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II - Acute and Chronic Inflammation Flashcards

1
Q

Vasoconstriction.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.33

A

Initial vascular response to injury

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2
Q

Acute inflammation(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71

A

Inflammation characterized by exudation of fluid and plasma protein and a predominantly neutrophilic leukocyte accumulation.

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3
Q

Chronic inflammation(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71

A

Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and deposition of connective tissue.

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4
Q

Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71

A

Five cardinal signs of inflammation

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5
Q

Transudate. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

A

An ultrafiltrate of blood which contains little protein, little or no cellular material and low specific gravity as a result of osmotic or hydrostatic imbalance across the vessel wall WITHOUT increase in vascular permeability.

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6
Q

Exudate(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

A

An extravascular fluid with high protein content. Its presence implies an increased vascular permeability, triggered by tissue injury and ongoing inflammatory reaction.

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7
Q

Vasodilation. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

A

Effect of histamine on vascular smooth muscle

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8
Q

Contraction of endothelial cells resulting in increased interendothelial spaces. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 74

A

The most common mechanism of increased vascular permeability.

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9
Q

Reactive or inflammatory lymphadenitis. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 74

A

Proliferation of lymphatic vessels and painful enlarged lymph nodes secondary to inflammation.

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10
Q

P and E-Selectins on endothelium with Sialyl-Lewis-X on leukocyte; Glycam-1, CD-34 on endothelium with L-selectin on leukocyte (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 36 *SEE SLIDE 2.1

A

Molecules in the endothelium and leukocyte responsible for this stage of vascular inflammatory response: Rolling

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11
Q

ICAM-1 on endothelium with CD11/CD18 integrins (aka, LFA-1, Mac-1) on leukocyte; VCAM-1 on endothelium with VLA-4 on leukocyte (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 36 *SEE SLIDE 2.1

A

Molecules in the lymphocyte responsible for this stage of vascular inflammatory response: Firm adhesion

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12
Q

PECAM-1/CD 31(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77 *SEE SLIDE 2.1

A

Molecules in the endothelium responsible for this stage of vascular inflammatory response:
Transmigration

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13
Q

Lymphocytes, MACROPHAGES and CYTOKINES (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 41

A

CELLS AND MOLECULES INVOLVED IN: Chronic transplant rejection

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14
Q

Lymphocytes, ANTIBODIES and COMPLEMENT (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 41

A

CELLS AND MOLECULES INVOLVED IN: Acute transplant rejection

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15
Q

Margination(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75

A

The process of leukocyte accumulation at the periphery of blood vessels

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16
Q

C, A, D, B, E (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 72

A 
Arrange the following steps in the inflammatory response:
A. Recruitment of leukocytes
B. Regulation of response
C. Recognition of injurious agent
D. Removal of agent
E. Resolution
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17
Q

C, B, D, A (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75

A

Arrange the steps in leukocyte recruitment:A. TransmigrationB. Rolling C. MarginationD. Firm adhesion

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18
Q

Opsonization (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75

A

Process of coating microorganisms with proteins that facilitate phagocytosis.

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19
Q

Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 78

A

A lymphocyte with ingested microorganism fused with lysosome is called _______.

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20
Q

Transmigration or diapedesis. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

A

The process of migration of the leukocytes through the endothelium.

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21
Q

Chemotaxis (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

A

Process of leukocyte migration toward sites of infection or injury along a chemical gradient.

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22
Q

Elastase(TOPNOTCH)

A

The most important lysosomal enzyme involved in bacterial killing.

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23
Q

Defensins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.40

A

A peptide leukocyte granule constituent which kills microbes by creating holes in their membranes.

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24
Q

Neutrophils(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

A

Predominant form of leukocyte during the first 6 - 24 hours of inflammation.

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25
Q

Monocytes(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

A

Predominant form of leukocyte during 24-48 hrs after the onset of inflammation.

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26
Q

Neutrophils(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

A

Predominant cellular infiltrate in bacterial infections

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27
Q

Lymphocytes (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

A

Predominant cellular infiltrate in viral infections

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28
Q

Eosinophils (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77

A

Predominant cellular infiltrate in allergic reactions

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29
Q

Lysosomal enzymes, reactive oxygen and nitrogen species.(TOPNOTCH)

A

Substances responsible for leukocyte-induced tissue injury

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30
Q

Leukocyte adhesion deficiency type 1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41

A

Defective synthesis of CD 18 B-subunit of leukocyte integrins LFA-1 and Mac-1, leading to impaired leukocyte adhesion and migration through endothelium.

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31
Q

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

A

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.

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32
Q

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

A

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

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33
Q

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

A

NADPH deficiency or defect resulting in decreased oxidative burst.

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34
Q

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

A

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.

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35
Q

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

A

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.

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36
Q

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

A

The richest sources of histamine

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37
Q

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

A

Causes vasoconstriction or vasodilation: SEROTONIN

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38
Q

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

A

Causes vasoconstriction or vasodilation: PROSTAGLANDINS

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39
Q

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

A

Two kinds of cells seen in granulomas

40
Q

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

A

Arachidonic acid metabolites/derivatives

41
Q

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

A

Arachidonic acid derivative that causes vasoconstriction and promotes platelet aggregration.

42
Q

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

A

Arachidonic acid metabolite implicated in increased vascular permeability and bronchospasm

43
Q

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

A

Arachidonic acid metabolite that causes chemotaxis and leukocyte adhesion.

44
Q

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

A

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

45
Q

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

A

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

46
Q

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

A

3 Functions of complement proteins

47
Q

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

A

Morphologic hallmarks of acute inflammation

48
Q

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

A

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.

49
Q

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

A

Fluid in a serous cavity is called ______.

50
Q

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

A

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)

51
Q

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

A

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

52
Q

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

A

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

53
Q

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

A

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.

54
Q

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

A

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.

55
Q

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

A

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

56
Q

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

A

Complement fragments which are anaphylotoxins.

57
Q

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

A

Complement fragment which aids in opsonization.

58
Q

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

A

Membrane attack complex

59
Q

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

A

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

60
Q

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

A

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

61
Q

Platelet aggregration, vasoconstriction (vasodilation in low concentration), bronchoconstriction, and increased venular permeability. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 89

A

Platelet-activating factor (PAF) is a phospholipid-derived mediator that is now known to have multiple inflammatory effects. What are these?

62
Q

Cyclooxygenase 1 and 2 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 85 *SEE SLIDE 2.6

A

Enzyme blocked by NSAIDS.

63
Q

Phospholipase A2 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 85 *SEE SLIDE 2.6

A

Enzyme inhibited by glucocorticoids

64
Q

Cytokines (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 86

A

Polypeptide products of many cell types that function as mediators of inflammation and immune response.

65
Q

Chemokines (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 87

A

They are a family of small structurally related proteins that act primarily as chemoattractants for different subsets of leukocytes.

66
Q

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

A

Major cytokines in acute inflmmation.

67
Q

Nitric oxide (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 80

A

A short-lived, soluble, free-radical gas produced by endothelial cells causing smooth muscle relaxation and vasodilation.

68
Q

Activated Hageman Factor / Factor XIIa(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.52

A

This component of the coagulation cascade initiates four systems involved in the inflammatory response, namely the kinin, clotting, fibrinolytic and complement systems.

69
Q

Chronic Inflammation(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 93-94

A

Inflammation characterized by infiltration with mononuclear cells, tissue destruction and repair involving angiogenesis and fibrosis.

70
Q

Kupffer cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

A

Macrophages in the liver

71
Q

Sinus histiocytes(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

A

Macrophages in the spleen and lymph nodes

72
Q

Microglial cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

A

Macrophages in the CNS

73
Q

Classical pathway. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

A

Pathway of macrophage activation induced by microbial products such as endotoxin, cytokines, or foreign substance to produce substance for host defense and inflammatory reactions

74
Q

Alternative pathway. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 95

A

Pathway of macrophage activation induced by cytokines produced by T lymphocytes and other cells with the principal function of tissue repair.

75
Q

Alveolar Macrophages (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 94

A

Macrophages in the lungs

76
Q

Caseating tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

A

Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli *SEE SLIDE 2.2

77
Q

Leprosy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

A

Acid-fast bacilli in macrophages, noncaseating granulomas

78
Q

Gumma (Syphilis)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

A

Microscopic to visible lesion, enclosing wall of histiocytes, plasma cell infiltrates, necrotic central cells without loss of cellular outline

79
Q

Cat-scratch Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

A

Rounded or stellate granuloma containing central granular debris and recognizable neutrophils, giant cells uncommon.

80
Q

Sarcoidosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

A

Noncaseating granulomas with abundant activated macrophages *SEE SLIDE 2.5

81
Q

Crohn’s disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

A

Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate *SEE SLIDE 2.3

82
Q

Epithelioid cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

A

Cells with pink, granular cytoplasm with indistinct boundaries.

83
Q

Giant cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

A

40-50 um in size, consisting of a large mass of cytoplasm and many nuclei. *SEE SLIDE 2.4

84
Q

TNF, IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.57

A

Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.

85
Q

Granulomatous inflammation. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

A

A form of chronic inflammation characterized by collections of activated macrophages, often with T lymphocytes.

86
Q

TB, Leprosy, syphilis, cat-scratch disease, sarcoidosis, Crohn’s disease, systemic mycoses (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

A

Diseases with granulomatous inflammation

87
Q

True. (TOPNOTCH)

A

True or false. Schistosomiasis may cause granulomatous inflammation

88
Q

True. (TOPNOTCH)

A

True or false. Histoplasmosis may cause granulomatous inflammation

89
Q

Serous inflammation. (TOPNOTCH)

A

A 5 y/o child touches a lit candle and develops a small blister on his right hand. The blister is an example of what type of inflammation?

90
Q

Tissue destruction (TOPNOTCH)

A

The hallmark of chronic inflammation

91
Q

Neutrophils (TOPNOTCH)

A

A 20 y/o male was admitted due to RLQ pain of 18 hours duration. Appendectomy and revealed an edematous and erythematous appendix. An infiltrate of what cells would be most likely seen?

92
Q

Increased blood flow (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 74

A

Heat and redness in acute inflammation is due to what pathogenetic mechanism?

93
Q

protein poor fluid (Morphologic patterns of acute inflammation) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 43-44

A

An 18 year old college student accidentally scalds his hand while ironing, where a large unruptured blister forms. What is seen in the blister? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) large necrotic center surrounded by neutrophils (D) epithelioid macrophages and giant cells

94
Q

large necrotic center surrounded by neutrophils (Morphologic patterns of acute inflammation) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 43-44

A

A 64 year old stroke patient at the ICU with a chest radiograph showing a cavitary lesion in the right lower lung lobe with fluid levels. What is seen in that lobe? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) extensive necrosis and neutrophilic infiltrates (D) epithelioid macrophages and giant cells

95
Q

eosinophilic meshwork of amorphous coagulum (Morphologic patterns of acute inflammation) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 43-44

A

A rheumatologist auscultates a friction rub in a 33 year old admitted lupus patient. What is seen in her pericardial cavity? (A) protein poor fluid (B) eosinophilic meshwork of amorphous coagulum (C) large necrotic center surrounded by neutrophils (D) epithelioid macrophages and giant cells

96
Q

giant cells surrounding refractile bodies (Granulomatous Inflammation) (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 56

A

A 33 year old female who underwent partial thyroidectomy for a colloid nodule 5 years ago underwent a completion thyroidectomy for persistent enlargement. On her present thyroid specimen, the original excision site shows a sutured area. Microscopic examination of that area will show (A) epithelioid cells with occasional giant cellssurrounding a necrotic center (B) neutrophils surrounding a necrotic center (C) protein poor fluid (D) giant cells surrounding refractile bodies

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