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Topnotch Pathology > II - Acute and Chronic Inflammation > Flashcards

II - Acute and Chronic Inflammation Flashcards

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 leukocyte 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 leukocytes B.Regulation of response C.Recognition of injurious agent D.Removal of agent E.Resolution.

A

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

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19
Q

Arrange the steps in leukocyte recruitment: A.Transmigration B.Rolling C.Margination D.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 6-24hours of inflammation.

A

Neutrophils(TOPNOTCH)

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27
Q

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

A

Monocytes(TOPNOTCH)

28
Q

Substances responsible for leukocyte-induced tissue injury.

A

Lysosomal enzymes, reactive oxygen and nitrogen species(TOPNOTCH)

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

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

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

32
Q

NADPH deficiency or defect resulting in decreased oxidative burst.

A

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

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

34
Q

Fluid in a serous cavity is called ______.

A

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

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

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

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

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

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

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

41
Q

Complement fragments which are anaphylotoxins.

A

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

42
Q

Complement fragment which aids in opsonization.

A

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

43
Q

Membrane attack complex.

A

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

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

45
Q

Enzyme blocked by NSAIDS.

A

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

46
Q

Enzyme inhibited by glucocorticoids.

A

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

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

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

49
Q

Major cytokines in acute inflammation.

A

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

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

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

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

53
Q

Macrophages in the liver.

A

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

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 epitheloid 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 cellular 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

40-50um 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

Topnotch Pathology (23 decks)

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