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Pathology 101 > Chapter II - Acute and Chronic Inflammation > Flashcards

Chapter II - Acute and Chronic Inflammation Flashcards

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1
Q

It is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.

A

Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.31

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2
Q

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

A

Acute inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

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3
Q

Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and fibrosis.

A

Chronic inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

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4
Q

Five cardinal signs of inflammation?

A

Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

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5
Q

Initial vascular response to injury?

A

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

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6
Q

An ultrafiltrate of blood which contains little protein. Results from arteriolar vasodilation and increased blood flow.

A

Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

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7
Q

Results from increased vascular permeability, leading to leakage of protein into tissues.

A

Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

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8
Q

Fluid accumulation in extravascular space.

A

Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

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9
Q

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

A

Selectins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

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10
Q

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

A

Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

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11
Q

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

A

PECAM-1/CD 31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

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12
Q

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

A

ICAM -1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

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13
Q

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

A

Sialyl-Lewis X modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

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14
Q

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

A

Sialyl-Lewis X-Modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

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15
Q

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

A

Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

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16
Q

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

A

CD-31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

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17
Q

The process of luekocyte accumulation at the periphery of blood vessels is called ______.

A

Margination(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

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18
Q

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

A

C, A, D, B, E(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35

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19
Q

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

A

C, B, D, A(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35

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20
Q

Process of coating microorganisms with proteins that facilitate phagocytosis.

A

Opsonization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.38

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21
Q

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

A

Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.39

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22
Q

The most important lysosomal enzyme involved in bacterial killing.

A

Elastase(TOPNOTCH)

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23
Q

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

A

Chemotaxis(TOPNOTCH)

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24
Q

The most important lysosomal enzyme involved in bacterial killing.

A

Elastase(TOPNOTCH)

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25
Q

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

A

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

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26
Q

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

A

Neutrophils(TOPNOTCH)

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27
Q

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

A

Monocytes(TOPNOTCH)

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28
Q

Substances responsible for leukocyte-induced tissue injury?

A

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

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29
Q

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

A

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

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30
Q

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.

A

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

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31
Q

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

A

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

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32
Q

NADPH deficiency or defect resulting in decreased oxidative burst.

A

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

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33
Q

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.

A

Serous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43

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34
Q

Fluid in a serous cavity is called ______.

A

Effusion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43

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35
Q

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

A

Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

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36
Q

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

A

Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

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37
Q

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

A

Suppurative (purulent) inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

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38
Q

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

A

Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

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39
Q

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.

A

Ulcer(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

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40
Q

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

A

Serotonin, Histamine(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

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41
Q

Complement fragments which are anaphylotoxins.

A

C3a, C5a (A for anaphylotoxin)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

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42
Q

Complement fragment which aids in opsonization.

A

C3b (b for binding)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

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43
Q

Membrane attack complex

A

C5b, C6-9(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

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44
Q

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

A

Membrane attack complex (C5b,C6-9)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

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45
Q

Enzyme blocked by NSAIDS.

A

Cyclooxygenase 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47

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46
Q

Enzyme inhibited by glucocorticoids

A

Phospholipase A2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47

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47
Q

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

A

Cytokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

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48
Q

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

A

Chemokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

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49
Q

Major cytokines in acute inflmmation.

A

TNF and IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

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50
Q

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

A

Nitric oxide(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.49

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51
Q

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

A

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

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52
Q

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

A

Chronic Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.53

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53
Q

Macrophages in the liver

A

Kupffer cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

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54
Q

Macrophages in the spleen and lymph nodes

A

Sinus histiocytes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

55
Q

Macrophages in the CNS

A

Microglial cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

56
Q

Macrophages in the lungs

A

Alveolar Macrophages(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

57
Q

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

A

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

58
Q

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

A

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

59
Q

Acid-fast bacilli in macrophages, noncaseating granulomas

A

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

60
Q

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

A

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

61
Q

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

A

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

62
Q

Noncaseating granulomas with abundant activated macrophages

A

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

63
Q

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

A

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

64
Q

Cells with pink, granular cytoplasm with indistinct boundaries.

A

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

65
Q

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

A

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

66
Q

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

A

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

67
Q

Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.

A

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

68
Q

It is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.

A

Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.31

69
Q

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

A

Acute inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

70
Q

Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and fibrosis.

A

Chronic inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

71
Q

Five cardinal signs of inflammation?

A

Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32

72
Q

Initial vascular response to injury?

A

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

73
Q

An ultrafiltrate of blood which contains little protein. Results from arteriolar vasodilation and increased blood flow.

A

Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

74
Q

Results from increased vascular permeability, leading to leakage of protein into tissues.

A

Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

75
Q

Fluid accumulation in extravascular space.

A

Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34

76
Q

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

A

Selectins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

77
Q

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

A

Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

78
Q

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

A

PECAM-1/CD 31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

79
Q

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

A

ICAM -1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

80
Q

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

A

Sialyl-Lewis X modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

81
Q

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

A

Sialyl-Lewis X-Modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

82
Q

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

A

Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

83
Q

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

A

CD-31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37

84
Q

The process of luekocyte accumulation at the periphery of blood vessels is called ______.

A

Margination(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36

85
Q

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

A

C, A, D, B, E(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35

86
Q

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

A

C, B, D, A(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35

87
Q

Process of coating microorganisms with proteins that facilitate phagocytosis.

A

Opsonization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.38

88
Q

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

A

Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.39

89
Q

The most important lysosomal enzyme involved in bacterial killing.

A

Elastase(TOPNOTCH)

90
Q

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

A

Chemotaxis(TOPNOTCH)

91
Q

The most important lysosomal enzyme involved in bacterial killing.

A

Elastase(TOPNOTCH)

92
Q

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

A

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

93
Q

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

A

Neutrophils(TOPNOTCH)

94
Q

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

A

Monocytes(TOPNOTCH)

95
Q

Substances responsible for leukocyte-induced tissue injury?

A

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

96
Q

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

A

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

97
Q

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.

A

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

98
Q

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

A

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

99
Q

NADPH deficiency or defect resulting in decreased oxidative burst.

A

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

100
Q

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.

A

Serous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43

101
Q

Fluid in a serous cavity is called ______.

A

Effusion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43

102
Q

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

A

Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

103
Q

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

A

Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

104
Q

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

A

Suppurative (purulent) inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

105
Q

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

A

Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

106
Q

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.

A

Ulcer(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44

107
Q

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

A

Serotonin, Histamine(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

108
Q

Complement fragments which are anaphylotoxins.

A

C3a, C5a (A for anaphylotoxin)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

109
Q

Complement fragment which aids in opsonization.

A

C3b (b for binding)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

110
Q

Membrane attack complex

A

C5b, C6-9(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

111
Q

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

A

Membrane attack complex (C5b,C6-9)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46

112
Q

Enzyme blocked by NSAIDS.

A

Cyclooxygenase 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47

113
Q

Enzyme inhibited by glucocorticoids

A

Phospholipase A2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47

114
Q

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

A

Cytokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

115
Q

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

A

Chemokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

116
Q

Major cytokines in acute inflmmation.

A

TNF and IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48

117
Q

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

A

Nitric oxide(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.49

118
Q

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

A

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

119
Q

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

A

Chronic Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.53

120
Q

Macrophages in the liver

A

Kupffer cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

121
Q

Macrophages in the spleen and lymph nodes

A

Sinus histiocytes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

122
Q

Macrophages in the CNS

A

Microglial cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

123
Q

Macrophages in the lungs

A

Alveolar Macrophages(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54

124
Q

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

A

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

125
Q

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

A

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

126
Q

Acid-fast bacilli in macrophages, noncaseating granulomas

A

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

127
Q

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

A

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

128
Q

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

A

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

129
Q

Noncaseating granulomas with abundant activated macrophages

A

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

130
Q

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

A

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

131
Q

Cells with pink, granular cytoplasm with indistinct boundaries.

A

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

132
Q

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

A

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

133
Q

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

A

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

134
Q

Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.

A

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

Pathology 101 (23 decks)

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