
2) mediastinal exploration (to evaluate nodes)
3) pleural tap & biopsy
4) tissue from metastatic sites
5) surgical staging |
|
|
Term
| What is the standard TNM staging? |
|
Definition
1) T = tumor
2) N = nodes
3) M = metastases |
|
|
Term
|
Definition
| 1) TX = tumor cells in secretions, no tumor seen
2) T0 = no primary tumor seen
3) T1 = small tumor w/ no other structures invaded
4) T2 = large tumor OR any size tumor invading pleura, associated w/ obstruction
5) T3 = any size tumor invading chest wall but not heart OR close to carina
6) T4 = any size tumor invading mediastinum or heart/great vessels, esophagus, vertebrae, carina, or associated w/ malignant effusion |
|
|
Term
|
Definition
| 1) NX = cannot assess regional nodes
2) N0 = no regional nodes
3) N1 = bronchial or hilar nodes on the side w/ tumor
4) N2 = mediastinal or subcarinal nodes
5) N3 = contralateral nodes, scalene or suraclavicular nodes
6) N4 = |
|
|
Term
|
Definition
| 1) MX = cannot be assessed
2) M0 = no distant metastases
3) M1 = distant metastases |
|
|
Term
| When are you a stage 1 cancer? |
|
Definition
T1 or 2 (IA w/ T1, IB w/ T2)
N0
M0 |
|
|
Term
| When are you a stage 2 cancer? |
|
Definition
T3, N0 (IIB)
T1 or 2, N1 (IIA, except IIB w/ T2)
M0 |
|
|
Term
| When are you a stage 3 cancer? |
|
Definition
T1, N 2,3 (IIIA, except IIIB w/N3)
T2. N 2,3 (IIIA, except IIIB w/N3)
T3, N 1,2,3 (IIIA, except IIIB w/ N3)
T4, N any (IIIB)
M0 |
|
|
Term
|
Definition
|
|
Term
| Which stages can be approached surgically? |
|
Definition
|
|
Term
| Can stage of cancer help w/ prognosis? |
|
Definition
|
|
Term
| *How often are patients considered resectable w/ lung cancer at diagnosis? |
|
Definition
|
|
Term
| *What is the overall 5y survival of a lung cancer patient w/ surgery? |
|
Definition
|
|
Term
| *What is the 5y survival overall for lung cancer? |
|
Definition
|
|
Term
| What is the theory for screening for lung cancer? |
|
Definition
earlier detection = earlier disease stage = better cure rate/survival
(~ to that of colon, cervix, prostate, breast cancer) |
|
|
Term
| What are the problems w/ screening for lung cancer? |
|
Definition
1) earlier study showed no benefit
2) who is the high risk group? |
|
|
Term
| Who are the 4 types of people that should get focused lung cancer screening? |
|
Definition
1) smoking pack years >30
2) obstructive airway disease
3) known ocupational/exposure risks
4) genetic risk (familial/gene markers) |
|
|
Term
| Why are those w/ a >30 pack/year Hx at a greater risk than those who smoke less/don't? |
|
Definition
| lung cancer risk is "dose dependent" |
|
|
Term
| Does the cancer risk for people who quit smoking ever reach that of non-smokers? |
|
Definition
|
|
Term
| What test is done to check for obstructive airway disease? |
|
Definition
|
|
Term
| Why are those with obstructive airway disease at a higher risk for lung cancer? |
|
Definition
| cancer risk increases w/ increasing obstruction |
|
|
Term
| What are the 3 general aspects of lung cancer? |
|
Definition
1) classification
2) age @ presentation
3) etiology & epidemiology |
|
|
Term
| What are the 6 parts of the pathology of cancer? |
|
Definition
1) anatomocal distribution
2) precursor leisons
3) tissue diagnosis
4) description of major histotypes
5) field effect in lung cancer
6) molecular alterations |
|
|
Term
| How are lung tumors classified? |
|
Definition
| on the basis of biological behavior & differentiation (encompasing epithelial, soft tissue, mesothelial tumors & lymphoproliferative disorders) |
|
|
Term
| What are the 2 major classifications of lung tumors (or really, any tumor)? |
|
Definition
|
|
Term
| What is the most common type of primary tumors in the lung? |
|
Definition
| malignant epithelial tumors |
|
|
Term
| How are small cell carcinomas different from non-small cell carcinomas? |
|
Definition
small cell: treated w/ chemo
non-small cell: treated w/ surgery (if of limited stage) |
|
|
Term
| What are the 3 non-small cell lung cancer types? |
|
Definition
1) squamous cell carcinoma
2) adenocarcinoma
3) large cell carcinoma |
|
|
Term
|
Definition
| tumors w/ combined features |
|
|
Term
| What are the 2 types of carcinoid tumors seen in the lung? |
|
Definition
|
|
Term
| Can there be secondary malignant tumors in the lung? |
|
Definition
|
|
Term
| Of the malignant tumors available to the lung, which have neuroendocrine differentiation? |
|
Definition
1) Lage cell w/ neuroendocrine features (subtype)
2) carcinoids |
|
|
Term
| Who is affected by lung cancer? |
|
Definition
middle aged/elderly
men
smoker |
|
|
Term
| What reflects the long latency of lung cancer development? |
|
Definition
| advanced age at presentation, considering exposure to cigarette smoking starts long before clinical presentation |
|
|
Term
| Why is there a long latency for lung cancer development? |
|
Definition
| necessity for genetic abnormalities & cloncal expansion |
|
|
Term
| What is the number one killer among cancers? |
|
Definition
|
|
Term
| Why is lung cancer the number one killer? |
|
Definition
| by virtue of it's advanced stage at presentation (highlighting that mortality is related to stage at presentation) |
|
|
Term
| What are the risk factors for lung cancer? |
|
Definition
1) smoking
2) environmental/occupational exposures to carcinogens (s.a. asbestos)
3) personal genome
4) aging
5) infections (s.a. HOPV => SqCC) |
|
|
Term
| How closely linked is the risk of lung cancer to smoking? |
|
Definition
| the incidence of lung cancer is proportional to the extent and duration of exposure to cigarette smoke |
|
|
Term
| Can lung cancer arise w/o the presence of smoking? |
|
Definition
| yes (tho only ~15% of lung cancer, and only a small subset is contributed to second hand smoke) |
|
|
Term
| Why so only some smokers develop lung cancer? |
|
Definition
| There are wide variations in the risk of developing lung cancer among patients w/ comparable smoke exposure - unclear, but it's probably due to a complex interplay of gender, genetic & environmental factors |
|
|
Term
| Of the non-smokers, who is most likely to have lung cancer, and what cancer type? |
|
Definition
adenocarcinoma
young females
(women may have increased incidence, but they have less mortality) |
|
|
Term
| What is the most common histotype of lung cancer? |
|
Definition
|
|
Term
| What is the second most common histotype of lung cancer? |
|
Definition
|
|
Term
| Which cancer histotypes have the highest associations w/ cigarette smoking? |
|
Definition
|
|
Term
| Which lung cancer type has the strongest association w/ smoking? |
|
Definition
| Small Cell (99%) > SqCC (98%) > Lg. CC (93%) > Adeno (82%) |
|
|
Term
| What are the 6 features types that differentiate the different lung cancer types? |
|
Definition
1) anatomical sites of origin
2) association w/ smoking
3) stages @ presentation & prognosis
4) sensitivity to chemo
5) clinical presentations
6) molecular abnormalities |
|
|
Term
| Which lung cancer type arises most frequently in non-smokers? |
|
Definition
| Adenocarcinoma (18%) > Lg. CC (7%) > SqCC (2%) > Sm. CC (1%) |
|
|
Term
| What proportion of the non-smokers within the adenocarcinoma cancer category have the BAC (bronchiolo-alveolar) subtype? |
|
Definition
|
|
Term
Which lung cancer types ten to be central (bronchial mucosa)?
Which lung cancer types tend to be more peripheral (bronchioles-alveoli)? |
|
Definition
central: SqCC, & SCC
peripheral: Adeno & LCC |
|
|
Term
| Why is it important to know the location of the tumors in the lung? |
|
Definition
1) reflects differences in cell of origin
2) dictates differences in clinical presentation |
|
|
Term
Sx
SqCC & SCC
Local Tumor Growth |
|
Definition
Cough
hemoptysis
stridor
atelectasis
pneumonia
dyspnea |
|
|
Term
Sx
Adeno & LCC
Peripheral tumor growth |
|
Definition
plueral effusion
chest pain |
|
|
Term
| Which lung cancer tumors are likely to metastasize? |
|
Definition
|
|
Term
Sx
Metastases
SCC, Adeno, LCC |
|
Definition
|
|
Term
| Which lung cancer type is likely to have paraneoplastic syndromes? |
|
Definition
|
|
Term
Sx
Paraneoplastic syndromes
SCC |
|
Definition
hyponatremia
Cushings
muscle weakness
etc. |
|
|
Term
| Which lung cancer histotypes are more prone to give clinical presentations secondary to the effect of the primary tumor? |
|
Definition
1) those located centrally
2) those that involve the hilum
3) those that invade the chest wall |
|
|
Term
| How does the clinical presentation depend on the intrinsic differences in biology & aggressiveness of the different lung cancer histotypes? |
|
Definition
| The aggressiveness is intrinsically driven and biology determines the likelihood to metastesize, grow fast, and have paraneoplastic syndromes. |
|
|
Term
| Which lung cancer histotype has the highest proliferative rate of all lung cancers? |
|
Definition
| Sm. CC ∴ most responsive to chemotherapy |
|
|
Term
| What is the treatment of choice for non-small cell lung cancers? |
|
Definition
| surgery (if viable option & stage is low) |
|
|
Term
| What lung cancer histotype tends to be found at a lower, more treatable stage? |
|
Definition
|
|
Term
| Is SmCC found generally at a low or high cancer stage? |
|
Definition
|
|
Term
| Is adenocarcinoma of the lung found generally at a high or low cancer stage? |
|
Definition
| higher than SqCC but lower than SmCC |
|
|
Term
| Of all the malignant lung tumors, which have the highest 5 year survival rates? |
|
Definition
| Carcinoid (83%) > BAC (42%) > ... > SmCC (5%) |
|
|
Term
| Which lung cancer histotypes have well known precursors? |
|
Definition
SqCC & Adeno: well-known
SmCC: not known |
|
|
Term
| What is the pathogenesis for SqCC? |
|
Definition
| Normal bronchial mucosa => squamous metaplasia => low grade dysplasia => high grade dysplasia => invasive SqCC |
|
|
Term
| What are the morphological criteria to consider in the progression of SqCC? |
|
Definition
1) degree of differentiation
2) cytological grade |
|
|
Term
| What happens in squamous metaplasia? |
|
Definition
| native ciliated bronchial epi. is replaced by squamous epi. |
|
|
Term
| What characterizes the increasing degree of dysplasia arising from the squamous metaplasia? |
|
Definition
| expansion of replicative component w/in the epi. @ the expense of the superficial, differentiated component |
|
|
Term
| What happens to the squamous metaplasia epi. w/ increasing dysplasia? |
|
Definition
increasing area of epi. is replased by dysplastic cells.
dysplastic cells: high N/C ratio, cariation in size & shape (pleomorphism), & high proliferative rate |
|
|
Term
|
Definition
| carcinoma in situ = highest pre-invasive grade of dysplasia, with the dysplastic cells occupying the full-thickness of epi. Apical maturation into differentiated squamous cells is either absent of negligable |
|
|
Term
| What in the genes parallels the morphological changes seen with increasing dysplasia? |
|
Definition
| increasing molecular abnormalities in genes controlling the cell cycle progression |
|
|
Term
| In which genes can molecular abnormalities in genes controlling the cell cycle occur? |
|
Definition
1) p53
2) Cyclin D & E
3) EGFR
4) telomerase activation
5) CDKs
6) chromosomal losses |
|
|
Term
| What is the pathogenesis of lung adenocarcinoma? |
|
Definition
| normal terminal bronchioles/alveoli => atypical adenomatous hyperplasia => bronchio-alveolar carcinoma growth pattern => invasive adenocarcinoma |
|
|
Term
| What are normal alveolar sacs composed of? |
|
Definition
| think membrane of flattened, elongated cytoplasm of alveolar type I pneumocytes, juxtaposed, thru a shared BM to endothelial cells |
|
|
Term
|
Definition
|
|
Term
| What occurs in atypical adenomatous hyperplasia? |
|
Definition
| an increase in the number & cytological grade of the alveolar lining pneumocytes takes place |
|
|
Term
| What happens to the alveolar septa as the alveolar lining pneumocytes changes to atypical adenomatous hyperplasia? |
|
Definition
| becomes progressively thickened secondary to fibrosis |
|
|
Term
| What happens in BAC compared to other adenocarcinomas of the lung? |
|
Definition
1) increased septal fibrosis & increased cytological atypia takes place
2) may occupy an entire lobe or lung (while other adenocarcinomas are found only in microscopic foci)
3) can occur by itself or w/ invasive adenocarcinoma
4) carcinoma that is entirely composed of non-invasive growth pattern ∴ ~ to CIS since does not breach BM |
|
|
Term
| What is the difference b/w adenomatous hyperplasia (AAH) & BAC? |
|
Definition
AAH:
1) < cytological atypia
2) thin septa
3) < 5mm
4) incidental finding
BAC:
1) > cytological atypia
2) fibrotic septa
3) > 5mm & may occupy lobe or lung
4) clinically evident |
|
|
Term
| What occurs to the alveolar outline in the transition from non-invasive to invasive adenocarcinoma? |
|
Definition
| progressive destruction & remodeling |
|
|
Term
| What happens w/ molecular alterations when the transition from non-invasive to invasive adencarcinoma? |
|
Definition
| increased molecular alterations inc. activation of oncogenes, loss of suppressor genes, & activation of telomerase |
|
|
Term
| What is needed before Tx for a malignant tumor can be initiated? |
|
Definition
| tissue diagnosis of malignancy |
|
|
Term
| What is the only non-invasive way to obtain lung tissue? |
|
Definition
| analysis of cells in sputum (sputum cytology) |
|
|
Term
| What invasive procedures are there for lung tissue biopsy? |
|
Definition
1) transthoracic sampling of lung for cells (fine needle aspiration) or tissue (fine needle biopsy)
2) diagnostic procedures during bronchoscopy (s.a. washing & brushing - for cytological specimen - or biopsy - for tissue) |
|
|
Term
| What dictates the sensitivity of the diagnostic techniques to obtain tissue/cells of the lung? |
|
Definition
| differences in anatomical distribution of the lung cancer |
|
|
Term
| When is the sensitivity for sputum cytology the highest? |
|
Definition
| central leison (i.e. SqCC & SCC - esp. SqCC) |
|
|
Term
| What can increase the sensitivity of sputum cytology for peripheral leisons (i.e. adeno & LCC)? |
|
Definition
| addition of washing & brushing |
|
|
Term
| How effective is bronchoscopy-based techniques at diagnosis of lung tumors? |
|
Definition
allows for diagnosis in ~70% of cases (the reamining need transthoracic sampling)
most sensitive for central leisons as well |
|
|
Term
| Which histotypes of lung cancer usually require fine needle aspiration? |
|
Definition
|
|
Term
| What does transthoracic aspiration have the highest sensitivity to? |
|
Definition
|
|
Term
| What decreases the sensitivity of transthoracic aspiration? |
|
Definition
|
|
Term
| How accurate is biopsy overall at distinguishing SCC from non-SCC? |
|
Definition
|
|
Term
| Does lung cancer hace a pathognomonic morphological feature to distinguish it from metastaes? |
|
Definition
| no (i.e. SqCC of the lung is not different from one of the larynx) |
|
|
Term
| How are lung tumors differentiated as primary or secondary if there is usually no distinction b/w a primary & metastatic tumor? |
|
Definition
clinical evaluation & extensive imaging studies is needed to R/O other possible primary sites
(& there is no substitute for clinical judgement since pathology is not 100% sensitive or specific) |
|
|
Term
|
Definition
| its ability to show squamous differentiation, highlighted by keratinization &/or intercellular bridges |
|
|
Term
| What characterizes SqCC w/ squamous cell differentiation highlighted by keratinization? |
|
Definition
| intracytoplasmic accumulation of intermediate filaments & progressive reducation of the N/C ratio => formation of elongated or spindly cells w/ deeply eosinophilic cytoplasm & absent/inconspicuous nucleus (squames) |
|
|
Term
| What characterizes SqCC w/ squamous cell differentiation highlighted by intercellular bridges? |
|
Definition
| by LM as thin intercellular striations that correspond ultrastructurally to the presence of desmosomes b/w interlocking cytoplasmic projections of adjacent cells |
|
|
Term
| What happens to the gradient of differentiation normally seen in squamous epithelium in SqCC? |
|
Definition
| replaced - typically growing in nests featuring an undifferentiated component of basaloid cells @ the periphery w/ progressive differentiation toward the center |
|
|
Term
| What are typically seen occupying the center of the tumor nests? |
|
Definition
| accumulating squames mixed w/ apoptotic & necrotic debris |
|
|
Term
| Can SqCC cause cavitation? |
|
Definition
| yes, even when small size (~1/3 of all SqCC causes cavitation) |
|
|
Term
| What dictates the grade of the SqCC leison? |
|
Definition
| ratio of different cell types & the degree of cytological atypia |
|
|
Term
| When can papillary SqCC arise? |
|
Definition
| recurrent laryngeal papillomatosis |
|
|
Term
|
Definition
| malignant epithelial tumor w/ glandular differentiation |
|
|
Term
| How does glandular differentiation manifest itself @ the architechtural level? |
|
Definition
| in the arrangement of cells around central lumens, as in the acini of exocrine glands |
|
|
Term
| What highlights glandular differentiation @ the single cell level? |
|
Definition
| ability of tumor cells to manufacture secretory molecules |
|
|
Term
| What secretory molecules are manufactured in lung adenocarcinoma? |
|
Definition
| mucins, molecules normally produced by Clara cells or surfactant |
|
|
Term
|
Definition
| a subtype of adenocarcinoma w/ distinct clinical, radiological, & pathological features |
|
|
Term
| What are the 4 main histological features of BAC (bronchioloavleolar cell carcinoma)? |
|
Definition
1) no stromal invasion
2) high incidence in non-smokers & women
3) peripheral
4) can remain stable for years or disseminate/recur to other lung fields (multifocal) |
|
|
Term
| Is BAC mucinous or serous? |
|
Definition
| can be either sybtype of BAC |
|
|
Term
|
Definition
1) over 1/2 have an asymptomatic nodule discovered incidentally
2) may mimic pneumonia due to lack of desmoplasia & lack of stromal invasion |
|
|
Term
|
Definition
| better survival compared to stage matched adenocarcinoma for leisons <3 cm |
|
|
Term
| Why is BAC possibly considered a pre-invasive phase of adenocarcinoma? |
|
Definition
| can have focal growth of BAC in conventional adenocarcinoma |
|
|
Term
| Is it called BAC if there is adenocarcinoma w/ focal BAC growth? |
|
Definition
no, it's only named BAC if all leisons & have exclusively BAC growth pattern
(any foci of invasion = NOT BAC since BAC ~ to CIS) |
|
|
Term
| Is it considered BAC still if the leisons are >3cm? |
|
Definition
| no => just adenocarcinoma at that point |
|
|
Term
| Why can there be pleural retraction seen in adenocarcinoma? |
|
Definition
| extensive tissue remodeling |
|
|
Term
|
Definition
| undifferentiated malignant tumor that lacks the cytological features of SCC & glandular or squamous differentiation |
|
|
Term
| What do tumor cells look like typically in LCC? |
|
Definition
| lg. nuclei, prominent nucleoli & a moderate amount of cytoplasm growing in solid and often discohesive sheets w/ prominent cell borders |
|
|
Term
| What is LCC oftenly misused for synonymously? |
|
Definition
| non-small cell lung carcinoma (it's NOT, it's a TYPE of NSCL) |
|
|
Term
| What is implyed by the diagnosis of LCC since it's a diganosis of exclusion? |
|
Definition
| absence of differentiation (∴ thorough sampling is necessary for a correct diagnosis) |
|
|
Term
| What is a variant of LCC that shows evidence of neuroendocrine differentiation by immunohistochemistry? |
|
Definition
| large cell neuroendocrine carcinoma |
|
|
Term
| What are the 3 lung tumor types that can show neuroendocrine differentiations? |
|
Definition
1) large cell neuroendocrine carcinoma
2) SCC
3) carcinoid (typical & atypical) |
|
|
Term
| What is the SCC tumor made of? |
|
Definition
| small sized cells w/ high proliferative & apoptotic reates, high N/C ratio, & distinct cytolocial features (inc. fine chromatin, crush artifact, & necrosis) |
|
|
Term
| How do the cells in SCC grow? |
|
Definition
| in nests separated by stroma that usually has a fine vascular netowrk (neuroendocrine architecture) |
|
|
Term
| What do the cells in a SCC tumor look like? |
|
Definition
1) high N/C ratio
2) scant rim of cytoplasm
3) finely granular chromatin
4) absent/rare nucleoli
5) round/spindly
6) exhibiting molding, crush artifact & extensive necrosis
7) high proliferative rate |
|
|
Term
| Why is SCC Tx modality limited to chemotherapy? |
|
Definition
|
|
Term
| Why does Dx of SCC rely on morphological features & not on immunohistochemistry? |
|
Definition
evidence of neuroendocrine differentiation may be absent in immunohistochemical evidence
(∴ it's the pathologists job to differentiate b/w SCC & NSCL & it's a very important distinction, w/ inter-observer reproducibility of ~95%) |
|
|
Term
def
typical carcinoid tumor |
|
Definition
| tumor w/ NE features histologically (nested pattern, high vascularity), cytologically (finely dispersed chromatin), immunohistochemically, & ultrastructurally, w/ a low proliferative rate & no necrosis |
|
|
Term
|
Definition
| very small typical carcinoids |
|
|
Term
Prognosis
typical carcinoid |
|
Definition
|
|
Term
| Are typical carcinoids associated w/ smoking? |
|
Definition
|
|
Term
| Are men or women more likely to get typical carcinoid? |
|
Definition
|
|
Term
| How are typical carcinoids typically found? |
|
Definition
| incidentally aince most often asymptomatic |
|
|
Term
| When are Sx for typical carcinoids more likely to occur? |
|
Definition
| centrally located typical carcinoids |
|
|
Term
Sx
typical carcinoids (if symptomatic) |
|
Definition
hemoptysis
duspnea
post-obstructive pneumonia (secondary to bronchial obstruction) |
|
|
Term
| What are the tumor cells characterized by in typical carcinoids? |
|
Definition
1) relatively low N/C ratio
2) prominent rim of granular cytoplasm
3) typical neuclear fatures
4) fine & homogeneously dispersed chromatin ("salt & pepper" pattern)
5) absent/very small nucleoli |
|
|
Term
| How are the tumor cells arranged in typical carcinoid tumors? |
|
Definition
| in nests, tightly juxtaposed to a rich capillary network |
|
|
Term
| How is the neuroendocrine differentiation of a typical carcinoid highlighted? |
|
Definition
1) strong immunoreactivity of tumor cells for neuroendocrine markers (inc. Synaptophysin & Chromogranin)
2) numerous neuroendocrine secretory granules are evident ultrastructurally |
|
|
Term
| How does central typical carcinoid tumor behave? |
|
Definition
1) undermine bronchial mucosa
or
2) grow as exophytic, endobronchial masses |
|
|
Term
| Do typical carcinoid tumors tend to be central or peripheral? |
|
Definition
|
|
Term
| What characterized atypical carcinoid tumors compared to typical carcinoids? |
|
Definition
1) much more aggressive behavior
2) higher incidence of lymph node metastases
3) worse prognosis
4) larger than typical carcinoid
5) similar morphological pattern
6) similar cytological features
7) *presence of necrosis &/or higher mitotic count |
|
|
Term
| How does necrosis in atypical carinoids typically occur? |
|
Definition
| punctate, comedo-like foci |
|
|
Term
| What distinguishes an atypical carcinoid from a SCC? |
|
Definition
|
|
Term
| How often is lung cancer multifocal? |
|
Definition
4-8%
(up to 20% in carcinoid tumors) |
|
|
Term
| If more than one tumor occurs in lung cancer, does it occur at the same time or develops over time? |
|
Definition
|
|
Term
| What is the incidence of a secondar primary lung tumor in survivors? |
|
Definition
| 1-2%/year (overall 7% of lung cancer) |
|
|
Term
| What is the incidence of a second primar tumor in head & neck cancer survivors? |
|
Definition
| 1-2%/year & includes lung cancer |
|
|
Term
| What causes the phenomenon of the incidence of a new primary tumor in survivors? |
|
Definition
field of carcinogenesis, composed of multiple pre-neoplastic leisons, created by exposure to smoking, involving the entire lower RT (the upper aero-digestive tract is involved if smoking & drinking)
any of the premalignant foci may progress & develop into overt invasive carcinoma |
|
|
Term
| Do molecular alterations differ b/w different lung cancer histotypes? |
|
Definition
|
|
Term
| What in lung cancer histotypes can characterize smoking related vs non-smoking related cancers? |
|
Definition
|
|
Term
| Which lung cancer histotype has a K-RAS mutation w/ smokers? |
|
Definition
|
|
Term
| Which lung cancer histotype has a Rb deletion? |
|
Definition
|
|
Term
| What other mutation are Rb deletions in SCC often found in association w/? |
|
Definition
|
|
Term
| Which lung cancer histotypes are associated w/ p53 mutations? |
|
Definition
| all (but highest frequency in SqCC & SCC) |
|
|
Term
| What is the difference b/w a p53 mutation in smokers vs non-smokers? |
|
Definition
| smokers have a predominance of G-C transversions over G-T transitions |
|
|
Term
| When can lung adenocarcinoma show a EGFR mutation? |
|
Definition
| non-smokers, women, Asian descent |
|
|
Term
| Why are there 2 pathogenic pathways for adenocarinoma involving EGFR & K-Ras mutations? |
|
Definition
| they are exclusive of eachother |
|
|
Term
| Can Rb deletions occur in NSCL? |
|
Definition
| yes, but are no where near as frequent as in SCC |
|
|
Term
| Why is it important in the patient's eyes for you to address smoking cessation? |
|
Definition
1) they expect to be encouraged to quit
2) failure to do so implies quitting isn't important |
|
|
Term
| With whom does the decision to quit smoking lie w/? |
|
Definition
|
|
Term
| What are the 5 A's for clinicians to do w/ each patient? |
|
Definition
1) Ask about tobacco use
2) advise tobacco users to quit
3) assess readiness to quit
4) assist w/ quit attempts
5) arrange follow up care |
|
|
Term
| What compunds are in tobacco smoke? |
|
Definition
| over 4800 compounds, 11 of which are known carcinogens |
|
|
Term
| What is nicotine's role in tobacco smoke? |
|
Definition
| addictive component (NOT carcinogenic) |
|
|
Term
| What are the health consequences of smoking? |
|
Definition
1) cancer
2) pulmonary disease
3) CV disease
4) reproductive effects
5) other |
|
|
Term
| How much does lung function improve just w/in 3 months of smoking cessation? |
|
Definition
|
|
Term
| When does cilia function return to normal after smoking cessation? |
|
Definition
|
|
Term
| What happens to CVD risk after 1 year smoking cessation? |
|
Definition
| down to 1/2 that of continuing smoker |
|
|
Term
| When is risk of stroke down to that of someone who's never smoked? |
|
Definition
|
|
Term
| When does lung cancer risk become half of a smoker after cessation? |
|
Definition
|
|
Term
| When is CVD risk of a smoker that of someone who's never smoked? |
|
Definition
|
|
Term
| When is lung cancer risk that of someone who's never smoked? |
|
Definition
|
|
Term
|
Definition
1) pleasure
2) arousal, enhanced vigilance
3) imporved task performance
4) anxiety relief |
|
|
Term
Effects
Nicotine of CV system |
|
Definition
1) increased HR
2) increased CO
3) increased BP
4) coronary vasoconstriction
5) cutaneous vasoconstriction |
|
|
Term
| What other effects does nicotine have on the body? |
|
Definition
1) appetite suppression
2) increased metabolic rate
3) skeletal muscle relaxation |
|
|
Term
|
Definition
| compulsive drug use w/o medical purpose in the face of negative consequences |
|
|
Term
| Why does discontinuation of nicotine lead to withdrawl Sx? |
|
Definition
| nicotine stimulates DA release => pleasurable feelings & repeated administration => tolerance |
|
|
Term
| When do nicotine w/drawl Sx occur? |
|
Definition
| start w/in 1-2 days of discontinuation & peak in the first week & subside w/in 2-4 weeks |
|
|
Term
|
Definition
1) irritability/anger/frustration
2) anxiety
3) restlessness/impatience
4) depression
5) insomnia
6) impaired performance
7) increased appetite/weight gain
8) cravings |
|
|
Term
| When assessing a patient's readiness to quit, what are the 5 stages of readiness that they could be categorized as? |
|
Definition
1) precontemplation
2) contemplation
3) preparation
4) action
5) maintenance |
|
|
Term
|
Definition
| not ready to quit in the next 6 months |
|
|
Term
| Why would a patient be in the precontemplation stage? |
|
Definition
1) struggle w/ ambivalence to change
2) not ready to change
3) pros outweigh the cons for them
4) may or may not be aware of need to quit |
|
|
Term
| What is the goal of the physician when dealing with a patient in the precontemplation stage? |
|
Definition
| move patient into contemplation stage |
|
|
Term
| What are the counseling strategies for a patient in the precontemplation stage to move them to contemplation? |
|
Definition
DO:
1) strongly advise quitting & provide info. on how to & why to quit
2) ask noninvasive questions to find out the reason for use
3) demonstrate emplathy & foster communication
4) leave decision to patient
Don't:
1) presuade/cheerlead
2) be judgemental
3) provide Tx plan |
|
|
Term
|
Definition
| considering quitting in the next 6 mo., but not ready in the next 30 days |
|
|
Term
| Why would a patient be in the contemplation stage? |
|
Definition
1) aware of need to quit
2) aware of benefits of quitting
3) struggle w/ ambivalence of change |
|
|
Term
| What is the physician's goal when dealing w/ a patient in contemplation? |
|
Definition
| move them to preparation stage |
|
|
Term
| What are the 5 R's to increase motivation of someone in the contemplation stage? |
|
Definition
1) relevance
2) risks
3) rewards
4) roadblocks
5) repetition
(leads to a tailored motivational message) |
|
|
Term
|
Definition
| ready to quit w/in the next 30 days |
|
|
Term
| What is the mindset of patients in the preparation phase? |
|
Definition
1) aware of need to & benefits of quitting
2) getting ready to take action |
|
|
Term
| What is the goal physician's dealing w/ patients in the preparation phase? |
|
Definition
|
|
Term
| What is the role of the physician in facilitating a patient in the preparation phase? |
|
Definition
1) praise patient's readiness to quit
2) assess tobacco use Hx
3) discuss key issues
4) facilitate the quitting process
5) congratulate the patient |
|
|
Term
| What about the patient's tobacco use Hx needs to be assessed? |
|
Definition
1) current use (types, brand, amount)
2) past use (duration, recent changes)
3) past quit attempts (number, date, length, methods used, compliance, reason for relapse) |
|
|
Term
| What are the 6 keys issues that must be discussed with patients in the preparation phase? |
|
Definition
1) reasons/motivation to quit/avoid relapse
2) confidence in ability to quit/avoid relapse
3) triggers for use
4) routines/situations associated w/ tobacco use
5) concerns about weight gain
6) concerns about w/drawl Sx |
|
|
Term
| What specifically regarding weight gain concerns should be addressed while counseling a patient in preparation? |
|
Definition
1) avoid strict dieting (exercise, nonfood rewards, increase water intake, sugarless gum)
2) pharmacotherapy is an option
3) specialists/program referral for more help |
|
|
Term
| How long do cravings for cigarettes last? |
|
Definition
| longer than most withdrawl Sx (several months/years) |
|
|
Term
| How can the physician facilitate the quitting process for a patient in preparation? |
|
Definition
1) discuss methods for quitting
2) set quit date
3) recommend tobacco use log
4) discuss coping strategies
5) provide medication counseling
6) discuss concept of "slip" vs relapse
7) offer to assist throughout quit attempt |
|
|
Term
| What needs to be addressed when discussing methods of quitting for a patient in preparation? |
|
Definition
1) pros & cons of available methods
2) pharmacotherapy is a Tx, not a crutch
3) importance of behavioral counseling |
|
|
Term
| Why is a tobacco use log helpful? |
|
Definition
1) helps patient understand when, why, & how much they're smoking
2) identifies activities or situations that trigger tobacco use
3) can be used to develop coping strategies to overcome the temptation to use tobacco |
|
|
Term
| What are the different coping strategies for when somone is having withdrawl/cravings after quitting smoking? |
|
Definition
1) cognitive (focus on retraining the way a patient thinks)
2) behavioral (involve specific actions to reduce risk for relapse) |
|
|
Term
| When should the physician follow up after the scheduled quit date for a patient? |
|
Definition
1) first week after quitting
2) first month after quitting
3) additional as needed |
|
|
Term
|
Definition
| actively trying to quit for good |
|
|
Term
| When is a patient in the action phase? |
|
Definition
| they have quit smoking sometime in the past 6 months and are taking steps to increase their success, tho may have withdrawl Sx/cravings |
|
|
Term
| When are patient's at risk for relapse in smoking? |
|
Definition
|
|
Term
| What is the goal of the physician dealing w/ patients in the active phase of smoking cessation? |
|
Definition
| remain tobacco free for at least 6 months |
|
|
Term
|
Definition
| tobacco free for 6 months |
|
|
Term
| What patients are in the maintenance phase? |
|
Definition
| former tobacco user, quit >6 mo. ago |
|
|
Term
| Are patients in the maintenance phase of smoking cessation still at risk for relapse? |
|
Definition
| yes, thus ongoing relapse prevention is needed |
|
|
Term
| What is the goal of the patient dealing w/ a patient in the maintenance phase of tobacco cessation? |
|
Definition
| remain tobacco free for life |
|
|
Term
| What are the 3 non-pharmacological methods for smoking cessation? |
|
Definition
1) cold turkey
2) unassisted tapering (reduce frequency, lower nicotine cigarettes, special filters)
3) assisted tapering (QuitKey - computer/telephone support) |
|
|
Term
| What are the 3 classes of FDA-approved drugs for smoking cessation? |
|
Definition
1) nicotine replacement therapy (gum, patch, lozence, nasal spray, inhaler)
2) psychotropics (sustained-release buproprion)
3) partial nicotinic receptor agonist (varenicline) |
|
|
Term
| What are the benefits of nicotine replacement therapy (NRT)? |
|
Definition
1) reduce physical withdrawl
2) wliminate immediate, reinforcing effects of nicotine in tobacco use
3) allows patient to focus on behavioral & paychological aspects of tobacco use
4) doubles quit rates |
|
|
Term
| What are the precautions in NRT? |
|
Definition
1) not approved for use in children/adolescents
2) stop all tobacco use prior to NRT initiation
3) patients w/ underlying CVD (s.a. recent MI, life-threatening arrythmias, severe/worsening angina, others)
4) patients w/ active TMJ disease (gum only)
5) pregnancy/lactation |
|
|
Term
|
Definition
resin complex of nicotine & polacrilin to form a sugar-free chewing gum containing buffering agents to enhance buccal absorption
(available in different flavors & strength - strength recommended based on cigarettes smoked/day) |
|
|
Term
| What is the schedule for nicotine gum usage? |
|
Definition
FIXED SCHEDULE (not as needed)
weeks 1;6: 1 piece/1-2 hrs (never exceed more than 24 pieces/day)
weeks 7-9: 1 piece/2-4hrs
weeks 10-12: 1 piece/4-8 hrs |
|
|
Term
| What is the technique for chewing nicotine gum? |
|
Definition
1) chew slowly
2) strop chewing at first sign of peppery, minty, or citrus taste/slight tingling in mouth (~15 chews)
3) let gum rest b/w cheek & gum
4) resume slow chewing when taste/tingling fades
5) repeat |
|
|
Term
| What can help improve chances of wuitting when being assisted by nicotine gum? |
|
Definition
1) use @ least 9 pieces of gum/day
2) don't eat or drink 15 minutes before/while using gum (can reduce effectivity)
3) chewing gum too rapidly can cause excessive nicotine release => SE |
|
|
Term
| Will chewing nicotine gum provide the same rapid satisfaction that smoking provides? |
|
Definition
|
|
Term
SE
chewing nicotine gum too rapid |
|
Definition
1) lightheadedness
2) N/V
3) irritation of throat/mouth
4) hiccups
5) indigestion |
|
|
Term
SE
nicotine gum (used correctly) |
|
Definition
1) mouth soreness
2) hiccups
3) dyspepsia
4) jaw muscle ache
5) may stick to dental work (discontinue if excessive sticking/damage to dental work occurs) |
|
|
Term
|
Definition
1) may satisfy oral cravings
2) may delay weight gain
3) can titrate therapy to manage w/drawl Sx
4) variety of flavors available |
|
|
Term
Disadvantages
nicotine gum |
|
Definition
1) may not be socially acceptable
2) difficult w/ dentures
3) must use proper chewing technique to minimize SE
4) frequent dosing can decrease compliance |
|
|
Term
| What formulations of nicotine lozenge are there? |
|
Definition
1) sugar-free
2) mint flavor
3) contains buffering agent to enhance buccal absorption
4) available in different strengths |
|
|
Term
| How is the dosage of nicotine lozenge determined? |
|
Definition
"time to first cigarette"
(more if smoke w/in 30 min of waking) |
|
|
Term
| What is the scheduled used for nicotine lozenge use? |
|
Definition
FIXED SCHEDULE (not as needed)
weeks 1-6: 1 lozenge/1-2 hrs (never use more than 20 lozenges in a day)
weeks 7-9: 1 lozenge/2-4 hrs
weeks 10-12: 1 lozenge/4-8 hrs |
|
|
Term
| What are the directions for use w/ nicotine lozenges? |
|
Definition
1) place in mouth & allow to dissolve slowly
2) do NOT chew or swallow
3) occasionally rotate to different areas of the mouth
(will completely dissolve w/in 20-30 min) |
|
|
Term
| What helps the success rate when using nicotine lozenges? |
|
Definition
1) use at least 9 lozenges daily in 1st 6 weeks
2) do not eat or drink 15 minutes before or while using nicotine lozenge (some foods can reduce effectiveness) |
|
|
Term
| Does the nicotine lozenge provide the same rapid satisfaction that smoking provides? |
|
Definition
|
|
Term
|
Definition
1) nausea
2) hiccups
3) cough
4) heartburn
5) headache
6) flatulence
7) insomnia |
|
|
Term
Advantages
nicotine lozenge |
|
Definition
1) may satisfy oral cravings
2) easy to use & conceal
3) patients can titrate therapy to manage withdrawl Sx
4) variety of flavors available |
|
|
Term
Disadvantages
nictoine lozenge |
|
Definition
1) GI SE
2) frequent dosing => less compliance |
|
|
Term
| Why does the transdermal nicotine patch work? |
|
Definition
1) nicotine is well absorbed thru the skin
2) delivery to systemic circulation avoids first-pass metabolism
3) plasma nicotine levels aare lower & fluctuate less than with smoking |
|
|
Term
| How often is the nicotine patch administered? |
|
Definition
| once daily (different strengths are available for tapering - start higher for heavier smokers) |
|
|
Term
| What are the directions for use with the nicotine patch? |
|
Definition
1) choose an area of skin on the upper body or upper outer part of the arm
2) make sure the area is clean, dry, hairless, & not irritated
3) apply patch to different area each day & do not use same area for at least one week
4) remove patch from protective puch & peel off half of backing from patch
5) apply adhesive side to skin and peel off remaining protective covering
6) press firmly w/ palm of hand for 10 seconds & make sure patch stick well, esp. around edges
7) wash hands to remove any nicotine that may have gotten on hands to avoid stinging/redness in eyes or nose
8) remove w/in 24 hrs to avoid skin irritation
9) remove any remaining adhesive on skin w/ rubbing alcohol or acetone
10) hidpose of used patch by folding in half to completely cover adhesive area |
|
|
Term
| Can water harm the nicotine patch? |
|
Definition
| not if applied correctly ∴ patients can bathe, swim, shower, exercise |
|
|
Term
| Can patients cut the patch to adjust the dose? |
|
Definition
| no since nicotine may evapoate from cut edges & the patch may be less effective |
|
|
Term
Precautions
nicotine transdermal patch |
|
Definition
1) keep out of the reach of children & pets (new & used patches)
2) remove patch before MRI procedures |
|
|
Term
SE
transdermal nicotine patch |
|
Definition
1st hour: mild itching, burning, tingling
after 1st hour: vivid dreams or sleep disturbances, headache, local skin reaction |
|
|
Term
| What causes the local skin reactions in transdermal nicotine patch use? |
|
Definition
(redness, burning, itching)
usually caused by adhesive - up to 50% of patients will experience this, but less than 5% will discontinue due to SE |
|
|
Term
| Due to local skin reactions, who should avoid using the nicotine transdermal patch?? |
|
Definition
| patients w/ dermatologic conditions |
|
|
Term
| When is redness normal/abnormal when associated w/ nicotine transdermal patch? |
|
Definition
redness for 24 hours after removal = normal
if skin stay red for more than 4 days or if it swells or a rash appears = abnormal (contact health care professional & don't apply new patch) |
|
|
Term
Advantages
nicotine transdermal patch |
|
Definition
1) provides contant nicotine levels
2) easy to use/conceal
3) fewer compliance issues |
|
|
Term
Disadvantages
nicotine transdermal patch |
|
Definition
1) patients cannot titrate dose
2) allergic rxns to adhesive can occur
3) patients w/ dermatologic conditions shouldn't use |
|
|
Term
| Why does the nicotine nasal spray work? |
|
Definition
| rapid absorption across nasal mucosa |
|
|
Term
| What is considered one dose of the the nicotine nasal spray? |
|
Definition
| 2 sprays (one spray in each nostril) |
|
|
Term
| What is the dosing schedule for the nicotine nasal spray? |
|
Definition
begin w/ 1-2 doses per hour & increase as needed to a max of 5 doses per hour
for termination, begin a gradual tapering over an additional 4-6 weeks |
|
|
Term
| For the best results with the nicotine nasal spray, how many doses should be used per day for the first 6-8 weeks? |
|
Definition
|
|
Term
| What is the directions for proper nicotine nasal spray use? |
|
Definition
1) press circle on sides of botle & pull to remove cap
2) prime the pump before 1st use via holding bottle & pressing bottom w/ thum into papertowel until fine spray is observed (6-8 times)
3) may need to prime the pump if nto used for 24 hours
4) blow nose
5) tilt head back slightly & insert tip of bottle into nostril as far as comfortable
6) breeathe thru mouth & spray once in each nostril (do NOT sniff or inhale while apraying)
7) if nose run, gently sniff to keep nasal spray in nose, but don't blow nose for 2-3 minutes
8) wait 5 minutes before driving or operating machinery (can cause tearing, coughing & sneezing)
9) avoid contact w/ skin, eyes & mouth (if occurs, rinse w/ water since niotine is absorbed thru skin & mucus membranes) |
|
|
Term
|
Definition
1st week: hot peppery feeling in back of the throat/nose, sneezing, coughing, watery eyes, runny nose
SE should lessen over a few days & regular use in the first week will help build tolerance to the irritant effects
if SE do not decrease after a week, contact health care professional |
|
|
Term
Advantages
nicotine nasal spray |
|
Definition
| patients can easily titrate therapy to manage withdrawl Sx |
|
|
Term
Disadvantages
nicotine nasal spray |
|
Definition
1) nasal/throat irritation
2) higher dependence potential
3) patients w/ chronic nasal disorders or severe reactive airway disease should not use the spray
4) frequent dosing => less compliance |
|
|
Term
| What does the nicotine inhaler inhalation system consist of? |
|
Definition
1) mouthpiece
2) cartridge w/ porous plug containing nicotine |
|
|
Term
| Where is the nicotine absorbed w/ a nicotine inhaler? |
|
Definition
|
|
Term
| What is the dosing regimen of the nicotine inhaler? |
|
Definition
1) start w/ 6 cartridges/day
2) increases as needed to max of 16 cartridges/day
3) use for min. of 3 weeks & max of 12 weeks
4) gradual dosage reduction over additional 6-12 weeks |
|
|
Term
| What are the directions for proper nicotine inhaler use? |
|
Definition
1) align marks on the mouthpiece
2) pull & separate mouthpiece in 2 parts
3) press nicotine cartridge firmly into bottom of mouthpiece until seal breaks
4) put top on mouthpiece & align marks to close
5) press down firmly to break top seal of cartridge
6) twist top to misalign marks & secure unit
7) during inhalation, nicotine is vaporized & absorbed across oropharyngeal mucosa
8) inhale into back of throat or puff in short breaths |
|
|
Term
| When is the nicotine in cartirdges of a nicotine inhaler depleted? |
|
Definition
| after ~ 20 min. or active puffinf (but cartridge doesn't have to be used all at once, and can retain potency for 24 hrs |
|
|
Term
| What happens with the mouthpiece after use w/ a nicotine inhaler? |
|
Definition
| its reusable, so clean regularly w/ mild detergent |
|
|
Term
|
Definition
1) mild irritation of the mouth or throat
2) unpleasant taste/cough
(will adapt to 1 & 2 in a short time)
3) other less common SE include: rhinitis, dyspepsia, hiccups, headache |
|
|
Term
| When may the nicotine inhaler might not be as effective? |
|
Definition
1) in very cold temps since delivery of nicotine vapor may be compromised
2) do not eat or drink for 15 minutes before or while using the inhaler since effectiveness may be reduced by some foods/drinks |
|
|
Term
| What can help with craving control at first w/ when using the nicotine inhaler? |
|
Definition
| use the inhaler longer & more often at first |
|
|
Term
Advantages
nicotine inhaler |
|
Definition
1) patients can easily titrate therapy to manage withdrawl Sx
2) inhaler mimics hand-to-mouth ritual of smoking |
|
|
Term
Disadvantages
nicotine inhaler |
|
Definition
1) initial throat/mouth irritation
2) cartridges should not be stored in very warm conditions or used in very cold conditions
3) caution w/ patients w/ underlying bronchospastic disease
4) frequent dosing => decreased compliance |
|
|
Term
|
Definition
| sustained release antidepressant for nicotine cessation in an oral formulation |
|
|
Term
|
Definition
| atypical antidepressant thought to affect levels of various neurotransmitters (DA & NE) |
|
|
Term
Clinical Effects
buproprion |
|
Definition
1) decreased craving for cigarettes
2) decreased Sx of nicotine withdrawl |
|
|
Term
| What is the absorption bioavailability of buproprion? |
|
Definition
|
|
Term
|
Definition
| extensive hepatic metabolism (CYP2B6) |
|
|
Term
| How is buproprion eliminated? |
|
Definition
|
|
Term
| What is the half life of buproprion? |
|
Definition
| 21 hours (metabolites 20-37 hrs) |
|
|
Term
|
Definition
1) patients w/ seizure disorder
2) patients on wellbutrin or MAOI
3) patients w/ a current or prior diagnosis of anorexia/bulemia
4) patients undergo abrupt discontinuation of alcohol or sedatives |
|
|
Term
|
Definition
1) Hx of seizures
2) Hx of cranial trauma
3) taking medication that lower seizure threshold (antipsychotics, antidepressants, theophylline, systemic steroids)
4) severe hepatic cirrhosis
5) pregnancy (only is clearly indicated) |
|
|
Term
| When should patients begin buproprion therapy for smoking cessation? |
|
Definition
| 1-2 weeks prior to their quit date to ensure plasma levels of drug are achieved |
|
|
Term
| What is the dosing schedule for buproprion? |
|
Definition
PO in the morning for first 3 days
then BID for 7-12 weeks |
|
|
Term
|
Definition
1) insomnia (avoid bedtime dosing)
2) dry mouth
3) tremor/skin rash (less common) |
|
|
Term
| Is dose tapering of buproprion needed when discontinuing Tx? |
|
Definition
|
|
Term
| When is buproprion therapy considered ineffective? |
|
Definition
| if no significant progress by 7th week ∴ discontinue and reevaluate & restart at a later date |
|
|
Term
|
Definition
1) PO formulation w/ BID dosing
2) may be beneficial for patients w/ depression |
|
|
Term
|
Definition
1) increased seizure risk
2) several CI & precautions |
|
|
Term
|
Definition
| non-nicotine cessation aid that's a partial nicotine receptor agonist available in PO formulation |
|
|
Term
|
Definition
| bind w/ high affinity & selectivity @ α4β2 neuronal nicotinic acetylcholine receptors => stimulation of low-level agonist activity & competitively inhibits binding of nicotine |
|
|
Term
Clinical Effects
varenicline |
|
Definition
1) decreased Sx of nicotine withdrawl
2) blocks dopaminergic stimulation responsible for reinforcement & reward associated w/ smoking |
|
|
Term
| How much of verinicline is absorbed? |
|
Definition
| virtually 100% after PO administration & is not affected by food |
|
|
Term
|
Definition
|
|
Term
|
Definition
| primarily renal thru glomerular filtration & active tubular secretion (92% excreted unchanged) |
|
|
Term
| Whatis the half life of verenicline? |
|
Definition
|
|
Term
| Can verenicline be used in pregnancy? |
|
Definition
only if potential benefit justifies potential risk
(unknown if excreted in breast milk) |
|
|
Term
| When should patients begin their verenicline drug therapy? |
|
Definition
| 1 week prior to smoking cessation |
|
|
Term
| How is verenicline dosed? |
|
Definition
Days 1-3: 1/2 dose once a day
Days 4-7: 1/2 dose twice a day
Weeks 2-12: full dose twice a day |
|
|
Term
| Why is dosing of verenicline increased gradually? |
|
Definition
| to minimize treatment related nausea & insomnia |
|
|
Term
|
Definition
1) nausea
2) sleep disturbance (insomnia, abnormal dreams)
3) constipation
4) flatulence
5) vomiting |
|
|
Term
| When should doses of verenicline be taken? |
|
Definition
| after eating w/ full glass of water |
|
|
Term
| Do the nausea & insomnia SE seen w/ verenicline occur throughout therapy? |
|
Definition
| no, usually temporary (if persist, contact health care provider) |
|
|
Term
| Is tapering of verenicline necessary upon discontinuation? |
|
Definition
|
|
Term
|
Definition
1) PO formulation w/ BID dosing
2) new MOA for persions who failed using other medications |
|
|
Term
|
Definition
1) mya induce nausea in 1/3 of patients
2) post-marketing surveillance data not available
3) FDA warnings (increase suicidal ideation, sm. increase CV events) |
|
|
Term
| What are 2 drugs considered second line pharacological smoking cessation therapy? |
|
Definition
1) clonidine
2) nortriptyline |
|
|
Term
| What herbal drug is available for smoking cessation? |
|
Definition
|
|
Term
|
Definition
| derived from indian tobacco plant leaves & is a partial nicotine agonist (tho no evidence to support use) |
|
|
Term
| Do the pharmacological nicotine cessation therapies work? |
|
Definition
| all of them increase smoking cessation rates compared to trying w/ placebo, but none are greater than 24% |
|
|
Term
| What combination pharmacotherapies are available for smoking cessation? |
|
Definition
1) combination NRT (long acting formulation + short acting formulation = patch + gum/lozenge/nasal spray/inhaler)
2) buproprion sr + NRT |
|
|
Term
| Is there any safety/efficacy concerns w/ NRT + buproprion or verenicline? |
|
Definition
|
|
Term
| Why is combination NRT effective? |
|
Definition
1) produces relatively constant levels of nicotine w/ long-acting formulation
2) allows for acute dose titration as needed for withdrawl Sx w/ short-acting formulations |
|
|
Term
| What is the most common occupational disease worldwide? |
|
Definition
|
|
Term
| What are the 5 patterns of lung occupational disease? |
|
Definition
1) dust macule deposition in the lungs
2) fibrotic lung disease
3) immunologic (or hypersensitivity pneumonia)
4) occupational asthma
5) toxic lung injury |
|
|
Term
| What are the 5 steps to approaching occupational lung disease? |
|
Definition
1) occupational Hx
2) explore the job
3) look at the home & environment
4) explore the workplace
5) patient evaluation |
|
|
Term
| When reviewing the occupational Hx of a patient, what are you looking for? |
|
Definition
1) CC & it's temporal relationship to any job
2) social Hx (smoking Hx, ALL jobs ever held/how long?, exposures to dust/fumes/chemical/irradiation) |
|
|
Term
| How should you ask the patient to decribe his/her job? |
|
Definition
1) description of actual job duties
2) potential for exposure
3) products manufactured
4) smilar illness in other workers |
|
|
Term
| What exploration of the home & environment needs to be done while evaluating occupational exposure? |
|
Definition
1) nearby industries
2) contaminated work clothes
3) all illness in neighbors
4) pollution/ozone
5) household chemicals
6) hobbies |
|
|
Term
| When exploring the workplace for possible exposures, what are you looking for? |
|
Definition
1) handling of substances (usual operation/clean up practices)
2) protective equipment
3) ventilation system
4) may need to hire occupational site investigator |
|
|
Term
| What should the patient be evaluated for when looking for occupational exposure? |
|
Definition
1) complete Hx & PE
2) PFTs
3) CXR
4) HRCTs
5) serum markers
6) biopsy/pathological exam (may not be required if Hx, PFTs, & CXR are sufficient) |
|
|
Term
| What does it mean if the occupational exposure belongs to the dust macules category? |
|
Definition
they are inhaled & retained in the lungs
1) little host reaction to foreign material
2) generally no clinical Sx
3) no PFT abnormalities
4) CXR may show scattered densities
5) no progressive lung disease ∴ no further clinical action required |
|
|
Term
| What occupation generally is associated w/ dust macules? |
|
Definition
|
|
Term
| What are common dust macules inhaled via occupational exposure? |
|
Definition
1) aluminum
2) antimony
3) barium
4) chromium
5) urban pollution, cigarette smoking
6) iron
7) rare earths
8) tin
9) titanium |
|
|
Term
| What are the 3 common fibrotic lung diseases caused by occupational exposure? |
|
Definition
1) silicosis
2) coal workers' pneumonoconiosis
3) asbestosis/asbestos related diseases |
|
|
Term
| What is the most common cause for pneumoconiosis in the world (but not US)? |
|
Definition
|
|
Term
| What occupations are at risk for exposure to silicosis? |
|
Definition
1) tunneling
2) hard rock mining
3) sandblasting
4) quarrying
5) stone cutting
6) grinding
7) foundry |
|
|
Term
|
Definition
| pneumoconiosis due to crystalline silica |
|
|
Term
| Where is crytalline silica found? |
|
Definition
| ubiquitous (major part of earth's crust) |
|
|
Term
| Why were dental technicians having increased occupational exposure? |
|
Definition
| prosthetic material contained silica, asbestos, vitallium, acrylic resins |
|
|
Term
| What are the clinical patterns seen w/ silicosis? |
|
Definition
1) silicoproteinosis
2) simple (chronic) silicosis
3) complicated silicosis
4) progressive massive fibrosis (PMF) |
|
|
Term
| Does more disease correlate w/ exposure in silicosis? |
|
Definition
|
|
Term
| Once the exposure has ended, can silicosis disease still progress? |
|
Definition
|
|
Term
def
acute silicosis (silicoproteinosis) |
|
Definition
| progressibe & often fatal reaction to massive silica exposure (rare today due to proper protection of high risk occupations) |
|
|
Term
|
Definition
hypoxia, resp. failure, lung edema
CXR: "ground glass" appearance (esp. in upper lobes) |
|
|
Term
Sx
chronic (simple) silicosis |
|
Definition
1) silicotic nodules present (esp. in upper lung)
2) "eggshell calcification" of hilar lymph nodes
3) increased CXR abnormalities w/ increased exposure, tho rarely have significant Sx
4) minimal to no change in PFTs |
|
|
Term
|
Definition
| progressive lung disease, even in absence of continued silica exposure |
|
|
Term
|
Definition
1) simple nodules coalesce => larger densities on CXR
2) cough, progressive dyspnea, hypoxia, cor pulmonale
3) PFTs indicate restrictive disease - may also show obstruction due to distortion of airways
4) + markers for autoimmune disease s.a. ANA & rheumatoid factor |
|
|
Term
|
Definition
| patients w/ silica exposure & RA where the nodules may be very large, but the disease is more benign |
|
|
Term
Sx
progressive massive fibrosis |
|
Definition
1) massive coalescence of upper lobe nodules
2) traction on lower lung by fibrosing upper lobes => retraction bullaw at lung bases
3) great vessel involvement as fibrosis progresses => SVC compromise => lack of adequate blood return to heart |
|
|
Term
Which silicosis clinical pattern is most fatal?
Why? |
|
Definition
| progressive massive fibrosis due to extensive lung disease & CV compromise |
|
|
Term
|
Definition
| silica poisons macs ∴ persons infected w/ TB have an increased risk of developing active TB & all patients w/ evidence of silicosis should have an annual PPD test |
|
|
Term
What part of the lung is most affected by TB?
silicosis? |
|
Definition
|
|
Term
| What disease is produced by non0fibrous silicates? |
|
Definition
| disease similar to fibrous silica (simple pnumoconiosis or complicated w/ PMF) |
|
|
Term
| What 3 agents are considered non-fibrous silicates? |
|
Definition
1) talc
2) kaolin
3) bentonite |
|
|
Term
Managenement
silicotuberculosis |
|
Definition
1) supportive care
2) annual PPD
3) evaulate for autoimmune disease
4) watch for hypoxemia
(if weight loss, think TB) |
|
|
Term
def
coal workers' pneumoconiosis (CWP)
(for workers comp) |
|
Definition
accumulation of coal dust in lungs
10+ yrs exposure, nodules on CXR
(no need to demonstrate disability or physiologic impairment) |
|
|
Term
| What are the common myths of CWP? |
|
Definition
1) all due to silicosis (false)
2) all due to smoking (false)
3) related to coal + infection (proabably false)
4) something autoimmune (maybe) |
|
|
Term
| What are the 3 formsof coal? |
|
Definition
1) anthracite (oldest, hardest, highest # disease)
2) bituminous
3) peat (newest, softest, least disease) |
|
|
Term
| Since depth of the mine determines the chance of disease, where is the risk the greatest? |
|
Definition
the further down you go (deep shaft mine)
(least w/ open strip mines) |
|
|
Term
| What increases the risk of miners getting CWP? |
|
Definition
1) type of coal
2) depth of mine
3) duration of exposure
(46% if anthracite, deep mine) |
|
|
Term
| Who as a non-miner is at risk for CWP? |
|
Definition
| those who are involved in crushing, sizing, washing, blending, loading ships, barges, RR cars of coal |
|
|
Term
|
Definition
| accumulation of coal dust in lungs |
|
|
Term
|
Definition
cough w/ blaskish sputum
CXR: fine nodules
PFTs usually normal (COPD common since many coal miners smoked) |
|
|
Term
| What disease is complicated CWP similar to? |
|
Definition
|
|
Term
| What are the common myths of complicated CWP? |
|
Definition
1) silica + coal dust
2) massive coal dust exposure w/ host reaction in susceptible individuals
3) infection + coal dust
4) can lead to PMF (progressive massive fibrosis) |
|
|
Term
| What are the differences seen on CXR of complicated CWP compared to simple CWP? |
|
Definition
simple: small opacities in lower lobe
complex: increasing size of opacities that may aggregate & may => PMF |
|
|
Term
| What does the CXR in CWP relate to? |
|
Definition
|
|
Term
| Who is as risk for occupational asbestosis? |
|
Definition
1) mining (mainly 3rd world countries)
2) manufacturing & shipping
3) naval veterans
4) brake lining
5) insulation (pipe fitters, boiler workers, plumbers, demolition, reconstruction) |
|
|
Term
| What are the 3 clinical pattern seen with asbestosis? |
|
Definition
1) pleural disease
2) asbestosis (fibrotic lung disease)
3) malignancies |
|
|
Term
Sx
asbestos pleural disease |
|
Definition
1) pleural plaques
2) diffuse pleural thickening (less common & less characteristic)
3) exudative, bloody pleural effusions |
|
|
Term
|
Definition
| thickened plaural in patches along lateral chest walls/diaphragm/mediastinal pleura & are often calcified & appear as hard white areas on CXR |
|
|
Term
|
Definition
| progressive fibrotic lung disease secondary to inhalation & lung reaction |
|
|
Term
|
Definition
| asbestos fibers are too large to be ingested by macs => cycle of inflam. & fibrosis |
|
|
Term
| Where in the lung is asbestosis generally more prominent? |
|
Definition
|
|
Term
|
Definition
1) "shaggy heart" border on CXR
2) dry cough, crackles on exam, exertional dyspnea
3) PFTs: restrictive (low lung volumes)
4) can result in clubbing, cor pulmonale, resp. failure |
|
|
Term
| What malignancies can be caused by asbestos exposure? |
|
Definition
1) bronchogenic (lung) cancer
2) malignant mesothelioma
3) laryngeal/GI cancers
4) bladder cancer |
|
|
Term
| What is asbestos synergistic w/ to cause bronchogenic cancer? |
|
Definition
|
|
Term
def
malignant mesothelioma |
|
Definition
| malignant tumor of the pleural mesothelial cells |
|
|
Term
| How is malignant mesothelioma distinguished from benign mesothelioma? |
|
Definition
| behavior (rather than cell types) |
|
|
Term
| Is prognosis of malignant mesothelioma better or worse than bronchogenic cancer? |
|
Definition
| worse since not responsive to radiation of chemo & difficult to surgically resect |
|
|
Term
def
hypersensitivity pneumonitis (HP)
aka allergic alveolitis |
|
Definition
| type II hypersensitivity rxn to a variety of ORGANIC dusts |
|
|
Term
| What is the classical HP? |
|
Definition
| farmer's lung (rxn to thermophyllic actinomyces & micropolyspora in moldy hay) |
|
|
Term
def
mushroom worker's lung |
|
Definition
| exposure to mushroom compost (micopolyspora) |
|
|
Term
|
Definition
| exposure to bark decay (cryptostroma sp.) |
|
|
Term
|
Definition
| exposure to moldy barley (aspergillus sp.) |
|
|
Term
|
Definition
| exposure to bird droppings |
|
|
Term
|
Definition
| exposure to fungal spores (thermophyllic actinomyces sp.) |
|
|
Term
| What is the key to making an HP diagnosis? |
|
Definition
| the clinical & temporal association of Sx to exposure |
|
|
Term
| What are the clues that farmer's lung is suspected? |
|
Definition
1) Sx occur 4-8 hrs after exposure
2) more common in spring when hay has been molding all winter & then forked out
3) Sx will resolve spontaneously w/in 18-24 hrs
4) repeated exposure => progressively more severe attacks
5) can lead to restrictive lung disease is continued exposure not avoided |
|
|
Term
|
Definition
fever, chills, sweating, coughing, dyspnea (~ to pneumonia)
PE: tachypnea, crackles
CXR: bilateral reticulonodular infiltrates |
|
|
Term
| What HP is seen in Detroit (since farmer's lung isn't very common here)? |
|
Definition
| Crack Lung (pulmonary disease caused by cocaine abuse) |
|
|
Term
| Does occupational asthma resemble typical asthma? |
|
Definition
| in all clinical & physiologic aspects |
|
|
Term
| What is the distinguishing feature of occupational asthma? |
|
Definition
| temporal relationship to work exposure (worse during day, improve away from work) |
|
|
Term
| What happens if a person with occupational asthma is not removed from the work environment? |
|
Definition
|
|
Term
| What occupations are commonly seen associated w/ occupational asthma? |
|
Definition
1) plastics manufacturing (TDI & TMA)
2) urethane foam (refrigeration)
3) hair care products
4) byssinosis (cotton bracts) |
|
|
Term
|
Definition
| wheezing, coughing, SOB - worsening in work place |
|
|
Term
| How is occupational asthma diagnosed? |
|
Definition
| spirometry beofre& after a work shift |
|
|
Term
| How prevalent is occupational asthma? |
|
Definition
|
|
Term
|
Definition
| responds to bronchodilators, but really needs to avoid exposure |
|
|
Term
| What soluble agents can cause toxic lung injury? |
|
Definition
1) HCl
2) ammonia
3) sulfer dioxide
4) phossgene |
|
|
Term
| Why do soluble agents less commonly cause lung injury? |
|
Definition
they're harsh upper airway irritants & person leaves exposure area due to noxious effects on eyes, nose, throat
(only when trapped in the area can produce lung injury) |
|
|
Term
Sx
accidental exposure to soluble agents |
|
Definition
diffuse alveolar damage
pulmonary edema |
|
|
Term
| What are examples of poorly soluble agents that can cause toxic lung injury? |
|
Definition
|
|
Term
| Why is lung injury due to oxides of nitrogen more commonly seen? |
|
Definition
| they have few noxious effects on the upper airway => more prolonged exposure => lung injury |
|
|
Term
| What is the classic disease caused by oxides of nitrogen toxic lung injury? |
|
Definition
|
|
Term
| Where does the exposure of oxides of nitrogen occur from in silo filler's disease? |
|
Definition
| from fresh cut hay (in the fall), where are yellow brown gas is often seen overlying the hay |
|
|
Term
| How fast do Sx occur in silo filler's disease? |
|
Definition
| nearly immediate w/ high exposure or eveolve over 18-24+ hours w/ lower level exposure |
|
|
Term
|
Definition
severe SOB
hypoxemia
CXR: bilateral diffuse lung infiltrates |
|
|
Term
| What is the pathology seen in silo filler's disease? |
|
Definition
ARDS type picture/diffuse alveolar damage (high exposure)
bronchiolitis obliterans (low level exposure) |
|
|
Term
|
Definition
oxygen & resp. support
corticosteroids |
|
|
Term
| What are the 5 causes of environmental/occupational lung diseae? |
|
Definition
1) biological dusts
2) toxic chemicals
3) inorganic dusts
4) infectious disease
5) resp. carcinogens |
|
|
Term
| What are the modifying factors for if/when/severity of environmental/occupational lung disease? |
|
Definition
1) state/nature of agent
2) particle size/concentration
3) length of exposure
4) coexistance of other lung disease |
|
|
Term
def
diffuse alveolar damage (DAD) |
|
Definition
| the pathological equivalent of adults resp. distress syndrome (ARDS) is a very common reaction to inhaled fumes & gases of many types (almonst any irritant gas in high enough concentration can propably produce a DAD) |
|
|
Term
|
Definition
1) rapidly developing & severe SOB only a few hours after toxic fume inhalation
2) CXR: diffuse bilateral alveolar infiltrates
3) severe hypoxemia |
|
|
Term
| What does the DAD lung look like grossly? |
|
Definition
| diffuse consolidation w/ loss of normal markings |
|
|
Term
| What does the DAD lung look like microscopically? |
|
Definition
| hyaline membranes in alveolar ducts & collapse of alveolar parenchyma |
|
|
Term
| What helps determine the etiology of DAD? |
|
Definition
| most instances only the Hx (since there is nothing specific about this clinical or pathological picture) |
|
|
Term
| What does DAD present as in an idiopathic setting? |
|
Definition
| acute interstitial pneumonia |
|
|
Term
| Since DAD is often rapidly progressive, what can it lead to? |
|
Definition
| resp. failure & mechanical vent. |
|
|
Term
| When is DAD seen as the terminal event? |
|
Definition
|
|
Term
| What are the key histological features of DAD? |
|
Definition
1) diffuse distribution
2) uniform temporal appearance
3) alveolar septal thickening due to organizing fibrosis (usually diffuse)
4) airspace organization (may be patchy or diffuse)
5) hyaline membranes (maybe focal or diffuse) |
|
|
Term
| What are the pertinent negatives seen w/ DAD? |
|
Definition
1) lack or granulomas, necrosis, pneumonia, abscess
2) lack of infectious agents
3) lack of prominent eosinophils, neutrophils
4) negative cultures |
|
|
Term
| Besides DAD, what can also be caused by most of the irritating agents than cause DAD? |
|
Definition
1) necrosis of airway epi.
2) BO (bronchiolitis obliterans)
3) bronchiectasis (occasionally) |
|
|
Term
| What are the 2 most common etiologies of necrotizing bronchitis & bronchiolitis? |
|
Definition
| fume & gas inhalation, and viral inf. |
|
|
Term
| What are most cases of BO secondary to? |
|
Definition
| fume inhalation caused by sulfer dioxide or oxides of nitrogen (silo filler's disease) |
|
|
Term
| How does BO appear in the acute form on histology? |
|
Definition
| tufts of granulation tissue in resp. bronchioles |
|
|
Term
| What causes BO development? |
|
Definition
1) sequal to DAD
or
2) if initial exposure is lower, may first appear as SOB developing several weeks after exposure |
|
|
Term
| What are the common fumes & gases that cause BO? |
|
Definition
ammonia
sulfer dioxide
nitrogen dioxide
chlorine
fire smoke
hydrogen selenide |
|
|
Term
| Why are many dusts considered to be "inert"? |
|
Definition
unlike crystalline silica, not all dust evokes a marked fibrotic response in the lung.
inert dusts produce macules |
|
|
Term
|
Definition
collections of macs & free dust particles surrounding smaller branchesof the pulmonary artery & sm. bronchioles
by def. are non-palpable |
|
|
Term
|
Definition
| techinically a macule that is palpable |
|
|
Term
| When will the macules seen due to inert dusts be visible grossly as colored leisons in the centers of lobules? |
|
Definition
| if the dust inhaled is pigmented |
|
|
Term
What color are the macules in coal workers?
hematite miners?
paint pigment titanium oxide?
tin? |
|
Definition
coal: black
heatite: red
titanium: white
tin: gray |
|
|
Term
| What is the most common form of dust macule? |
|
Definition
| black centrilobular pigment seen in cigarette smokers & urban dwellers |
|
|
Term
def
coal cowrkers pneumoconiosis (CWP) |
|
Definition
| accumulation of coal dust in the lungs and the tissues' reaction to its presence |
|
|
Term
| What is necessary for establishing a diagnosis of CWP? |
|
Definition
1) Hx of exposure to coal dust (usually at least 10 years underground)
2) certain relatively characteristic abnormalities on the CXR |
|
|
Term
| When is CWP most likely seen? |
|
Definition
| face workers, followed by transportation, maintenance and surface workers of the coal mine |
|
|
Term
| What is the overal prevalence in CWP? |
|
Definition
|
|
Term
|
Definition
almost no Sx
(cough & blackish sputum, but those are nonspecific since almost all coal miners have this) |
|
|
Term
| What is complicated CWP aka? |
|
Definition
| PMF (progressive massive fibrosis) |
|
|
Term
|
Definition
SOB
DOE (dyspnea on exertion)
exercise hypoxemia
hypercapnia (preterminal finding) |
|
|
Term
|
Definition
| from the more complicated cases of simple CWP |
|
|
Term
|
Definition
| unrelated CV & pulmonary disease (usually presents in older miner) |
|
|
Term
| How does simple CWP present in CXR? |
|
Definition
| fine nodulation (usually smaller than silicosis) |
|
|
Term
| What does PMF look like on CXR? |
|
Definition
| nodules that may coalesce |
|
|
Term
| What happens in PMF after contact has ended? |
|
Definition
|
|
Term
| What happens to the PFTs in simple CWP? |
|
Definition
| subtle abnormalities, most of which are attributed to miner's smoking habit |
|
|
Term
| What happens to the PFTs in PMF? |
|
Definition
| both restrictive & obstructive change in PFTs
w/ decreased DLCO and increased A-a gradient (∴ parenchymal problem) |
|
|
Term
| What is the pathogenesis of CMP? |
|
Definition
1) coal dust is inhaled and deposited in alveoli
2) macs ingest and convey toward the resp. bronchioles & pulmonary lymphoid tissue |
|
|
Term
| Since CWP doesn't produce profound changes to lung structure, why does it occasionally progress to PMF? |
|
Definition
possibly:
1) response to total dust load
2) inf. including both TB & NTM
3) immunological hypthesis (mac activation w/ production of a fibroblast growth factor & collagen formation) |
|
|
Term
| What things are seen pathologically in CWP? |
|
Definition
1) macules
2) nodules
3) massive fibrosis
4) caplan's leisons
5) intersitial fibrosis |
|
|
Term
| How does coal dust macules appear grossly? |
|
Definition
| black nonpalpable sports in the centers of the lobules |
|
|
Term
| What are the coal dust macules in CWP formed by microscopically? |
|
Definition
| accumulations of dust along the walls of resp. bronchioles |
|
|
Term
| What happens to the airspace around the coal dust macules in CWP? |
|
Definition
| frequently are enlarged in a pattern resembling centrilobular empysema ("focal emphysema") |
|
|
Term
|
Definition
| pigmented leisons that are partially collagenized (∴ palpable) |
|
|
Term
| What is deposited at the center of nodules in CWP? |
|
Definition
|
|
Term
| What causes the nodules seen in CWP? |
|
Definition
coal dust alone?
coal dust + silica?
unclear |
|
|
Term
| Where are PMF leisons most likely found? |
|
Definition
| bilaterally are are more common in upper lung zones |
|
|
Term
| What is at the center of the pigmented PMF leisons? |
|
Definition
|
|
Term
| What are the 2 forms of PMF seen microscopically? |
|
Definition
1) coalscence of many nodules
2) single large leison |
|
|
Term
| Is simple pneumoconiosis progressive after removal from the dust? |
|
Definition
|
|
Term
|
Definition
| fibrotic disease of the lungs caused by the inhalation of dust containing silicon dioxide |
|
|
Term
| Who is usually affected by silicosis? |
|
Definition
1) hard rock miners
2) sand blasters
3) foundry workers
4) pottery workers
5) abrasive soaps
6) rubber & glass manufacturers
7) users of diatomaceous earth
8) historically: flintlock gun makers, grindstone makers, knife grinders |
|
|
Term
| What happens to the risk of silicosis with increased duration of exposure? |
|
Definition
|
|
Term
| Is prognosis of CWP or silicosis w/ similar radiographic category the same, better, or worse? |
|
Definition
| death rate of silicosis is double CWP |
|
|
Term
| What occupations are associated w/ exposure to silica? |
|
Definition
1) mining/quarrying/tunneling thru siliceous rock
2) engraving & polishing of stone/stonecutting
3) use/manufacture or silica-containing abrasives & fillers
4) work in foundries
5) ceramic and refractory manufacture
6) sandblasting & grinding |
|
|
Term
|
Definition
no Sx usually
can complain of: cough, sputum production (tho usually related to chronic bronchitis) |
|
|
Term
| What are the 2 threats of simple silicosis? |
|
Definition
1) development of complicated disease
2) development of TB |
|
|
Term
|
Definition
Sx of restrictive disease:
dyspnea, paroxysmal cough, and eventually cor pulmonale
clubbing & basal rales are infrequent
bulla formation if airway obstruction |
|
|
Term
| Does silicosis continue to progress after contact has stopped? |
|
Definition
|
|
Term
|
Definition
| multiple small nodules, usually in upper lobes |
|
|
Term
|
Definition
| larger nodules that eventually coalesce to involve much of an entire hemithorax |
|
|
Term
| What is seen on CXR in the hilar nodes in silicosis? |
|
Definition
| "eggshell calcification" - calcification of the periphery of the hilar node |
|
|
Term
| What happens to PFTs in silicosis? |
|
Definition
| restrictive process (decreased VC, TLC, compliance) and later, obstruction also occurs |
|
|
Term
| What is the pathogenesis of silicosis? |
|
Definition
possibly:
1) silica particle is ingested by a mac, that subsequently dies & degenerates => release of proteolytic enzymes that attack the lung while the silica particle is re-ingested by another mac that dies => stimulated fibrosis
2) alveolar macs are activated => production of fibroblast growth factors & IL-1. Lymphocytes also participate by proliferating and elaborating additional cytokines => further stimulating fibrosis |
|
|
Term
| What explains why silicosis continues to progress even after the exposure has ceased? |
|
Definition
| there is no good body mech to remove silica particles |
|
|
Term
| What are reactions can the lung have to silicosis? |
|
Definition
1) silicotic nodules
2) conglomerate nodules
3) PMF
4) caplan's nodules
5) scleroderma & other CT
6) mycobacterial inf.
7) alveolar lipoproteinosis |
|
|
Term
| Do the macules produced by silicosis resemble those of iron or coal? |
|
Definition
| yes, but the dust is colorless |
|
|
Term
| What happens to silicotic macules? |
|
Definition
| rapidly fibrose overall macules are relatively rare) |
|
|
Term
| What are the classical leisons of silicosis? |
|
Definition
|
|
Term
| What do silicotic nodules look like grossly? |
|
Definition
| round, hard, typically blue/green (may have other colors if other dusts are present) |
|
|
Term
| What do silicotic nodules look like microscopically? |
|
Definition
| fairly sharply demarkated round borders & a whorled collagenous center w/ a more or less prominent infiltrate of dust laden macs around the periphery |
|
|
Term
| What is seen pathologically in the hilar lymph nodes in silicosis? |
|
Definition
enlarged, extremely fibrotic
may calcify in an egg shell pattern (visible on CXR)
note: silicotic nodules may be found in the hilar lymph nodes of coal miners & those with silica exposure w/ no parenchymal nodules |
|
|
Term
| What causes the pathology seen in the hilar lymph nodes in silicosis? |
|
Definition
| concentration of silica in lymph nodes |
|
|
Term
| What is needed before silicosis can be diagnosed? |
|
Definition
| parenchymal silicotic nodules are present |
|
|
Term
| What can cause silica proteinosis? |
|
Definition
| exposure to very high levels of silica, acutely |
|
|
Term
| What is the histological process of silica proteinosis similar to? |
|
Definition
alveolar proteinosis (with filling of alveoli by granular pink debris)
in silica proteinosis finely divided bifringent material is usually present in large amounts & there is commonly an interstital inflam. infiltrate (not seen in alveolar proteinosis) |
|
|
Term
|
Definition
| fibrotic lung disease caused by inhalation of asbestos fibers |
|
|
Term
| What are the clinical effects of asbestosis? |
|
Definition
1) pulmonary fibrosis
2) increased bronchogenic carcinoma
3) mesothelioma
4) GI tract neoplasms
5) benign pleural plaques & effusions |
|
|
Term
|
Definition
| mainly in contruction (cements, tiles, felts, etc) |
|
|
Term
| Who is at risk for asbestosis? |
|
Definition
| plumbers, demolition workers, electricians, boiler room workers |
|
|
Term
| How prevalent is asbestosis? |
|
Definition
1967 - almost 50% of all autopsies has asbestos bodies
1990 - declined to 35%
(increased chance of exposure w/ increased duration of exposure) |
|
|
Term
|
Definition
DOE (dyspnea on exertion) & dry cough
=> hyperventilation & profound hypoxemia
by the time Sx develop, several years of fibrosis has already occured
death from cor pulmonale occurs w/in 15 years of disease onset |
|
|
Term
| What can hasten the death of those w/ asbestosis? |
|
Definition
| GI or pulmonary neoplasms |
|
|
Term
| Does all asbestosis progress? |
|
Definition
| not if exposure is terminated early (but advanced forms will progress dispite removal from exposure) |
|
|
Term
|
Definition
| linear markings, mainly in lower lung fields, often given the heart a "shaggy" appearance. Pleural plaques & effusions may also be seen |
|
|
Term
| What happens to the PFTs in asbestosis? |
|
Definition
| almost purely restrictive (decreased VC & TLC, decreased compliance, decreased DLCO, increased A-a gradient) |
|
|
Term
|
Definition
| result of mechanical irritation or injury to tissues by asbestos fibers => mechanisms similar to CWP & silicosis w/ added fact that asbestos fibers can directly stimulate fibroblasts to make CT elements |
|
|
Term
| Why doesn't the inhalation of most glass fibers result in pneumoconiosis? |
|
Definition
| large sixe & inability to penetrate deeply into alveoli as asbestos fibers can (tho some new ultrafine fiberglass has been able to produce asbestos like results) |
|
|
Term
| How is asbestos found in the lung? |
|
Definition
| as a bare fiber or as an asbestos body |
|
|
Term
|
Definition
| a fiber of asbestos to which the lung has added a coating of iron-protein |
|
|
Term
| Can asbestos bodies be seen microscopically? |
|
Definition
| yes, by LM (while uncoated fibers can only been seen by EM) |
|
|
Term
|
Definition
| mineral particle w/ iron-protein coats (asbestos body is one class of ferruginous body) |
|
|
Term
| How can asbestos bodies be reliably distinguished from other ferruginous bodies? |
|
Definition
| by LM appearance, tho doesn't indicate what type of asbestos constitutes the body core |
|
|
Term
| What is needed to determine that a fiber found in the lung tissue is asbestos? |
|
Definition
| EM techniques s.a. morphology, defraction, and energy dispersive xray spectroscopy |
|
|
Term
| What is an indication of extensive asbestos exposure? |
|
Definition
| the observation of asbestos bodies in a tissue section (since tissue sections are insensitive detectors of these structures) - tho they just indicate exposue (i.e. ARE NOT IN AND OF THEMSELVES DISEASE) |
|
|
Term
| Can asbestosis be distinguished from idiopathic interstitial fibrosis? |
|
Definition
| yes, by distinct clinical & CXR features |
|
|
Term
| What benign parenchymal leisons are associated w/ asbestos exposure? |
|
Definition
fibrosis of small airways
asbestosis |
|
|
Term
| What benign pleural leisons are associated w/ asbestos exposure? |
|
Definition
pleural effusion
pleural fibrosis
pleural plaques
pleural pseudotumors |
|
|
Term
| What neoplasms as associated w/ asbestos exposure? |
|
Definition
malignant mesothelioma
carcinoma of the lung
others? |
|
|
Term
| What is the gross appearance of asbestosis? |
|
Definition
| similar to that of IIF (idiopathic interstitial fibrosis) w/ the formation of revised airspaces & honeycombing & commonly seen is pleural thickening. |
|
|
Term
| Where in the lung does asbestosis tend to be more severe? |
|
Definition
|
|
Term
| What is the microscopic appearance of well-established asbestosis? |
|
Definition
indistinguishable from IIF except for the presence of asbestos bodies in tissue
the fibrotic component consists of a variable pattern of interstitial collagen & inflam. cells |
|
|
Term
| What must be seen to diagnose asbestosis microscopically? |
|
Definition
| diffuse fibrosis + asbestos bodies |
|
|
Term
| What can asbestosis progress to? |
|
Definition
| resp. insufficiency & cor pulmonale |
|
|
Term
| What does asbestosis predispose the development of? |
|
Definition
| lung cancer (30-40% develop carcinoma) |
|
|
Term
| What pleural leisons are caused by asbestos exposure? |
|
Definition
| pleural plaques, pleural fibrosis, pleural effusions, and pleural pseudotumors (rounded atelectasis) |
|
|
Term
| How soon after asbestos exposure do pleural effusions occur? |
|
Definition
| early after initial exposure, but are subclinical usually (may produce pain & resp. distress) |
|
|
Term
| What do the pleural biopsies of patients w/ a pleural effusion induced by asbestos exposure reveal pathologically? |
|
Definition
| nondescript fibrosis & inflam. |
|
|
Term
| What happens to the visceral pleura w/ asbestos exposure? |
|
Definition
| fibrosis can occur by itself or in conjuncture w/ asbestosis |
|
|
Term
| What is seen pathologically in the visceral pleura of a patient exposed to asbestos? |
|
Definition
| nonspecific pattern of fibrosis & inflam., but may contain asbestos bodies in underlying tissue |
|
|
Term
| What can occur on the parietal pleural (chest wall) * diaphragm of a patient w/ asbestos exposure? |
|
Definition
|
|
Term
| What do pleural plaques look like grossly? |
|
Definition
| hard white masses of collagen that may be knobbed or flat |
|
|
Term
| What do pleural plaques look like microscopically? |
|
Definition
| typical appearance of acellular collagen arranged in a so-called basket weave configuration |
|
|
Term
| So pleural plaques cause disease? |
|
Definition
| no, they are just clinical markers of exposure, but occasionally plaques adherent to underlying lung produce restriction |
|
|
Term
def
pseudotumors (rounded atelectasis) |
|
Definition
| infoldings of lung caused by scarring of the overlying pleura, often associated w/ a plaque |
|
|
Term
| Do pseudotumors produce disease? |
|
Definition
| no, but are often mistaken for tumors on CXR |
|
|
Term
| **Is there an apparent direct association b/w asbestosis induced benign pleural disease & the development of malignant mesothelioma? |
|
Definition
| No (i.e. no precursor relationship) |
|
|
Term
| Can asbestos exposure induce benign pleural neoplasms? |
|
Definition
| yes, but are rare - localized fibrous mass |
|
|
Term
| What is the latency of mesothelioma? |
|
Definition
| 20-40 years (minimum 15 yrs) |
|
|
Term
| What is seen on gross appearance of a malignant mesothelioma? |
|
Definition
mesothelioma typically surrounds viscera (lung or bowel) and invades from the external surface w/ metastases present in half of cases, tho usually small & clinically insignificant
(diffusely involves the pleura to encase the lung)
its a soft, gray-white mass, marked over lower lobes, lines pleural cavity & fissues, vary rarely invades, but causes cavitation |
|
|
Term
| What is seen microscopically in malignant mesothelioma? |
|
Definition
a wide variety of histopathological appearances:
epithelial types may form tubules & papillae lines by cuboidal cells (adenocarcinomas have columnar cells)
they may be composed of cells resembling large polygonal mesothelial cells of the type seen in pleural effusions
usually combinations of patterns occur (s.a. papillary, glanular, sarcomatous resembles adenocarcinoma & fibrosarcoma) |
|
|
Term
| What is done to confirm or exclude an asbestos etiology of mesothelioma? |
|
Definition
| mineralogic analysis (b/c can occur w/o Hx or mineralogic evidence, esp. in women) |
|
|
Term
Prognosis
malignant mesothelioma |
|
Definition
|
|
Term
| What is the largest problem in asbestos-related disease? |
|
Definition
|
|
Term
| What does smoking + asbestos exposure do to a person's risk for lung cancer? |
|
Definition
| increases is synergistically |
|
|
Term
| What is the common predisposing condition that leads to lung carcinoma from asbestos exposure? |
|
Definition
|
|
Term
def
extrinsic allergic alveolitis (hypersensitivity pneumonitis) |
|
Definition
| type III & IV hypersensitivity response to the inhalation of a variety of organic dusts, tho the process is often referred to by a name indicating the specific occupation or setting involved (s.a. farmer's lung) |
|
|
Term
| What species is usually responsible for extrinsic allergic alveolitis (EAA)? |
|
Definition
| thermophilic actinomycetes |
|
|
Term
|
Definition
|
|
Term
def
mushroom worker's lung |
|
Definition
| exposure to mushroom compost |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| exposure to coffee bean dust |
|
|
Term
|
Definition
| exposure to various isocyanates |
|
|
Term
def
bird fancier's lung & pigeon breeder's lung |
|
Definition
| exposure to bird droppings |
|
|
Term
|
Definition
| exposure to fungal spores |
|
|
Term
| How soon after exposure will patients with EAA experience Sx? |
|
Definition
|
|
Term
|
Definition
4-8 hrs post exposure: fever, chills, malaise, unproductive cough, SOB
Sx abate after a few hours, but subsequent attacks become more severe & last longer |
|
|
Term
| What ultimately happens in EAA if the patient never seeks Tx or removal from allergen? |
|
Definition
| irreversible restrictive lung disease develops |
|
|
Term
| What normally improves the outcome of EAA? |
|
Definition
|
|
Term
| What is the pathogenesis of EAA? |
|
Definition
| typye II & IV hypersensitivity rxn results in intestitial changes w/ physiological impairemtn typical of restrictive disease + granuloma formation |
|
|
Term
| What is the pathology seen in the acute phase of EAA? |
|
Definition
| form of interstitial pneumonia, tho acute phase is poorly defined |
|
|
Term
| What occurs pathologically in the chronic phase of EAA? |
|
Definition
1) interstitial infiltrate of lymphocytes & plasma cells w/ a distinct tendency to be worse around bronchioles
2) granulomas are present in 3/4 of cases and may resemble sarcoid granulomas, but as usually not as well formed & may be seen in airspaces as well as interstitium. They tend to be accentuated around small airways => small airway obstruction (BOOP) |
|
|
Term
| How long do the pathological changes seen in the chronic phase of EAA last for after exposure? |
|
Definition
|
|
Term
| What can develop if EAA continues for long periods of time? |
|
Definition
| interstitial fibrosis & even honeycombing |
|
|
Term
| What provides a clue that EAA is the cause of the interstitial fibrosis & honeycombing? |
|
Definition
| Schaumann bodies may be found to provide an important clue to Dx |
|
|
Term
| What are the 5 classes of anticoagulants? |
|
Definition
1) AT III catalyzers
2) Vit K antagonist
3) Factor 10a inhibitors (direct & indirect)
4) Direct thrombin inhibitors (DTIs)
5) Fibrinolytic (thromolytic) agents |
|
|
Term
| What are the AT III catalyzers? |
|
Definition
|
|
Term
| What is the Vit K antagonist? |
|
Definition
|
|
Term
| What is the indirect factor Xa inhibitor? |
|
Definition
|
|
Term
| What are the 3 direct factor Xa inhibitors? |
|
Definition
1) Rivaroxaban
2) Apixaban |
|
|
Term
|
Definition
1) Lepirudin
2) Argatroban
3) Bivalirudin
4) Desirudin
5) Dabigitran
(DTIs were made in the LAB to DEStroy BIG clots)
(Aragog was a BIG, Rude(in) spider that died) |
|
|
Term
| What are the fibrinolytic (thrombolytic) agents? |
|
Definition
1) Tissue Plasminogen Activators (TPA) s.a. Tenecteplase, Reteplase, Aletplase (Plase for plasminogen)
2) streptokinase |
|
|
Term
| Why is there a need to overlap warfarin w/ another immediate-acting anticoagulant (s.a. heparin)? |
|
Definition
1) Warfarin prevents the synthesis of new clotting factors, and has no effect on previously made CFs
2) Half life of previously made CFs are long (esp. factor II), so warfarin won't have an effect for several days if given alone
∴ there is a need for a short-acting supplementation to warfarin, for at least the first few days |
|
|
Term
|
Definition
| activates plasminogen to plasmin => degradation of thrombus matrix => thrombus lysis |
|
|
Term
| What is the only fibrinolytic agent approved for use with a pulmonary embolism (PE)? |
|
Definition
|
|
Term
| What is the only time a thrombolytic agent (more specifically alteplase) can be used in a PE? |
|
Definition
| EARLY in a confirmed PE w/ hemodynamic compromise (massive PE) |
|
|
Term
| Can thrombolytics be used in patient's w/ submassive PE (meolytically stable, but w/ evidence of ventricular dysfunction)? |
|
Definition
controversial, so just say no.
There is lack of mortality benefit, and a risk of bleeding ∴ NEVER use w/ a patient in ICU |
|
|
Term
|
Definition
| BLEEDING (esp. CNS bleeding) |
|
|
Term
|
Definition
1) intracranial disease
2) uncontrolled HTN
3) major surgery/trauma |
|
|
Term
MOA
HIT (heparin induced thrombocytopenia) |
|
Definition
| heparin interacts w/ platelet PF-4 => formation of antigenic complex => IgG recognition & binding of hep-PF4 complex => platelet activation |
|
|
Term
Effect
platelet activation due to HIT |
|
Definition
1) drop in platelet count (>50% drop)
2) prothrombotic condition => promotion of platelet aggregation (BAD) |
|
|
Term
| How soon after heparin introduction can HIT be seen? |
|
Definition
| usually >4 days (can be sooner, can be delayed) |
|
|
Term
|
Definition
The 4 "Ts"
1) Thrombocytopenia
2) Timing
3) Thrombosis
4) oTher causes of platelet fall |
|
|
Term
|
Definition
discontinue all heparin
begin regimen of DTI |
|
|
Term
| Is there a risk of HIT w/ both UFH & LMWH? |
|
Definition
| yes, tho there is a greater risk w/ UFH |
|
|
Term
|
Definition
monitoring of platelet counts whenever heparin is given
(the lower the platelet count, the greater the risk for HIT) |
|
|
Term
| Is it possible to have HIT w/o a thrombus? |
|
Definition
|
|
Term
| Which anticogaulants are renally dependent? |
|
Definition
AT III catalyzer: LMWH
Indirect Xa Inh: Fondaparinux
Direct Xa Inh: Rivaroxaban, Apixaban DTIs: Lepirudin, Bivalirudin, Desirudin, Dabigatran |
|
|
Term
| Which anticoagulants are NOT renally dependent? |
|
Definition
AT III catalyzer: UFH
Vit K antagonist: warfarin
DTI: argatroban
(Ur-ine W-AR and you pee your pants w/b your scared - not b/c you have kidney problems) |
|
|
Term
| What 3 anticoagulants have reversing agents? |
|
Definition
|
|
Term
| What is the reversing agent for both UFH & LMWH? |
|
Definition
| protamine (tho a complete reversal for UFH & a partial reversal for LMWH) |
|
|
Term
| What is the reversing agent for warfarin? |
|
Definition
| 1) Immediate: FFP (fresh frozen plasma) - to replace CFs directly
2) Later onset: Vit K1 replacement via IVPB (8hrs) or PO (24hrs) |
|
|
Term
| Can you give subq Vit K1 replacement for warfarin reversal? |
|
Definition
| yes, but not recommended due to erratic & delayed absorption |
|
|
Term
| Why isn't IM Vit K1 replacement given for warfarin reversal? |
|
Definition
|
|
Term
What are the only anticoagulants w/o reversing agents where it's not such a big deal?
Why? |
|
Definition
DTIs since they have short half lives (except Dabigatran)
Any anticoagulants w/o reversal & long half life = potentially very bad |
|
|
Term
|
Definition
1) PO formulation (only DTI)
2) No monitoring necessary (only DTI)
3) INR effect is negligable
4) Less stroke/systemic embolism compared to warfarin |
|
|
Term
|
Definition
| 1) increased GI bleeding in patients >75 y (due to decreased CLCr)
2) long half life w/ no reversing agent |
|
|
Term
|
Definition
| prophylaxis & Tx of TED (thromboembolic disease) |
|
|
Term
|
Definition
| prophylaxis to new clot formation & TED |
|
|
Term
|
Definition
| prophylaxis & Tx of VTD (venous thromboembolic disease) |
|
|
Term
|
Definition
1) more effective in post-hip/knee arthroplasty than enoxaparin (LMWH)
2) as effective as other bleeding agents
3) as effective as warfarin in AFIB |
|
|
Term
|
Definition
1) as effective in post-hip/knee arthroplasty than enoxaparin (LMWH)
2) as effective as other bleeding agents
3) more effective than warfarin in AFIB |
|
|
Term
SOA
lepirudin & argatroban (IV) |
|
Definition
| anticoagulation in patients w/ HIT |
|
|
Term
|
Definition
1) patients w/ HIT requiring percutaneous coronary intervention (PCI)
2) patients w/ non-HIT unstable angina undergoing PCI |
|
|
Term
|
Definition
| prophylaxis of venous thromboembolism after total hip arthroplasty |
|
|
Term
|
Definition
| ↓risk of stroke & systemic embolism in patients w/ atrial fibrillation |
|
|
Term
UFH vs LMWH
chain length?
MOA?
monitoring?
half life? |
|
Definition
chain length:
UFH = long; LMWH = short
MOA:
monitoring:
UFH = PTT required; LMWH = n/a
half life:
UFH = 40 min - 3 hrs; LMWH = 3-4 hrs |
|
|
Term
UFH vs LMWH
Elimination/Metabolism?
Administration Route?
Bioavailability?
Reversal? |
|
Definition
Elimination/Metabolism:
UFH = heparinase & RE; LMWH = renal
Administration Route:
UFH = subq & IV; LMWH = subq
Bioavailability:
UFH = subq 20%; LMWH = 90-100% (no FPM)
Reversal:
BOTH by protamine - UFH = complete; LMWH = partial |
|
|
Term
| What is the subq adminitration of LMWH convenient for? |
|
Definition
1) outpatient
2) bridge therapy w/ surgical procedures |
|
|
Term
| Which heparin formulation has a greater risk of HIT? |
|
Definition
|
|
Term
| Which anticoagulation therapy is ideal for pregnant patients? |
|
Definition
|
|
Term
| Why must PTT be monitored while on UFH, but not on LMWH? |
|
Definition
PTT measures changes/sensitivity to CF II, and UFH has more effect on CF II than LMWH
(ratio of Xa:II - UFH = 1:1; LMWH = 3:1) |
|
|
Term
| What does INR values indicate? |
|
Definition
| how thick the blood is (increasing INR => thinner blood) |
|
|
Term
| What drug increases INR while on warfarin? |
|
Definition
|
|
Term
| What 5 disease states increase INR while on warfarin (make the blood thinner)? |
|
Definition
1) liver dysfunction
2) hyperthyroidism
3) acute decompensated HF
4) acute inf.
5) protracted diarrhea |
|
|
Term
| What 2 disease states decrease INR while on warfarin (i.e. increase thickness of blood)? |
|
Definition
1) short bowel syndrome
2) hypothyroidism |
|
|
Term
|
Definition
| the space b/w the mesothelium of the parietal & visceral pleura |
|
|
Term
|
Definition
| the interstitial fluid of the parietal pleura |
|
|
Term
| What is the pleural fluid composed of? |
|
Definition
| low protein filtrate from systemic vessels that enter the parietal pleural interstitial space & leaks thru the mesothelium |
|
|
Term
| What are the mechanisms to prevent fluid accumulation in the pleural space? |
|
Definition
1) balance of Starling forces favors resorption of fluib by visceral pleura
2) active solute-coupled fluid pumps in the mesothelium
3) lymphatic drainage |
|
|
Term
| What is the normal volume of pleural fluid? |
|
Definition
| 0.1-0.2 ml/kg of body weight |
|
|
Term
| What are the characteristics of pleural fluid? |
|
Definition
1) colorless & clear
2) protein <1.5 g/dL
3) cell count ~ 1500 cells/μL
4) mainly monocytes w/ variable lymphocytes, PMNs, & mesothelial cells |
|
|
Term
| What can increase to cause pleural fluid accumulation? |
|
Definition
1) increase in hydrostatic pressure (CHF)
2) increased permability of microvascular circulation due to inflam. mediators (pneumonia) |
|
|
Term
| What can decrease to cause pleural fluid accumulation? |
|
Definition
1) oncotic pressure (nephrotic syndrome)
2) pressure in pleural space (lung collapse or lobar atelectasis) |
|
|
Term
| What can be impaired/rupture and lead to pleural fluid accumulation? |
|
Definition
1) impaired lymphatic drainage due to occlusion from stroma to mediastinal lymph nodes (malignancies)
2) movement from fluid from peritoneal space thru diaphragmatic lymphatics or defects (liver disease, pancreatitis)
3) rupture of thoracic duct
4) rupture of esophagus
5) iatrogenic introduction from central catheters |
|
|
Term
Sx
pleural fluid accumulation |
|
Definition
dyspnea
pleuritic chest pain
PE: dullness to percussion, absence of fremitus, diminished/absent breath sounds, friction rub |
|
|
Term
| What are the most common causes of pleural effusions? |
|
Definition
1) CHF
2) pneumonia
3) cancer
4) PE
5) viral disease
6) coronary-artery bypass surgery
7) cirrhosis w/ ascites |
|
|
Term
| What are the indications to do a thoracentesis? |
|
Definition
1) any undiagnosed pleural effusion to establish pleural effusion
2) relief of Sx due to large pleural effusion
3) drainage of infected fluid |
|
|
Term
| What lab values can be obtained from a thoracentesis of pleural fluid? |
|
Definition
1) pH
2) protein
3) LDH
4) glucose
5) can: albumin, cholesterol, amylase
6) cell count/differential
7) gram/AFB stains
8) culture
9) cytology |
|
|
Term
| When is a pleural biopsy indicated w/ a pleural effusion? |
|
Definition
| exudate of unknown etiology, esp. if malignancy or TB is suspected |
|
|
Term
| What are the 2 types of biopsies that can occur on the pleura? |
|
Definition
1) closed biopsy (performed by pulmonologist)
2) open biospy (performed by thoracic surgeons) |
|
|
Term
|
Definition
| random sample of pleura (rarely performed) |
|
|
Term
| What is the closed biopsy esp. useful for? |
|
Definition
|
|
Term
|
Definition
| allows visual inspection of pleura to provide a definitive Dx |
|
|
Term
| What is open pleural biopsy esp. helpful for? |
|
Definition
|
|
Term
| When is the answer to Tx of pleural effusion just observation? |
|
Definition
| if there isn't a substantial amount og pleural fluid on ultrasound or radiography |
|
|
Term
| When is the Tx plan for pleural effusion diuresis & observation? |
|
Definition
| If the patient has CHF w/ no asymmetry in the pleural effusion, chest pain, or fever |
|
|
Term
| When is the Tx plan for a pleural effusion to treat for CHF, cirrhosis, or nephrosis? |
|
Definition
| if after thoracocentesis the fluid comes back as transudative |
|
|
Term
| When should you test the pleural fluid for TB markers? |
|
Definition
| if after thoracocentesis the pleural fluid is exudative and lymphocytic |
|
|
Term
| When should you be worried about PE causing the pleural effusion? |
|
Definition
| if after thoracocentesis the fluid is exudative, but not lymphocytic, and no other cause is established |
|
|
Term
| When will a transudative pleural effusion occur? |
|
Definition
| when systemic factors that influence the formation and absorption of pleural fluid are altered (s.a. CHF & cirrhosis) |
|
|
Term
| When will a transudative pleural effusion occur? |
|
Definition
| when local factors that influence the formation and absorption of pleural fluid are altered (s.a. pneumonia & malignancy) |
|
|
Term
| What criteria is used to differentiate a transudate from an exudate? |
|
Definition
|
|
Term
|
Definition
1) an effusion is exudative if any occur (serum values available):
a) protein:serum protein ratio >0.5
b) LDH:serum LDH ratio >0.6
c) total pleural fluid LDH > 2/3 the ULN for serum LDH
2) effusion is exudative if any occur (serum values unavailable):
a) LDH > 45% of serum ULN
b) cholesterol > 45 mg/dL
c) protein > 2.9 g/dL |
|
|
Term
| What are 4 disease states than can cause a transudative pleural effusion? |
|
Definition
1) CHF
2) hepatic disease
3) nephrotic syndrome
4) peritoneal dialysis |
|
|
Term
| Can any CHF cause a transudative pleural effusion? |
|
Definition
|
|
Term
| When can CHF cause exudative pleural effusion? |
|
Definition
|
|
Term
| What happens to the pleural effusion if it's a c/w heart failure? |
|
Definition
1) serum-pleural fluid albumin difference is >1.2 g/dL
2) serum-pleural fluid protein difference >3.1 g/dL |
|
|
Term
| How often is pleural effusion seen w/ hepatic disease s.a. cirrhosis & ascites? |
|
Definition
| 5% (generally right sided) |
|
|
Term
| What are the characteristics of nephrotic syndrome that can cause pleural effusion? |
|
Definition
| bilateral, small, generally aymptomatic |
|
|
Term
| If there is a pleural effusion that is asymmetric, has dyspnea, or pleuritic pain, what Dx should you be thinking of? |
|
Definition
| PE (hypercoaguable state) |
|
|
Term
| What are the 3 most common causes of exudative pleural effusions? |
|
Definition
1) paraneumonic
2) malignancy
3) PE |
|
|
Term
| What are 3 common causes of exudative pleural effusion? |
|
Definition
1) TB
2) collagen vascular (SLE, RA)
3) trauma |
|
|
Term
| What are 7 uncommon causes of exudative pleural effusion? |
|
Definition
1) drug
2) asbestos
3) radiation
4) dressler's syndrome
5) chylothorax
6) pancreatitis
7) esophageal rupture |
|
|
Term
| How is the differential Dx of an exudate made? |
|
Definition
1) cell count
2) glucose
3) pH
4) LDH
5) amylase |
|
|
Term
| What is on the DD w/ an exudative pleural effusion w/ neutrophils >50% of cell count? |
|
Definition
acute process:
parapneumonic
PE
pancreatitis |
|
|
Term
| What is on the DD w/ an exudative pleural effusion w/ lymphocytes >50% of cell count? |
|
Definition
chronic process:
TB
malignancy |
|
|
Term
| What is on the DD w/ an exudative pleural effusion w/ eosinophils >10% of cell count? |
|
Definition
blood or air in pleural space
drugs
Churg-Strauss
(not common in cancer or TB) |
|
|
Term
| What is on the DD w/ an exudative pleural effusion w/ Hct 1-20% of cell count? |
|
Definition
|
|
Term
| What is on the DD w/ an exudative pleural effusion w/ glucose <60 mg/dL? |
|
Definition
complicated parapneumonic effusion
malignancy
RA
(uncommon in in TB or lupus pleuritis) |
|
|
Term
| What is on the DD w/ an exudative pleural effusion w/ pH < 7.20? |
|
Definition
complicated parapneumonic effusion
empyema
RA
malignancy (life expectancy <30 d & chemical pleurodesis unlikely to be effective) |
|
|
Term
| What is on the DD w/ an exudative pleural effusion w/ LDH >500? |
|
Definition
complicated parapneumonic effusion
RA
malignancy (shortened life expectancy & chemical pleurodesis less likely to be effective) |
|
|
Term
| What is on the DD w/ an exudative pleural effusion w/ high amylase? |
|
Definition
pancreatitis (often left sided)
esophageal rupture |
|
|
Term
def
parapneumonic effusions |
|
Definition
| effusions associated w/ pneumonia |
|
|
Term
| Why is Dx & proper Tx of parapneumonic effusions important? |
|
Definition
| to prevent loculation & fibrosis of pleural space |
|
|
Term
| When should patients w/ pneumonia have a thoracocentesis? |
|
Definition
| w/ you have an effusion that layers to >10 mm on lateral decubitus xray |
|
|
Term
| What are the 4 possible labels of a parapneumonic effusion based on the thoracentesis? |
|
Definition
1) typical parapneumonic effusion
2) borderline parapneumonic effusion
3) complicated parapneumonic effusion
4) empyema |
|
|
Term
def
typical parapneumonic effusion |
|
Definition
pH > 7.2
glucose > 40 mg/dL
(-) gram/culture
not associated w/ loculation |
|
|
Term
Tx
typical parapneumonic effusion |
|
Definition
|
|
Term
def
borderline parapneumonic effusion |
|
Definition
pH 7.0-7.2
glucose > 40 mg/dL
(-) Gram/culture |
|
|
Term
Tx
borderline parapneumonic effusion |
|
Definition
repeat toracentesis in 6-12 hrs
if no change/improvement in pH: Tx as typical parapneumonic effusion
if pH or glucose worsen: Tx as complicated parapneumonic effusion |
|
|
Term
def
complicated parapneumonic effusion |
|
Definition
pH <7.0
glucose <40 mg/dL
(+) Gram/culture
can become loculated |
|
|
Term
Tx
complicated parapneumonic effusion |
|
Definition
| placement of a chest tube ± thrombolytics |
|
|
Term
|
Definition
| pus obtained at thoracentesis |
|
|
Term
|
Definition
chest tube ± thrombolytics
often needs surgical decortication after healing |
|
|
Term
| How is a malignant pleural effusion diagnosed? |
|
Definition
1) cytological examination (if malignancy expected) - yield is only good for adenocarcinoma
2) if negative, open pleural biopsy needed |
|
|
Term
| What are the 3 most common malignancies that cause pleural effusions? |
|
Definition
1) lung
2) breast
3) lymphoma |
|
|
Term
| What can be helpful if lymphoma is suspected? |
|
Definition
|
|
Term
| When should TB be the suspected cause of exudative pleural effusion? |
|
Definition
| if exudate has lymphocytosis |
|
|
Term
| Why can Dx of TB be difficult? |
|
Definition
| <40% have positive culture & 30% will have (-) initial TB skin test |
|
|
Term
| How can TB pleural effusions be confirmed? |
|
Definition
either:
1) an adenosine deaminase >40 U/L
2) IFN >140 pg/ml
3) PCR for TB
4) closed pleural biopsy |
|
|
Term
|
Definition
| spontaneous respolve w/o Tx, but >50% will develop pulmonary/extrapulmonary TB |
|
|
Term
| What is seen in a chylothorax? |
|
Definition
presence of milky fluid in the pleural space
triglyceride level >110 mg/dL |
|
|
Term
| What causes a chylothorax? |
|
Definition
| disruption of the thoracic duct s.a. lymphoma, penetrating trauma of the neck/thorax, surgical procedures |
|
|
Term
|
Definition
presence of blood in the pleural space
Hct >50% of blood Hct |
|
|
Term
|
Definition
generally trauma
can be to rupture of blood vessel/tumor |
|
|
Term
|
Definition
| presence of gas in the pleural space |
|
|
Term
| When will a pneumothorax occur? |
|
Definition
| when there is a communication either b/w the alveoli & pleural space or the outside of the thoracic cavity & the pleural space |
|
|
Term
| Why does air enter the cavity when there is communication b/w the pleural space & the alveoli or outside the thoracic cavity? |
|
Definition
| pressure of the pleural space is (-) wrt atm & the alveolar pressure |
|
|
Term
| What are the 5 types of pneumothorax? |
|
Definition
1) iatrogenic
2) traumatic
3) primary spontaneous
4) secondary spontaneous
5) tension |
|
|
Term
def
iatrogenic pneumothorax |
|
Definition
| consequence of a diagnostic therapeutic procedure |
|
|
Term
| What are the most common causes of iatrogenic pneumothorax? |
|
Definition
1) central line placement
2) thoracentesis
3) bronchoscopy |
|
|
Term
def
traumatic pneumothorax |
|
Definition
| result of penetrating or nonpenetrating injury to the chest |
|
|
Term
def
primary spontaneous pneumothorax |
|
Definition
| spontaneous pneumothorax w/o any underlying disease |
|
|
Term
| What usually causes primary spontaneous pneumothorax? |
|
Definition
| rupture of apical pleural blebs or cystic spaces which lie within or immediately under the visceral pleura |
|
|
Term
| What are the risk factors for primary spontaneous pneumothorax? |
|
Definition
tall
thin body habitus
tobacco abuse |
|
|
Term
Sx
primary spontaneous pneumothorax |
|
Definition
acute chest pain & dyspnea
PE: may have decreased breath sounds |
|
|
Term
Tx
primary spontaneous pneumothorax |
|
Definition
needle aspiration of air
prevent recurrance via thoracoscopy w/ bullectomy & pleurodesis |
|
|
Term
| What is the recurrance rate of a primary spontaneous pneumothorax? |
|
Definition
30-50%
(pleurodesis is Tx if this occurs) |
|
|
Term
def
secondary spontaneous pneumothorax |
|
Definition
| spontaneous pneumothorax w/ underlying lung disease |
|
|
Term
| What is the most common cause of secondary spontaneous pneumothorax? |
|
Definition
|
|
Term
| Besides COPD, what are other common causes of secondary spontaneous pneumothorax? |
|
Definition
1) PCP in AIDS
2) asthma
3) CF
4) lymphangioleiomyomatosis
5) TB sclerosis
6) mechanical ventilation |
|
|
Term
| Is the prognosis for secondary spontaneous pneumothorax better or worse? |
|
Definition
| worse (more life-threatening) since they already have diminished lung capacity |
|
|
Term
Tx
secondary spontaneous pneumothorax |
|
Definition
chest tube
may undergo pleurodesis |
|
|
Term
|
Definition
| when the intrapleural pressure exceeds atm pressure throughout expiration => decreased ventilation, hypoxemia, decreased venous return & decreaed CO |
|
|
Term
| When are tension pneumothorax most common? |
|
Definition
| mechanically ventilated patients |
|
|
Term
|
Definition
acutely ill w/ dyspnea, tachycardia, tachypnea, distended neck veins, & hypotension
PE: decreased breath sounds on effected side, trachea deviated |
|
|
Term
|
Definition
MEDICAL EMERGENCY
place large bore needle into the pleural space thru the second anterior intercostal space |
|
|
Term
|
Definition
| inability of the resp. system to provide adequate oxygen for the body tissue needs |
|
|
Term
| Why can the reason behind resp. failure be so complicated? |
|
Definition
| any lung or chest wall pathology can lead to resp. failure & may be multifactorial |
|
|
Term
| What is the first thing used to evaluate resp. failure? |
|
Definition
|
|
Term
| What are the 2 major categories of resp. failure? |
|
Definition
1) hypoxia w/ hypercarbia (inadequate ventilation)
2) hypoxia predominating |
|
|
Term
| What are the values of ABG that indicate hypoxia w/ hypercarbia? |
|
Definition
| 1) low PaO2
2) high PaCO2 |
|
|
Term
| What is the problem in hypoxia w/ hypercarbia resp. failure? |
|
Definition
| inadequate ventilation (increased PaCO2) & oxygenation |
|
|
Term
| What are the 3 types of problems associated w/ hypoxia w/ hypercarbia resp. failure? |
|
Definition
1) CNS
2) chest wall
3) airways |
|
|
Term
| What are the ABGs seen in hypoxemia predominating resp. failure? |
|
Definition
| 1) love PaO2
2) no change PaCO2 (until the end) |
|
|
Term
| What is the problem in hypoxemia predominating resp. failure? |
|
Definition
| inability to get oxygen thru the resp. system & out to needy tissues |
|
|
Term
| What are the 4 types of problems seen w/ hypoxemia predominating resp. failure? |
|
Definition
1) circulatory, cardiac
2) Hb
3) intrinsic lung disease
4) ARDS |
|
|
Term
| What are the 5 mechanisms of hypoxia? |
|
Definition
1) low environmental oxygen
2) severe hypoventilation
3) shunting
4) ventilation/perfusion mismatch
5) diffusion defect |
|
|
Term
| What causes low environmental oxygen? |
|
Definition
1) altitude
2) poisonings of Hb (CO, cyanide, etc)
3) another plant's atm? |
|
|
Term
|
Definition
| decreased ventilation => increased alveolar CO2 |
|
|
Term
| What does the elevated PaCO2 due to hypoventilation cause? |
|
Definition
| displacement of PaO2 in the alveolus |
|
|
Term
| What values indicate hypoventilation is responsible for hypoxia? |
|
Definition
| if hypoventilating =>
increased PaCO2
decreased PaO2
check A-a gradient. If normal, implies hypoventilation is the sole mechanism for hypoxia |
|
|
Term
|
Definition
extreme mismatch of ventilation & perfusion, where an area of the lung has 0 ventilation, but continues to recieve perfusion (V/Q = 0)
This results in hypoxemia b/c unoxygenated blood is being sent to the left side of the heart |
|
|
Term
| What is an example of shunting? |
|
Definition
| leison block bronchi, but doesn't interfere w/ blood perfusion |
|
|
Term
| Can shunting be corrected by 100% oxygen? |
|
Definition
|
|
Term
def
dead space ventilation |
|
Definition
| opposite end of the spectrum of V/Q mismatch - areas of the lung are ventilated, but do not recieve perfusion (V/Q = infinity), tho rarely causes hypoxemia on its own |
|
|
Term
| What causes hypoxemia due to shunting? |
|
Definition
| admixture of shunted, poorly oxygenated blood into the circulation |
|
|
Term
| What one of the tests for shunting? |
|
Definition
| give a patient 100% O2 to see if the PaO2 will rise |
|
|
Term
| What is the most common cause for hypoxemia? |
|
Definition
|
|
Term
| What can cause a V/Q mismatch? |
|
Definition
| any lung or airway disease |
|
|
Term
| When is worse hypoxemia seen w/ V/Q mismatch? |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| problem moving oxygen from the lung onto the capillaries |
|
|
Term
| How common is diffusion defect for hypoxemia? |
|
Definition
| very common part of a variety of lung diseases (pneumonia, inflam. lung disease, ILD, etc) is almost NEVER is the primary cause for hypoxemia |
|
|
Term
| What are the 4 systems that can malfunction to give a hypercapneic resp. failure? |
|
Definition
1) CNS
2) CW malformation/injury
3) CW malfunction
4) airways |
|
|
Term
| How can the CNS lead to hypercapneic resp. failure? |
|
Definition
| signal to resp. system fails |
|
|
Term
|
Definition
| ventilation = resp. rate * TV (tidal volume) |
|
|
Term
ABGs
CNS induced hypercapneic resp. failure |
|
Definition
|
|
Term
| What can cause the CNS singal to resp. system to fail? |
|
Definition
1) CNS depressants
2) CNS trauma
3) stroke (rare) - only when the brainstem is directly affected
4) Ondine's curse |
|
|
Term
|
Definition
| a very rare malady involving failure of the central pathways regulating resp. where there is no resp. effort unless the person is conscious & actively deciding to breathe (problematic during sleep) |
|
|
Term
| How can chest wall malformation/injury lead to hypercapneic resp. failure? |
|
Definition
| changes the structure of the CW => ventilatory efforts inadequate to remove CO2 & pull in adequate O2 |
|
|
Term
| What are causes of chest wall malformation/injury? |
|
Definition
1) kyphosis (AP spinal deformity)
2) scoliosis (side to side spinal deformity)
3) hyperinflation
4) flail chest |
|
|
Term
| How does hyperinflation affect the structure of the CW? |
|
Definition
| pushes the diaphragm down into an inefficient position/diaphragm fiber length for an effective contraction in ventilation |
|
|
Term
|
Definition
| after multiple rib fractures (at least 3), a section of the chest wall move paradoxically w/ resp., wasting ventilatory effort |
|
|
Term
| What can affect the ability of the chest bellows to achieve adequate ventilation? |
|
Definition
| variety of neural, muscular, & neuromuscular pathologies |
|
|
Term
| What disease states can affect CW function and lead to hypercapneic resp. failure? |
|
Definition
1) high spinal cord injury
2) amyotrophic lateral sclerosis (Lou Gehrig's disease)
3) Guillain Barre Syndrome
4) Polio and post-polio syndrome, West Nile Virus
5) Myasthenia Gravis
6) Muscular Dystrophies |
|
|
Term
def
amyotrophic lateral sclerosis |
|
Definition
| loss of anterior horn cells, brainstem bulbar => progressive neuron loss => resp. failure |
|
|
Term
def
Guillain Barre Syndrome |
|
Definition
| an acute demyelinating neuropathy, often post viral => progressive paralysis that may last for months |
|
|
Term
| How can polio & post-polio syndrome, west nile virus cause hypercapneic resp. failure? |
|
Definition
| may affect brain (encephalitis), anterior horn cells, or peripheral neuromuscular behavior => loss of function => eventual return of function, but to varying degrees |
|
|
Term
|
Definition
| decrease in AchRs @ neuromuscular junction => sudden onset of resp. failure (when occurs, tho, doesn't occur often) |
|
|
Term
|
Definition
| progressive muscular weakness caused by numerous genetic types |
|
|
Term
| How can airway malformation lead to hypercapneic resp. failure? |
|
Definition
| any factor that compromises the airway lumen can lead to hypercapneic resp. failure |
|
|
Term
| What can compromise the upper airway and lead to hypercapneic resp. failure? |
|
Definition
1) obstruction (tumor, foreign body, scarring)
2) inflam. (airway injury)
3) vocal cord pathology |
|
|
Term
| What can compromise the lower airways and lead to hypercapneic resp. failure? |
|
Definition
1) obstruction (tumor, foreign body, scarring)
2) inflam. (from inhalant injury)
3) obstructive airway disease (chronic or reversible) |
|
|
Term
| What COPD patients are more likely to have hypercapneic resp. failure? |
|
Definition
| COPD patients who are predominately chronic bronchitis (clue bloaters) or late stage emphysema |
|
|
Term
| What reversible airway disease can lead to hypercapneic resp. failure? |
|
Definition
| severe attacks of asthma => early rise of PaCO2 => late fall of PaO2 |
|
|
Term
| What malformations can lead to primarily hypoxemic resp. failure? |
|
Definition
1) CV factors
2) lung pathology |
|
|
Term
| What CV factors can lead to primarily hypoxemic resp. failure? |
|
Definition
1) cardiac failure (L or R sided)
2) vascular compromise |
|
|
Term
| How can L sided heart failure lead to hypoxemic resp. failure? |
|
Definition
| back pressure to pulmonaary circular => inadequate CO/tissue delivery |
|
|
Term
| How can R sided HF cause hypoxemic resp. failure? |
|
Definition
| inadequate flow thru lungs => reduced blood delivery to the L heart |
|
|
Term
| What can cause vascular compromise and lead to hypoxemic resp. failure? |
|
Definition
1) thrombi/emboli
2) inflam. (vasculitis)
3) fibrosis |
|
|
Term
| What pathophysiological processes intrinsic to the lung can leads to hypoxemia resp. failure? |
|
Definition
1) loss of ventilatory units (V/Q mismatch)
2) DECREASED lung compliance => increased elastic load & increased work of breathing
3) gas diffusion problems
4) hypoxiv vasocontriction |
|
|
Term
| What pathological processes of the lung can lead to hypoxemia resp. failure? |
|
Definition
1) inf. (extensive pneumonia or less extensive in patients w/ underlying disease)
2) inflam. & fibrotic lung diseases
3) neoplasms |
|
|
Term
| How is noraml fluid circulated in the pulmonary interstitium/alveoli? |
|
Definition
| small amount of fluid continuously filters into the pulomary interstitium and is removed by lymphatics, where the rate of fluid movement is described by the Starling equation |
|
|
Term
|
Definition
| Qf = Kf[(Pmv - Pi) - σ(πmv - πi)]
Q = fluid flow/filtration rate
K = filtration coefficient
(Pmv - Pi) = blanace b/w microvasculat & interstitial hydrostatic pressure
σ = osmotic reflection coefficient
(πmv - πi) = the balance b/w oncotic pressure in the vasculature vs. the interstitium of the lung |
|
|
Term
| What is the net result of the Starling forces on the pulmonary interstitial fluid of a normal lung? |
|
Definition
| interstitium & alveolar spaces remain "dry" |
|
|
Term
| What are the 3 mechanisms of pulmonary edema? |
|
Definition
1) increased vascular hydrostatic pressure
2) decreased vascular oncotic pressure
3) damage or distruption of the alveolar/capillary membrane (leak) |
|
|
Term
| What is the result of a increase in vascular hystrostatic pressure, decrease in vascular oncotic pressure, or damage/disruption of the alveolar/capillary membrane? |
|
Definition
fluid will initially collect in the interstitial spaces of the lung (interstitial edema)
if large quantities of fluid enter the pulmonary interstitium => fluid enters the alveoli (alveolar edema) |
|
|
Term
| What is cardiogenic pulmonary edema? |
|
Definition
| pulmonary microvascular hydrostatic pressure increases due to failure of the left ventricle to pump forward adequately => normal oncotic/lymphatic defences are overwhelmed |
|
|
Term
| What causes cardiogenic pulmonary edema? |
|
Definition
MI
cardiomyopathies
L sided valvular heart disease |
|
|
Term
Tx
cardiogenic pulmonary edema |
|
Definition
| Tx the cardiac problem and the edema will resolve |
|
|
Term
| What is non cardiogenic pulmonary edema? |
|
Definition
| acute widespread injury to the pulmonary endothelium => fluid leaks into the interstitium |
|
|
Term
| What is the most common cause of non-cardiogenic pulmonary edema? |
|
Definition
| ARDS (acute resp. distress syndrome) |
|
|
Term
| Why is it important to distinguish b/w cardiogenic & noncardiogenic pulmonary edema? |
|
Definition
| b/c of the difference in management approaches to the 2 types of edema |
|
|
Term
| How is cardiogenic vs. noncardiogenic pulmonary edema distinguished? |
|
Definition
by passing a balloon tipped catheter via a vein to the right ride of the heart & out into the pulmonary circulation, "wedging" the balloon in the pulmonary capillary bed.
(tho the clinical picture and presentation may give the Dx and this invasive procedure may not be needed) |
|
|
Term
| What is seen in a cardiogenic pulmonary edema due to the invasive balloon tipped catheter procedure? |
|
Definition
| the pulmonary capillary pressure is INCREASED due to the back pressure from the dysfunctional L heart |
|
|
Term
| What is seen in a noncardiogenic pulmonary edema due to the invasive balloon tipped catheter procedure? |
|
Definition
| the pulmonary capillary wedge pressure will be low to normal |
|
|
Term
|
Definition
| acute lung injury leading to widespread pulmonary infiltrates, hypoxemia, and reduction of lung compliance w/o evidence of L ventricular failure |
|
|
Term
|
Definition
the end result of injury to the lung from multiple etiologies s.a.
1) sepsis
2) shock
3) pneumonia
4) aspiration of gastic contents
5) inhalation of toxic agents
6) narcotic OD
7) pancreatitis
8) emboli (blood, amniotic fluid, fat) |
|
|
Term
| What is the pathogenesis of ARDS? |
|
Definition
| injury to alveolar capillary membrane => interstitial edema => alveolar edema => accumulation of PMNs, macs, cell debris, & fibrin => hyaline membrane formation |
|
|
Term
| What are the 3 possible outcomes to ARDS? |
|
Definition
1) death due to resp. insufficiency
2) recovery, but significant restrictive impairment
3) recovery w/ minimal impairment (rare) |
|
|
Term
|
Definition
1) progressive hypoxic resp. failure
2) CXR: bilateral infiltrates
3) low pulmonary capillary wedge pressure (PCWP)
4) often - multiorgan system dysfunction |
|
|
Term
|
Definition
1) support w/ oxygen
2) mechanical ventilation
3) Tx underlying cause if possible
4) fluids, Abx, vasopressors, etc. |
|
|
Term
| How is a patient's resp. failure evaluated? |
|
Definition
1) Hx & PE when possible to suggest etiologies
2) ABGs
3) CXR to suggest etiology
4) specific testing to determine the underlying pathophysiology suggested by initial evalutation |
|
|
Term
| What is learned by obtaining the ABGs of a patient in resp. failure? |
|
Definition
1) presence/absence of hypercarbia
2) degree of hypoxemia |
|
|
Term
| What specific testing can be done on a patient in resp. failure to determine underlying pathophysiology? |
|
Definition
1) microbiologic studies
2) neuromuscular evaluation
3) CNS assessment
4) past/present studies diagnosing specific lung diseases (s.a. COPD, etc)
etc |
|
|
Term
|
Definition
| 1) supplemental oxygen as needed to keep SaO2 >90%
2) assess need for mechanical ventilation & institiute if needed
3) Tx underlyign disease
4) supportive care |
|
|
Term
| What values are tested to assess the need for mechanical ventilation in patients w/ resp. failure? |
|
Definition
1) hypercarbia
2) acidosis
3) poor resp. muscle strength
4) rapid resp. muscle strength (>40 breaths/min)
5) signs of fatigue
6) poor oxygenation |
|
|
Term
| What supportive care can be given to patients w/ resp. failure? |
|
Definition
1) fluids
2) nutrition
3) blood products
4) body positioning
5) Tx of complicating conditions |
|
|
Term
| What are the 3 goals of mechanical ventilation? |
|
Definition
1) oxygenation
2) ventilation
3) don't hurt the patient |
|
|
Term
| How is oxygenation maximized in mechanical ventilation? |
|
Definition
| V/Q matching (opening more alveoli & get them oxygen) |
|
|
Term
| How is ventilation optimized in mechanical ventilation? |
|
Definition
| work of breathing - move the lungs to lear CO2 if patient can't do it |
|
|
Term
| What is the most common cause of mechanical ventilation injury to patients? |
|
Definition
| VILI (ventilator induced lung injury) |
|
|
Term
| What ABG levels are affected by ventilation? |
|
Definition
|
|
Term
| What is oxygenation a product of? |
|
Definition
| FIO2 & the number of open alveoli (open more alveoli by increasing the pressure on them) |
|
|
Term
|
Definition
1) barotrauma/volutrauma
2) patient comfort/synchrony
3) CO/venous return
4) glottic opening/VAP/aspiration
5) glottic damage/tracheal stenosis
6) over/undersedation |
|
|
Term
| What are the possible points of ventilatory control? |
|
Definition
1) start/stop inspiration
2) start/stop exhalation
3) frequency
4) flow rate (into circuit) |
|
|
Term
| What is the active process in mechanical ventilation (what does the machine do)? |
|
Definition
inspiration
(the patient's body does expiration) |
|
|
Term
| Does the mode of ventilation (frequency, flow, etc.) matter? |
|
Definition
| no, not as long as there is adequate alveolar distention (for O2), adequate work of breathing (for CO2), & you aren't hurting the patient |
|
|
Term
| What are the 2 modes of volume cycled (positive pressure) ventilation? |
|
Definition
1) controlled mechanical ventilation (CMV)
2) assist control ventilation (AC) |
|
|
Term
|
Definition
| 1) RR is fixed
2) TV is set
3) % oxygen is set (FIO2) |
|
|
Term
|
Definition
| 1) RR, TV, & FIO2 set like in CMV
2) any patient ventilatory efforts will be assisted |
|
|
Term
| What is the rationale for positive end expiratiory pressure use? |
|
Definition
| increased work needed to open alveoli |
|
|
Term
| What causes inspiration/expiration during spontaneous breathing? |
|
Definition
inspiration is due to the pressure difference b/w pressure at the mouth (atm) & pressure in the alveoli (-)
expiration is by passive recoil |
|
|
Term
| How is alveolar pressure different in mechanical ventilation? |
|
Definition
pressure at the mouth is positive during inspriation & alveoli are at atm pressure to create a pressure difference to cause flow
expiration is again, passive |
|
|
Term
| What can cause problems w/ alveolar pressure? |
|
Definition
1) w/ disease alveoli may fill w/ material other than air (V/Q mismatch(
2) there may be collapse or atelectasis of alveoli
filling these alveoli w/ air requires more work: work to open the alveoli, then work to fill them with air |
|
|
Term
def
PEEP (positive end expiratory pressure) |
|
Definition
| a valve is inserted in the expiratory side of the ventilator circuite to keep the pressure at end-expiration >0 |
|
|
Term
|
Definition
| it assists w/ alveolar recruitment & helps avoid collapsing of alveoli, improving the ability to get oxygen to the patient, so PEEP is often added to mechanical ventilation (esp. in very hypoxic patients) |
|
|
Term
| What is the normal value of PEEP? |
|
Definition
|
|
Term
| Since ventilation = RR x TV, how can ventilation be manipulated? |
|
Definition
RR can be manipulated in any mode
TV can be manipulated in any mode, but the mode determines how you do it |
|
|
Term
| What happens if you close the inspiratory valve w/o opening the expiratory valve? |
|
Definition
inspiratory pause => to obtain plateau pressure
the resulting pressure wave will show an initial high pressure (pressure peak) then decay to a lower pressure (plateau pressure) |
|
|
Term
| What does the initial peak pressure represent? |
|
Definition
| the work done to overcome airway resistance |
|
|
Term
|
Definition
| R = (Ppeak - Pplateau)/flow |
|
|
Term
| What does the plateau pressure represent? |
|
Definition
| work done to overcome the elastic forces of the lung & CW |
|
|
Term
|
Definition
| C = (Vexhaled total - any PEEP)/Pplateau |
|
|
Term
| What is demonstrated by the pressure-volume loop? |
|
Definition
| hysterestis b/w inspiration & expiration |
|
|
Term
| What do changes in the pressure volume loop indicate? |
|
Definition
changes in compliance
1) lower compliance => R shift (stiff lung)
2) higher compliance => L shift (floppy lung) |
|
|
Term
| What pressure value is never exceeded in the lung? |
|
Definition
|
|
Term
| What value of TV is not exceeded? |
|
Definition
| >8 cm/kg ideal body weight (not acutal) |
|
|
Term
| What 4 complications can occur w/ mechanical ventilation? |
|
Definition
1) barotrauma
2) CV
3) dynamic hyperinflation/auto PEEP
4) VAP (ventalator associated pneumonia) |
|
|
Term
| What causes barotrauma w/ mech. vent.? |
|
Definition
| since nomral breathing is negative pressure, the postive pressure on mech. vent. can lead to rupture of alveoli |
|
|
Term
|
Definition
| air can leak along the pulmonary interstitium, track up the mediastinum, into the pleural space (pneumothorax) and even into the subq tissues => can be fatal |
|
|
Term
| Is the alveolar damage obtained from mech. vent. barotrauma permanent? |
|
Definition
|
|
Term
| How is barotrauma prevented in mech. vent.? |
|
Definition
| monitoring pressure measurements & modifying ventilator settings as needed |
|
|
Term
| How can mech. vent. lead to CV issues? |
|
Definition
| if very high intrathoracic pressures are created, there can be compression of the veins returning to the heart => decreased ventricular filling (lower pre-load) in the R ventricle => less blood coming through the pulmonary circulation to the L ventricle => decreased CO => hypotension |
|
|
Term
| How can mech. vent. cause dynamic hyperinflation (auto PEEP)? |
|
Definition
| if inadequate time is allowed for exhalation => build up of volume & pressure in the lungs => CV complications |
|
|
Term
| When is dynamic hyperinflation due to mech. vent. most likely to occur? |
|
Definition
| in patient's w/ obstructive lung diseases (they need linger expiratory times) |
|
|
Term
|
Definition
pop the patient off the ventilator to relieve pressure
reset the ventilator to decrease resp. rate, decreaed TV, or increaed inspiratory flow rate (allows for more expiration time) |
|
|
Term
| What causes ventilatory associated pneumonia (VAP)? |
|
Definition
1) placing a cuffed endotracheal tube from the mouth thru the vocal cords eliminated the nomral upper airway defense mechanism
2) secretions can pool on the top of the cuff and leak into the airways |
|
|
Term
| Why is VAP often severe and hard to treat? |
|
Definition
| patients on mech. vent. are in ICU, which is a hotbed for aggressive & highly Abx resistant bacteria |
|
|
Term
| Why is it often difficult to detect VAP? |
|
Definition
| patient is on a mech. vent. b/c they have a serious lung problem and it can be difficult to detect new pneumonia |
|
|
Term
|
Definition
1) sit patient at 45 degreee angle
2) wash hands b/w patients
3) use Abx jusiciously (not freely)
4) avoid aspiration of gastric contents by close monitoring of any tube feeding |
|
|
Term
| When should removal from the ventilator be considered? |
|
Definition
| when the patient is awake & stable |
|
|
Term
| What is the best method to determine the patient's "readiness" to be weaned from the ventilator? |
|
Definition
disconnect the ventilator & monitor the patient as they breathe humidified oxygen or air.
if they fail, restart the ventilator
if they are able to breathe easily for at least 30 min, remove the ET tube |
|
|
Term
| How does a pulmonary embolism (PE) form? |
|
Definition
| deep vein thrombosis (deep venous system clots) => clot sheds/breaks off => travel thru the venous system to the vena cava to the right heart => pulmonary circulation |
|
|
Term
| What venous systems are often the source of PE? |
|
Definition
| deep venous systems of the femoral, iliac & pelvic venous systems |
|
|
Term
| What are the 3 risk factors for a DVT (deep vein thrombus)? |
|
Definition
Virchow's triad:
1) stasis
2) endothelial injury
3) hypercoaguable state |
|
|
Term
| What clinical scenarios should physicians be on the lookout for PE? |
|
Definition
1) bedridden
2) post-op
3) orthopedis procedures
4) underlying malignancy
5) pregnancy
6) immobitily (inc. immoble occupations: bus, car, plane, etc) |
|
|
Term
|
Definition
tachypnea
tachycardia
hypoxia
dyspnea (esp. sudden onset)
pleuritic pain (esp. sudden onset)
cough
signs/Sx of DVT
fever
hemoptysis
syncopy (fainting)
hypotension
death |
|
|
Term
| Why is it bad that PE is over AND under diagnosed? |
|
Definition
over: => excess therapy
under: => morbidity/mortality |
|
|
Term
| What is point of the risk assessment tools for PE s.a. Wells criteria, clinical risk assessment score, Canadian score, Charlotte ruless? |
|
Definition
| give a probability that the patient has a PE |
|
|
Term
| What are the components of the intial patient evaluation upon suspected PE? |
|
Definition
1) CXR
2) electrocardiogram
3) ABGs |
|
|
Term
| Why is a CXR important in the initial evaluation for suspeced PE? |
|
Definition
1) possible to find PE (tho usually subtle or absent)
2) more useful for R/O other diseases s.a. pneumothorax or pneumonia that have similar Sx |
|
|
Term
| Why is an electrocardiogram important in the initial evaluation for suspeced PE? |
|
Definition
1) NOT useful in Dx of PE since finding are non-specific
2) most useful in R/O acute MI or pericardial effusion (present w/ similar Sx)
3) troponin is prognostic, not diagnostic |
|
|
Term
| Why is obtaining ABGs important in the initial evaluation for suspeced PE? |
|
Definition
| 1) NOT specific to rule in PE
2) helpful since majority of PE patients have PaO2 <80 and the absence of hypoxia => another Dx |
|
|
Term
| What should be the initial diagnostic procedures that lead a physician to suspect PE? |
|
Definition
1) high clinical suspicion w/ high clinical scores
2) R/O other possible diagnoses
3) V/Q scan (as suggested by PIOPED trial) to look for areas of no perfusion
4) consider d-dimer measurement |
|
|
Term
|
Definition
| a product of fibrinolysis |
|
|
Term
| Why might a d-dimer measurement in the initial diagnostic testing for suspeced PE be a good thing? |
|
Definition
1) finbrinolysis is always occuring when there are clots
2) a (-) result is strong evidence that a PE is NOT present (<500 ng/L via ELISA - don't do rapid assays since less sensitive)
3) a (+) result inducates need for further diagnostic testing |
|
|
Term
| What are the 4 possible diagnostic tests that can be done to R/I PE? |
|
Definition
1) pulmonary angiogram
2) V/Q scan
3) venous imaging (look for source of PE)
4) spiral CT angiography |
|
|
Term
| What is the "god standard" for PE Dx (tho rarely done)? |
|
Definition
|
|
Term
| What will a (+) pulmonary angiogram for PE show? |
|
Definition
| an intravascular filling defect in the area of the clot |
|
|
Term
| What are the risks of comolications associated w/ pulmonary angiogram? |
|
Definition
1) hypotension
2) arrythmias
3) arterial rupture
4) dye reaction |
|
|
Term
| How does a V/Q scan work? |
|
Definition
nuclear markers introduced & the chest in scanned in 2 modes: one for perfusion, one for ventilation.
This test requires patient holds their breath, the lab be open, and there are no abnormalities on CXR |
|
|
Term
| How can the results of V/Q scan help Dx of PE (or R/O)? |
|
Definition
1) (-) or low probability scan (no areas of perfusion defect) virtually excludes PE
2) (+) or high probability scan (area of lung w/ lack of perfusion, but normal ventilation - V/Q mismatch) suggests PE is VERY LIKELY(85-90%)
(most scans are indeterminate, which doesn't help at all) |
|
|
Term
| How often does doppler ultrasouns find DVT in PE suspected patients? |
|
Definition
~1/2 (high false +)
only sm. amount of proven PE will have a (+) venous imaging test |
|
|
Term
| Why might a venous imaging in the diagnostic testing for suspeced PE be a good thing? |
|
Definition
may exclude other Dx
(venograms are the "gold standard", but rarely used) |
|
|
Term
| What test is the most used PE dianostic test? |
|
Definition
|
|
Term
| What test was set up to evaluate the efficacy of CT angiography in PE? |
|
Definition
| PIOPED II (results were inconclusive, but there have been improvements since, inc. faster speed & more images) |
|
|
Term
| What are the clinicans looking for to detect PE in spiral CT angiography? |
|
Definition
| intravacular filling defect |
|
|
Term
Advantages
spiral CT angiography for PE Dx |
|
Definition
1) high sensitivity & specificity
2) esp. good for central emboli, but also good for segmental & subsegmental
3) cost effective
4) (+) test => Tx of PE |
|
|
Term
Disadvantages
Spiral CT angiography |
|
Definition
1) poor for small segmental emboli
2) required 15-25sec breath hold
3) more radiation exposure than V/Q scan
4) requires IV contrast |
|
|
Term
| What is the diagnostic protocol for PE? |
|
Definition
1) clinical score risk
2) d-dimer
3) V/Q or CT
4) ultrasound leg study
5) consider angiography |
|
|
Term
| What are the 4 therapeutic options for a PE? |
|
Definition
1) anticoagulation
2) IVC filter
3) surgical embolectomy
4) thrombolytic agents |
|
|
Term
| What are the options for anticoagulation? |
|
Definition
1) heparin & derivatives
2) Vit K antagonists
3) thrombin inhibitors
4) new therapies |
|
|
Term
|
Definition
| a very long molecule of which only a small portion accomplishes anticoagulation |
|
|
Term
Advantages/Disadvantages
UFH (unfractionated heparin) |
|
Definition
Ad: cheap, familiar
Dis: difficult to dose, has significant complications inc. bleeding & thrombocytopenia |
|
|
Term
def
LMWH (low molecular weight heparin) |
|
Definition
| a smaller molecule than UFH |
|
|
Term
| What are the advantages of LMWH over UFH? |
|
Definition
1) dosing is weight based & more predictable
2) less complications |
|
|
Term
|
Definition
| pentasaccharide w/ only the active anti-thrombin portion of heparin |
|
|
Term
|
Definition
| alternative anticoagulation for patients who develop HIT (heparin induced thrombocytopenia) |
|
|
Term
def
HIT (heparin induced thrombocytopenia) |
|
Definition
it's an Ab mediated rxn:
heparin binds to PF4 => epitope => Ab binding |
|
|
Term
|
Definition
1) decreaed platelets (usually >50% drop)
2) skin leisons at heparin site
3) acute systemic reactions |
|
|
Term
|
Definition
1) monitor platelet count for at least 14 days
2) if acute systemic reaction: immediate platelet count
3) non heparin anticoagulants s.a. Agatroban (direct thrombin inhibitor) or fondaparinux |
|
|
Term
| What are the 2 common DTI (direct thrombin inhibitors)? |
|
Definition
|
|
Term
| What is the mainstay of long term oral anticoagulation therapy? |
|
Definition
| Vit K antagonists since effectiveness well-established |
|
|
Term
| What are the Vit K antagonists? |
|
Definition
| warfarin & its derivatives, coumadin |
|
|
Term
|
Definition
| interfere w/ Vit K carboxylation of factors II, VII, IX, & X |
|
|
Term
|
Definition
| pregnancy (teratogenic - fetal bone abnormalities b/c can cross the placenta) |
|
|
Term
|
Definition
1) narrow therapeutic window
2) variable dose response
3) DDIs
4) lab controls not well standardized
5) non-adherence, non-compliance |
|
|
Term
| What has helped somewhat to standardize the monitoring of warfarin therapy? |
|
Definition
| INR (international normalized ratio) |
|
|
Term
| What are the current monitoring methods of warfarin? |
|
Definition
1) PT time (since CF factors affected are those on the extrinsic coagulation pathway)
2) INR (patient PT/normal PT) |
|
|
Term
| What new drugs are in development as anticoagulants? |
|
Definition
1) DTIs
2) thrombomodulin
3) agents modifying fibrinolysis |
|
|
Term
| When is anticoagulation therapy indication? |
|
Definition
1) prophylaxis for high risk patients 2) Tx of PE (start UFH or LMWH while work up is in progress)
3) Tx of DVT |
|
|
Term
|
Definition
|
|
Term
DOC
anticoagulation therapy |
|
Definition
|
|
Term
| When is an embolectomy indicated? |
|
Definition
1) patients w/ severe CV compromise secondary to PE
2) saddle block embolus or large PE in compromised patient |
|
|
Term
| What are the challenges of a embolectomy? |
|
Definition
1) high risk procedure
2) hard to arrange quickly |
|
|
Term
DOC
anticoagulation in pregnancy, cancer |
|
Definition
|
|
Term
|
Definition
| an umbrella like basket that is inserted into the vena cava to catch & filter out any clots coming from the legs or pelvic area |
|
|
Term
| What are the indications for an IVC filter? |
|
Definition
1) failure of anticoagulation therapy
2) CI to anticoagulation |
|
|
Term
| What are the complications associated w/ IVC filter? |
|
Definition
1) limb edema
2) filter blockage w/ development of venous collaterals |
|
|
Term
| How does normal pulmonary circulation usually compare to normal systemic cirulation in regards to pressure w/in the system, resistance to blood flow, and capacitance to handle increased blood flow? |
|
Definition
Pulonary:
1) low pressure w/in system
2) low resistance to blood flow
3) high capacitance
systemic:
1) high pressure w/in system
2) high resistance to blood flow
3) low capacitance |
|
|
Term
| What causes pulmonary HTN? |
|
Definition
| variety of reasons - resistance to blood flow in the lungs increases => increased pressure from R heart needed to move blood thru lungs => dilation of R heart & possibly R heart failure => increased pressure in the jugular veins, edema of the legs, and potential engorgement of the liver or ascites |
|
|
Term
|
Definition
| fluid in peritoneal cavity |
|
|
Term
|
Definition
early disease: asymptomatic
progressive disease: dyspnea, fatigue, chest heaviness, chest pain, leg edema, abdominal swelling, syncopy |
|
|
Term
|
Definition
|
|
Term
|
Definition
1) lungs: clear - unless underlying lung disease
2) heart: loud 2nd heart sound (P2) due to late closure of the pulmonic valve, murmurs if the dilation of the RV affects tricuspid or pulmonic heart valve
3) signs of RV HF: edema, ascites, hepatomegaly, JVD (jugular venous distension) |
|
|
Term
| What are the 5 classes of pulmonary HTN? |
|
Definition
I: idiopathic
II: due to L heart disease
III: hypoxemia related
IV: chronic thromboemolic diseae
V: miscellaneous |
|
|
Term
| What are causes of miscellaneous pulmonary HTN? |
|
Definition
1) inflam./infiltrative lung diseases (sarcoidosis, Langerhan's histocytosis, lymphangioleiomyomatosis)
2) compression of pulmonary vessels (adenopathy, tumor, fibrosis in the mediastinum) |
|
|
Term
Tx
miscellaneous pulmonary HTN |
|
Definition
| Tx underlying disease & reassess for improvement, tho in some cases Tx specifically for pulmonary HTN may be indicated (esp. sarcoidosis) |
|
|
Term
| What are the causes of chronic thromboembolic disease pulmonary HTN? |
|
Definition
1) thromboembolic obstruction of proximal pulmonary arteries
2) thromboembolic obstruction of distal pulmonary arteries
3) PE due to tumor, parasites, foreign material |
|
|
Term
Tx
chronic thromboembolic diseae pulmonary HTN |
|
Definition
| Tx disease by pulmonary endarterectomy |
|
|
Term
def
pulmonary endarterectomy |
|
Definition
| chronic clots are physically pulled out of the pulmonary circulation, improving blood flow |
|
|
Term
| What are causes of hypoxemia related pulmonary HTN? |
|
Definition
1) COPD
2) ILD
3) sleep disordered breathing
4) alveolar hypoventilation syndromes
5) chronic exposure to high altitude
6) developmental abnormalities associated w/ hypoxemia |
|
|
Term
Tx
hypoxemia related pulmonary HTN |
|
Definition
initial approach: Tx underlying disease
beneficial: oxygen supplementation |
|
|
Term
| Why is there controversy on whether to Tx the pulmonary HTN in patients w/ hypoxemia related pulmonary HTN? |
|
Definition
| drugs may increase pulmonary blood flow, but may worsen hypoxemia bc of increased V/Q mismatch |
|
|
Term
| What causes pulmonary HTN due to L heart disease? |
|
Definition
1) L sided atrial or ventricular disease
2) L sided valvular heart disease |
|
|
Term
| How can L sided heart disease lead to pulmonary HTN? |
|
Definition
| high pressures from a bad L heart => high pressures in the pulmonary venous system => high pressures in pulmonary capillaries => high pressures in pulmonary arteries |
|
|
Term
Tx
pulmonary HTN due to L heart disease |
|
Definition
medications for heart failure
repair of abnormal valves |
|
|
Term
| What are the conditions associated w/ idiopathic pulmonary HTN? |
|
Definition
1) idiopathic pulmonary HTN
2) familial pulmonary HTN
3) related conditions (collagen vascular diseases, congenital systemic to pulmonary shunts, portal HTN, HIV inf., drugs/toxins, hemoglobinopathies)
4) pulmonary veno-occlusive disease
5) persistent pulmonary HTN of the newborn |
|
|
Term
| Is there usually underlying disease associated w/ idiopathic pulmonary HTN? |
|
Definition
|
|
Term
| Who is more likely to be affected by idiopathic pulmonary HTN? |
|
Definition
|
|
Term
Prognosis
untreated idiopathic pulmonary HTN |
|
Definition
|
|
Term
| What is the pathogenesis of idiopathic pulmonary HTN? |
|
Definition
| imbalance of mediators => increased thromboxin A2, 5-HT, and endothelin => decreased IL-12, NO, & VIP (vasoactive intestinal peptide) => vasoconstriction => intimal proliferation => thrombosis |
|
|
Term
Sx
idiopathic pulmonary HTN |
|
Definition
early: asymptomatic
progressing: exertional dyspnea, chest discomfort => exercise intolerance, syncopy |
|
|
Term
PE findings
idiopathic pulmonary HTN |
|
Definition
1) JVD
2) loud P2
3) systolic murmur
4) pulmonary regurgitation murmur
5) mumur of tricuspid regurgitation
6) hepatospenlomegaly (pulsatile)
7) ascites
8) peripheral edema |
|
|
Term
| What 4 basic tests will be done on a patient w/ pulmonary HTN? |
|
Definition
1) ECG
2) CXR
3) PFTs
4) echocardiogram
5) R heart catheterication |
|
|
Term
| What will be seen on an ECG of a patient w/ pulmonary HTN? |
|
Definition
|
|
Term
| What will be seen on the CXR of a person w/ pulmonary HT? |
|
Definition
| may show enlargement of the pulmonary artereies &/or cardiomegaly |
|
|
Term
| What is the purpose of PFTs on a person w/ pulmonary HTN? |
|
Definition
R/O obstructive or restrictive lung diseases
(not diagnostic) |
|
|
Term
| What PFT findings can be seen in a patient w/ pulmonary HTN? |
|
Definition
| 1) mild decrease in TLC & FVC
2) marked decreaed in DLCO |
|
|
Term
| What will the findings on an echocardiogram reflect in a patient w/ pulmonary HTN? |
|
Definition
1) LV: normal ejection fraction, no hypertrophy of wall
2) LA: normal
3) RA: enlargement
4) RV: enlargement
5) intraventricular septum: flattened
6) tricuspid regurgitation |
|
|
Term
| What can be estimated from the measurements of the ardiac images on an echocardiogram? |
|
Definition
|
|
Term
| What is the only test for firm Dx of pulmonary HTN? |
|
Definition
|
|
Term
def
pulmonary HTN (PH)
via R heart catheterization |
|
Definition
1) mean pressure ≥ 25 mmHg
2) mean PA pressure ≥ 30 mmHg w/ exercise
3) systolic PA pressure ≥ 40 mmHg |
|
|
Term
def
pulmonary arterial HTN (PAH)
via R heart catheterization |
|
Definition
1) mean PA ≥ 25 mmHg or ≥ 30 w/ exercise
2) PCWP ≤ 15 mmHg
3) PVR ≥ 3 mmHg(min/L) or 240 dyn(sec)(cm-5) |
|
|
Term
| What additional testing needs to be done on those individuals documents to have PAG? |
|
Definition
1) r/o autoimmune (blood work)
2) CT scan for ILD if suggested by PFTs
3) r/o HIV
4) r/o chronic thromboembolic disease (V/Q scan, CT angiography)
5) r/o portal HTN (LFTs, hepatitis profile, imaging)
6) r/o sleep disordered breathing (polysomnography)
7) r/o L to R shunt ("bubble study" - invasive) |
|
|
Term
| What is the diagnostic algorhythm for pulmonary HTN? |
|
Definition
1) PAH suspected based on PE & Hx
2) CXR, ECG, PFTs
3) surface echocardiogram
4) R heart catheterization |
|
|
Term
| What are the 2 "tests" to assess severity & prognosis of pulmonary HTN? |
|
Definition
1) WHO functional classification of dyspnea
2) six minute walk test |
|
|
Term
| What are the 4 functional classifications of dyspnea according to WHO? |
|
Definition
I: ordinary activity doesn't cause Sx
II: slight limitation of physical activity. Ordinary activity causes Sx.
III: marked limitation of physical activity. Less than ordinary activity causes Sx
IV: inability to carry out any physical activity w/o Sx. Dyspnea or fatigue may be present at rest.
(survival & severity is worse w/ increasing score) |
|
|
Term
|
Definition
| patient walks a measured course for 6 minutes while oxygen saturation & HR are monitored (survival is worse in those whose walking distances are short) |
|
|
Term
|
Definition
1) supplemental oxygen
2) diuretics
3) anticoagulation |
|
|
Term
| What are the newer medical therapies for PAH Tx? |
|
Definition
1) calcium channel blockers (vasodilators)
2) endothelin receptor antagonists (counter increased ET activity)
3) phosphodiesterase-5 inhibitors (counter increased 5-HT)
4) prostacyclin derivatives (counter increased thromboxane A2)
5) NO acutely (lacking in PAH) |
|
|
Term
| What ar etherapy decisions based on for PAH? |
|
Definition
| Sx & function class of the patient (tho degree of pressure elevation is important) |
|
|
Term
|
Definition
|
|
Term
|
Definition
1) convention measures
2) assess for response to calcium channel blockers; start oral med if positive
3) if not responsive to CCBs, try phosphodiesterase-5 inhibitor or endothelin receptor antagonist (both PO) |
|
|
Term
|
Definition
1) convention measures
2) ERA &/or PDEi + inhaled prostacyclin |
|
|
Term
|
Definition
1) convention measures
2) start IV or subq prostacyclin derivative
3) EAR or PDEi |
|
|
Term
| What are the benefits to medical therapy for PAH? |
|
Definition
1) based on known pathophysiologic mechs.
2) improve Sx & QOL
3) improve survival
4) combination therapy may further improve patients |
|
|
Term
| Since early Dx of PAH saves lives, how can physicians help to produce earlier Dx? |
|
Definition
1) screening echo for high risk patients
2) evaluate unexplained dyspnea carefully
3) echo performed by experienced cardiologist
4) early referral to PH center |
|
|
Term
| Who is at high risk for PAH? |
|
Definition
1) family Hx PAH
2) CT disease
3) liver disease, cirrhosis, portal HTN
4) HIV
5) sickle cell |
|
|
