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INFLAMMATION1. In acute inflammationa. A hallmark is reduced vascular permeabilityb. Vasodilation is a late manifestationc. Extravasation involves movement of leukocytes from interstitial tissue to the vessel lumend. Chemotaxis is migration of leukocytes along a chemical gradiente. Selectins have a minor role2. In acute inflammation which event occurs firsta. Arteriolar dilatationb. Arteriolar constriction – vasodilatation follows transient arteriolar constriction lasting a few secondsc. Oedemad. Leucocyte migratione. Blood flow stasis3. The first vascular response to injury isa. Slowing of the circulationb. Venular dilationc. Recruitment of vascular bedsd. Capillary engorgemente. Arteriolar vasoconstriction – vasodilatation follows transient arteriolar constriction lasting a few seconds4. leukocytes move into tissues from the vasculature (extravasation)a. by the action of actin and myosin - correctb. predominantly as monocytes on the first day post injury - neutrophilsc. in response to C3bd. in response to the Fc fragment of IgG e. largely in the arterioles – in venules5. Regarding chemical mediators of inflammationa. Histamine is derived from plasma – and serotonin released from preformed stores from mast cells, basophils and plateletsb. C3b is within macrophages – synthesized in liverc. The kinin system is activated in platelets – on platelets?d. Nitric oxide is preformed in leukocytes – short half life, lasts secondse. Serotonin is preformed in mast cells – actually not in humans! It is preformed and in platelets and neuroendocrine cells6. Chronic inflammation isa. Always preceded by acute inflammation – no, can result from low-grade persistent insultb. Characterized by hyperaemia, oedema and leukocyte infiltrationc. Most frequently results in resolutiond. The factors underlying monocyte infiltration are the same as for acute inflammatione. ?7. In the triple response the reactive hyperaemia is due to:- something wrong with the question, reactive hyperaemia is due to an increase in blood flow after re-establishment after occlusion. The redness in the triple response is erythema.a. Blushingb. Exercisec. Arteriolar dilation – true (if the question read initial then it would be incorrect, the initial is due to capillary dilation)d. Inflammatory mediatorse. Still present after sympathectomy – trueTripple response = normal response to injury w/ red reaction, wheal and flare. Reddening in 10sec due to capillary dilation, then oedema due to permeability, then flare due to arterioloar dilation. Because it is an axon reflex with antidromic conduction sympathectomy or higher nerve block doesn’t effect (although local block will prevent flare)8. regarding chronic inflammation all of the following are true EXCEPT:a. it can be caused by persistent infectionsb. it primarily involves tissue destructionc. it may contribute to the formation of athersclerosisd. it involves mononuclear inflammatory cellse. it can be caused by exposure to toxic agents9. Regarding leucocyte adhesion and transmigration during acute inflammation:a. There is reduced binding of integrinsb. Transmigration is mediated by E-selectinc. Leukocyte adhesion deficiency type II is associated with resistance to bacterial infectiond. Leukocyte rolling is reducede. There is initial redistribution of pre-formed adhesion molecules to the cell surface10. In acute inflammationa. Vasoconstriction is the primary eventb. Direct injury is due to histaminec. Vascular leakage occurs mainly by formation of endothelial gaps in arteriolesd. There is outpouring of a transudate due to increased vascular permeabilitye. Leukocyte dependent injury occurs mainly in arterioles11. In chronic inflammation:a. The most important cells are lymphocytes – are present, but macrophages more importantb. Mast cells are not involved – plasma cells are (?Mast cells)c. Is always associated with tissue damage – associated with mononuclear cells (Macrophages), tissue destruction and attempts at healing (angiogenesis and fibrosis)d. The most important cells are neutrophils – monocytes -> macrophagese. Caseous necrosis is only seen in tuberculosis – characteristic of, not indicative12. granulomatous inflammatory reactions:a. can be caused by syphilitic infections - trueb. are a type II hypersensitivity reactionc. predominantly contain eosinophils with a modified “epithelial like” appearance – modified macrophages with epithelioid appearance (enlargement and flattening)d. are surrounded by natural killer cellse. are not associated with inert foreign bodies – can be e.g. silicosis, foreign body granuloma around sutures13. Leukotrienes play a role in all of the following EXCEPT:a. Chemotaxisb. Vasoconstriction c. Platelet aggreagation – don’t cause thisd. Bronchospasm – more potent than histaminee. Increased permeability14. Platelet activating factora. Is produced by platelets – this is true, also mast cells, leukocytes and endotheliumb. Induces bronchodilation - bronchoconstrictionc. Increases vascular permeability – at extremely low concentrations potent vasodilator and increases permeability (100-10,000 more potent than histamine)d. Decreases leukocyte adhesion - increasese. Is not produced by mast cells15. A preformed mediator of inflammation is:a. Prostaglandinb. Histaminec. Leukotriened. Nitric oxidee. Platelet activating factor16. Interleukin 1 causes:a. Neutropeniab. Decreased sleepc. Decreased prostaglandin synthesisd. Increased collagen synthesis - Vascular endothelium and leukocytes -> inflammationFibroblasts (promote proliferation and collagen synthesis) -> repair, Fever, Anorexia, Lethargy, Neutrophilia, Corticotrophin and corticosteroid releasee. Decreased leukocyte adherence17. With regard to the acute inflammatory response, which is the most common mechanism of vascular leakage?a. Endothelial cell contractionb. Junctional retractionc. Direct injuryd. Leukocyte-dependent leakagee. Regeneration indothelium18. With regard to the role of complement in the acute inflammatory response, which is INCORRECT?a. C5a is a powerful chemotactic agent for neutrophils, monocytes and eosinophilsb. C5a increases leukocyte adhesion to endothelium by activating leukocytesc. C3a and C5a are called anaphylatoxins because they cause mast cell degranulationd. C3a activated the lipooxygenase pathway in leukocytes – C5a does…e. C3 and C5 can be activated in inflammatory exudates by lysosomal enzymes19. Granulomatous inflammationa. May sometimes be a component of the acute inflammatory responseb. Indicates the presence of tuberculosisc. Consists in part of microscopic aggregates of transformed lymphocytesd. Is always associated with the presence of giant cells – often, especially if oldere. May result from non-immune mechanisms – foreign body granuloma20. In acute inflammation, all of the following are true EXCEPT:a. There is contraction of endothelial cellsb. There is a mononuclear infiltrate – this seems true, neutrophils first 6-24, then monocytes 24-48c. There is induction of adhesion molecules on endotheliumd. There is production of arachadonic acid metabolitese. Cytokines induce a systemic acute phase response21. Cellular events in acute inflammation include all of the following EXCEPT:a. Redistribution of preformed adhesion molecules to the cell surface of leukocytesb. Adhesion and transmigration of leukocytes to endotheliumc. Leukocyte activationd. Margination of macrophages to vessel wallse. Extracellular release of lysosomal enzymes and products of arachidonic acid metabolism22. Which is true of chronic inflammation?a. Macrophages have a half life of 5 daysb. It commonly follows acute inflammationc. Frequently resolvesd. It is characterized by increased vascular permeability and oedemae. Has the same chemotactic factors as for acute inflammation23. Which is not chemotactic?a. Histamine – just causes vasodilatation, increased permeability (and endothelial activation)b. C5a - powerfulc. Leukotriene B4 – main leukotriened. Bacterial polypeptides - truee. Cytokines - definitiely24. The alternative pathway of complement activation can be triggered by:a. IgG antigen-antibody complexesb. Properdinc. Microbial surfacesd. Lysosomal proteasese. C5-9 Membrane attack complex25. Which factor ties together activation of the clotting cascade, kinins and the fibrinolytic system?a. Stuart Factorb. Prothrombinc. Plasminogend. Factor XII – aka Hageman factor -> XIIa:1. induces the intrinsic pathway, 2. prekallikrein -> kallikeini. autocatalytic loop-> XIIii. HMWK - > bradykinin (dilation/permeability)iii. C5->C5a3. pasminogen -> plasmin (fibrinolytic), plasmin also C3->C3ae. Kallikrein26. Which of the following statements regarding prostaglandins is INCORRECT?a. Prostacyclin and thromboxane A2 are synthesized from the same precursorb. Leukocyte adhesion is mediated by thromboxane A2 - selectinsc. Vasodilation is mediated by PGEd. Vasoconstriction is mediated by LTD4e. Chemotaxis is mediated by HETE27. Chronic inflammationa. Is characterized by prolonged duration and usually results in resolutionb. Is associated with structural changes in microvasculature leading to exudation of proteinsc. Is characterized by angiogenesis <- true, as part of the healingd. Features infiltration by polymorphonuclear cells, mast cells and lymphocytes – may have infiltration from these cells… e. Is usually associated with markedly symptomatic response to persistent infection by certain microorganisms – low grade response to28. In chronic inflammation the life span of tissue macrophages is closest to:a. 4-8 hoursb. 1 dayc. 8 daysd. 2-4 weekse. 2 months29. With regard to chemical mediators of inflammation:a. Are solely derived from plasmab. Leukotrienes are preformed mediatorsc. Nitric oxide results in vasodilationd. Source of serotonin is leukocytese. Histamine results in vascular leakage30. Regarding chemical mediators of inflammation:a. Histamine exerts its proinflammatory effects mainly on venules – arteriolar dilation, venule leakageb. C5a, LTB4, IL8 are chemotactic - IL8 is a chemokinec. Fever and pain are mediated by prostaglandins, IL1, TNF and kinins (?kinins – pain, not fever)d. Oxygen metabolites are important in host defence – definitely truee. All of the above31. Vascular changes in acute inflammation include:a. Slowing of the circulation leading to leukocyte margination - trueb. Initial transient vasodilation of arterioles – initial transient arteriolar vasoconstrictionc. Decreased hydrostatic pressure caused by vasodilation - increasedd. Leakage of high protein fluid into vessels – out ofe. Increased osmotic pressure within vessels - outside32. Leukocyte extravasation occurs in the following order:a. Activation, rolling, transmigration, adhesionb. Rolling, activation, adhesion, immigrationc. Adhesion, rolling, activation, transmigrationd. Rolling, activation, adhesion, transmigratione. Transmigration, adhesion, activation, rolling33. In acute inflammation, which is the correct sequence of events with regard to vascular flow and caliber?a. Vasodilation, margination, stasis, vasoconstrictionb. Vasoconstriction, stasis, margination, vasodilationc. Vasodilation, stasis, vasoconstriction, marginaitond. Vasoconstriction, vasodilation, stasis, marginatione. Vasodilation, vasoconstriction, stasis, margination34. The epithelioid cells of follicular granulomas are:a. Reticularb. Fibroblastsc. Modified macrophagesd. Plasma cellse. Lymphocytes35. Vascular permeability in inflammation is increased by:a. C3b and C3bI - opsinisationb. C3b - opsinisationc. C3a and C5a – via histamine release (anaphylatoxins)d. C5-9 – C6-9 are important in MAC formation (multiples of C9’s)e. C3bI – iC3b impt in opsinisation36. Regarding acute inflammation:a. Occurs in apoptosisb. Increased vascular permeability resulting in increased colloid osmotic pressure and reduced hytdrostatic pressurec. Leukocyte migration through blood vessels is required by binding to selectin and integrin receptorsd. Causes venule dilation but not arteriole dilatione. Typically produces transudate – normally exudate37. Mononuclear phagocytesa. Are the predominant cells in three day old woundsb. Are common in liver, spleen and pancreasc. Produce fibroblast growth factord. Secrete interferon-ge. Have a half-life of one day38. With regard to the leukocyte extravasation of the acute inflammatory response, which of the following is INCORRECT?a. ELAM-1 is a selectin found on endothelium – aka E-selectinb. E and P-selectins bind to oligosaccharides found on neutrophils and monocytesc. L-selectin is found on neutrophils, monocytes and lymphocytesd. ICAM-1 belongs to the immunoglobulin family of molecules, and is found on leukocytes – ICAM is an intergrin ligand found on endolthelial cellse. VCAM-1 binds to integrins39. Phagocytosisa. Occurs in 2 steps – 3 steps: recognition, engulfment and killingb. C5a is an opsonin – C3b and iC3bc. IgM is a potent opsonind. Bacterial killing occurs by mainly O2 dependent mechanismse. Doesn’t occur without opsonisation ................
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