Term
| True or false: CD4 T cells' activation of CD8 T cells requires co-stimulation from the same antigen presenting cell |
|
Definition
| True, CD8 T cells aren't fully effective until stimulated by CD4 T cells (Th1) bound to the same APC |
|
|
Term
| CD40-CD40R binding on an APC induces expression of this co-stimulatory transmembrane protein, which binds to CD8 cells |
|
Definition
|
|
Term
| CD4 T cells bound to B cells via MHC II secrete these three interleukins to aid in B cell activation |
|
Definition
|
|
Term
| These factors in order, make up the "intrinsic pathway" of clot formation |
|
Definition
| XII, XI, IX, VII, X-> with V, forms the prothrombin activator that cleaves prothrombin to form thrombin, which can then auto-catalyze prothrombin-thrombin formation and primary removes 4 peptides from fibrinogen to enable the formation of fibrin polymers, the clot |
|
|
Term
| This factor activates factor X directly |
|
Definition
| Factor VII, making up the "extrinsic pathway" of clot formation, it itself is activated by the release of tissue factor from damaged endothelium and/or inflammatory cells |
|
|
Term
| What is the clinical significance of an elevated PT? |
|
Definition
| Liver dysfunction, as factors VII, X, prothrombin and fibrinogen are all synthesized in the liver, also, monitoring warfarin therapy with PT is useful as warfarin depresses synthesis of the above factors for hours after administration |
|
|
Term
| aPTT is most useful in monitoring anti-coagulant therapy with this agent. |
|
Definition
| Heparin, a set of glycoprotein polymers that bind to factor IX, X, Thrombin etc. and prevent them from activating fibrinogen ultimately |
|
|
Term
| A fast, IgE mediated response to antigen triggering vasoactive amines (i.e. histamine) |
|
Definition
| Type 1 hypersensitivity reaction, mild as hayfever or serious as anaphylactic shock |
|
|
Term
| IgM and IgG-complement membrane attack complexes form in response to antigen that causes lysis or phagocytosis, ie cytotoxic response |
|
Definition
| Type II hypersensitivity reaction |
|
|
Term
IgG antibody and antigen activate complement (immune complexes), which attracts neutrophils, which release lysosomal enzymes.
|
|
Definition
| Type III hypersensitivty reactions, like SLE |
|
|
Term
| CD4+ T Cell mediated reaction, sensitized lymphocytes encounter antigen and release cytokines causing inflammation. |
|
Definition
| Type IV hypersensitivity reaction, like in DMI, hashimoto's thyroiditis, guillan-barre, can be remembered with the four T's: T-cells, Transplant rejection, Touch (contact dermatitis), TB skin tests |
|
|
Term
| Released by CD4+ cells following exposure to antigen, this cytokine recruits macrophages to the site of reaction, increasing the number of epithelioid cells |
|
Definition
| Interferon-gamma, ultimately leads to granuloma formation |
|
|
Term
| What are the two fates of granulomata? |
|
Definition
|
|
Term
| The systemic changes associated with inflammation, especially in pts who have infections are collectively called the (), or the () |
|
Definition
| acute phase response or systemic inflammatory response syndrome |
|
|
Term
| Which bacterial product is usually the cause of SIRS? |
|
Definition
| lipopolysaccharide from the cell wall of gram - bacteria, or LPS |
|
|
Term
| T or F: Fever is a respone to substances called pyrogens that act by stimlating prostaglandin synthesis in the vascular and perivascular cells of the hypothalamus |
|
Definition
|
|
Term
| T or F: LPS can be considered an exogenous pyrogen |
|
Definition
|
|
Term
| What two cytokines are usually thought of as endogenous pyrogens? |
|
Definition
|
|
Term
| Which enzymes are stimulated by pyrogens to produce prostaglandins from amino acids? |
|
Definition
|
|
Term
| Name one hypothesis for the + effect of fever on bacterial infection |
|
Definition
| Fever may induce heat shock proteins that enhance lymphocyte responses to microbial antigens |
|
|
Term
| T or F: CRP, fibrinogen, and serum amyloid A protein are all considered acute phase reactants |
|
Definition
|
|
Term
| What is the biochemical basis for measuring the erythrocyte sedimentation rate? |
|
Definition
| The rise in fibrinogen during acute inflammation causes erythrocytes to form stacks that sediment more rapidly per unit gravity than do individual erythrocytes, hence the ESR is elevated in systemic inflammation |
|
|
Term
| What cytokines are responsible for leukocytosis from rapid release of leukocytes from the post-mitotic marrow pool? |
|
Definition
|
|
Term
| T or F: Viral infections such as infectious mononucleosis, mumps and reubella produce leukocytosis by virtue of an increase in the number of eosinophils |
|
Definition
|
|
Term
| T or F: High levels of TNFa cause disseminated intravascular coagulation |
|
Definition
|
|
Term
| LPS and TNFa induce () expression on endothelial cells, which initiates coagulation; the same agents inhibit natural anticoagulation mechanisms by decreasing the expression of () |
|
Definition
| Tissue factor, tissue factor pathway inhibitor |
|
|
Term
| T or F: cytokines cause liver injury and impaired liver function |
|
Definition
|
|
Term
| In sepsis, overproduction of () by cytokine activated cardiac myocytes and vascular SM cells leads to heart failure, loss of perfusion and pressure and ultimatle hemodynamic collapse |
|
Definition
|
|
Term
| T or F: Tissue injury in response to LPS can also result from the activation of neutrophils before they exit the vasculature |
|
Definition
|
|
Term
| The clinical triad of (), (), and () is described as septic shock |
|
Definition
| DIC, hypoglycemia and cardiovascular collapse |
|
|
Term
| Lung damage from acute systemic inflammation is commonly referred to as () |
|
Definition
| Acute respiratory distress syndrome |
|
|
Term
| T or F: Sepsis is the leading cause of death in US ICUs |
|
Definition
|
|
Term
| T or F: 70% of sepsis cases are caused by gram negative rods bacteria |
|
Definition
|
|
Term
| Which TLR is responsible for recognizing LPS? |
|
Definition
|
|
Term
| T or F: TLR4 directly inhibits TFPI in endothelial cells of vasculature inducing a hypercoagulable state |
|
Definition
|
|
Term
| T or F: LPS cannot directly activate compliment, it must first activate neutrophils and monocytes |
|
Definition
| False, it can directly activate compliment |
|
|
Term
| In addition to IL1 and TNFa, what other cytokine is predominately involved in response to LPS? |
|
Definition
|
|
Term
| T or F: Even in the non-progressive stage of shock vital organ perfusion is compromised |
|
Definition
| False, it is maintained, once signs of organ dysfunction arise the progressive stage has been reached, survival is not possible at the irreversible stage |
|
|
Term
| () undergo reactive changes whenever they are challenged by microbial agents, cell debris or foreign matter introduced into wounds or circulation. |
|
Definition
|
|
Term
| Acute lymphadenitis is most often seen in the () region due to microbial drainage from the teeth or (), and in the axillary region and inguinal region secondary to infections in the () |
|
Definition
| cervical, tonsils, upper and lower extremities |
|
|
Term
| T or F: The abdominal symptoms of mesenteric lymphadenitis mimic those of appendicitis |
|
Definition
|
|
Term
| T or F: Systemic viral infections rarely produce lymphadenopathy, but system bacterial infections usually produce it. |
|
Definition
| False, in children especially systemic viral infections can cause lymphadenopathy |
|
|
Term
| The macroscopic appearance of a lymph node in lymphadenitis is (), () and engorged. There is a prominence of () follicles, with large () containing numerous mitotic figures. |
|
Definition
| gray-red, swollen, lymphoid, germinal centers |
|
|
Term
| When pyogenic organisms cause lymphadenitis, the centers of the follicles undergo (), sometimes the entire node can be turned into a (). Less severe reactions show a () infiltrate in the follicles and neutrophils can be found in the () |
|
Definition
| necrosis, suppurative mass, neutrophilic, lymphoid sinuses |
|
|
Term
| T or F: Inflamed lymph nodes undergo hyperplasia but not hypertrophy |
|
Definition
|
|
Term
| Lymph nodes with acute lymphadenitis are enlarged because of () and edema. As a consequence they are (tender/not tender) due to capsule stretch |
|
Definition
| Cellular infiltration, tender |
|
|
Term
| Sometimes an inflamed lymph node can penetrate the skin and cause (), particularly when the nodes have undergone () necrosis. |
|
Definition
| Draining sinuses or sinus fistulas, suppurative |
|
|
Term
| The tonsils and adenoids are lymphoid tissue, also known as: |
|
Definition
|
|
Term
| Follicular hyperplasia in non-specific lymphadenitis is caused by stimul of this () arm of the immune system. It is distinguished by the appeariance of large, round or oblong ()-cell rich (), aka (), surrounded by a collar of small, resting naive B cells called the () |
|
Definition
| Humoral (antibodies), B cell germinal centers, secondary follicles, mantle zone |
|
|
Term
| Within germinal centers two distinct regions are visible, a dark zone containing proliferating () cells and a light zone composed of B cells with () or cleaved nuclear contours, aka () |
|
Definition
| B, irregular, centrocytes |
|
|
Term
| () macrophages are present throughout the follicle in lymphadenitiis, so named because they are filled with phagocytosed nuclear debris. |
|
Definition
|
|
Term
| In lymphadenitis, there is often striking () of the mononuclear phagocytic cells in the lymphatic () |
|
Definition
|
|
Term
| Specific causes of follicular hyperplasia include: |
|
Definition
| Rheumatoid arthritis, toxoplasma and early HIV |
|
|
Term
| What 3 features can distinguish follicular hyperplasia due to systemic inflammation from follicular lymphoma? |
|
Definition
| In follicular hyperplasia there is preservation of lymph node architecture like sinusoids and interfollicular T-cell zones, marked variation in size and shape of lymphoid nodules and the presence of frequent mitotic figures, phagocytic macrophages and light and dark zones. These things tend to not be in neoplastic nodes. |
|
|
Term
| Follicular hyperplasia is sometimes accompanied by (), where marginal zone B cells accumulate in a rim external to the mantle zone of germinal centers. The marginal zone B cells are sometimes called () due to the folded nuclei and are probably memory B cells. |
|
Definition
| Marginal zone B-cell hyperplasia |
|
|
Term
| () in lymphadenitis is seen in stimuli that cause a cellular immune response.It is characterized by reactive changes within the T-cell regions of the lymph node that encroach on the B-cell follicles. |
|
Definition
| Paracortical lymphoid hyperplasia |
|
|
Term
| The interfollicular regions of the lymph node, during paracortical lymphoid hyperplasia, contain a number of activated () cells, three to four times the size of resting lymphocites, round nuclei, open chromatin several nucleoli and moderate amounts of pale cytoplasm. There is also hypertrophy of () cells and a mixed infiltrate composed of () and sometimes (). |
|
Definition
| T cells, vascular endolthelial, macrophages, eosinophils |
|
|
Term
| Paracortical lymphoid hyperplasia is most often seen in: |
|
Definition
| Drug-induced reactions like Dilantin, acute viral infections esp. mononucleosis, and post-vaccine, if the reaction is especially vigorous further study is needed to rule out neoplasm |
|
|
Term
| () or reticular hyperplasia refers to the distention and prominence of lymphatic sinusoids. This form of hyperplasia is nonspecific but may be prominent in nodes draining cancers, such as () of the breast. The lining lymphatic endothelial cells are markedly (hypertrophied/hyperplasia), resulting in distention of the sinuses. |
|
Definition
| Sinus histiocytosis, carcinoma, hypertrophied |
|
|
Term
| The three main components of the innate immune system are: |
|
Definition
| The complement system, professional phagocytes e.g. neutrophils and macrophages, natural killer cells |
|
|
Term
| In the () system about 20 different proteins work together to destroy invaders and signal other immune system players that an attack is starting. |
|
Definition
|
|
Term
| Proteins of the complement system are produced mainly by the () but are present in high concentrations in the blood and tissues. () is the most abundant protein of the complement system and is a part of all three pathways. |
|
Definition
|
|
Term
| The alternative pathway is antibody (dependent/independent) involves C3 being spontaneously hydrolyzed to form () and (). |
|
Definition
|
|
Term
| In the alternative pathway, C3() reacts with a molecule on a bacteria's surface, then binds with protein (), the protein () converts protein B to protein Bb to make C3bBb, which is also known as the enzyme () |
|
Definition
|
|
Term
| In the alternative pathway, C3 convertase works on () to break it into C3a and C3b, at which point C3b can again be activated by protein (), creating a positive feedback loop. |
|
Definition
|
|
Term
| In the lectin pathway, the response is dependent on (), a carbohydrate molecule on the surface of many pathogens including yeast, viruses, bacteria and parasites. () binds the mannose of these cells. |
|
Definition
| Mannose, mannose-binding lectin |
|
|
Term
| MBL binds with (), which together bind the surface of the pathogen and convert C3 into C3b and regenerating the cycle. |
|
Definition
| mannose-binding lectin associated serine protease |
|
|
Term
| The classical pathway is () dependent, requiring either () or () to initiate the cascade |
|
Definition
| Antibody, IgM or some IgG molecules |
|
|
Term
| In the classical pathway, two or more () complexes, each comprised of around 30 proteins, must congregate and become activated. IgM uses its () region to bind the antigen and its () region to bind the C1 aggregate. |
|
Definition
|
|
Term
| In the classical pathway, once IgM binds 2+ C1 complexes, () and () complex to create C3 convertase. |
|
Definition
|
|
Term
| How does IgM activation of the classical pathway differ from IgG activation of the classical pathway? |
|
Definition
| IgM is a pentamer, meaning it can bind up to 5 C1 complexes on its Fc regions at once. IgG is a monomer, and can only bind one, so at least 2 IgGs must be attached both the antigen and each to a C1 to activate the pathway, in short there must be a lot of IgG in the serum to activate the classical pathway |
|
|
Term
| T or F: Antibodies extend the functional capacity of the complement system by enabling its activation for any antigen that has an antibody |
|
Definition
|
|
Term
| All three pathways of the complement system terminate in the creation of (), which can cut () into its component parts, () and (). () combines with C6-9 to form the (). The () portion of the MAC polymerizes on the surface of the antigen and forms a pore in the cell membrane, leading to lysis. |
|
Definition
| C3 convertase, C5, C5a and C5b, C5b, membrane attack complex, C9 |
|
|
Term
| These two complement proteins () and (), lead to a local inflammatory response by acting as chemoattractants, attracting activated macrophages and (). They're also called () and contribute to anaphylactic shock. |
|
Definition
| C3a and C5a, neutrophils, anaphyltoxins |
|
|
Term
| () can be clipped to become inactivated (), which cannot create a MAC but does opsonize the foreign element such that phagocytes are more likely to digest the material. |
|
Definition
|
|
Term
| In the alternative pathway, lots of complement proteins protect against errant behavior. () can be deactivated by enzymes on human cell membranes and () can be destroyed by proteins after coming into contact with () on human cells, finally () can remove the MAC if it does end up on a human cell |
|
Definition
| C3b, C3 convertase, Decay accelerating factor (DAF), CD59 |
|
|
Term
| () inhibitor prevents self-activation of the classical pathway |
|
Definition
| C1 esterase, usually antibodies bind to human cells only in pathology |
|
|
Term
| () are the phagocytic cells of the tissues and are found in lungs, skin, intestines and any other tissue exposed to the outside world. |
|
Definition
|
|
Term
| Macrophages at rest function as garbage collectors, clearing tissues of naturally dying cells, they express few () receptors thus making them poor APCs for CD4+ T cells |
|
Definition
|
|
Term
| When activated by () secreted by () and () cells, macrophages start to phagyctose more of the surrounding material and up-regulate their production of MHC II, making them better APCs. |
|
Definition
| Interferon-gamma, CD4, natural killer |
|
|
Term
| () and () can hyperactivate macrophages via direct contact, where macrophages become solely phagocytic and growing in size, via increasing the number of () in the cytosol as well as production of (). Lysosomal contents can also be ejcted onto parasites too big to phagocytose. |
|
Definition
| LPS, mannose, lysosomes, reactive oxygen species |
|
|
Term
| Hyperactivated macrophages secrete (), which can kill virus-infected cells and tumor cells and activate other immune system cells. They also produce () which can activate NK cells. |
|
Definition
|
|
Term
| () are the phagocytes of the blood, they live only () days at a time once exiting the bone marrow and die by apoptosis. They (do/do not) act as an APC. They are activated in tissues and are inactive in blood. |
|
Definition
|
|
Term
| Neutrophils in circulaiton express a surface protein called (), of which Sialyl Lewis-x is an example. Endothelial cells of the circulatory systme express a membrane protein called (). When () and () are secreted by macrophages, however, endothelial cells produce selectins along with ICAM. |
|
Definition
| Selectin ligand or SLIG, ICAM, IL-1 and TNF-a |
|
|
Term
| Selectin proteins on the surface of vascular endothelium and selectin ligands on the neutrophil act like velcro and slow down the circulating neutrophils (rolling), where they look for () or (), triggering the appearance of () on the neutrophil surface to bind ICAM. |
|
Definition
| C5a, LPS, integrin (LFA-1) |
|
|
Term
| The process by which neutrophils squeeze through vascular endothelial cells into tissues is called () and is aided by the () protein on the endothelial cells |
|
Definition
|
|
Term
| Neutrophils are attracted to sites of infection by: |
|
Definition
| f-met peptides, C5a, IL-8, LTB4, Kallikrein |
|
|
Term
| () ingest antigens in tissues and carry them to the lympho nodes for presentation. They are the best APC's. |
|
Definition
|
|
Term
| () cells are produced in the bone marrow and live for no more than a week. They circulate as inactive lymphocytes but are activated during infection and enter tissues in the same way neutrophils do, just with different proteins. |
|
Definition
|
|
Term
| Name NK cells two main functions in fighting infection: |
|
Definition
| Secrete cytokines like IFN-gamma and IL-2, destroy infected cells or tumor cells, bacteria, parasites and fungi by inducing apopotosis with granzymes and perforins or through Fas-FasL interactions |
|
|
Term
| NK Cells are inhibited by a receptor that recognizes () molecules on cell surfaces, which are found everywhere in the human body except RBCs. THey lack () cell receptors and thus do not use MHC to identify infected cells. They are activated by the cytokines (), (), (), (), and () |
|
Definition
| MHC 1, T cell receptors, LPS, IFN alpha, IFN beta, TNF, IL-12 |
|
|
Term
| Macrophages secrete (), () and (), important proteins in the alternative pathway of complement activation |
|
Definition
|
|
Term
| The most common cause of lymphangitis is: |
|
Definition
|
|
Term
| Systemic manifestations of septicemia or bacteremia are: |
|
Definition
|
|
Term
| Nodular lymphangitis is caused by (), a subcutaneous mycotic infection, leading toa chain of suppurating lymphocutaneous nodules |
|
Definition
|
|
Term
| Lymphedema is caused by () of lymphatic drainage, leading accumulation of interstitial fluid in the area (distal/proximal) to the obstruction |
|
Definition
|
|
Term
| Persistence of lymphedema leads to () subcutaneous interstitial fibrous tissues, with subsequent enlargement of the affected part, induration, () appearance of the skin and ulceration |
|
Definition
|
|
Term
| List seven common causes of lymphedema: |
|
Definition
| Breast lymphedema secondary to malignancy (peau d'orange), surgery that removes lymph nodes, LGV, filariasis from Wucheria bancroftii, postirradiation, postinflammatory thrombosis and scarring, chylous ascites following rupture of obstructed lymphatics |
|
|
Term
| Treatment for lymphedema is: |
|
Definition
| Apply complex decongestive therapy: elevation, limb massage and compression |
|
|
Term
| Most inherited immunodeficiency diseases are caused by () gene defects |
|
Definition
|
|
Term
| Inherited problems with complement components, the () response can be impaired, and accumulation of () occurs |
|
Definition
|
|
Term
| () is responsible for recruitment of inflammatory cells, smooth muscle contraction, histamine release and chemotactic signals. |
|
Definition
|
|
Term
| () is responsible for binding to the pathogen's surface and signaling macrophages to increase phagocytic activity, binding immune-complexes and formation of the MAC |
|
Definition
|
|
Term
| When an encapsulated bacteria is coated with antibodies and (), macrophages are more efficient at phagyctosing those bacteria. IgM binds its () region to the antigen and its () region to the complement complex, leading to a cascade effect where () is activated. |
|
Definition
| C3b, Fab, Fc, C3 convertase |
|
|
Term
| T or F: Even without complement, it is very difficult for antibody-antigen binds to be reversed. |
|
Definition
| False, it is more reversible without complement |
|
|
Term
| Defects in () increase susceptibility to a wide range of pyogenic infections due to loss of opsonization. |
|
Definition
|
|
Term
| () is an inherited immune deficiency resulting from a deficiency of adenosine deaminase, interrupting DNA synthesis and lymphocte production. |
|
Definition
| Severe combined immune deficiency (SCID |
|
|
Term
| DiGeorge syndrome results from a () deletion, resulting in a failure to develop the () and () pharyngeal pouches |
|
Definition
|
|
Term
| () syndrome presents with tetany, recurrent viral and fungal infections due to a T-cell deficiency, heart and great vessel defects |
|
Definition
|
|
Term
| The most common form of SCID is a defective () receptor, an X-linked disorder |
|
Definition
| IL2 leading to less T-cell activation |
|
|
Term
| Mutations in the region on chromosome 6p23 can result in these two types of inherited immune deficiences. |
|
Definition
| MHC I and MHC II deficiency |
|
|
Term
| This inherited immune deficiency is X-linked, and results in a defective antibody response to polysaccharide antigens, and is associated with eczema and thrombocytopenia. |
|
Definition
| Wiskott-Aldrich, defect in the WASP gene |
|
|
Term
| There are many different complement deficiencies, but defects in C3 or C5-C9 can all result in susceptibility to bacterial infection, especially () spp. |
|
Definition
| Neisseria (meningitis and gonorrhea) |
|
|
Term
| Patients with () and () deficiencies have diseases resembling systemic lupus erythematosus or other autoimmune diseases. () deficiency is the most common complement defect and is frequently asymptomatic. |
|
Definition
|
|
Term
| Hereditary angioedema is associated with which complement defect? |
|
Definition
| C1 inhibitor, this is a rare deficiency |
|
|
Term
| Mutations in the gene for () tyrosine kinase disrupt B cell development, making individuals more susceptible to bacterial and viral infection. |
|
Definition
| Btk, X-linked agamma-globulinemia |
|
|
Term
| Defects in the CD40L prevent (), necessary to make IgG, IgA and IgE, a process initiated by CD4 T cells. What disease is this seen in? |
|
Definition
| Isotype switching, X-linked hyper IgM syndrome, since IgM predominates |
|
|
Term
| Inherited deficiencies in IgA synthesis predispose to what type of infections? |
|
Definition
| Respiratory infections especially, any infection of mucosal membranes |
|
|
Term
| Defects in () and () lead to immune complex deposition in the blood, lymph and ECF, which can directly damage tissues as well as activating phagocytes causing further inflammation and tissue damage. |
|
Definition
|
|
Term
| () inhibits the conversion of C3-C3b, if absent C3 reserves are rapidly depleted. |
|
Definition
|
|
Term
| () normally enhances the alternative pathway. without it, patients have heightened susceptibility to Neisseria due to inhibition of MAC and bacterial lysis. |
|
Definition
|
|
Term
| () or CD59 normally inhibits the alternative pathway. Defects lead to enhanced activation of the alternative pathway and autoimmune-like conditions, like paroxysmal nocturnal hemoglobinuria. |
|
Definition
| Decay-accelerating factor due to complement-mediate lysis of erythrocytes. |
|
|
Term
| T or F: overactivity of vasoactive C2 fragment leads to increased capillary permeability and can lead to death from epiglottis swelling. |
|
Definition
|
|
Term
| Patients with severe liver disease are at risk for what type of infections? |
|
Definition
| Pyogenic bacterial infections from a loss of complement synthesis |
|
|
Term
| Complement protein () opsonizes, while () and () act as anaphylactic agents |
|
Definition
|
|
Term
| () are leukocytes well suited for working under anaerobic conditions in diseased tissues. |
|
Definition
|
|
Term
| Trace the lineage of PMNs starting in the bone marrow: |
|
Definition
| Pluripotent stem cell, myeloblast, promyelocyte, myelocyte, metamyelocyte, band, PMN |
|
|
Term
| Hypersegmented PMNs are a sign of () or () deficiency |
|
Definition
|
|
Term
| Under normal conditoins, () of the PMN pool is in the marrow, () in the vessels, and the remainder in () |
|
Definition
|
|
Term
| () graniules contain the myeloperoxidase enzyme, as well as lysozyme and other degradative enzymes. They are formed at the () stage. |
|
Definition
| Primary or azurophilic, promyelocyte |
|
|
Term
| () granules contain lactoferrin and proteases, nucleases, and lipases, formed at the () stage |
|
Definition
| secondary or specific, myelocyte |
|
|
Term
| T or F: like macrophages, PMNs can regenerate granules and survive in tissues for weeks |
|
Definition
| False, once the granules are gone they die and are digested |
|
|
Term
| List some surface receptors PMns have that can recognize common pathogen antigens. |
|
Definition
| Mannose, sialic acid, glycan, LPS, C3b |
|
|
Term
| Phagocytosis by PMNs is aided by the binding of () antibodies to the bacteria. Then the () is triggered, resulting in the production of microbicidal agents like (), (), and (). |
|
Definition
| IgG, respiratory burst, superoxide, hydrogen peroxide, nitric oxide |
|
|
Term
| Hydrogen peroxide is more toxic than superoxide to bacteria but can be circumvented by what bacterial strategy? |
|
Definition
Catalase, which can break H202 into water, produced by
S. aureus for instance |
|
|
Term
| Over production of () in an acute inflammatory reaction can cause the hypotension seen in septic shock from vasodilation of peripheral blood vessels. |
|
Definition
|
|
Term
| The most important oxygen-dependent mechanism of killing microorganisms after engulfing them is the production of () ion from chloride and hydrogen peroxide, catalyzed by () |
|
Definition
| hypochlorite, myeloperoxidase |
|
|
Term
| People deficient in myeloperoxidase can kill bacteria slowly due to the (), but catalase positive organisms or organisms with this enzyme () that inactivates superoxide radical formation, frequently cause disase. |
|
Definition
| respiratory burst, superoxide dismutase |
|
|
Term
| Oxygen-independent mechanisms of killing bacteria are important under anaerobic conditions, list some of these methods. |
|
Definition
| Lactoferrin chelates iron from bacteria, lysozyme degrades peptidoglycan in the cell wall, cationic protiens that damage cell membranes and low pH |
|
|
Term
| Organisms like (), () and () are all preferentially ingested by macrophages instead of PMNs, remaining viable and multiplying within these cells in granulomas |
|
Definition
| M. tuberculae, brucella, toxoplasma gondii |
|
|
