Blood Surface Interactions (Part 1) - Exam 3 Flashcards

1
Q

How does heparin work?at

A

No direct inhibition of coag; accelerates action of antithrombin
Direct activation of other blood components

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2
Q

What blood components does heparin activate?

A
Platelets
Factor XII
Complement system
Neutrophils
Monocytes
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3
Q

What allergic response can occur from heparin?

A

HIT

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4
Q

HIT

A

Heparin Induced Thrombocytopenia

Causes bleeding

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5
Q

What percent of patients receiving heparin develop HIT?

A

2-5% of patients receiving heparin

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6
Q

HITT

A

Heparin Induced Thrombocytopenia and Thrombosis

causes thrombosis

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7
Q

What percent of patients develop HITT?

A

0.1-0.2% of patients receiving heparin

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8
Q

What is the mechanism for HIT and HITT?

A

Heparin binds to PF4 and induces IgG formation

Heparin/PF4-IgG complex activates plts

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9
Q

PF4

A

Platelet factor 4

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10
Q

What does the formation of heparin/PF4-IgG result in?

A

Decreases circulating number of platelets

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11
Q

HIT is defined as what percent decrease in platelets?

A

40-50% decrease

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12
Q

What does HITT involve?

A

Decrease in number of platelets and any evidence of thrombosis

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13
Q

What does quick exposure of whole blood mass to biomaterials of ECC result in?

A

Plasma protein adsorption on to surface of ECC
Contact activation of blood
Emboli formation
Increased Interstitial fluid

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14
Q

How fast does plasma protein adsorption onto the surface of ECC occur?

A

Very quick

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15
Q

What does the amount of plasma proteins absorbed onto ECC depend on?

A
  1. Protein and intrinsic surface activity of biomaterial
  2. Wettability
  3. Hydrophilic/ hydrophobic ratio
  4. Surface chemistry
  5. surface electrical properties
  6. roughness/ porosity
  7. subsurface features
  8. distribution of function receptor sites
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16
Q

What does activation of blood correlate with?

A

Physical/Chemical properties of biomaterial

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17
Q

Is plasma protein adsopriton onto surface of ECC predictable?

A

No; correlation is made retrospectively

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18
Q

What does contact activation of blood to ECC stimulate?

A

Coagulation cascade
Complement system
Alteration of cell signaling substances

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19
Q

Contact activation of blood to ECC exposes receptor sites for what?

A

Blood cells
Plasma proteins (FXII, Complement protein 3)
Platelets

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20
Q

Surgery Emboli Formation Sources: Wound Debris

A
Fibrin
Fat
Calcium
Cellular debris
Other foreign material
Air emboli
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21
Q

Surgery Emboli Formation Sources: Surgical Manipulation

A
Plaque debris (arterial cannulation, XC)
Air emboli (cannulation, incomplete deairing)
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22
Q

Blood Activation/Trauma Emboli Formation Sources

A

Fibrin emboli
Macroaggregates of proteins and lipoproteins
Fat flobules
Platelet and Leukocyte aggregates

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23
Q

Homologous Blood (unfiltered) Emboli Formation

A

Platelet & Leukocyte aggregates
Fibrin
Lipid precipitates
red cell debris

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24
Q

Crystalloid Solutions: emboli formation

A

Inorganic debris

dust

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25
Q

Roller Pumps: Emboli Formation

A

Spallation

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26
Q

Embolic Material

A
Fibrin
Fat (Free/denatured lipoproteins/chlyomicrons)
Denatured protein
Platelet aggreagtes
Leukocyte aggregates
Red cell debris
Gas (Nitrogen, oxygen)
Foreign material (Ca, Tissue debris, sutures)
Spallated material
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27
Q

What type of fats can be embolic material?

A

Free fat
denatured lipoproteins
Chylomicrons

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28
Q

Chylomicrons

A

a droplet of fat present in the blood or lymph after absorption form the small intestine

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29
Q

What is the accumulation of interstitial fluid proprotional to?

A

Duration of bypass

30
Q

What can cause increased interstitial fluid?

A

Increased capillary permeability

31
Q

CPB can result in

A

Whole Body Inflammation

Temporary Organ Dysfunction

32
Q

What are the Five Protein Systems

A
Contact Activation System
Intrinsic Coagulation System
Extrinsic Coagulation System
Fibrinolysis
Complement Activation
33
Q

What are the four proteins involved with plasma contact activation?

A

Factor XII
Prekallikrein
HMWK
Factor XI

34
Q

What does FXII do when activated by contact with ECC?

A

Adsorbed onto foreign surface of ECC

Changes shape produces active protease FXIIa and XIIf

35
Q

What must be present for FXII to be adsorbed onto foreign surface of ECC?

A

Prekallikrein and HMWK

36
Q

What does active protease FXIIa do?

A
  1. Cleaves prekallikrein to kellikrein
  2. Cleaves HMWK to bradykinin
  3. Activates FXi to FXIa
37
Q

What is a strong neutrophil agonist?

A

Kallikrein

38
Q

What is a weak neutrophil agonist?

A

FXIIa

39
Q

What must be present for FXIIa to activate FXI to FXIa?

A

Kallikrein and HMWK must be present

40
Q

What does FXIa do?

A

Activates intrinsic coagulation cascade; results in thrombin production

41
Q

How is the intrinsic coagulation cascade initiated?

A

Plasma contact activation; initiated directly by blood contact with the ECC

42
Q

How is the exntrinsic coagulation cascade initiated?

A

By the expression of tissue factor on nonvascular cells

43
Q

What are the 2 forms of tissue factor?

A
  1. Cell bound tissue factor

2. Soluble plasma tissue factor

44
Q

What does tissue factor do?

A

Binds to and activates FVII; which activates FX

45
Q

What are the actions of thrombin?

A

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

46
Q

How many proteins are involved in the complement system?

A

30+ proteins; most inactive enzyme precursors

47
Q

What pathways are involved in the complement system?

A

Classical Pathway
Alternative pathway
Terminal Pathway

48
Q

How is the classical pathway of the complement system activated?

A

Antigen-antibody complexes

49
Q

How is the alternative pathway of the complement system activated?

A

C3b (a produce of classical pathway)

Inititated by spontaneous activation on a continuous basis

50
Q

What is alternative pathway

A

A feedback loop for amplification

51
Q

What is the terminal pathway in the complement system?

A

Classical and alternative merge at the level of C3 convertase production

52
Q

What do the end products of the complement system do?

A

Work to prevent/ limit damage from invading organism or toxins

53
Q

How does the end produce membrane attack complex work to prevent damange from invading organism?

A
Opsonization
Lysis
Agglutination
Neutralization of viruses
Chemotaxis
Activation of mast cells and basophils
Inflammation
54
Q

Describe opsonization.

A

Neutrophils and macrophages activated

They engulf bacterial to which antigen-antibody complex is attached

55
Q

Describe Lysis.

A

Final product called lytic complex or terminal complement complex. Creates a pore in the cell membrane of bacteria or other invading organisms that allows the influx of ions and water into the cell

56
Q

Describe agglutination

A

Complement produces change surface of invading organisms; organisms adhere to each other

57
Q

Neutralization of viruses

A

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

58
Q

What causes chemotaxis of neutrophils and macrophages?

A

C5a

59
Q

What happens during chemotaxis?

A

Large number of phagocytes migrate to the area

60
Q

What are mast cells nad basophils activated by?

A

C3a, C4a, C5a

61
Q

What do mast cells release?

A

Histamine and other substances into local fluids

62
Q

What does activation of mast cells and basophils result in?

A

Increased local blood flow and increased leakage of fluid and protein into the tissue

63
Q

What does inflammation result in?

A

INcreased capillary permeability
Altered vasomotor tone
Impaired cardiac function

64
Q

What does the activation of classical and alternative pathway result in?

A
Cellular damange
Endothelial and leukocyte activation
Histamine release
Increased vascular permeability
Generalized inflammatory response
Platelet activation
65
Q

What 4 things initiate the classical pathway?

A

Surface contact activation of FXII
Heparin-protamine Complexes
Ischemia reperfusion
Blood-air interface

66
Q

What 3 things activate the alternative pathway?

A

Contact with foreign surface
Activated pericardium and suction blood
Ischemia reperfusion

67
Q

What activates complement system?

A

Classical and alternative pathways

68
Q

What are 3 anaphylatoxins with vasoactive properties?

A

C3a, C4a, C5a

69
Q

What is a major neutrophil agonist?

A

C5a

70
Q

What results in opsonization?

A

C3b, C4b

71
Q

What does the terminal complement complex do?

A

Accelerates thrombin formation via action on prothrombinase complex
Activates platelets