II - Acute and Chronic Inflammation Flashcards

master everything (67 cards)

1
Q

pathology

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

pathology

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

pathology

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

pathology

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

pathology

Initial vascular response to injury?

A

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

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6
Q

pathology

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

pathology

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

pathology

Fluid accumulation in extravascular space.

A

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

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9
Q

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

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

pathology

The most important lysosomal enzyme involved in bacterial killing.

A

Elastase(TOPNOTCH)

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23
Q

pathology

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

A

Chemotaxis(TOPNOTCH)

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24
Q

pathology

The most important lysosomal enzyme involved in bacterial killing.

A

Elastase(TOPNOTCH)

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25
# pathology A peptide Leukocyte granule constituent which kills microbes by creating holes in their membranes.
Defensins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.40
26
# pathology Predominant form of leukocyte during the first 6 - 24 hours of inflammation?
Neutrophils(TOPNOTCH)
27
# pathology Predominant form of leukocyte during 24-48 hrs after the onset of inflammation?
Monocytes(TOPNOTCH)
28
# pathology Substances responsible for leukocyte-induced tissue injury?
Lysosomal enzymes, reactive oxygen and nitrogen species.(TOPNOTCH)
29
# pathology 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
30
# pathology 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
31
# pathology Results from a defect in the protein involved in membrane docking and fusion.
Chediak-Higashi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
32
# pathology NADPH deficiency or defect resulting in decreased oxidative burst.
Chronic Granulomatous Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.42
33
# pathology 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, 8th ed. p.43
34
# pathology Fluid in a serous cavity is called ______.
Effusion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43
35
# pathology This type of inflmmation results from greater vascular permeability that allows larger molecules to pass the endothelial barrier.
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
36
# pathology Histologically, appears as an eosinophilic meshwork of threads or sometimes an amorphous coagulum.
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
37
# pathology 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, 8th ed. p.44
38
# pathology 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, 8th ed. p.44
39
# pathology 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, 8th ed. p.44
40
# pathology Vasoactive amines that are preformed molecules in secretory granules of mast cells, basophils and platelets.
Serotonin, Histamine(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
41
# pathology Complement fragments which are anaphylotoxins.
C3a, C5a (A for anaphylotoxin)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
42
# pathology Complement fragment which aids in opsonization.
C3b (b for binding)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
43
# pathology Membrane attack complex
C5b, C6-9(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
44
# pathology 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, 8th ed. p.46
45
# pathology Enzyme blocked by NSAIDS.
Cyclooxygenase 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
46
# pathology Enzyme inhibited by glucocorticoids
Phospholipase A2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
47
# pathology Polypeptide products of many cell types that function as mediators of inflammation and immune response.
Cytokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
48
# pathology They are a family of small structurally related proteins that act primarily as chemoattractants for different subsets of leukocytes.
Chemokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
49
# pathology Major cytokines in acute inflmmation.
TNF and IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
50
# pathology A short-lived, soluble, free-radical gas produced by endothelial cells causing smooth muscle relaxation and vasodilation.
Nitric oxide(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.49
51
# pathology 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
52
# pathology Inflammation characterized by infiltration with mononuclear cells, tissue destruction and repair involving angiogenesis and fibrosis.
Chronic Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.53
53
# pathology Macrophages in the liver
Kupffer cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
54
# pathology Macrophages in the spleen and lymph nodes
Sinus histiocytes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
55
# pathology Macrophages in the CNS
Microglial cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
56
# pathology Macrophages in the lungs
Alveolar Macrophages(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
57
# pathology A focus of epiheloid cells, rimmed by fibroblasts, lymphocytes, histiocytes, occasional giant cells.
Noncaseating tubercle, Tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
58
# pathology Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli
Caseating tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
59
# pathology Acid-fast bacilli in macrophages, noncaseating granulomas
Leprosy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
60
# pathology Microscopic to visible lesion, enclosing wall of histiocytes, plasma cell infiltrates, necrotic central cells without loss of cellulr outline
Gumma (Syphilis)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
61
# pathology 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
62
# pathology Noncaseating granulomas with abundant activated macrophages
Sarcoidosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
63
# pathology Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate
Chron disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
64
# pathology Cells with pink, granular cytoplasm with indistinct boundaries.
Epitheloid cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
65
# pathology 40-50 um in size, consisting of a large mass of cytoplasm and many nuclei.
Giant cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
66
# pathology Necrotic material which appears amorphous, structureless, granular debris, with complete loss of cellular details.
Caseous necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
67
# pathology Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.
TNF, IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.57