Blood surface interactions part 2 Flashcards

1
Q

Identify the 5 key blood cell types involved in the response to ECC

A

 Platelets  Neutrophils  Monocytes  Lymphocytes  Endothelial Cells

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2
Q

what causes Platelet Initial / Early Activation (4 things)

A

 Surface contact with ECC
 Heparin increases sensitivity
 Circulating thrombin is a powerful agonist and probably initial activator
 Platelet-activating factor (PAF)

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3
Q

what causes Platelets Late Activation (7 things)

A

 Activated Complement (C5b – C9)  Plasmin  Hypothermia  Interleukin-6
 Cathepsin G  Serotonin  Epinephrine

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4
Q

Platelets Response to Activation

A

 Immediate shape change
express pseudo pods
express surface receptors GPIIb/IIIa GPIb
secrete receptor P selectin from granules

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5
Q

GPIIb/IIIa receptors bind to

A

surface absorbed fibrinogen–use

fibrinogen as bridge to bind to other platelets

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6
Q

P-selectin receptors bind to

A

monocytes & neutrophils to form aggregates

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7
Q

Some platelets release a variety of chemicals and proteins called

A

thromboxane-A2, platelet factor 4, Beta-thromboglobulin, serotonin, etc.

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8
Q

principal agonists of neutrophil activation

A

kallikrein and C5a

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9
Q

other agonists involved in neutrophil activation

A

factor XIIa, heparin, MAC, interleukin 1 Beta, interleukin 8, TNF

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10
Q

when neutrophils activated release contents of granules which are….. (9 of them)

A

ysosomal enzymes, elastase, myeloperoxidase, hydrogen peroxide, hydroxyl radicals, hypochlorous acid, hypobromous acid, acid hydrolases, collagenases

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11
Q

types of receptors expressed when neutrophils are activated

A

Express MAC-1 (CD11b/CD18) & CD11c/CD18 receptors

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12
Q

what do neutrophil receptors bind to

A

binds to fibrinogen, complement fragment, endothelial cells, collagen. binds with factor X and fibrinogen to facilitate thrombin formation

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13
Q

neutrophil L selectin receptor

A

binds with P-selectin expressed by endothelial cells and platelets

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14
Q

neutrophils contribute to what kind of injury

A

reperfusion injury

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15
Q

Monocyte Activation

A

low activation during CPB by  C5a

 thrombin  bradykinin

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16
Q

monocytes form conjugates with

A

platelets via GMP-140 and express

tissue factor

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17
Q

monocyte activation effect on tissue factor

A

Delayed increase of tissue factor seen 20 hours post CPB

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18
Q

monocyte activation releases what cytokines

A

IL-6 and IL-8 during and post CPB  IL-1, IL-2, IL-4 post CPB

19
Q

lymphocyte response to bypass

A

 Number of cells - reduced first week after bypass  Cell responsiveness to mitogens / other agonist –
reduced
Increases susceptibility of postoperative infections. Septic shock  Endocarditis

20
Q

activation agents for endothelial cells

A

 thrombin,C5a,variouscytokines,TNF

21
Q

endothelial cells produce

A

 prostacyclin,heparansulfate,thrombomodulin,protease
nexin-1, protein S, tissue factor pathway inhibitor, t-PA
 vasoactivesubstanceslikenitricoxide,endothelin,PAF, histamine, norepinephrine, bradykinin

22
Q

activated endothelial cells express what receptors

A

tissuefactor,P-selectin,E-selectin,ICAM-1,VCAM-1

23
Q

effect of activated endothelial cells

A

 Synthesize tissue factor to generate thrombin  Initiate fibrinolysis  Contribute to the overall acute inflammatory response
 Allow fluid and leukocytes to enter the interstitial space

24
Q

Possible Contributions to Bleeding After Cardiopulmonary Bypass Non-Platelet Related Causes

A

Hyper fibrinolysis
Heparin excess (inadequate neutralization, rebound)
Hypothermia
Protamine excess
Consumption of soluble coagulation factor(s)
Decreased von Willebrand’s factor

25
Q

Possible Contributions to Bleeding After Cardiopulmonary Bypass Platelet Related Causes

A

Thrombocytopenia
Aspirin-induced platelet dysfunction
Impaired aggregation response to agonists (epinephrine, collagen, ADP, thrombin
Selective loss of youngest (most functional) platelets
Platelet fragmentation / loss of membrane receptors
Impaired platelet-mediated clot retraction
Plasmin-induced platelet activation / dysfunction
Platelet activation / dysfunction induced by C5b-9

26
Q

XII Hageman factor percentage of normal conc. needed for coag.

A

none

27
Q

XI Plasma thromboplastin antecedent percentage of normal conc. needed for coag.

A

20

28
Q

IX Christmas factor percentage of normal conc. needed for coag.

A

40

29
Q

VIII Antihemophilic factor percentage of normal conc. needed for coag.

A

30

30
Q

VII Proconvertin, serum prothrombin conversion percentage of normal conc. needed for coag.accelerato

A

25

31
Q

X Stuart factor percentage of normal conc. needed for coag.

A

40

32
Q

V Proaccelerin, labile factor percentage of normal conc. needed for coag.

A

40

33
Q

II Prothrombin percentage of normal conc. needed for coag.

A

40

34
Q

I Fibrinogen percentage of normal conc. needed for coag.

A

100 mg/dl

35
Q

Terumo coating

A

XCoating(poly(2-methoxyethylacrylate)(PMEA)-noheparin)

36
Q

Medtronic coating

A

 Carmeda(heparincoating–covalentbonded)

 Trillium(heparincoating–covalentbonded)  Balance® Biosurface (hydrophilic polymer coating-no heparin)

37
Q

Maquet coating

A

 Bioline(combinedalbuminandheparincoating)  Softline® (hydrophilic & hydrophobic polymer coating-no heparin)

38
Q

Sorin coating

A

P.h.i.s.i.o(syntheticphosphorylcholine-noheparin)

39
Q

Preop administration of corticosteroids attenuates

A

complement activation

40
Q

Aprotinin inhibits

A

plasmin directly high dose partially inhibits kallikrein – platelet sparing

41
Q

W-aminocarboxylic acids inhibit

A

inhibit cleavage of plasminogen to plasmin

42
Q

Platelet anesthesia

A

Reversible inhibition of platelets during procedure  Eptifibatide (Integrilin) with or without nitric oxide  Nitric oxide provides partial protection

43
Q

Complement inhibition drugs

A

 Pexelizumab  TP10