Immunology L6 Acute Inflammation

Front 1

What is the hallmark of acute inflammation?

Back 1

influx of PMNs (neutrophils) into the tissues

Front 2

What are the 5 cardinal signs of Acute Inflammation?

Back 2

Heat
Redness
Edema
Pain
Loss of Function

Front 3

What do clotting factors and badykinin do?

Back 3

these potentiate the inflammatory response, they come from tissue damage

Front 4

What do C5a and C3a do in acute inflammation?

Back 4

these are anaphylatoxins, used to promote mast cell degranulation.

causes histamine release from mast cells

Front 5

What does bradykinin result in?

Back 5

this results in an increase in vascular permeablility

vasodilation, pain, and SM contraction

Front 6

What dose complement activation result in?

Back 6

increase in vascular permeability

chemotaxis (C3a, C5a)

opsonization (C3b)

Cell lysis (C5b, C6, C7,C8, C9's)

Front 7

What does Thromboxane do?

Back 7

this causes vasoconstriction

platelet aggregation

Front 8

What do prostaglandins do?

Back 8

increases vascular permeability

vascular diliation

neutrophil chemotaxis

pain/fever

Front 9

what do Leukotrienes do?

Back 9

increases vascular permeability

bronchoconstriction

Front 10

What are the 5 effects of the Three major cytokines IL-1, IL-6 TNF's

IMPORTANT QUESTION

Back 10

These all result in:

fever

hypoferremia

fibrinogen and complement synthesis (acute phase proteins)

Lower albumin synthesis

increase in certain white cell lines

Front 11

What does IL-12 do?

Back 11

this comes from distressed macrophages that cant handle their stuff.

this activates NK cells to come kill them

Front 12

What does IL-8 do?

Back 12

this is a chemoattractant for WBC's

Front 13

What are the 3 proinflammatory cytokines?

Back 13

IL-1, IL-6, TNF- (anything?)

Front 14

What do the proinflammatory cytokines do to the liver? what are the 3 proinflammatories?

Back 14

these promote the secretion of acute phase proteins. including: Haptoglobin, C-reactive protein, serum amyloid A, and fibrinogen

(the 3 proinflammatory ones of IL-1, IL-6, and TNF)

Front 15

What two tests are used to measure inflammation?

Back 15

the erythrocyte sedimentation rate. A FASTER ESR rate indicates inflammation response. (due to fibrinogen)

Also, serum CRP levels

(All of these are created by the liver, under the promotion of IL-1, IL-6, and TNF)

Front 16

What are the functions of CRP?

Back 16

opsonin

activates compliment

simulates release of cytokines from phagoctyes.

Front 17

What are the uses of CRP clinically?

Back 17

this is used to assess and monitor the presence, severity, and course of inflammatory responses

Front 18

What is the purpose of inflammation in general? why does vasodilation occur?

Back 18

the purpose is to get proteins and cells from the blood into the interstitial spaces to fight the infection or injury

Front 19

What molecules mediate Extravasation?

Back 19

This is done by CAM's. like selectin and integrin

Front 20

What is rolling adhesion? what molecules are involved?

Back 20

this is a weak interaction between WBC's and endothelial cells via Selectins binding to Mucins.

Front 21

What helps increase the affinity of integrins on WBC's for integrin ligands on endothelial cells?

Back 21

this is done by chemokines activating the high-affinity integrins of WBC's. this promotes binding of WBC's to vascular walls.

Front 22

What is upregulated in endothelial cells by TNF and IL-1?

Back 22

this upregulates the expression of E- and P- selectins, (which are used to slow down WBC's in rolling adhesion)

Front 23

What is LAD-1?

Back 23

this is a failure of WBC's to express an integrin (so prevents stable adhesion, or activation by chemokines)

Front 24

What is LAD-2?

Back 24

this is a failure of the endothelial cells to express E and P- selectins. this prevents the slow rolling binding phase of WBC adhesion.

Front 25

When PTs have a leukocyte adhesion deficiency, what are some of the clinical signs?

Back 25

high WBC counts and recurrent apustular bacterial infections from an early age.

diagnosed shortly after birth with delayed umbilical cord separation

Front 26

What are the 3 clinical findings in CSF during menningitus?

Back 26

High neutrophils, High levels of protein (acute phase proteins), and low glucose (from all the bacteria and stuff using it up)

Front 27

What is an example of an Endotoxin?

Back 27

LPS

Front 28

What does endotoxin do upon its release? what is the pathway?

Back 28

this will bind to LBP (polysaccharide binding protein)

this complex then binds CD-14

CD-14+LPS/LBP then activates the secretion of various proinflammatory mediatiors (IL-1, IL-6, TNF, leukotrienes, chemokines, Platelet activating factor, and NO)

Front 29

What happens to inflammation in the CNS?

Back 29

this can cause the bacteria to extravate into the CSF...where inflammation occurs, and bacteria flourishes.

produces symptoms of stiff neck, fever, and severe headache

(occurs in the subarachnoid space)

Front 30

What happens to inflammation in the periphery?

Back 30

this results in endotoxin being released into the blood stream.

This causes the same release of cytokines, (IL-1, IL-6, TNF, PAF , IL-8) but also activates the clotting pathway.

can result in Disseminated Intravascular coagulation (DIC) and thrombocytopenia (as they are all in use).

Presents as Petechiae