test 9 part 2

Question 1

Non-specific inflammation

Answer 1

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

Question 2

4 signs of inflammation

Answer 2

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

Question 3

Stages of inflammation

Answer 3

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

Question 4

components of inflammation and duration

Answer 4

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

Question 5

Major players in inflammation

Answer 5

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

Question 6

Inflammation mediated by variety of

Answer 6

• chemical mediators

- derived from plasma proteins and/or cells

Question 7

Chemical Mediators

Answer 7

• 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

Question 8

Chemical mediators that cause vasodilation

Answer 8

• Nitric Oxide

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

Question 9

Chemical mediators that increase vascular permeability

Answer 9

• C3a and C5a
• Bradykinin
• Leukotrienes

Question 10

Chemical mediators that cause chemotaxis, leukocyte recruitment and activation

Answer 10

• C5a
• Leukotriene B4
• Chemokines
• Interleuken-1

Question 11

Chemical mediators that cause fever

Answer 11

• Interleuken-1

Question 12

purpose of Vascular change

Answer 12

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

Question 13

Vasodilation

Answer 13

• 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

Question 14

increased capillary permeability

Answer 14

• Allows antibodies and clotting factors to leave the blood

Question 15

Vasodilation and increased

permeability: Histamine

Answer 15

• 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

Question 16

Vasodilation and increased

permeability: Kinins

Answer 16

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

Question 17

Vasodilation and increased

permeability: Prostaglandins

Answer 17

• Lipid
• š Released by damaged cells
• š Stimulate emigration of phagocytes

Question 18

Vasodilation and increased

permeability: Leukotrienes

Answer 18

• š Basophils and mast cells produce

- š Increase permeability

Question 19

Vasodilation and increased

permeability: Complement

Answer 19

• š Stimulate histamine release
• š Attract neutrophils
• š Promote Phagocytosis

Question 20

Clotting and inflammation

Answer 20

• 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

Question 21

Neutrophils and Inflammation

Answer 21

• 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)

Question 22

Extravasation

Answer 22

• movement of leukocytes from vessel lumen to interstitial space

Question 23

Cellular Events

Answer 23

• 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

Question 24

4 characteristics of inflammation

Answer 24

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)

Question 25

Fever

Answer 25

- 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

Question 26

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

Answer 26

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

Question 27

Systemic Inflammatory Response After Bypass (SIRAB) injuries

Answer 27

``` 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 ```

Question 28

SIRAB risk factor

Answer 28

- š Risk factor – Length of CPB | - š Frequently a risk factor, but not necessarily

Question 29

Common causes of SIRAB

Answer 29

-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

Question 30

Contact activation end result

Answer 30

- 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.

Question 31

Generalized big pictures with CPB and inflammation

Answer 31

- 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

Question 32

Immune system and bypass

Answer 32

- 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