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Perf Tech II (exam 3) > Topic 12a Blood Surface Interactions > Flashcards

Topic 12a Blood Surface Interactions Flashcards

1
Q

% of patients receiving Heparin that develop HIT

A

2-5% of patients receiving heparin

Causes bleeding

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2
Q

% of patients receiving Heparin that develop HITT

A

0.1-0.2% of patients receiving heparin

Causes thrombosis

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3
Q

HIT and HITT mechanisms ?

A

Heparin binds to PF4 (platelet factor 4) and induces formation of IgG antibodies

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4
Q

PF4-IgG complex activates platelets and does what to them ? With HIT and HITT?

A

Decreases circulating number of platelets
HIT defined as 40-50% decrease
HITT involves decrease AND any evidence of
thrombosis

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5
Q

plasma protein adsorption onto surface of ECC amount?

A
  • very quick

* amount adsorbed depends on [protein] & intrinsic surface activity of biomaterial

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6
Q

plasma protein adsorption onto surface of ECC correlation?

A

correlation between physical / chemical

properties of biomaterial and activation of blood are made retrospectively–not possible to predict the response

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7
Q

plasma protein adsorption onto surface of ECC depends on what characteristics of the surface?

A
  • wettability
  • hydrophilic / hydrophobic ratio
  • surface chemistry
  • surface electrical properties
  • roughness / porosity
  • subsurface features
  • distribution of functional receptor sites
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8
Q

contact activation of blood expose receptor sites on what? (3)

A
  • blood cells
  • plasma proteins (factor XII & complement protein 3)
  • platelets
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9
Q

emboli formation can be caused by what? (5)

A

*surgery
*blood activation (fibrin emboli, macroaggregates of proteins and, lipoproteins, fat globules)
*homologous blood (if not filtered- fibrin, RBC debris, platelet and leukocyte aggregates)
*crystalloid solutions (debris/dust)
roller pumps (spallation)

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10
Q

Increased interstitial fluid formation caused by what?

A

increased capillary permeability

accumulation proportional to duration of bypass

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11
Q

Five protein systems in whole body coagulation?

A 
Contact Activation System
Intrinsic Coagulation
Extrinsic Coagulation
Fibrinolysis
Complement Activation
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12
Q

Plasma Contact Activation: Four proteins involved?

A

factor XII
prekallikrein
high-molecular-weight kininogen (HMWK)
factor XI

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13
Q

For factor XII to be absorbed onto foreign surface of ECC - what two things must be present?

A

prekallikrein & HMWK must be present

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14
Q

Once factor XII changes shape it produces what?

A

active protease factor XIIa and XIIf

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15
Q

Factor XIIa cleaves prekallikrein into what?

A

to kallikrein (strong neutrophil agonist)

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16
Q

Factor XIIa Activates factor XI to XIa: what must be present? and what does XIa activate ?

A

kallikrein & HMWK must be present

factor XIa activates intrinsic coagulation cascade–thrombin production

17
Q

Factor XIIa cleaves HMWK into what?

A

to bradykinin ( potent vasodilator )

18
Q

Factor XIIa is an agonist of what?

A

factor XIIa weak neutrophil agonist

19
Q

Intrinsic Coagulation Cascade initiated by what?

A

Initiated by plasma contact activation

Initiated directly by blood contact with the ECC

20
Q

Extrinsic Coagulation Cascade initiated by what?

A

Initiated by the expression of tissue factor on

nonvascular cells

21
Q

What are the two forms of tissue factor that are expressed when extrinsic coagulation cascade is initiated?

A

cell bound tissue factor

soluble plasma tissue factor

22
Q

Binds to and activates factor VII activates what factor?

A

factor X

23
Q

Thrombin Actions (4)

A

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

24
Q

Compliment system made up of how many proteins ?

A

30+ proteins–most inactive enzyme precursors

25
Q

Complement Pathway entails 3 paths?

A

Common Pathway
Alternative Pathway
Terminal Pathway

26
Q

Alternative Pathway initiated by what two things?

A

Initiated by C3b (a product of the classical pathway)
Initiated by spontaneous activation on a continuous basis
Feedback loop for amplification

27
Q

Terminal Pathway does what?

A

Classical and Alternative merge at the level of C3 convertase production

28
Q

Classical Pathway initiated by what?

A

Initiated by antigen-antibody complexes

29
Q

End Product-Membrane Attack Complex

Works to prevent / limit damage from invading organism or toxin by what? (7)

A 
opsonization
lysis
agglutination
neutralization of viruses
chemotaxis
activation of mast cells and basophils
inflammation
30
Q

End Product-Membrane Attack Complex OPSONIZATION does what?

A

neutrophils & macrophages activated

they engulf bacteria to which antigen-antibody complex is attached

31
Q

End Product-Membrane Attack Complex

LYSIS final product?

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

32
Q

End Product-Membrane Attack Complex

AGGLUTINATION does what?

A

complement products change surface of invading organisms

•organisms adhere to each other

33
Q

End Product-Membrane Attack Complex

neutralization of viruses how?

A

products can attack structures of some

viruses and render them non-virulent

34
Q

C5a causes what of neutrophils

and macrophages?

A

chemotaxis

large number phagocytes migrate to area

35
Q

mast cells and basophils are activated by what?

A

activated by C3a, C4a, & C5a

36
Q

mast cells and basophils release what?

A

cells release histamine and other substances

into local fluids

37
Q

mast cells and basophils results in what?

A

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

38
Q

inflammation does what to vasomotor tone, cap permeability and cardiac function ?

A

increased capillary permeability
altered vasomotor tone
impaired cardiac function

Perf Tech II (exam 3) (3 decks)

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