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Perf Tech II > Test 3 Immunity Part 2 > Flashcards

Test 3 Immunity Part 2 Flashcards

0
Q

Inflammation response to tissue damage

A

Pathogens, abrasions, chemical irritations, distortion/cell disturbance, extreme temps

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1
Q

Nonspecific inflammation

A

Response to is same as burn, radiation, infection, etc

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2
Q

4 signs of inflammation

A

Redness, pain, heat, swelling

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3
Q

Goal of inflammation

A

Dispose of microbes, toxins, foreign materials

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4
Q

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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5
Q

Factors that cause vasodilation and increased permeability

A

Histamine, kinins, prostaglandins, leukotrienes, complement

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6
Q

Histamine release

A

Released by mast cells in the tissues
Release in blood is stimulated by basophils and platelets
Causes increased dilation and permeability

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7
Q

Kinins

A

Polypeptides
Increase permeability and vasodilation
Act as chemotactic phagocytes
Ex. Bradykinin a

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8
Q

Prostaglandins

A

Lipid released by damaged cells

Stimulated emigration of phagocytes

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9
Q

Leukotrienes

A

Produced by basophils and mast cells

Increase permeability

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10
Q

Complement

A

Stimulate histamine release
Attract neutrophils
Promote phagocytosis

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11
Q

Clotting factors move into tissues causing

A

Initiation of clotting cascade

Fibrinogen converted to fibrin- forms fibrin mesh–localizes and traps invading organisms–blocks spread of organisms

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12
Q

When do phagocytes appear?

A

Within one hour of start of inflammatory process

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13
Q

What causes neutrophils to stick to blood vessel walls

A

Increased blood flow

  • squeeze through blood Vessel walls to tissues (emigration)
  • depends on chemotaxis
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14
Q

Neutrophils attempt to destroy via…

A

Phagocytosis

  • monocytes follow neutrophils (transform into macrophages)
  • monocytes are more potent phagocytes than neutrophils
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15
Q

What happens when macrophages die?

A

Leave collection of dead cells and fluid (pus)

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16
Q

4 signs of inflammations due to vasodilation and increased permeability

A
  1. Heat
  2. Redness (large amount of blood in infected area, local temp increase, increased speed of metabolic process, more heat released)
  3. Swelling (increased permeability, more fluid in area)
  4. Pain (neuron injury or increased pressure (edema))
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17
Q

Fever aids in…

A

Helps inhibit growth of microbes
Helps speed up body reactions
Aids in repair

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18
Q

Fever cause

A

Body toxins increase body temp

Trigger release of interleukin 1 (causes fever)

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19
Q

Two major components of inflammation

A

Vascular reaction and cellular reaction

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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

Inflammation components

A
  1. Circulating white cells (neutrophils, monocytes, eosinophils, lymphocytes, basophils, platelets)
  2. Connective tissue cells (mast cells, fibroblasts, macrophages, lymphocytes)
  3. Extracellular matrix: structural fibrous proteins, adhesive glycoproteins, proteoglycans, basement membrane of capillary
23
Q

Chemical factors that mediate inflammation are derived from…

A

Plasma proteins/cells

Produced in response to or activated by inflammation

24
Mediators at site of injury in acute inflammation
Leukocytes | Plasma proteins
25
Components of acute inflammation
1. Dilation ofcapillaries and surrounding blood vessels (increases flow) 2. Structural changes in capillaries-allows plasma and leukocytes to enter interstitial space 3. Emigration of leukocytes from capillaries where they accumulate in focus of injury --activation to eliminate offending agent
26
Stimuli for acute inflammation
1. Infections and microbial toxins (bacterial, girl, parasitic) 2. Trauma 3. Physical and chemical agents (thermal injury, irradiation, environmental chemicals) 4. Tissue necrosis 5. Foreign bodies (splinters, dirt, sutures) 6. Immune reactions
27
Purpose of vascular changes
Maximize movement of plasma proteins and appropriate circulating cells into site of injury or infection Happens by vasodilation and increased capillary permeability
28
Mechanism of vasodilation
- Early manifestation - arterioles involved first, followed by openings of new capillary beds - induced by histamine and NO
29
Mechanism of increased capillary permeability
- movement of protein rich fluid into intravascular tissue and concentration of RBCs (viscosity change) - physical changes in endothelial structure of capillaries
30
Result of increased capillary permeability
Osmotic and 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, and cells to migrate
31
Result of vasodilation
Increased blood flow which leads to increased redness and warmth of tissue
32
Extravasation
Movement of leukocytes from vessel lumen to interstitial space
33
Margination
Movement of leukocytes toward wall of capillary
34
Rolling
Leukocytes tumble along endothelium, adhere transiently, then attached. Endothelium completely lined with white cells
35
Transmigration (diapedesis)
Insert pseudopods into junctions between endothelial cells- move through junction
36
Chemotaxis
- Locomotion along chemical gradient | - most common exogenous agents are bacterial products
37
Order of cellular events
1. Extravasation 2. Margination 3. Rolling 4. Transmigration (diapedesis) 5. Chemotaxis
38
Endogenous agents for chemotaxis
Components of complement (C5a) Products of lipoxygenase pathway (leukotriene B4) Cytokines
39
Leukocyte activation induced by...
Microbes Necrotic cells Antigen/antibody complexes Cytokines
40
Results of leukocyte activation
Production of arachnidonic acid metabolites Degranulation and secretion of lysosomal enzymes Secretion of cytokines Modulation of surface receptors Phagocytosis
41
Origin of clinical mediators
Plasma or cells -plasma derived must be activated -cell derived stored in intra cellular granules Production triggered by microbial products or host proteins (complement)
42
Chemical mediators actions
Bind to specific receptors on target cells One mediator may stimulate release of other mediator Can act on more than one target Short lived Potential to cause GREAT HARM
43
Systemic inflammatory response to CPB: SIRS
common systemic response to wide variety of insults Induced in all patients on bypass -incidence and severity is variable -degree and type of response is unpredictable -risk factor is length of CPB
44
Indications of SIRS
``` Body temp below 36 or above 38 HR>90bpm Respiratory rate >20/min PaCO2 12000 cells/mm2 -or <10% immature neutrophils ``` Need two of the above to diagnose SIRS
45
SIRAB
Systemic inflammatory response after bypass CPB produces whole body inflammation Injuries: pulmonary, renal, gut, CNS, myocardial dysfunction, coagulopathy, hemolysis, fever, increased susceptibility to infection, leukocytosis
46
Most common culprits for SIRAB
Contact with foreign surface area Other factors: altered arterial blood flow patterns, sheer stress, cardiotomy suction, tissue ischemia, reperfusion, hypothermia, relative anemia, anticoagulants
47
Contact activation
Blood passes through ECC | Activation of contact proteins (coagulation factors XI and XII, prekallikriens, high molecular weigh kininogen)
48
End result of contact activation
Formation of bradykinin Conversion of plasminogen into plasmin Initiate fibrinolysis Triggers classical complement cascade
49
Immune system and bypass
Postop: patients more acceptable to infection Serum immunoglobulins and complement decreased Decreased chemotaxis ability of granuloyctes Decreased NK cells Decreased CD3+ and CD4+ cells Increased CD8+ cells Leukocyte numbers decreased for up to a week post bypass

Perf Tech II (4 decks)

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