II - Acute and Chronic Inflammation (with pics) Flashcards Preview

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Flashcards in II - Acute and Chronic Inflammation (with pics) Deck (96)
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31

Caused by a defect in fucose metabolism resulting in absence of sialyl-lewis X, the oligosaccharide on leukocytes that binds to selectins on activated endothelium.

Leukocyte adhesion deficiency type 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41

32

Results from a defect in the protein involved in membrane docking and fusion.

Chediak-Higashi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41

33

NADPH deficiency or defect resulting in decreased oxidative burst.

Chronic Granulomatous Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.42

34

Type of inflammatory mediators that are normally sequestered in intracellular granules and can be rapidly secreted by granule exocytosis or are synthesized de novo in response to a stimulus.

Cell-derived mediators.(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 82

35

Type of mediators that are produced mainly in the liver and are present in the circulation as inactive precursors that must be activated by proteolytic cleavages to acquire their biologic properties.

Plasma-derived mediators. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83

36

The richest sources of histamine

Mast cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83

37

Causes vasoconstriction or vasodilation: SEROTONIN

Vasoconstriction (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 45

38

Causes vasoconstriction or vasodilation: PROSTAGLANDINS

Vasodilation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 46

39

Two kinds of cells seen in granulomas

Epithelioid cells (activated macrophages with pink, granular cytoplasm, resembling epithelial cell) and giant cells (TOPNOTCH) Robbins, 9th ed. P. 46

40

Arachidonic acid metabolites/derivatives

Prostaglandin, prostacyclin, thromboxane, leukotrienes, lipoxin. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 84 *SEE SLIDE 2.6

41

Arachidonic acid derivative that causes vasoconstriction and promotes platelet aggregration.

Thromboxane A2 (TXA2) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 84

42

Arachidonic acid metabolite implicated in increased vascular permeability and bronchospasm

LTC4, LTD4, and LTE4 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 84

43

Arachidonic acid metabolite that causes chemotaxis and leukocyte adhesion.

Leukotriene B4 (LTB4) and hydroxyeicosatetraenoic acid (HETE). (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 84

44

Cytokines that induce systemic acute-phase response associated with infection or injury, and are implicated in sepsis.

TNF, IL-1 (and IL-6) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 86

45

The cytokines that are important mediators of acute-phase reaction causing fever.

TNF, IL-1 (and IL-6) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 99

46

3 Functions of complement proteins

Inflammation, opsonization and phagocytosis, and cell lysis. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

47

Morphologic hallmarks of acute inflammation

Vasodilation and accumulation of leukocytes and fluid in the extravascular tissue. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

48

Type of acute inflammation characterized by the outpouring of watery, relatively protein-poor fluid derived from the serum or endothelial lining of peritoneal, pleural, and pericardial cavities.

Serous inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

49

Fluid in a serous cavity is called ______.

Effusion (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

50

This type of inflammation results from greater vascular permeability that allows larger molecules like fibrin to pass the endothelial barrier. Often seen in inflammation of body cavity linings, such as meninges, pericardium, and pleura. May lead to resolution or organization (scarring)

Fibrinous inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

51

Histologically, appears as an eosinophilic meshwork of threads or sometimes an amorphous coagulum.

Fibrinous inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

52

This type of inflammation is manifested by the presence of large amounts of purulent exudate consisting of neutrophils, necrotic cells, and edema fluid.

Suppurative (purulent) inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

53

Focal collections of pus that may be caused by seeding pyogenic organisms into a tissue or by secondary infections of necrotic foci. Has a central necrotic region rimmed by a layer of preserved neutrophils and dilated vessels.

Abscess (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 90

54

It is an excavation of the surface of an organ or tissue that is produced by necrosis of cells and sloughing of inflammatory necrotic tissue.

Ulcer (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 91

55

Vasoactive amines that are preformed molecules in secretory granules of mast cells, basophils and platelets.

Serotonin, Histamine (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83

56

Complement fragments which are anaphylotoxins.

C3a, C5a (A for anaphylotoxin) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

57

Complement fragment which aids in opsonization.

C3b (b for binding)(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

58

Membrane attack complex

C5b, C6-9 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

59

Deficiency of the terminal components of complement predisposes to what infection.

Neisseria infections. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

60

It is the cytolytic endproduct of the complement cascade, which forms a transmembrane channel causing osmotic lysis of target cells.

Membrane attack complex (C5b,C6-9) (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89