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II - Acute and Chronic Inflammation Flashcards

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2
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

p.31

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3
Q

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

A

Acute inflammation

p.32

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4
Q

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

A

Chronic inflammation

p.32

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5
Q

Five cardinal signs of inflammation?

A

Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)

p.32

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6
Q

Initial vascular response to injury?

A

Vasoconstriction.

p.33

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7
Q

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

A

Transudate

p.34

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8
Q

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

A

Exudate

p.34

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9
Q

Fluid accumulation in extravascular space.

A

Edema

p.34

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10
Q

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

A

Selectins

p.36

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11
Q

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

A

Integrins

p.37

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12
Q

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

A

PECAM-1/CD 31

p.37

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13
Q

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

A

ICAM -1

p.37

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14
Q

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

A

Sialyl-Lewis X modified glycoprotein

p.36

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15
Q

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

A

Sialyl-Lewis X-Modified glycoprotein

p.36

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16
Q

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

A

Integrins

p.37

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17
Q

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

A

CD-31

p.37

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18
Q

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

A

Margination

p.36

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19
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

p.35

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20
Q

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

A

C, B, D, A

p.35

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21
Q

Process of coating microorganisms with proteins that facilitate phagocytosis.

A

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

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22
Q

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

A

Phagolysosome

p.39

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23
Q

The most important lysosomal enzyme involved in bacterial killing.

A

Elastase

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24
Q

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

A

Chemotaxis

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25
Q

The most important lysosomal enzyme involved in bacterial killing.

A

Elastase

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26
A peptide Leukocyte granule constituent which kills microbes by creating holes in their membranes.
Defensins p.40
27
Predominant form of leukocyte during the first 6 - 24 hours of inflammation?
Neutrophils
28
Predominant form of leukocyte during 24-48 hrs after the onset of inflammation?
Monocytes
29
Substances responsible for leukocyte-induced tissue injury?
Lysosomal enzymes, reactive oxygen and nitrogen species.(TOPNOTCH)
30
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
31
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
32
Results from a defect in the protein involved in membrane docking and fusion.
Chediak-Higashi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
33
NADPH deficiency or defect resulting in decreased oxidative burst.
Chronic Granulomatous Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.42
34
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
35
Fluid in a serous cavity is called ______.
Effusion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43
36
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
37
Histologically, appears as an eosinophilic meshwork of threads or sometimes an amorphous coagulum.
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
38
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
39
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
40
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
41
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
42
Complement fragments which are anaphylotoxins.
C3a, C5a (A for anaphylotoxin)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
43
Complement fragment which aids in opsonization.
C3b (b for binding)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
44
Membrane attack complex
C5b, C6-9(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
45
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
46
Enzyme blocked by NSAIDS.
Cyclooxygenase 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
47
Enzyme inhibited by glucocorticoids
Phospholipase A2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
48
Polypeptide products of many cell types that function as mediators of inflammation and immune response.
Cytokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
49
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
50
Major cytokines in acute inflmmation.
TNF and IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
51
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
52
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
53
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
54
Macrophages in the liver
Kupffer cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
55
Macrophages in the spleen and lymph nodes
Sinus histiocytes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
56
Macrophages in the CNS
Microglial cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
57
Macrophages in the lungs
Alveolar Macrophages(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
58
A focus of epiheloid cells, rimmed by fibroblasts, lymphocytes, histiocytes, occasional giant cells.
Noncaseating tubercle, Tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
59
Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli
Caseating tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
60
Acid-fast bacilli in macrophages, noncaseating granulomas
Leprosy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
61
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
62
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
63
Noncaseating granulomas with abundant activated macrophages
Sarcoidosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
64
Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate
Chron disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
65
Cells with pink, granular cytoplasm with indistinct boundaries.
Epitheloid cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
66
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
67
Necrotic material which appears amorphous, structureless, granular debris, with complete loss of cellular details.
Caseous necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
68
Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.
TNF, IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.57

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