Topic 12 Immune Response & Inflammation part 2 Flashcards

(46 cards)

1
Q

Non-specific response to tissue damage:

A

Response to cut is the same as a burn/radiation/infection, etc.
(Pathogens, Abrasions, Chemical irritations, Distortion / cell disturbance, Extreme temps)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Inflammation 4 signs

A

Redness
Pain
Heat
Swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 stages of Inflammation

A
  1. Vasodilation - Increase permeability of blood vessels
  2. Emigration - Movement of phagocytes from blood to interstitial fluid
  3. Tissue repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Factors that cause vasodilation and increased

permeability:

A

Histamine, Kinins, prostaglandins, leukotrienes, Complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Histamine

A

Mast cells in the tissues release
Basophils and platelets stimulate the release of
histamine in the blood
Causes increased dilation and permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Kinins induce/act as what?

A

Polypeptides
Induce vasodilation and increase permeability
Act as chemotaxic agent phagocytes
Ex: bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Prostaglandins

A

Lipid
Released by damaged cells
Stimulate emigration of phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Leukotrienes

A

Basophils and mast cells produce

Increase permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Complement

A

Stimulate histamine release
Attract neutrophils
Promote Phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Within 1hour of start of inflammatory process

what appears?

A

Phagocytes appear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Fibrinogen converted to fibrin forms what?

A

Forms fibrin mesh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Inflammation Neutrophils stick to blood vessel wall with increased blood flow – and do what?

A

Squeeze through blood vessel wall to tissues-“emigration”

Depends on chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Neutrophils attempt to destroy via what?

A

phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Monocytes follow neutrophils and do what?

A

Transform into macrophages
More potent phagocytes than neutrophils.
Eventually macrophages die

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Redness of inflammation is caused by?

A

Large amount of blood in damaged area
Local temperatures increase
Metabolic reactions speed up
More heat released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Swelling of inflammation is caused by?

A

Increased permeability

More fluid in the area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pain caused by inflammation is caused by?

A

Symptom of inflammation–neuron injury or increased pressure (edema)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Fever in inflammation is caused by and do what?

A

Bacteria toxins increase body temperature
Trigger release of interleukin-1 (cause fever)
Helps to inhibit the growth of some microbes
Helps to speed up body reactions
Aids in repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Inflammation two major components

A

vascular reaction

cellular reaction

20
Q

Acute inflammation

A

rapid onset / short duration / emigration of

neutrophils

21
Q

chronic inflammation

A

long duration / lymphocyte involvement /

proliferation of blood vessels / tissue necrosis

22
Q

Components of acute inflammation (3)

A

*dilation of capillaries and surrounding blood
vessels–increase blood flow
*structural changes in capillaries-allow plasma proteins and leukocytes to enter interstitial space
*emigration of leukocytes from capillaries where they accumulate in focus of injury-activation to eliminate offending agent

23
Q

Stimulation for acute inflammation

A
Infections and microbial toxins
Trauma
Physical and chemical agents
Tissue necrosis
Foreign bodies
Immune reactions
24
Q

Vascular changes do what?

A

Maximize movement of plasma proteins and
appropriate circulating cells into the site of injury or infection
Vasodilation
Increased capillary permeability

25
Vasodilation what is involved first?
Arterioles involved first, followed by opening of new capillary beds
26
Increased Capillary Permeability results in what?
Osmotic & hemodynamic changes force fluid into interstitial space (results stasis) / neutrophils begin adhering to endothelium and moving into interstitial space / physical openings in endothelium allow more fluid / protein / cells to migrate
27
Margination
movement of leukocytes toward the wall of the capillary
28
Rolling:
leukocytes tumble slowly along endothelium, adhere transiently, then are finally attached–endothelium completely lined with white cells
29
Transmigration (diapedesis):
insert pseudopods into junctions between endothelial cells–move through the junction
30
Chemotaxis:
migrate thru interstitial fluid to source of problem
31
Extravasation:
movement of leukocytes from vessel lumen to interstitial space
32
Chemotaxis how does it work?
Locomotion along chemical gradient Most common exogenous agents are bacterial products Common endogenous agents
33
Common endogenous agents of chemotaxis (3)
- components of complement (C5a) - products of lipoxygenase pathway (leukotriene B4) - cytokines
34
Results of Leukocyte activation (5)
production of arachidonic acid metabolites degrannulation and secretion of lysosomal enzymes secretion of cytokines modulation of surface receptors phagocytosis
35
Leukocyte activation induced by what?
microbes / products necrotic cells / antigen-antibody complexes / cytokines
36
Chemical mediators plasma derived must what?
plasma-derived must be activated
37
Cell-derived chemical mediators usually stored where?
usually stored in intracellular granules
38
Once activated and the chemical mediators released have what life span?
most are short lived
39
Production of active mediators triggered by microbial products or host proteins (complement, etc.)
chemical mediators
40
SIRS
systemic inflammatory response - common systemic response to a wide variety of insults
41
2 or more of these must be present to diagnosis SIRS (4)
``` Body temp above 38*C or below 36*C HR >90 BPM Respiratory Rate >20/min Or PaCO2 12,000 cell/mm2 Or <10% immature neutrophils ```
42
Widely accepted that SIRS is induced in what % of patients undergoing bypass?
ALL Incidence and severity or type of response-variable Most have a few clinical symptoms Minority develop severe hemodynamic changes or organ failure after bypass. Risk factor–Length of CPB
43
Most common culprit of SIRAB is ?
``` = contact with foreign surface Other factor: Altered arterial blood flow patterns Sheer stress (blood pumps) Cardiotomy suction Tissue ischemia Reperfusion Hypothermia Relative anemia anticoagulants ```
44
What contact proteins are activated during SIRAB?
Coagulation factors XII and XI Prekallikrein High molecular weight kininogen
45
End result of SIRAB: formation of what? converts what?
Formation of bradykinin Conversion of plasminogen into plasmin Initiates fibrinolysis Triggers classical complement cascade
46
Chemokine mediated generalized whole boy inflammation response
Activates vascular endothelium | Further neutrophil-mediated injury