CH 2 - Acute Inflammation Flashcards Preview

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Flashcards in CH 2 - Acute Inflammation Deck (203)
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1

Thick, yellow fluid draining from a breast fissure is

a purulent exudate.

2

Purulent exudates and effusions are associated with

pathologic conditions such as pyogenic bacterial infections, in which the predominant cell type is the segmented neutrophil (polymorphonuclear leukocyte).

3

Mast cells are

granulated cells that contain receptors for IgE on their cell surface. They are additional cellular sources of vasoactive mediators, particularly in response to allergens.

4

B lymphocytes and plasma cells are

mediators of chronic inflammation and provide antigen-specific immunity to infectious diseases.

5

Complement proteins

act upon one another in a cascade, generating biologically active fragments (e.g., C5a, C3b) or complexes (e.g., C567).

6

Products of complement activation cause

local edema by increasing the permeability of blood vessels. They also promote chemotaxis of leukocytes and lyse cells (membrane attack complex) and act as opsonins by coating bacteria.

7

Kinins

are formed following tissue trauma and mediate pain transmission.

8

The most potent chemotactic factors for leukocytes at the site of injury are

(1) complement proteins (e.g., C5a); (2) bacterial and mitochondrial products, particularly low molecular weight N-formylated peptides; (3) products of arachidonic acid metabolism (especially LTB4); and (4) chemokines (e.g., interleukin-1 and interferon g

9

Plasmin is

a fibrinolytic enzyme generated by activated Hageman factor (clotting factor XII).

10

Histamine is

one of the primary mediators of increased vascular permeability.

11

During acute inflammation, neutrophils (PMNs) adhere to

the vascular endothelium.

12

What happens to PMNs after they adhere to the vascular endothelium?

They flatten and migrate from the vasculature, through the endothelial cell layer, and into the surrounding tissue.

13

About 24 hours after the onset of infarction, PMNs are observed to do what?

infiltrate necrotic tissue at the periphery of the infarct.

14

What is the of the PMNs in acute inflammation?

function is to clear debris and begin the process of wound healing.

15

Lymphocytes and plasma cells are

mediators of chronic inflammation and provide antigen specific immunity to infectious diseases.

16

Fibroblasts and macrophages regulate what?

scar tissue formation at the site of infarction.

17

Forces that regulate the balance of vascular and tissue fluids include

(1) hydrostatic pressure, (2) oncotic pressure, (3) osmotic pressure, and (4) lymph flow.

18

Inflammatory edema

1) an increase in the permeability of the endothelial cell barrier results in local edema. 2) Vasodilation of arterioles exacerbates fluid leakage 3) vasoconstriction of postcapillary venules increases the hydrostatic pressure in the capillary bed potenti

19

Vasodilation of venules

decreases capillary hydrostatic pressure and inhibits the movement of fluid into the extravascular spaces.

20

Acute inflammations’ effect on plasma oncotic pressure

it is not associated with changes in plasma oncotic pressure

21

Hageman factor

(clotting factor XII) provides a key source of vasoactive mediators.

22

Activation of Hageman

plasma protein at the site of tissue injury stimulates (1) conversion of plasminogen to plasmin, which induces fibrinolysis; (2) conversion of prekallikrein to kallikrein, which generates vasoactive peptides of low molecular weight referred to as kinins;

23

Septicemia (bacteremia) denotes

the clinical condition in which bacteria are found in the circulation. It can be suspected clinically, but the final diagnosis is made by culturing the organisms from the blood.

24

In patients with endotoxic shock

lipopolysaccharide released from Gram-negative bacteria stimulates monocytes/macrophages to secrete large quantities of TNF alpha.

25

LPS causes

direct cytotoxic damage to capillary endothelial cells.

26

Suppurative inflammation

describes a condition in which a purulent exudates is accompanied by significant liquefactive necrosis. It is the equivalent of pus.

27

Chronic inflammation

is nonsuppurative.

28

Fibrinoid necrosis is observed in areas of

necrotizing vasculitis.

29

Granulomatous inflammation is seen in patients with

tuberculosis.

30

Reactive gliosis is

a normal response of the brain to injury and infection but is not visible on the cut surface of the brain at autopsy.