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Perf Tech II (exam 3) > Topic 12 Immune Response & Inflammation part 2 > Flashcards

Topic 12 Immune Response & Inflammation part 2 Flashcards

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)

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2
Q

Inflammation 4 signs

A

Redness
Pain
Heat
Swelling

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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
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4
Q

Factors that cause vasodilation and increased

permeability:

A

Histamine, Kinins, prostaglandins, leukotrienes, Complement

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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

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6
Q

Kinins induce/act as what?

A

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

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7
Q

Prostaglandins

A

Lipid
Released by damaged cells
Stimulate emigration of phagocytes

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8
Q

Leukotrienes

A

Basophils and mast cells produce

Increase permeability

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9
Q

Complement

A

Stimulate histamine release
Attract neutrophils
Promote Phagocytosis

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10
Q

Within 1hour of start of inflammatory process

what appears?

A

Phagocytes appear

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11
Q

Fibrinogen converted to fibrin forms what?

A

Forms fibrin mesh

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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

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13
Q

Neutrophils attempt to destroy via what?

A

phagocytosis

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14
Q

Monocytes follow neutrophils and do what?

A

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

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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

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16
Q

Swelling of inflammation is caused by?

A

Increased permeability

More fluid in the area

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17
Q

Pain caused by inflammation is caused by?

A

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

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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

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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
Q

Vasodilation what is involved first?

A

Arterioles involved first, followed by opening of new capillary beds

26
Q

Increased Capillary Permeability results in what?

A

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
Q

Margination

A

movement of leukocytes toward the wall of the capillary

28
Q

Rolling:

A

leukocytes tumble slowly along endothelium, adhere transiently, then are finally attached–endothelium completely lined with white cells

29
Q

Transmigration (diapedesis):

A

insert pseudopods into junctions between endothelial cells–move through the junction

30
Q

Chemotaxis:

A

migrate thru interstitial fluid to source of problem

31
Q

Extravasation:

A

movement of leukocytes from vessel lumen to interstitial space

32
Q

Chemotaxis how does it work?

A

Locomotion along chemical gradient
Most common exogenous agents are bacterial products
Common endogenous agents

33
Q

Common endogenous agents of chemotaxis (3)

A
  • components of complement (C5a)
  • products of lipoxygenase pathway (leukotriene B4)
  • cytokines
34
Q

Results of Leukocyte activation (5)

A

production of arachidonic acid metabolites
degrannulation and secretion of lysosomal enzymes
secretion of cytokines
modulation of surface receptors
phagocytosis

35
Q

Leukocyte activation induced by what?

A

microbes / products necrotic cells / antigen-antibody complexes / cytokines

36
Q

Chemical mediators plasma derived must what?

A

plasma-derived must be activated

37
Q

Cell-derived chemical mediators usually stored where?

A

usually stored in intracellular granules

38
Q

Once activated and the chemical mediators released have what life span?

A

most are short lived

39
Q

Production of active mediators triggered by microbial products or host proteins (complement, etc.)

A

chemical mediators

40
Q

SIRS

A

systemic inflammatory response - common systemic response to a wide variety of insults

41
Q

2 or more of these must be present to diagnosis SIRS (4)

A 
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
Q

Widely accepted that SIRS is induced in what % of patients undergoing bypass?

A

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
Q

Most common culprit of SIRAB is ?

A 
= 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
Q

What contact proteins are activated during SIRAB?

A

Coagulation factors XII and XI
Prekallikrein
High molecular weight kininogen

45
Q

End result of SIRAB: formation of what? converts what?

A

Formation of bradykinin
Conversion of plasminogen into plasmin
Initiates fibrinolysis
Triggers classical complement cascade

46
Q

Chemokine mediated generalized whole boy inflammation response

A

Activates vascular endothelium

Further neutrophil-mediated injury

Perf Tech II (exam 3) (3 decks)

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