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Perf tech II > test 9 part 2 > Flashcards

test 9 part 2 Flashcards

1
Q

Non-specific inflammation

A
  • Response to cut is the same as a burn/ radiation/ infection, etc.
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2
Q

4 signs of inflammation

A
  • Redness
    -š Pain
    š- Heat
    š- Swelling
  • Goal to dispose of microbes/ toxins / foreign materials
  • prevents spread
  • prepare for repair
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3
Q

Stages of inflammation

A
  1. Vasodilation
    - Increase permeability of blood vessels (fluid moves out = edema)
  2. Emigration
    - Movement of phagocytes from blood to interstitial fluid (neutrophiles and macrophages that gobble them up)
  3. Tissue repair
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4
Q

components of inflammation and duration

A
  • vascular reaction
  • š cellular reaction
  • acute
    - rapid onset / short duration / emigration of neutrophils
  • chronic
    - long duration / lymphocyte involvement / proliferation of blood vessels / tissue necrosis
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5
Q

Major players in inflammation

A
  • circulating white cells (neutrophils / monocytes / eosinophils)
  • connective tissue cells (mast cells)
  • extracellular matrix (structural fibrous protein)
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6
Q

Inflammation mediated by variety of

A
  • chemical mediators

- derived from plasma proteins and/or cells

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7
Q

Chemical Mediators

A
  • Originate from plasma or cells
  • Usually bind to specific receptors on target cells
  • One mediator may stimulate the release of other mediators
  • Mediators can act on more than one target
  • š Once activated and released, most are short lived
  • š Most have the potential to cause GREAT HARM
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8
Q

Chemical mediators that cause vasodilation

A
  • Nitric Oxide

- Histamine (from mast cells, basophils, and platelets)

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9
Q

Chemical mediators that increase vascular permeability

A
  • C3a and C5a
  • Bradykinin
  • Leukotrienes
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10
Q

Chemical mediators that cause chemotaxis, leukocyte recruitment and activation

A
  • C5a
  • Leukotriene B4
  • Chemokines
  • Interleuken-1
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11
Q

Chemical mediators that cause fever

A
  • Interleuken-1
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12
Q

purpose of Vascular change

A
  • Maximize movement of plasma proteins and appropriate circulating cells into the site of injury or infection
    - vasodilation and increase capillary permeability
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13
Q

Vasodilation

A
  • Early manifestation
  • š Arterioles involved first, followed by opening of new capillary beds
  • š Induced by variety of mediators (histamine / nitric oxide)
  • Allows more blood into an area
  • š Helps remove microbial toxins and dead cells
  • Result: Increased blood flow which increases REDNESS and WARMTH of tissue
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14
Q

increased capillary permeability

A
  • Allows antibodies and clotting factors to leave the blood
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15
Q

Vasodilation and increased

permeability: Histamine

A
  • š Mast cells in the tissues release
  • š Basophils and platelets stimulate the release of histamine in the blood
  • š Causes increased dilation and permeability
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16
Q

Vasodilation and increased

permeability: Kinins

A
  • š Polypeptides
  • š Induce vasodilation and increase permeability
  • š Act as chemotaxic agent for phagocytes
  • š Ex: bradykinin
17
Q

Vasodilation and increased

permeability: Prostaglandins

A
  • Lipid
  • š Released by damaged cells
  • š Stimulate emigration of phagocytes
18
Q

Vasodilation and increased

permeability: Leukotrienes

A
  • š Basophils and mast cells produce

- š Increase permeability

19
Q

Vasodilation and increased

permeability: Complement

A
  • š Stimulate histamine release
  • š Attract neutrophils
  • š Promote Phagocytosis
20
Q

Clotting and inflammation

A
  • š Clotting factors move into tissues
  • š Initiate the clotting cascade
  • š Fibrinogen converted to fibrin
    - š Localizes and traps invading organisms
    - š Blocks spread of organism
  • Within 1hour of start of inflammatory process
21
Q

Neutrophils and Inflammation

A
  • Neutrophils (first to respond) stick to blood vessel wall with increased blood flow
    - š Squeeze through blood vessel wall to tissues (emigration)
  • š Neutrophils attempt to destroy via phagocytosis
  • š Monocytes follow neutrophils
  • š Transform into macrophages
  • Macrophages die (pus)
22
Q

Extravasation

A
  • movement of leukocytes from vessel lumen to interstitial space
23
Q

Cellular Events

A
  • š Margination: movement of leukocytes toward the wall of the capillary
  • š Rolling: leukocytes tumble slowly along endothelium, adhere transiently, then are finally attached – endothelium completely lined with white cells
  • š Transmigration (diapedesis): insert pseudopods into junctions between endothelial cells – move through the junction
  • š Chemotaxis: migrate thru interstitial fluid to source of problem
24
Q

4 characteristics of inflammation

A
  1. Heat
  2. Redness
    š - Large amount of blood in damaged area
    š -š Local temperatures increase
    š -š Metabolic reactions speed up
    š -š More heat released
  3. Swelling
    š -š Increased permeability
    š -š More fluid in the area
  4. Pain
    š -š Symptom of inflammation – neuron injury or increased pressure (edema)
25
Q

Fever

A
  • š Bacteria toxins increase body temperature
  • š Trigger release of interleukin-1 (cause fever)
  • š Helps to inhibit the growth of some microbes
  • š Helps to speed up body reactions
  • š Aids in repair
26
Q

2 or more present for diagnosis of Systemic Inflammatory Response (SIRS):

A
  • SIRS – common systemic response to a wide variety of insults
  • š Body temp above 38C or below 36C
  • š HR >90 BPM
  • š Respiratory Rate >20/min
    - š Or PaCO2 <32mmHg
  • š Leukocyte count >12,000 cell/mm2
27
Q

Systemic Inflammatory Response After Bypass (SIRAB) injuries

A 
š- CPB produces “whole body” inflammatory response
-š Wide spectrum of injuries
š         -Pulmonary
šš          -Renal
šš          -Gut
šš          -Central Nervous system
š         š -Myocardial dysfunction
š         š -Coagulopathy
š         š -Hemolysis
šš          -Fever
š         š -Increase susceptibility to infection
š         š -Leukocytosis
š- All come within the “catch-all” terms of SIRS
28
Q

SIRAB risk factor

A
  • š Risk factor – Length of CPB

- š Frequently a risk factor, but not necessarily

29
Q

Common causes of SIRAB

A

-š Set in motion cytokine mediated events that activate vascular endothelium
- š Most common culprit = contact with foreign surface
-š Altered arterial blood flow patterns
-š Sheer stress (blood pumps)
š- Cardiotomy suction
š- Tissue ischemia
š- Reperfusion
š- Hypothermia
š- Relative anemia
š- anticoagulants

30
Q

Contact activation end result

A
  • š Activation of contact proteins
    - š Coagulation factors XII and XI
    - š Prekallikrein
    - š High molecular weight kininogen
  • š End Result
    - š Formation of bradykinin
    - š Conversion of plasminogen into plasmin
    - š Initiates fibrinolysis
    - š Triggers classical complement cascade.
31
Q

Generalized big pictures with CPB and inflammation

A
  • š Multiple inflammatory mediators are released upon exposure to ECC
  • š Disrupt homeostasis
  • š Generalized whole body inflammatory response
    - šActivates vascular endothelium
    - šFurther neutrophil-mediated injury (tissue damage)
  • š None occur alone
  • š Stimulate or catalyze other reactions in cycle of SIRAB
32
Q

Immune system and bypass

A
  • š Post operatively –
    - š Shown patients more susceptible to infections
  • š Noted serum immunoglobulins and complement are decreased
  • š Chemotaxic ability of granulocytes are decreased
  • š NK cells are decreased
    - Number and Function
  • š CD3+ and CD4+ cells are decreased
  • š CD8+ cells are slightly increased
  • š Leukocyte number remains low for about 1 week post bypass

Perf tech II (16 decks)

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