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Perf Tech II > Blood Surface Interactioms Part 1 > Flashcards

Blood Surface Interactioms Part 1 Flashcards

0
Q

HIT

A

Heparin induced thrombocytopenia
2-5% patients recieving heparin
Causes bleeding

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1
Q

Blood components directly activated by heparin

A 
Platelets
Factor VII
Complement 
Neutrophils
Monocytes
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2
Q

HITT

A

Heparin induced thrombocytopenia and thrombosis

0.1-2% patients receiving heparin

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3
Q

HIT and HITT mechanism

A

Heparin binds platelet factor 4 and induces formation of IgG
Heparin/PF4-IgG complex activates platelets
-decreases number of circulating platelets
-HIT defined as 40-50% decrease in platelets
-HITT involves decrease AND any sign of thrombosis

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4
Q

Plasma proteins absorb onto surface of ECC. Factors affecting absorption:

A

Very quick
Amount absorbed depends on concentration and intrinsic surface activity of biomaterial
Cannot predict response of loos to biomaterial
Wettability
Hydrophilic/hydrophobic ratio
Roughness
Subsurface features
Distribution of functional receptor sites

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5
Q

Contact activation of blood

A

Stimulates coagulation cascade
Stimulates complement system
Alteration of cell signaling substances
Expose receptor sites for: blood cells, plasma proteins (factor XII, CP3), platelets

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6
Q

Emboli formation

A
  1. Surgery
  2. Wound debris: fibrin, fat, calcium, cellular debris, foreign material, air emboli
  3. Surgical manipulation: plaque debris ( arterial cannulation, cross clamp), air emboli (cannulation, incomplete deairing)
  4. Blood activation and trauma: fibrin emboli, macroaggregates of proteins and glycoproteins, fat globules, platelet and leukocyte aggregates
  5. Nonfiltered homologous blood: platelet and leukocyte aggregates, fibrin, lipid precipitates, red cells debris
  6. Crystal loud solution: inorganic debris, dust
  7. Roller pumps: spallation
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7
Q

Embolic material on CPB

A 
Fibrin 
Fat
Denatured protein
Platelet aggregates
Leukocyte aggregates
Red cell debris
Gas(nitrogen, oxygen)
Foreign material (calcium, tissue debris, suture material)
Spallated material
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8
Q

Increased interstitial fluid

A

Increased capillary permeability

Accumulation proportional to duration of bypass

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9
Q

End results of blood exposure to ECC

A

High number of different reactions: changes composition of blood–changed blood reaches every organ, tissue, cell
Change in blood composition triggers normal endothelial cells- additional blood proteins converted to active enzymes, stimulated to expose various receptors, stimulated to release granule contents, stimulated to synthesize new enzymes and chemicals

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10
Q

2 major results

A

Whole body inflammation

Temporary organ dysfunction

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11
Q

5 key protein systems

A 
Contact activation system
Intrinsic coagulation
Extrinsic coagulation
Fibrinolysis 
Complement actovation
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12
Q

Four proteins of platelet contact activation

A

Factor XII
Prekallikrein
High molecular weight kininogen (HMWK)
Factor XI

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13
Q

Proteins activated by contact with ECC

A

Factor XII: absorbed onto foreign surface of ECC (prekallikrein and HMWK must be present)
Factor XI: changes shape producing active protease factor XIIa and XIIf

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14
Q

Functions of active protease factor XIIa

A
  1. Cleaves prekallikrein to kallikrein (kallikrein strong neutrophil agonist, factor XIIa is weak neutrophil agonist)
  2. Cleaves HMWK to bradykinin (potent vasodilator)
  3. Activates factor XI to XIa (kallikrein and HMWK must be present, activates intrinsic coagulation cascade-thrombin production)
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15
Q

Initiation of intrinsic coagulation cascade

A

Initiated by plasma contact activation

Initiated directly by blood contact with ECC

16
Q

Initiation of extrinsic coagulation cascade

A

Initiated by expression of tissue factor on nonvascular cells
2 forms: cell bound tissue fiber, soluble plasma Tissue factor
Binds to and activates factor VII which activates factor X

17
Q

Thrombin actions

A

Production of fibrin from fibrinogen
Cross-linking fibrin
Activating platelets
Stimulating production of tissue plasminogen activator (tPA) by endothelial cells

18
Q

Factors in fibrinolysis

A

Extrinsic: tPA and urokinase
Intrinsic: factor XIIa, kallikrein, HMWK
Exogenous: streptokinase

19
Q

Initiation of classical pathway in complement system

A

Antigen-antibody complexes

20
Q

Initiation of alternative pathway in complement system

A

C3b (product of classical pathway)
Spontaneous activation on continuous basis
Feedback Loop for amplification

21
Q

Terminal pathway of complement system

A

Classical and terminal merge at level of c3 convertase production
End products work to prevent/limit damage from invading organism or toxin

22
Q

MAC: opsonization

A

Neutrophils and macrophages activates

Engulf bacteria to which antigen-antibody complex is attached

23
Q

MAC: Lysis

A

Final product called lyric complex or terminal complement complex
Creates pore in cell membrane of bacteria or invading organism that allows influx of water and ions into the cell

24
Q

MAC: Agglutination

A

Complement products change surface of invading organisms

Organisms adhere to each other

25
Q

MAC: Neutralization of viruses

A

Products can attack structures of some viruses and render them non-virulent

26
Q

MAC: chemotaxis

A

C5a causes chemotaxis of neutrophils and macrophages

Large number of phagocytes migrate to area

27
Q

MAC: activation of mast cells and basophils

A

Activated by C3a, C4a, C5a
Cells release histamine and other substances into local fluids
Results in increased local blood flow and increased leakage of fluid and protein into the tissue

28
Q

MAC: inflammation

A

Increased capillary permeability
Altered vasomotor tone
Impaired cardiac function

29
Q

Action of classical and alternative pathways on CPB

A 
Cellular damage
Endothelial and leukocyte activation
Histamine release
Increased vascular permeability
Generalized inflammatory response
Platelet activation
30
Q

CPB classical pathway activation methods

A

Surface contact activation of factor XII
Heparin-protamine complexes
Ischemia reperfusion
Blood-air interface

31
Q

Anaphylotoxins with vasoactive properties

A

C3a, c4a, c5a

32
Q

Major neutrophil agonist

A

C5a

33
Q

Opsonization complement proteins

A

C3b, c4b

34
Q

Terminal complement complex actions

A

Accelerates thrombin formation via action on prothrombinase complex
Activates platelets

Perf Tech II (4 decks)

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