Term
| What results from failure of the heart to pump enough blood to meet the body's needs? |
|
Definition
|
|
Term
| What are the two types of CHF? Explain them. |
|
Definition
Diastolic: Abnormal relaxation of the heart leads to a decrease in CO (from hypertrophied heart muscle)
Systolic: Heart muscle dilated and muscle becomes weak and thin. Internalization of B1 antibodies disrupt a arrestin system of B recpetors.
Disruption of urocortin system: a paptide w/ positive inotrope effects. |
|
|
Term
| What type of CHF is more difficult to treat?? What type of CHF after an MI? |
|
Definition
| Diastolic is more difficult to treat. Systolic after MI |
|
|
Term
|
Definition
-Decreased ventricular performance
-Inadequate organ perfusion or O2 delivery
-Decrease in CO
-Venous congestion: liver, lungs, limbs
-Decrease in cardiac reserve |
|
|
Term
| What causes venous congestion in CHF patients? |
|
Definition
| Fluid backs up because it does not have a "large push" behind it, and cannot move through the body the way it should |
|
|
Term
| Goals of THX in CHF patinet? |
|
Definition
Control fluid/na absorption
Optimize myocardial contractile function (1*)
Minimize cardiac workload
Decrease pulmonary/vascular congestion |
|
|
Term
| CHF happens from a result of____?? |
|
Definition
| a compenssatory mech to increase CO and tissue perfusion |
|
|
Term
| What are the compensatory changes of the heart in CHF?? |
|
Definition
Frank-Starling Curve
Increase in SNS activity
Volume loading is increased: Increased plasma volume |
|
|
Term
Which Statement is true of the heart in CHF??
A.The heart is engorged bc it is insufficient
B.The heart is insufficient bc it is engorged |
|
Definition
| A. The heart becomes enlarged when it is not working correctly. |
|
|
Term
What happens if you increase LVEDP too dreastically? What about when you decrease ventricular performance??
(hint, remember graph**) |
|
Definition
Increase congestion with increased LVEDP
Low Ventricular Performance: Inadequate perfusion |
|
|
Term
| What are the pathophysiological changes that occur in CHF (ie. SV, reflexes) |
|
Definition
SV is decreased
Baroreceptor increase
SNS becomes activated
Vasoconstriction occurs
Tachycardia |
|
|
Term
| How are the pathophysiological changes of a CHF patient accounted for by a cardiac glycoside?? |
|
Definition
Increase Stroke Volume (+ inotrope)
Deactivate baroreceptor
SNS depressed
Vasodilation, Bradycardia
RAS is shut down
Sodium/H2O excreted. |
|
|
Term
|
Definition
| Generic term to desribe group of drugs called cardiac glycosides. |
|
|
Term
Cardiac glycosides:
2 major drugs. Preferred
How do they differ from one another
What are their indications? |
|
Definition
Digoxin**/Digitoxin
Differ in pharmacokinetics/toxiciites
CHF for + inotrope
Supra-Ventricular arrythmias; anti-arrytmic effects |
|
|
Term
| Where do arrytmias usually arise in supra-ventricular arrytmias?/ |
|
Definition
| Upstream from the ventricle in the atrium AV node |
|
|
Term
| Stages of CHF for cardiac glycosides? |
|
Definition
|
|
Term
How do cardiac glycosides work in CHF?
(primary/secondary actions)
Starling curve?? |
|
Definition
1*increase myocardial contractility by + inotrope effect. Effect directly on the myocardium muscle. Upward shift of the starling curve
2*Reverse compensatory mechanisms |
|
|
Term
| Mechanism of action of Cardiac glycosides |
|
Definition
-Bind/Inhibit NaKatpAse (maintain na,k in cell)
-More intracellular Ca for contraction bc of inter-relationship between NaKaptase andn Na/Ca exchanger |
|
|
Term
PDE inhibitors in CHF
What stage
Drug names |
|
Definition
Stage D
Imanrinone/Milrinone |
|
|
Term
MOA of PDE inhibitors in CHF?
-Heart/Periphery??
-Pre/afterload?? |
|
Definition
Increase cAMP by inhibiting PDE in heart muscles(metabolizes cAMP)
Increases Contraction
In periphery: vasodilation/afterload reduction. |
|
|
Term
|
Definition
|
|
Term
Dopamine in CHF
-MOA (pre/afterload??)
-Stage |
|
Definition
+ inotrope
B1 receptors
Stage D
Afterload reduction @ pre-junctional D2 receptors; activation of these receptors decrease NE release (decreases vasocontriction, reduces BP) |
|
|
Term
Dobutamine in CHF
-MOA
-Stage |
|
Definition
Racemic mixture. Stage D
-Alpha 1 agonist AND antagonist. Actions cancel
-B1 agonist + inotrope
Powerful. His friend example. |
|
|
Term
Beta Blockers in CHF?
Stage?
MOA? |
|
Definition
Stage B & C. CI in severe
-Initially decrease contractile force, but increase after several months
-Block E/NE @ B1
-May involve inverse agonist effects of cetrain beta blockers
-Decrease mortality |
|
|
Term
Carvedilol in CHF?
MOA
Pre/Afterload?? |
|
Definition
B1+B2 antagonist
Alpha 1 antagonist
Vasodilator/Prevents against sudden cardiac death
Block NEon arterial vessels (alpha)
Block NE on heart (BB)
Preload AND afterload reduction
Inhibits free radical generation*** |
|
|
Term
Systemic Vasodilators in CHF?
Stage?
MOA |
|
Definition
Cornerstone of THX in CHF
Stages B/C
Preload reduction-venodilation eases congestion
Afterload Reduction-arterial dilation
Increase SV and decrease cardiac workload |
|
|
Term
Organic Nitrates in CHF?
Pre/Afterload |
|
Definition
Hydralizine
Afterload Reduction
Decrease TPR |
|
|
Term
ACE inhibitors in CHF:
Mechanism |
|
Definition
Interfere w/ volume loading (RAS)
Afterload reduction (vasodilate/block AT) |
|
|
Term
|
Definition
Blocks vasoconstrictie effects of AT-2 subtype receptor 1
Afterload reduction/Preload reduction |
|
|
Term
Calcium Channel Blockers in CHF:
-MOA
-Drugs |
|
Definition
Block movement of calcium, no movment of calcium into arterial side
Decrease afterload
Dihydropyridines and Diltiazem (NOT verapamil) |
|
|
Term
|
Definition
Alpha 1 receptor blocker
Decrease afterload
Interfere w/ Ne/E on blood vessels (decrease constriction) |
|
|
Term
Diuretics in CHF
Stage, Drugs, MOA |
|
Definition
Preload reduction
Thiazides/HCTZ.MILD CHF
Loop Diuretics. MORE SEVERE
Aldosterone antagonists (K sparing)
Get rid of the fluid-decrease preload |
|
|
Term
|
Definition
This is a natural occurring naturetic hormone, goes to endogenous peptide in the ventricles.
Activates guanylate cyclase
Naturesis/Diuresis; preload reduction
Vasodilation: Decreases afterload
Stage D CHF
Efficacy Debatable |
|
|
Term
|
Definition
Glycosides
Dobutabmine
Dopamine
Nesiritide |
|
|
Term
|
Definition
| 1. Diuretic 2. ACE inhbitor 3. BB 4. Vasodilator 5. Glycosides 6. Nesiritide 7. Inotropes |
|
|
Term
|
Definition
A: High Risk w/ No symptoms
B: Structureal heart disease, no symptoms
C: Structoral disease, previous or current problems
D: Refractory symptoms causing special intervention |
|
|
Term
| Use of glycosides for SVA: relationship to atrial rhythm? |
|
Definition
| Useful w/ or w/o atrial rhythm. |
|
|
Term
| Conduction path of AP in the heart: |
|
Definition
| SA node->Atria->AV node->HIS bundle->bundle branches->Purkinje->Ventricular myocardium |
|
|
Term
| What is the pacemaker of the hart? |
|
Definition
|
|
Term
| Describe A-flutter; A-Fib |
|
Definition
Flutter:AP in atrium has random firing; some make it to ventricle, some don't. Fills w/ blood more than usual. Leads to erratic pulse
A-fib: Flutter gone nuts. Atral so many random paths that ventricle can't keep up (NOT LIFE THREATENING) |
|
|
Term
| Describe: Ventricular Arrythmias and V-Fib |
|
Definition
Ventricular tachycardia, there is an additional pacemaker in the ventricle
V-Fib: No coordinated contraction of ventricle, pt will die |
|
|
Term
Autonomic Innervation of the heart:
Sympathetic/Parasympathetic |
|
Definition
Sympathetic-everywhere
Parasympathetic- AV/SA nodes (NOT in V) |
|
|
Term
Automaticity
Conduction Velocity
ERP
APD |
|
Definition
Automaticity: To what degree AP fire @ SA node. Automatic
CV: Speed which AP travels
ERP: Period which 2nd Ap cannot occur
APD: Time between AP onset/finish |
|
|
Term
| Effects of Epinephrhin/NE @ SA/AV nodes?? |
|
Definition
|
|
Term
| Glycosides Direct/Indirect Effect on cardiac tissues. --Facts-- |
|
Definition
Indirect-ANS. Usually small doses (increase vagal tone and decrease symp tone)
Direct- Higher dose |
|
|
Term
| SA NODE: DIRECT/INDIRECT EFFECTS |
|
Definition
Indirect: Decrease Automaticity
Direct: Increase Automaticity |
|
|
Term
|
Definition
| Both: Decrease CV; Increase ERP |
|
|
Term
|
Definition
Indirect: Decrease ERP, Decrease APD
Direct: Increase ERP, Inrease APD |
|
|
Term
| Ventricles and Perkinje: INDIRECT, DIRECT |
|
Definition
Indirect: Minor
Direct: Decrease ERP, Decrease APD, Increase actopic |
|
|
Term
| More important THX effect: Direct or Indirect? |
|
Definition
| Indirect. Usually more therapeutically important, however often direct. This is confusing???! |
|
|
Term
| What do ACH, NE do the automaticity of the heart? |
|
Definition
ACH- Decrease HR
NE- Increase HR |
|
|
Term
| What do SVA arise from? How do glycosides work? Describe what happens |
|
Definition
Primarly from AV node effects; slow the CV through the AV dose and decrease the # of AP that go through AV node (acts as a gate)
Slows ventricular rate
Effects on AV node occur irrespective of whatever happens in the atria. |
|
|
Term
| Toxiciites of Glycosides: |
|
Definition
Low TI
Cardiac effects
Direction action on ventricle can lead to ectopic beats/delayed after depolarizations, AV block, A-V tachycardia/fibrillation
Myocardial K loss: over0inhibition of Na/K
GI: N/V/Anorexia
Neurological-neuromuscular
Headache/fatigue/Clurred vision, abnormal color perception |
|
|
Term
Pharmacokinetics of Glycosides
Appreciable differences in: |
|
Definition
Protein bindng
Oral effectiveness
Metabolism
Onset/Offset of action between glycosides
H2O solubility |
|
|
Term
| Relationship of the slope of phase 4 and HR? |
|
Definition
|
|
Term
| Factors that increase the rate of phase 4 depolarization? |
|
Definition
Ischemia
Catechols
Digitalis
Atropine |
|
|
Term
| Factors that decrease rate of phase 4 depolarization? |
|
Definition
Quinidine
Procainamide
Lidocaine
Phenytoin
Propranolol
Ach |
|
|
Term
What two factors cause a decrease in MDP?
What is MDP |
|
Definition
Acidosis
Digitalis
Maximum diastolic pressure |
|
|
Term
| What two places in the heart show automaticity? |
|
Definition
|
|
Term
| Goals of anti-arrythmic drugs in automaticity? |
|
Definition
| Restore normal automaticity and elminate ectopic pacemakers |
|
|
Term
| Fedan's favorite sentence? |
|
Definition
| All anti-arrythmics with exception of glycosides and bertyllium have selective suppression of ectopic pacemakers |
|
|
Term
| What often happens to CV in diseased cells? What does this result in? |
|
Definition
It is often changed, usually slowed.
Often results in arrythmias |
|
|
Term
| What is CV proportional to? |
|
Definition
AP amplitude (mV)
Delta V/Delta T of AP upstroke/membrane responsiveness |
|
|
Term
| Relationship between max diastolic potential and CV?? |
|
Definition
| One increases, the other increases (same w/ decreases) |
|
|
Term
| What do phenytoin and quinidine do to CV/MP? |
|
Definition
Phenytoin: Increases speeed
Quinidine: decreases speed
This is why each one of these increases HR/Decreases HR |
|
|
Term
| How can anti-arrythmics achieve normality of CV within cells? |
|
Definition
Increase CV of diseased
Decrease CV of normal |
|
|
Term
| How can anti-arrythmics alter ERP?? |
|
Definition
Lengthen the ERP in diseased cells
Shorten the ERP in normal cells |
|
|
Term
| What happens to the ERP in arrythmic patients? |
|
Definition
| Can result in adjacent fibers having different ERP, wave front/depolarization varies amongst differet cells. |
|
|
Term
|
Definition
Establish uniformity of ERP in adjacent areas of coalescence of ERP
Most often increase ERP in normal cells, and shorten ERP of diseased |
|
|
Term
| Goals of anti-arrythmic thx in the re-entry model: |
|
Definition
Decrease CV in blocked region (convert uniD block to biD block)
Increase CV i blocked region (abolish uniD block)
Increase ERP @ "A"--a penetrating re-entrant will not excite cells. |
|
|
Term
| Types of supraventricular arrythmias: |
|
Definition
|
|
Term
Class 1A Sodium Channel Blockers: (AA)
-Action
-Drugs |
|
Definition
Decrease membrane responsiveness
Increase ERP, APD
Quinidine, Procainamide, Disopyramidine |
|
|
Term
Sodium Channel Blockers 1B: (AA)
-Action
-Drugs |
|
Definition
Little Effect on membrane responsiveness
Decrease ERP, Decrease APD
Lidocaine, Phenytoin, Mexilitine, Moricizine |
|
|
Term
Sodium Channel Blockers type 1C: (AA)
-Action
-Drugs |
|
Definition
Decrease membrane responsiveness
-Flecainide, Morcizine |
|
|
Term
Class 2 Vaughn Williams
-Drug
-Action |
|
Definition
Beta Blocker
Propranolol
Think about what happens when you block B in heart @ SA/AV node (decrease automaticity) |
|
|
Term
Class 3 Vaughn Williams
-Drug
-Action |
|
Definition
Potassium Channel Blockade
Prolong repolarization
-Increase APD
-Increase ERP
Betrylium, amniodorone, dronedrenet, sotalol, defetilide |
|
|
Term
Class 4 Vaughn Williams
-Drug
-Action |
|
Definition
Calcium Blokcers
Verapamil
Diltazem
Bepridil
NOT diphenhydropyridines |
|
|
Term
| What do supraventricular arrythmias interfere with? |
|
Definition
| Conduction and contraction |
|
|
Term
| What system can help mediate actions of some AA drugs? |
|
Definition
|
|
Term
| What is the focus of atrial arrythmias?? Where does this effect occur? |
|
Definition
Protecting the ventricle from the irregular rhythem.
AV node is where this effect occurs |
|
|
Term
AA Drugs:
Drugs that decrease membrane responsiveness.
What is the class, which drugs, ERP/APD |
|
Definition
Sodium Channel Blockers 1A
Increase ERP/APD
Quinidine, Procainamide, Disopyramide |
|
|
Term
| Dissociation kinetics of 1A sodium channel blockers |
|
Definition
| Medium dissociation kinetics |
|
|
Term
| Indications for 1A sodium channel blockers? |
|
Definition
Broad Spectrum
-supraventricular/ventricular arrythmias
Short and long term treatment |
|
|
Term
| Indirect actions of 1A Sodium channel blockers? |
|
Definition
Anti-muscarinics (atropine-like)
Inhibits ach action
Results transiently in some patients in increased CV and decreased ERP @ AV (undesirable)
In A-fib patinets, can be a paradoxical increase in ventricular rate as atrial rate as atrial rate decreases and AV CV increase |
|
|
Term
| Direct actions of 1A Sodium Channel Blockers |
|
Definition
DESIRED EFFECT
-Effects Atria, Purkinje, AV Node
-Decrease CV (decrease membrane responsiveness)
-Increase ERP, Increase APD
-Converts a unidirectional block to a bi-directional block |
|
|
Term
| Side Effects of Quinidine (class??) |
|
Definition
Sodium Channel 1A block:
It is an isomer of quinine (malaria)
SE= cinchonism (tinnitus, headache, visual disturbances, impaired hearing, vertigo)
Hypersensitivity rxn |
|
|
Term
| SE of Sodium 1A blockers (AA) |
|
Definition
HOTN
Decreased myocardial contracility
AV block from direct effects
Ejection of arterial emboli (propylactic anti-coag given before conversion to sinus rhythm) |
|
|
Term
| Which sodium 1A channel blocker has a decreased chance of causing HOTN? |
|
Definition
|
|
Term
| What can 2 drugs that both lower CV cause? |
|
Definition
|
|
Term
| What happens in AV block? Is this a god thing? |
|
Definition
| Conduction through the AV node is completely stopped, in arrythmias you want to slow conduction through this to decrease incidence of ventricular tachycardia, however, you do not want to block completely |
|
|
Term
AA drugs w/ little effect on membrane responsiveness:
-Class
-Drugs
-ERP/APD |
|
Definition
Sodium Channel Blocker 1B
Phenytoin, Lidocaine, Mexilitine, Moricizine
-ERP/APD both decreased |
|
|
Term
Dissociation kinetics for 1B drugs?
What drugs are these? |
|
Definition
Fast Dissociation Kinetics
Phenytoin, Lidocaine, Mexilitine, Moricizine |
|
|
Term
| Indications for 1B sodium channel blockers? |
|
Definition
|
|
Term
| Use of lidocaine and phenytoin for ventricular arrythmias? |
|
Definition
Emergency treatment
Digitalis induced arrythmias (bc of their effects on ERP/APD--both; and AV/CV--phenytoin) |
|
|
Term
| Effects of Digitalis on ERP/APD; AV/CV |
|
Definition
ERP and APD are increased
AV and CV are decreased ???? I THINKS |
|
|
Term
| Indications for Mexilitene |
|
Definition
| Symptomatic ventricular arrythmias |
|
|
Term
| Indications for Moricizine |
|
Definition
| Similar structure to lidocaine; life treatening ventricular arrythmias |
|
|
Term
| Indirect actions of Sodium channel 1B blockers? |
|
Definition
|
|
Term
| Direct actions of Sodium Channel 1B blockers? |
|
Definition
Decrease ERP/APD @ Ventricle/Perkinje
Lidocaine: CV |
|
|
Term
|
Definition
Opposite of Quinidine.
So quinidine=High ERP/APD/ LOW CV
Phenytoin=Low ERP/APD/ HIGH CV |
|
|
Term
| What does phenytoin do to uni-directional block? |
|
Definition
|
|
Term
| What is an off label use for phenytoin? |
|
Definition
|
|
Term
| Similarities/Differences between phenytoin and glycosides (ERP,APD, CV, etc) |
|
Definition
|
|
Term
AA drugs that decrease membrane responsiveness?
-Class
-Drugs
-Dissociation??
-Effect on ERP/APD???? |
|
Definition
Sodium Channel Blocker 1C
-Flecaininde, Moricizine
-Slow dissociation
-Decreased ERP/APD |
|
|
Term
| Indications for Class 1C sodium channel blockers? |
|
Definition
| Life threatening, malignant atrial and ventricular arrhythmias |
|
|
Term
| Indirect actions of Class 1C sodium channel blockers? |
|
Definition
|
|
Term
| Direct action of 1C sodium channel blockers |
|
Definition
Slow conduction volume @ AV/Ventricle/Purkinje
Little efficacy elsewhere |
|
|
Term
| SE of Flecainide? What type of drug is this? |
|
Definition
Pro arrythmic ffects which can be fatal
- Inotropic effect may worsen CHF |
|
|
Term
| Class 2 anti-arrytmics: Drugs |
|
Definition
|
|
Term
| Indications for BB as anti-arrythmic drugs? |
|
Definition
Supraventricular arrythmias
Arrythmias caused by adrenergic mechanism
Digitalis-induced arrythmias |
|
|
Term
| Indirect action of Class 2 anti-arrhythmic (beta blockers) |
|
Definition
BB @ AV mimics vagal activation (PNS)
ERP is increased @ AV; decreased @ atria
CV is decreased @ AV node--basis (decreased automaticity throughout) |
|
|
Term
| Direct effect of class 2 anti-arrhythmic (Beta Blockers) |
|
Definition
High doses, propranolol ONLY leads to an interferece w/ propogation
Quinidine-like effectss(class 1A) |
|
|
Term
| SE/Caustions w/ Beta blockers in AA thx? |
|
Definition
|
|
Term
Class 3 AA Drugs:
-Drug Name
-Effect |
|
Definition
Prolong repolarization
Bretylium, Amniodarone, Dronendarone (amni. analog), sotalol, ibutilide, and dofetilitide |
|
|
Term
| Indications of Potassium channel blockers in AA therapy? |
|
Definition
Life threatening ventriicular arrythmias(amniodarone, dronaarone, sotalol)
Atrial Flutter (ibutilide, Dofentilide) |
|
|
Term
| What is special about sotalol in AA therapy? |
|
Definition
Sotalol: L isomer is non-selective BB w/ Class 2 effects.
D isomer is anti-arrythmic |
|
|
Term
| Direct actions of Potassium channel blocker in AA? |
|
Definition
Increase ERP
Increase APD
Decrease AV/CV
raises the electrical threshold needed to cause fibrillation |
|
|
Term
| SE/Cautions of Potassium Channel Blockers in AA |
|
Definition
Amniiodarone: pulmonary fibrosis
Dronedarone introduced to avoid this
Ibutilide: AV Block |
|
|
Term
| Which potassium channel blockers are used for a fib, and which for v fib? |
|
Definition
"ILIDE"-A fib (ibutilide, dofetilide)
Amniodarone, Dronedarone, Sotalol |
|
|
Term
| What happens when bertyllium is first administered to a patient? |
|
Definition
NE is released
Pro-arrtymic
Increases HR
This is why it is included in his fave sentence |
|
|
Term
Class 4 drugs for AA:
-Drugs
-Action |
|
Definition
Slow calcium channels
Verapamil, Diltiazem, bepridil |
|
|
Term
| Indications for slow calcium channels in AA therapy: |
|
Definition
| Supraventricular arrythmias |
|
|
Term
| Indirect actions of calcium channel blockers in AA? |
|
Definition
Little.
Verapamil has weak alpha blocker activity |
|
|
Term
| Direct actions of calcium channel blockers in AA therpay: |
|
Definition
SA/AV nodes (Slow response fibers)
Decrease CV, Increase ERP |
|
|
Term
| What calcium channel blocker is NOT used in AA therapy? Why? |
|
Definition
Dihydrapyridines--fast response @ phase 4 allow them to become ectopic pacemakers
Spontaneous movement of Ca into cell
Additional anti-arrythmic activity |
|
|
Term
| If patient has CHF, what Calcium channel blocker may worsen their condition? |
|
Definition
| Verapamil (decreases contraction) |
|
|
Term
| What is adenosine? How does it act? |
|
Definition
| An endogenous substance formed from ATP metabolsim. Receptors for adenosine (A1 type) |
|
|
Term
| Indications for adenosine in AA therapy? |
|
Definition
| Acute treatmetn of supraventricular arrythmias |
|
|
Term
| Direct actions of adenosine in AA therapy? |
|
Definition
Activates K channesl in SA/AV node
Action in AV node similar to ACH--Decrease CV, Increase ERP |
|
|
Term
|
Definition
|
|
Term
| How does the heart satisfy increasing O2 needs? |
|
Definition
| Increase coronary blood flow. |
|
|
Term
| How does atherosclerosis effect O2 delivery and work capacity of the ventricle? |
|
Definition
| Decreases O2 delivery, decreases work capacity |
|
|
Term
| What is the only way to increase O2 perfusion? |
|
Definition
| Increase coronary blood flow! |
|
|
Term
|
Definition
Coronary Arteries
Coronary Arterioles
Many Branches
Muscles
Contract
Vessels are squeezed closed by contracting muscles |
|
|
Term
| What happens to the ventricle when AP's occur? |
|
Definition
| Muscles contract, Aortic vales open (pressure is higher), blood expelled |
|
|
Term
| If you decrease HR do you need more or less time for coronary blood flow?? |
|
Definition
More time.
Decreased HR, so you need more time to get the same oxygen out |
|
|
Term
| Passive factors that effect CBF: |
|
Definition
-Arterial-venous pressure gradient (aortic sinus to coronary sinus in the right atrium)
-Duration of diastole (peak flow period)
-LVEDP (change in vessel architecture as ventricle distends) |
|
|
Term
| What is autoregulation in relation to coronary blood flow? |
|
Definition
| The intrinsic ability of the coronary bed to maintain constant CBF in presence of change in perfusion pressure |
|
|
Term
| What does autoregulation "link" |
|
Definition
| Coronary Blood flow and myocardial metabolism |
|
|
Term
| What are mediators of autoregulation |
|
Definition
-PO2 (decrease results in dilation)
-Adenosine
-NO |
|
|
Term
| How does PO2 effect autoregulation? |
|
Definition
| Decreased PO2 will result in a arteriolar vasodilation |
|
|
Term
| How does adenosine relate to autoregulation in the heart? |
|
Definition
| It is a coronary casodilator released from myocardial cells in high amounts as myocardial O2 consumption and work increase |
|
|
Term
| What does NO do in auto-regulation? |
|
Definition
| Released from endothelium VERY potent CV SM relaxant. Free radical gas |
|
|
Term
| What effect can autoregulation have on drug effects? |
|
Definition
| Can predominate and override drug effects |
|
|
Term
| Adenosine and ATP relationship in the heart contraction? |
|
Definition
| The more the heart contracts, the more ATP that is broken down, and this forms adenosine. A vasodilator.. |
|
|
Term
| What are the determinants of myocardial O2 consumption (MVO2)? |
|
Definition
-Wall tenstion (Increase LVEDP, Increase Tension, Increase O2 need)
-Myocardial contractility (Incrase O2)
-Increased heart rate (increase 02)
-Myocardial contractility and HR are also increased by SNS (physical exercion/exercise) |
|
|
Term
|
Definition
| Chest pain that indicates O2 demand is >>O2 provided |
|
|
Term
|
Definition
Stable Angina
Variant/Prinzmetals Angina |
|
|
Term
What happens in stable angina?
-Types of attack
-Supply/Demand |
|
Definition
Attacks provoked by physical or emothional strain
Increase in sympathetic outflow
The demand is >> supply
Atherosclerotic coronary artery + Increased O2 demand |
|
|
Term
| Variant/Prinzmetals Angina. what happens |
|
Definition
Occurs @ rest/ REM sleep
Due to coronary artery vasospasm
NOT due to an increase in O2 demand, supply is simply cut off |
|
|
Term
| Unstable angina: what is it? |
|
Definition
Exertaional and variable components
Have both stable and prinzmetals |
|
|
Term
| Therapeutic goals for angina patinets? |
|
Definition
Decrease myocardial O2 demands (esp in stable)
Increase myocardial O2 supply (esp variant)
-Prevent ischemia/Chest pain
-Increase exercise tolerance |
|
|
Term
| Organic Nitrates in Angina. Indications |
|
Definition
-Stable Angina: prophylaxis/treat acute ischemic attacks PO
-Acute MI and Coronary vasospasm in variant angina (variant) |
|
|
Term
Organic Nitrate Drugs for Angina:
-Dosage form/Facts |
|
Definition
NTG: prototype. Tab/Cap/Patch/IV
Amyl Nitrite: Inhalation
Isosorbide Mono/Dinitrate: Oral |
|
|
Term
| Why can isosorbide be taken daily for prophylaxis and NTG is only for short action emergencies? |
|
Definition
| Isosorbide is NOT metabolized first bass |
|
|
Term
|
Definition
Relax vascular SM, no DIRECT effect on the tissue
Formation of NO by myochondrial aldehyde dehydrogenase
Stimulation of gunaylate cyclase by S nitrosthiols and NO
Make cGMP, which decreases intracellular calcium |
|
|
Term
| What are the preferred therapeutic options for stable angina? (1*,2*,3*) |
|
Definition
1* Reduce preload reduction by dilation of venous captince vesssels (large veins)
Central pooling of blood, decreases LVEDP
Therefore, myocardial demand is decreased
2*Coronary artery dilation, increase O2 supply
3* Afterload reduction, dilate vessels on the arterial side (decrease TPR, decreases work done by heart) Decreases O2 demand |
|
|
Term
| What are some limitations associated with organic nitrites? |
|
Definition
Arterial dilation and HOTN caused by higher than needed doses evokes unwanted effeects:
-Decrease in BP, decreases o2 supply (passive factor)
-Decrease BP, Increase HR (O2 demand) |
|
|
Term
| Why do you give organic nitrates after MI? |
|
Definition
| Prevention of coronary vasospasm by relaxing smooth muscle. Prevention of coronary vasospasm |
|
|
Term
| Side effects of organic nitrates: |
|
Definition
| Headache, postural HOTN, methemoglobinemia |
|
|
Term
|
Definition
Deplation of cysteine/SH groups
Down regulation of ADH activity |
|
|
Term
Pharmacokinetics of organic nitrates:
-Routes
-Onset
-Duration |
|
Definition
Routes: SL, PO, Topical (ointment/patch)
metab by liver in first pass, so don't last that long.. hepatic glutathione organic nitrate reductase. AND renal excretion
-Onset 5 mintutes
-Duration 30 minutes |
|
|
Term
| Drug interactions associated with organic nitrates? |
|
Definition
PDE-5 inhibitors. Impotence
Increase NTG effects |
|
|
Term
| Beta blockers for treatment in angina |
|
Definition
| Long range prophylaxis. NOT for acute atacks |
|
|
Term
| MOA of BB in angina therpay |
|
Definition
B1 blockade of cardiac tissue and coronary SM
Inverse agonist= nadalol/metoprolol (reduce constitutive activity) |
|
|
Term
| What is a secondary reason BB are important in anti-anginal therapy? |
|
Definition
The ischemic zone is dilated, so you block B receptors and unmask alpha ones
Re-distribution of blood flow
When HR is decreased, Perfusion is increased, contractility in muscle is decreased, O2 supply is incrased |
|
|
Term
| What are limitations of BB in anti-anginal therapy? |
|
Definition
Myocardial depression: a problem if heart failure is presnet
Rebound ischemia, after sudden withdrawal
Other BB SE |
|
|
Term
| What happens with chronic use of Beta Blockers? So what happens when you withdraw use? |
|
Definition
Upregulation of Beta receptors
Therefore, when you stop taking them, you have a high number of receptors.
Ne/E stimulate receptors, and can cause rebound ischemia |
|
|
Term
| Is combined use of a BB and Nitrate useful in anti-anginal therapy? Why? |
|
Definition
Yes.
Negative actions of each drug cancel
(BB increase LVEDP and Nitrates reduce it)
Positive effects remain and add (Decrease O2 demand-BB; Increase supply-NTG) |
|
|
Term
| Calcium channel blockers used as anti-anginals |
|
Definition
Verapamil/Bepridil
Diltiazem
Nifedipine/Nicardipine/Nisoldapine |
|
|
Term
| Indications for Calcium Channel Blockers |
|
Definition
Variant angina
Stable angina (alone or w/ NTG/BB) |
|
|
Term
| Slow/L type calcium channels in calcium channel blockers? Where do they effect? in the heart-- |
|
Definition
-SA/AV node
-Plateau of myocardial AP |
|
|
Term
| What happens to automaticity/CV/Myocardial contractility in calcium channel blockers? |
|
Definition
Decrease automaticity
Decrase CV @ AV
Decrease contractility |
|
|
Term
| What to L-Type/Slow calcium channels do in vascular smooth muscle? WHat happens when you block them? |
|
Definition
Extracellular Calcium enters cell via L-type. Ca required for contraction. Coronary vasospasm: membrane depolarizes, opens L type chennels, more calcium in/ Contraction
Block this entry, no constriction, relax vasospastic SM |
|
|
Term
| Therapeutic goals/uses of calcium channel blockers depend on what?? |
|
Definition
|
|
Term
| Focus of calcium channel blocker use in variant angina?? |
|
Definition
Primary muscle is the coronary SM.
-Inhibit the coronary vasospasm and relax SM
-Dilate collateral vessels |
|
|
Term
| Focus of calcium channel blocker use in stable angina? (drugz too) |
|
Definition
1*Focus on myocardial performance
-Decrease myocardial O2 demand
-Afterload is decreased by all agents
-Decrease myocardial contractility/HR=verapamil
2* Increase Oxygen Supply
-Coronary artery dilation
-Increase CBF--all agents |
|
|
Term
| Type of tissues effected by calcium channel blockers? |
|
Definition
| Arterial vascular SM is more sensitive than venous SM (coronary arterial is particularly sensitive) |
|
|
Term
| Tissue Sensitivities of Calcium Channel Blockers: Verapamil, Diltiazem, Nifedipine. |
|
Definition
Verapamil: AV>>Myocarium>>Vasc. SM
Diltiazem:Vasc SM>>Myocardium (small AV effect)
Nifedipine:Vasc SM>>Myocardium. No AV. Potent vasodilator |
|
|
Term
| Which calcium channel blocker is an anti-arrythmic? What does this mean it can't be used in? Why? |
|
Definition
Verapamil.
CI in CHF. Decreases heart function |
|
|
Term
| Which calcium channel blocker is good for prinzetals/variant angina? Why? |
|
Definition
Dihydropyridines/Nifedipine
Potent vasodilator |
|
|
Term
| What can verapamil often be combined with to offset congestion?? How does this work? |
|
Definition
Nitrates. They dilate venous side (pre-load which leads to congestion)
-This offsets the ability of verapamil to worsen CHF |
|
|
Term
| What can verapamil be combined with to also decrease contractility? Is this safe? |
|
Definition
|
|
Term
| Which calcium channel blockers can be combined with beta blockers? |
|
Definition
|
|
Term
|
Definition
| Chronic angina patinets whom other anti-angina drugs havan't been effective |
|
|
Term
|
Definition
1*Block late sodium channels (1*)
2* Partial fatty acid oxidation inhibitor (more efficient O2 use, decreases metabolic rate of the heart, and decreases myocardial O2 demand. |
|
|
Term
| What drugs can ranolazine be combined with? |
|
Definition
Beta Blockers
Calcium Channel Blockers
Organic Nitrates |
|
|
Term
| What within the body are considered the first line of defense against bleeding? |
|
Definition
|
|
Term
| If blood is exposed to the endothelial matrix of an injury, what is activated?? |
|
Definition
Contact activation (intrinsic path)
Tissue Factor (extrinsic path) |
|
|
Term
| How are platelets activated, what happens once they are activated? What molecule facilitates this? |
|
Definition
| They are exposed to the injury, once activated: aggregate and adhere. Change shape. Empty their contents (ADP, TXA2, +FB). Activation facilitated by thrombin |
|
|
Term
| Vitamin K dependent Clotting factors? |
|
Definition
|
|
Term
| What is the binding site for fibrinogen on the platelet plug?? |
|
Definition
|
|
Term
| What is Unfractionated Heparin? |
|
Definition
| Mixture of high molecular weight negatively charged acidic monosaccharides extracted from animal byproducts |
|
|
Term
| Mechanism of Action of UFH |
|
Definition
Indirect Thrombin Inhibitor
Binds to Anti-Thrombin 3 (via an 18 polysaccharide sequence needed for its binding for thrombin). Accelerates interactions of AT3 w/ the factors |
|
|
Term
|
Definition
| Inhibits proteases: thombin (2A) and 10A and other endopeptidease enzymes |
|
|
Term
| Is UFH used in inpatient or outpatient settings? |
|
Definition
|
|
Term
| Heparin inhibits clotting by in vivo or in vitro?? |
|
Definition
|
|
Term
| What effect does heparin have on lab tests such as APTT. Is this for extrinsic or intrinsic path? |
|
Definition
Prolongs APTT.
APTT is for intrinsic path |
|
|
Term
| What effect does heparin have on already formed clots? |
|
Definition
|
|
Term
How is UFH administered?
Binding?
Metabolism? |
|
Definition
Parenterally
Binds to plasma proteins
Initially rapid O order metabolism, followed by a slower 1st order renal clearance |
|
|
Term
| Indications for anti-coagulants?? |
|
Definition
-Pre/Post surgical management of DVT/ Pulmonary Thrombosis and arterial and heart valve emboli
-Venous Stasis: lenghty hospital immobilization
-Unstable angina/post MI: In conjunction w/ anti-platelet and or fibrinolytic drugs to prevent re-infarction.
-Disseminated IV coagulation |
|
|
Term
|
Definition
1*
-Hemorrhage (visible or occult in internal organs)
-Thrombocytopenia (increase bleeding time/HIT)
2* Hypersensitivity, fever, anaphylaxis |
|
|
Term
|
Definition
Heparin Induced Thrombocytopenia:
-Formation of IgG antibodies against platelet factor 4/heparin complex
-Irreversibly activates platelets/thrombin
-Widespread deposit of microthromi in skin can lead to skin necrosis and gangrene, and anaphylactic reactions. |
|
|
Term
| What is thrombocytopenia? |
|
Definition
| Decreased platelet count with an increased bleeding tendancy |
|
|
Term
| Treatment of a heparin toxicity? |
|
Definition
Decrease dose
Discontinue
Prontamine |
|
|
Term
|
Definition
"Antidote" for increased bleeding-heparin
-Chemical antagonist
-Basic + charge low MW proeteins that bind - to UFH to neutralize anti-coagulant effect |
|
|
Term
| How is protamine administered? |
|
Definition
|
|
Term
| Contraindications/cautions for ALL anti-coagulants |
|
Definition
GI ulserative leasions
Occult Bleeding
Severe HTN (recent eye, brain,sc surg)
Visceral carcinoma
Threatened abortion
CI w/ anti-platelet drugs
Psence of thrombocytopenia |
|
|
Term
| What is often a sign of increased bleeding in patients? |
|
Definition
|
|
Term
| What patients would use a low dose warfarin? What about a high dose? |
|
Definition
Low-risk patients
High risk patients (ie hip surg) |
|
|
Term
| What is low molecular weight heparin? |
|
Definition
| Produced by chemical depolymerization of UFH to give polysaccharide chains. MW is still 2,000-9,000 |
|
|
Term
|
Definition
Dalteparin
Tinzaparin
Enoxaparin
Fondaparinux |
|
|
Term
| What is special about fondaparinux? |
|
Definition
It's symthetic
Protamine is NOT effective |
|
|
Term
|
Definition
Indirect thorombin inhibitor
Dependent on interaction with AT3
Contain the pentasaccharide needed to bind to AT3, but NOT to the 18 sequence saccharide needed for binding thrombin. Xa selective |
|
|
Term
| What does LMWH have a higher activity for: anti-factor 10A or Anti-thrombin?? |
|
Definition
anti-10A selective
Bleeding is less
Thrombin is still inhibited though, because factor 10 is upstream of it |
|
|
Term
| What pentasaccharide sequence does fondaparinux have? |
|
Definition
|
|
Term
| Which is better, LMWH or UFH? |
|
Definition
|
|
Term
| UFH/ LMWH which is unit based and which is mg based? |
|
Definition
LMWH is mg based
UFH is unit based |
|
|
Term
Pharmacokinetics of LMWH:
-Bioavailability
-Compared to UFH?? |
|
Definition
-Greater bioavailability and longer lasting than UFH
-Dose-independent clearance pharmacokinetics
-Predictable relationship btwn dose/response: control w/o lab tests |
|
|
Term
|
Definition
HIT occurance is less
Protamine somewhat effective (all but fondaparinux) |
|
|
Term
|
Definition
Resembles vitamin K
S and R
all are derivatives of "4 hydroxy coumarin"
Indan 1,3 dienes: not in US (>>toxicity and no adv against warfarin) |
|
|
Term
| Does warfarin act in vitro or in vivo?? |
|
Definition
|
|
Term
|
Definition
Vitamin K antagonist that inhibits VKOR reaction, which recycles vitamin K.
Postribosomal gamma carboxylation of glutamic acid (glu-> gla=carboxyglutamine) also requires vitamin K; factors involving this are defective and unable to complex w/ calcium during coagulation
Inhibition of vitamin K recycling inhibits all of the vitamin K dependent clotting factors (2,7,9,10, C,S,Z) |
|
|
Term
INR
APTT
What are these, what do they monitor? |
|
Definition
INR-Protrhombin Time (normalized from lab->lab)
Good for extrinsic factor
APTT:Partial thromboplastin time, monitors intrinsic path |
|
|
Term
| What is the first factor that is stopped during warfarin's action? WHY? |
|
Definition
| 7. Because this factor has the fastest turnover rate |
|
|
Term
| Is warfarin used inpatient or outpatient? |
|
Definition
|
|
Term
| Is onset of warfarin immediate or delayed? |
|
Definition
| Delayed, even when given IV |
|
|
Term
Pharmacokinetics of warfarin?
-DF
-Absorption
-Bound to?
-Pregnancy
-Metabolism |
|
Definition
By mouth. Rapidly/complete absorption
Protein bound (95%)-may be displaced
CI in pregnancy, crosses the placents
Hepatic metabolsm P450 |
|
|
Term
Warfarin toxicity
Treatment? |
|
Definition
1*hemorrhage
2* idiosyncratic rxns in some
No antidote: But should dc warfarin, administer vitamin K1; hours required to synthesize fxnl factors
In emergencies you can give FFP that contains functional factors |
|
|
Term
|
Definition
Same as heparin, but in addition:
-CI in preggerz
-CI in HIT patinets bc it also inhibits protein C (2,7,9,10,C,S,Z)--which is a protease and endogenous regulatory anticoagulant that inactivates Va and VIIa |
|
|
Term
|
Definition
| A protease and endogenous regulatory anticoagulant that inactivates 5A and 7A |
|
|
Term
|
Definition
| Oral anti-coagulant that is not yet FDA approved |
|
|
Term
|
Definition
It is a small molecule that directly inhibits 10A
Prevention of venous thombosis
Alternative to warfarin
No monitoring required |
|
|
Term
MOA of the direct thrombin inhbitors?
When are they used?
Antidode? |
|
Definition
-AT2 is NOT involved; inhibit thrombin directly and inhibit protease activty
-Used when throbocytopenia is present
-NO antidotes for these drugs |
|
|
Term
| Do Direct thrombin inhibtiors cause HIT? Why? |
|
Definition
| No. They don't, because there are no-upstream clotting factors that are inhibited |
|
|
Term
-Lepirudin, Bivalirudin, and desirudin
Drug Class
Fact about them
How are they administered |
|
Definition
Anti-coagulant
Direct Thrombin Inhibitors
Leeches/Bat Saliva
IV |
|
|
Term
Argatroban
-Class
-Administration
-Fact |
|
Definition
Synthetic anti-thrombin based on arganine
IV |
|
|
Term
Dabigatran
-DF
-Class
-Facts |
|
Definition
New oral medication
Alternative to warfarin
Direct thrombin inhibitors
Patients can eat green veggies
Low monitoring needed
**Expensive** |
|
|
Term
| Indication for anti-platelet drugs? |
|
Definition
Prevent thrombi in arterial blood
1. Prosthetic heart valves
2. MI
3. Comination therapy w/ anti-coag and fibrinolytic
4. PCTA (percutaneous transluminal angioplasty--STENT)
5. Prevention/Treatment of thrombotic stroke |
|
|
Term
| Why must you use platelet inhibitors when patient: has prosthetic heart valves/MI |
|
Definition
-Platelets stick to prosthetic valves
-Prophylaxis/treatment of thrombosis early in tx is important |
|
|
Term
Aspirin: MOA
What does this do to platelets? |
|
Definition
Acetylates/Irreversibly inhibits COX
-Prevents TXAs which promotes platelet adhesion and formation (Inhibits + feedback to activate other platelets)
-Platelets cannot synthesize COX
-Platelet adhesion and aggregation is inhibited |
|
|
Term
Aspirin:
What effect does COX inhibition have on endothelial cells? |
|
Definition
Prevents PGI2/prostacyclin formation
Endothelial cells make COX de novo |
|
|
Term
| What happens to platelet selectivity when you increase the dose of aspirin? |
|
Definition
| You lose platelet selectivity |
|
|
Term
Dipyridamole
-MOA
-Often used with |
|
Definition
Anti-platelet
Inhibits platelet PDE (platelets don't release their cotent, no feedback, increase camp, inhibit aggregation, release)
-Not very effective alone, sometimes used w/ aspirin and warfarin |
|
|
Term
Platelet ADP receptor (P2Y12) inibitors:
Drug names |
|
Definition
Clopidogrel
Ticlopidine
Prasugrel |
|
|
Term
MOA of Platelet ADP receptor (P2Y12) inhibitors
-How are they given |
|
Definition
Irreversible inhibits platelet ADP receptors and ADP induced exposure of platelet memnrane to glycoprotein 2B/3A and fibrinogen binding to active platelets
Orally Active |
|
|
Term
Ticlodipine:
Indication
Bound?
SE
Onset
Fact |
|
Definition
Aspirin Alternative
Used for prevention/treatment of thromboembolic stroke; PCI
Binds to plasma proteins, metabolized by the liver
SE=GI disturbancees/potential life threatening neutropenia and blood dyscrasias
Onset: 4 days
Pro-drug: metabolites must be formed. |
|
|
Term
|
Definition
Anti-Platelet (P2Y12 inhibitor)
Safer than ticoldipine
Must be actived
ADR w/ PPI (CYP2c19) |
|
|
Term
Prasurgrel
-Compared to Clopidogrel and Ticlopidine |
|
Definition
Similar to ticodipine and clopidogrel but is more potent and faster acting
Also a prodrug
Metabolized by a different cyp, no adr! |
|
|
Term
Glycoprotein 2B/3A inhibitors:
Drug Names
How are they given |
|
Definition
Given IV
Abciximab
Epifibatide
Tirofiban |
|
|
Term
| Side effect of anti-platelets: |
|
Definition
|
|
Term
Abciximab:
Drug type
How does it work
What type of inhibition is this |
|
Definition
Monoclonal antibody (=mab)
Blocks binding of fibrinogen & Von willebrand factor to GP2b/3A complex which inhibits platelet activation
Non-competative inhibition |
|
|
Term
Epifibatide
-Drug Type
-MOA |
|
Definition
| Cyclic hepatapeptide that is a competative inhibitor of glycoprotein 2B/3A |
|
|
Term
|
Definition
| Small molecule that is a derivative of tyrosine that is a compatative inhibitor of glycoprotein 2B/3A |
|
|
Term
|
Definition
Used for thromboCYTHEMIA (an increased platelet count)
Produces a thrombocythemic effect by inhibiting development of megakaryocytes--the platelet precursor. |
|
|
Term
|
Definition
Intermittent claudication (leg cramps caused by poor muscle circulation)
Works by inhibiting platelet aggregation and vasodilation (also good for MI) |
|
|
Term
| What are drug eluding stants? |
|
Definition
| The stents are impregnated with drugs that are slowly released (anti-platelet) |
|
|
Term
|
Definition
Used in drug eluding stents
Immunosupressant that blocks activation of B/T cells (inhibits growth of tissue) |
|
|
Term
|
Definition
Used in drug-eluding stents
An antineoplastic agent that inhibits blood vessel cell division |
|
|
Term
|
Definition
Like a chinese finger trap
When you withdraw, they're short but big in diameter
Drugs are embedded in fabric |
|
|
Term
|
Definition
Antisthesis of coagulation system:
Restricts the clot propogation and it involved in thrombous dissolution |
|
|
Term
| What are the therapeutic goals of fibrinolysis? |
|
Definition
| Proteolysis/lysing of fored clots while avoiding degredation of circling coagulating factors (fibrinogenolysis) which gives rise to a lytic state and hemmorrhage |
|
|
Term
| What are plasinogen activators? |
|
Definition
TPA.
Proteases which initiate fibronolysis
Released by endothelium and inhibited by PA1-1 |
|
|
Term
|
Definition
| Fibrin. To form a complex between itself and Plasinogen. Than plasminogen is activated to plasmin |
|
|
Term
|
Definition
| Degrade the fibrin clot OR fibrinogenolysis of circulating factors |
|
|
Term
| What inhibits plasin activity in the plasma? |
|
Definition
|
|
Term
| How is plasmin activated? |
|
Definition
| By binding of Plasinogen to TPA |
|
|
Term
| MOA of fibrinolytic drugs |
|
Definition
|
|
Term
| What are the 1st generation fibrinolytic drugs? |
|
Definition
|
|
Term
|
Definition
NOT fibrin specific
Cause appreciable systemic fibrogenolysis and bleeding
Streptokinase is NOT an enzyme
Urokinase is an enzyme |
|
|
Term
| 2nd generation fibrinolytics: |
|
Definition
Aletplase
Bind to fibrin; confers specificity of action to the clot; this specificity is NOT absolute
Decreases systeic fibronogenolysis;; bleeding is decreased but not eliminated |
|
|
Term
| 3rd generation fibrinolytic |
|
Definition
Reteplase; enecteplase
Structureal modifications increase fibrin specificity/kinetics
Modeled on alteplase |
|
|
Term
| Indications for fibrinolytic drugs: |
|
Definition
-Pulmonary embolism, DVT, arterial thrombosis
-MI |
|
|
Term
| Why do you give fibrinolytic drugs after MI? |
|
Definition
-Establish re-canalization
-Early therapy is essential to minimize damage to myocardial cells
-Anti-coagulants and antiplatelet drugs usually co-administered to prevent re-thrombosis and infarction
-Ischemic stroke |
|
|
Term
Streptokinase
-Fact
-MOA
-Origin
-How is it given |
|
Definition
-1st generation fibrinoglytic agent
-NOT an enzyme
-Forms a 1:1 complex with plasminogen, exposing the active site that activates additional plasminogen in plasmin
-Obtained from B hemolytic streptococci, therefore, it is antigenic
-IV or IC injection |
|
|
Term
Urokinase
-MOA
-Origin
-Main use |
|
Definition
Two chain urokinase-type plasminogen activator "tCU-PA"
-an endogenous enzyme which activates plasminogen directly
-Recombinant DNA from human cultured DNA cells--NOT antigenic
Main use is pulmonary embolism |
|
|
Term
What is alteplase?
T1/2. How is this significant
Efficacy compared to kinases? |
|
Definition
A single chain peptide that is converted to two chain dimer upon exposure to fibrin.
-5-8 minutes, you may need to give it many times to prevent re-thrombosis
-More effective than kinases |
|
|
Term
Reteplase
-generation
-Origin
-MOA
-Onset/Potency/binding compared to alteplase |
|
Definition
3rd generation fibrinolytic
Derivative of alteplase
Contains domain necessary for binding to fibrin and the protease domanin of TPA
More rapid onset, more potent than alteplase
More specific binging and action than alteplase |
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Term
Tenecteplase
-generation
-Derivative
-Specificity/T1/2 compared to alteplase |
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Definition
Alteplase deriviative
AA substitution
More specific, longer lasting than alteplase |
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Term
| ADR of fibrinolytic drugs? |
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Definition
Bleeding
Break down clotting factors
Lytic state |
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Term
| CI/Cautions of fibrinolytic drugs? |
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Definition
Similar to other anti-coagulants
If patient has risk for bleeding. Caution |
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Term
Anti-Fibrinlytic drugs:
-What are they used for
-Names |
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Definition
-Antidotes for fibrinolytics
-Aminocaptroic acid/ Tranexamic acid |
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Term
| Anti-fibrinolytic drug actions |
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Definition
-Inhibit plasminogen activation/plasmin activation
-Lysine binding sites of plasminogen/plasmin binding sites are
blocked by anti-fibrinolytic drugs
-Activation is inhibited |
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Term
| Indication of anti-fibrinolytic drugs? |
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Definition
| Dental procedures in hemopheliacs |
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Term
| What type of medications ar viagra, cialis, levitra. How do they work? |
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Definition
PDE inhibitors
Interfere with metabolism of cGMP |
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Term
| How do PDE-5 inhibitors interact with organic nitrates? |
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Definition
| Both increase amount of cGMP in the system. Extensive HOTN |
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Term
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Definition
Bocks pre junctional alpha 2 blockers
Results in an increase of NE release incnetral nor adrenergic nuclei
May increase penile blood flow
May increase BP/HR (opposite of clonadine, alpha 2 agonist)
-Less effective than other PDE's
Occurs in brain. CNS reactions |
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