Week 6 Patho Plfsom

Front 1

Definition of inflammation

Back 1

Inflammation is fundamentally a protective response, designed to rid the organism of both the initial cause of cell injury (e.g., microbes, toxins) and the consequences of such injury (e.g., necrotic cells and tissues).

Front 2

What are the 5 characteristics of inflammation

Back 2

rubor, calor, tumor, dolor, functio lasea

Front 3

What are the stimuli for acute inflammation?

Back 3

infection, trauma, penetrating wounds, autoimmunity, allergy

Front 4

What are the vascular events in inflammation?

Front 5

What leads to incrased vascular permeability and edema?

Front 6

What are the mediators of vascular changes during acute inflammation?

Back 6

histamine, NO, arachidonic acid metabolites

Front 7

Where is histamine preformed?

Back 7

mast cells in tissue. Basophils in blood

Front 8

histamine causes________.

Back 8

dialation of arterioles and increased permiability of venules

Front 9

What triggers mast cell degranulation?

Back 9

injury, anaphylotoxins, chemokines, substance P

Front 10

What are the components of the Lewis Triple Response?

Back 10

Flush: capillary dilation. Flare: arteriolar dilation. Weal: exudation, edema (increased capillary permeability) All within a couple minutes

Front 11

What state is NO?

Back 11

a soluble gas

Front 12

Endothelial NO is referred to as

Back 12

eNOS

Front 13

neuronal NO is referred to as nNOS

Front 14

phagocyte NO is referred to as iNOS

Front 15

What is the synthesized form of NO?

Back 15

L-arginine by nitric oxide synthase

Front 16

NO

Back 16

is a potent vasodilator and antimicrobial

Front 17

What is sodium notroprusside?

Back 17

used for rapid pressure reduction in arterial hypertension. Generates NO.

Front 18

What are metabolites of arachidonic acid called?

Back 18

eicosanoids

Front 19

Where is arachadonic acid located?

Back 19

lipid membranes

Front 20

What cells can produce eicosanoids?

Back 20

all except erythrocytes

Front 21

Are eicosanoids autocoids?

Back 21

Yes

Front 22

What is an autocoid?

Back 22

short-range hormone. Short range and short half life

Front 23

Arachidonic acid is derived from conversion of ________

Back 23

linolenic acid

Front 24

E-selectin

Back 24

on endothelium

Front 25

P-selectin

Back 25

on endothelium and platelets, is preformed and stored in Weible Palade bodies

Front 26

L-selectin

Back 26

leukocytes

Front 27

What are the ligands for E-and P-selectins

Back 27

sialylated glycoproteins

Front 28

What are the ligands for L-selectin?

Back 28

Glycan-bearing molecules such as GlyCAM-1, CD34, MadCam-1

Front 29

VLA-4

Back 29

leukocyte integrin, binds to VCAM-1

Front 30

LFA1 and MAC1

Back 30

leukocyte integrins that bind ICAM

Front 31

What are the immunoglobulin family (endothelial surface) adhesion molecules?

Back 31

ICAM1, VCAM-1,

Front 32

What are the mucin-like glycoproteins

Back 32

heparan sulfate (endothelium), Ligands for CD44 on leukocytes. All bind chemokines

Front 33

What is chemotaxis in leukocyte attraction?

Back 33

When leukocytes follow towards the site of injury in the tissue along a chemical gradient of chemo-attractants

Front 34

What are exogenous chemoattractants?

Back 34

bacterial products (N formyl-methionyl peptides)

Front 35

What are endogenous chemoattractants?

Back 35

anaphylatoxins (C5a), leukotrienes (LTB4), chemokines (IL-8)

Front 36

What is Wiskott-Aldrich Syndrome?

Back 36

a defect in the morphological response and trafficking defect of antigen presenting cells. Thrombocytopenia, eczema and increased susceptibility to infection

Front 37

What are the steps of mission phagocytosis?

Back 37

recognition, attachment, engulfment, fusion

Front 38

What is Chediak-Higashi syndrome?

Back 38

defect of the formation and function of neutrophil granules

Front 39

Neutrophil orientation and CHS

Back 39

Neutrophils of CHS patients fail to orient themselves during chemotaxis resulting in delayed diapedesis

Front 40

chronic granulomatous disease (CDG)

Back 40

a defect of NADPH oxidase system and therefore inability to undergo oxidative burst and production of hydrogen peroxide

Front 41

Genetics of CDG

Back 41

heterogenous disorder caused by defects of any of the four subints of NADPH oxidase. 70% are due to X-linked defect of gp91 phox. 2nd most due to autosomal recessive defect of p47 phox

Front 42

Exudation

Back 42

vascular changes and fluid leakage during acute inflammation lead to edema

Front 43

Transudate

Back 43

result of hydrostatic or osmotic imbalance. Unltrafiltrate of plasma, low protein content, sg <1.015

Front 44

Exudate

Back 44

result of inflammation, vascular permeability increases. High protein content. Sg > 1.020

Front 45

What is RBC concentration and Leukocyte margination

Back 45

after much of the fluid of blood has left due to increased vascular permeability, the leukocytes tend to collect on the arterial walls while RBCs concentrate in the center of the arteries or venules

Front 46

What does antihistamine block?

Back 46

The Lewis Triple Response

Front 47

Without B2, what will happen?

Back 47

Tethering and rolling will likely still occur, but adhesion probably won't occur

Front 48

Metallic taste in mouth is characteristic of_______

Back 48

GERD

Front 49

What is rolling?

Back 49

movement of WBC's along the endothelial surface

Front 50

What is adhesion?

Back 50

Adherence of WBC's to the endothelial cell surface

Front 51

What is transmigration/diapedesis

Back 51

movement of WBC's across the endothelium

Front 52

serous

Back 52

thin and watery

Front 53

fibrinous

Back 53

fibrous exudate

Front 54

suppurative/purulent

Back 54

pus exudate

Front 55

What are the vascular events in inflammation?

Back 55

Front 56

What leads to incrased vascular permeability and edema?

Back 56

Front 57

Back 57

Front 58

Mast

Back 58

Mast

Front 59

Neutrophil

Back 59

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