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Pharmacology II - CP > Coagulation and Dissolution of a Blood Clot > Flashcards

Coagulation and Dissolution of a Blood Clot Flashcards

1
Q

Normal hemostasis definition

A

balance between generation of hemostatic clots and uncontrolled thrombus formation

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2
Q

Extrinsic pathway

A

plasma mediated, initiation of hemostasis

key: tissue factor

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3
Q

Intrinsic pathway

A

amplifies and propagates hemostasis

key: thrombin

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4
Q

Common pathway

A

results in an insoluble fibrin clot

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5
Q

Preoperative coagulation testing should be based on

A

patient’s history and planned surgery

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6
Q

Hemostasis is regulated by interactions between

A

blood vessel walls, circulating platelets, and clotting proteins in the plasma

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7
Q

Fibrinolysis definition

A

orderly breakdown of a stable blood clot

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8
Q

Mechanisms of normal hemostasis

A

vasoconstriction, platelet plug, clot formation, clot dissolution

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9
Q

Initiation stage of clot formation

A

binding of platelets to collagen tissue factor dependent

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10
Q

Propagation stage of clot formation

A

recruitment of platelets to growing thrombus, amplification of clotting cascade

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11
Q

Stabilization stage of clot formation

A

platelet- platelet interaction, fibrin deposition

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12
Q

Damage to the endothelium exposes the ECM and causes

A

vasoconstriction/contraction

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13
Q

What can induce prothrombotic endothelial changes?

A

thrombin, hypoxia, and high fluid sheer stress

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14
Q

3 major phases of platelet plug formation

A

adhesion, activation, and aggregation

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15
Q

Normal concentration of platelets

A

150,000 - 400,000 per microliter

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16
Q

Spontaneous bleeding can occur when platelet levels are

A

< 50,000 u/L, lethal is < 10,000 u/L

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17
Q

Life of a platelet

A

8 - 12 days

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18
Q

Where are platelets formed and what is another name for platelets?

A

In the bone marrow; thrombocytes

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19
Q

Inhibitors of platelets

A

adenosine, insulin, NO, PGE2, PGI2

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20
Q

Activators of platelets

A

adrenaline, cholesterol, GAS6, ICAMs, IGF1, PGE2, sCD40L, thrombopoietin, vWF

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21
Q

4 types of platelets

A

secretory, aggregating, procoagulant, coated

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22
Q

Platelet receptors

A

ADP, TXA2, fibrinogen/vWF, vW factor, collagen

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23
Q

Platelet adhesion mechanism

A

exposure to sub-endothelial matrix proteins allows platelets to undergo conformational change to adhere to the vascular wall

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24
Q

Von Willebrand Factor (produced, released, and primary function)

A

produced in the endothelium and platelets
released by endothelial cells and activated platelets
primary function is to bind to other proteins

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25
Q

Glycoprotein IIb/IIIa deals with

A

platelet to platelet

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26
Q

Glycoprotein Ib/factor IX/factor V receptor complex deals with

A

platelet to vessel wall

27
Q

Glycoprotein Ib-V-IX Complex

A

binds von Willebrand Factor, allowing platelet adhesion and platelet plug formation at sites of vascular injury

28
Q

Von Willebrand Factor is mainly activated in conditions of

A

high blood flow and shear stress

29
Q

Which factor goes hand in hand with von willebrand factor?

A

factor VIII

30
Q

What are 3 “red flags” that could indicate von willebrand disease?

A

women with heavy menstrual periods, frequent nose bleeds, and gum bleeding with teeth brushing

31
Q

Type 1 vWD

A

failure to secrete vWF into circulation or vWF clear quickly
can be treated with DDAVP

32
Q

Type 2 vWD

A

decreased ability to bind to GPIb and VIII

33
Q

Type 3 vWD

A

complete absence of production of VWF

34
Q

Platelet type/pseudo vWD

A

defect of the platelet’s GPIb receptor (vWF is normal)

35
Q

What medications are GPIIb/IIIa inhibitors?

A

abciximab (ReoPro), eptifibatide (Integrilin), tirofiban (Aggrastat)

36
Q

GPIIb/IIIa inhibitor action

A

blocks ability of fibrinogen to form around aggregated platelets so no platelet to platelet bridging can occur

37
Q

Which GPIIb/IIIa inhibitor is irreversible?

A

Abciximab

38
Q

Which medications do we use that are thromboxane A2 inhibitors?

A

Aspirin

Naproxen

39
Q

Aspirin action

A

inhibits ability of COX enzyme to synthesize the precursors of thromboxane within platelets

40
Q

What do P2Y12 receptors do?

A

further amplify the response to ADP and draw forth the completion of aggregation

41
Q

What are ADP receptor antagonists?

A

ticlopidine (ticlid), clopidogrel (plavix), prasugrel (efient), ticagrelor (brilinta), cangrelor (kengrexal)

42
Q

What completes the formation of a platelet plug?

A

platelet aggregation

43
Q

blood clot formation

A

fibrinogen breaks down to produce fibrin that becomes cross linked into a stable mesh activating coagulation factors initiating the coagulation cascade

44
Q

the key step in blood clotting is the conversion of ___ to ___ by ____

A

fibrinogen; fibrin; thrombin

45
Q

alpha angle on ROTEM

A

tells how strong the clot will get

46
Q

Intrinsic pathway is triggered when

A

blood contacts a negatively charged surface

47
Q

Extrinsic pathway is activated when

A

blood contacts cells outside the vascular endothelium

48
Q

activation of which factor converges the extrinsic and intrinsic pathways?

A

factor X

49
Q

Which two factors are glycoproteins and not enzymes?

A

vWF and tissue factor III

50
Q

Which two factors are NOT synthesized in the liver?

A

Calcium (IV) - diet

Von willebrand - endothelial and platelets

51
Q

Which factors are vitamin K dependent for utilization?

A

factors II, VII, IX, and X

52
Q

prothrombin gets activated to

A

thrombin

53
Q

thrombin activates fibrinogen to form

A

fibrin

54
Q

clot lysis occurs when plasminogen is activated to

A

plasmin

55
Q

what activates plasminogen?

A

t-PA (tissue plasminogen activator)

56
Q

plasmin digests

A

fibrin fibers, fibrinogen, factor V, factor VIII, prothrombin, factor XII

57
Q

What is increased in DIC?

A

fibrinogen degradation products

58
Q

thrombolytics action

A

possess fibrinolytic effects or enhances the body’s fibrinolytic system by converting endogenous plasminogen to plasmin

dissolves newly formed clots

59
Q

prothrombin time (PT)

A

evaluates extrinsic pathway

reagents vary so INR is used for standardization

60
Q

partial thromboplastin time (PTT)

A

indicates performance of the intrinsic pathway

61
Q

ACT

A

reliable for high heparin concentrations

influenced by hypothermia, thrombocytopenia, coagulation deficiencies

62
Q

Viscoelastic testing (TEG and ROTEM)

A

global assay for whole blood clotting

63
Q

1 mg of protamine will inhibit

A

1 mg (100 units) of heparin

64
Q

normal value for ACT

A

80 - 150 seconds

Pharmacology II - CP (12 decks)

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