II - Acute and Chronic Inflammation Flashcards Preview

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Flashcards in II - Acute and Chronic Inflammation Deck (108):
1

It is a response of vascularized tissues to infection and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.

Inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 69

2

The first step in a typical inflammatory reaction

Recognition of offending agent (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 70

3

The main components of inflammation

Vascular reaction and cellular response. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 72

4

The sequential steps in a typical inflammatory reaction

Recognition of offending agent, recruitment of leukocytes and plasma proteins, removal of agent, regulation of response, repair.(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 70

5

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

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

6

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

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

7

Five cardinal signs of inflammation

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

8

Initial vascular response to injury

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

9

Three major components of acute inflammation

Vasodilation, increased permeability, leukocyte emigration. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73

10

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.

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

11

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

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

12

Denotes an excess fluid in the interstitial tissue or serous cavities

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

13

Effect of histamine on vascular smooth muscle

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

14

The most common mechanism of increased vascular permeability.

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

15

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

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

16

State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Rolling

Selectins (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

17

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

Integrins(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

18

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

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

19

State the endothelial adhesion molecule responsible for this stage of vascular inflammatory response:Intercellular adhesion

ICAM -1(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

20

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:E-Selectin

Sialyl-Lewis X modified glycoprotein (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

21

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:P-Selectin

Sialyl-Lewis X modified glycoprotein (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

22

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:ICAM-1

Integrins (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

23

State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:CD-31

CD-31(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76

24

The process of leukocyte accumulation at the periphery of blood vessels

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

25

Arrange the following steps in the inflammatory response:A. Recruitment of leukocytesB. Regulation of responseC. Recognition of injurious agentD. Removal of agentE. Resolution

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

26

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

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

27

Process of coating microorganisms with proteins that facilitate phagocytosis.

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

28

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

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

29

The process of migration of the leukocytes through the endothelium.

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

30

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

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

31

The most important lysosomal enzyme involved in bacterial killing.

Elastase(TOPNOTCH)

32

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

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

33

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

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

34

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

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

35

Predominant cellular infiltrate in Pseudomonas infection.

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

36

Predominant cellular infiltrate in viral infections

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

37

Predominant cellular infiltrate in allergic reactions

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

38

Sequential steps in phagocytosis

Recognition and attachment of particle to be ingested, engulfment and formation of phagocytic vacuole, killing or degradation of ingested material. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.78

39

First step in phagocytosis

Recognition and attachment of particle to be ingested(TOPNOTCH) Robbins Basic Pathology, 9th ed. P.78

40

Substances responsible for leukocyte-induced tissue injury

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

41

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

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

42

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

43

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

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

44

NADPH deficiency or defect resulting in decreased oxidative burst.

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

45

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

46

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

47

The richest sources of histamine

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

48

Effects of histamine of arterioles and venules

Dilation of arterioles and increases permeability of venules. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83

49

Arachidonic acid metabolites/derivatives

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

50

Arachidonic acid derivative that causes vasoconstriction and promotes platelet aggregration.

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

51

Arachidonic acid metabolite implicated in increased vascular permeability and bronchospasm

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

52

Arachidonic acid metabolite that causes chemotaxis and leukocyte adhesion.

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

53

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

54

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

55

3 Functions of complement proteins

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

56

Morphologic hallmarks of acute inflammation

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

57

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

58

Fluid in a serous cavity is called ______.

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

59

This type of inflmmation results from greater vascular permeability that allows larger molecules to pass the endothelial barrier.

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

60

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

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

61

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

62

Focal collections of pus that may be caused by seeding pyogenic organisms into a tissue or by secondary infections of necrotic foci.

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

63

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

64

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

65

Complement fragments which are anaphylotoxins.

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

66

Complement fragment which aids in opsonization.

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

67

Membrane attack complex

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

68

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

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

69

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

70

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

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

71

Enzyme blocked by NSAIDS.

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

72

Enzyme inhibited by glucocorticoids

Phospholipase A2 (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 85

73

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

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

74

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

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

75

Major cytokines in acute inflmmation.

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

76

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

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

77

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

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

78

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

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

79

Macrophages in the liver

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

80

Macrophages in the spleen and lymph nodes

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

81

Macrophages in the CNS

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

82

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

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

83

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

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

84

Macrophages in the lungs

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

85

A focus of epitheloid cells, rimmed by fibroblasts, lymphocytes, histiocytes, occasional giant cells.

Noncaseating tubercle, Tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56

86

Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli

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

87

Acid-fast bacilli in macrophages, noncaseating granulomas

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

88

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

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

89

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

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

90

Noncaseating granulomas with abundant activated macrophages

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

91

Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate

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

92

Cells with pink, granular cytoplasm with indistinct boundaries.

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

93

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

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

94

Necrotic material which appears amorphous, structureless, granular debris, with complete loss of cellular details.

Caseous necrosis (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 98

95

Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.

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

96

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

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

97

Diseases with granulomatous inflammation

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

98

True or false. Schistosomiasis may cause granulomatous inflammation

True. (TOPNOTCH)

99

True or false. Histoplasmosis may cause granulomatous inflammation

True. (TOPNOTCH)

100

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?

Serous inflammation. (TOPNOTCH)

101

The hallmark of chronic inflammation

Tissue destruction (TOPNOTCH)

102

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?

Neutrophils (TOPNOTCH)

103

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

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

104

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

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

105

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

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

106

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

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

107

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

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

108

What is expected in the involved intestine of a patient with Chron disease? (A) eosinophilic network of amorphous coagulum (B) foci of neutrophils with necrotic debris (C) occasional noncaseating granulomas with dense chronic inflammatory infiltrate (D) pockets of protein poor fluid

occasional noncaseating granulomas with dense chronic inflammatory infiltrate (Granulomatous Inflammation) (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56