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Final HEME > hypercoagulation state scheme > Flashcards

hypercoagulation state scheme Flashcards

1
Q

what is virchows triad?

A

venous stasis
vascular injury
hypercoagulability

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2
Q

what is the most common acquired thrombophilia?

A

antiphospholipid antibody syndrome

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3
Q

what are the two vasodilators that inhibit platelet aggregation?

A

NO and prostacyclin

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4
Q

what are the two vasoconstrictors that facilitate platelet aggregation?

A

endothelin 1

thromboxane A2

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5
Q

is vascular smooth muscle unitary or multiunit?

A

both

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6
Q

what binds to Ca in vascular smooth muscle to cause contraction?

A

calmodulin

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7
Q

how many ways does Ca enter vascular smooth muscle cells

A

3!

voltage gated. IP3, ligand gated g proteins

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8
Q

what causes vascular smooth muscle to use less ATP than skeletal muscle for contraction?

A

Latch state: myosin dephosphorylated while still attached

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9
Q

what releases endothelin 1?

A

damaged vascular endothelium

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10
Q

what releases thromboxane A2?

A

platelets

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11
Q

how is NO produced?

A

from L-arginine through nitric oxide synthase

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12
Q

what is serum?

A

plasma minus the clotting factors

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13
Q

what is the buffy coat?

A

WBCs that make up 1% of Hct

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14
Q

what is plasma?

A

ECF + plasma proteins: albumin, fibrinogen, and globulins

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15
Q

what is the purpose of albumin?

A

transport protein

prevents edema

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16
Q

what clotting substances do platelets release?

A

thromboplastin and plasmin

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17
Q

what does thromboplastin do?

A

converts prothrombin to thrombin

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18
Q

what does thrombin do?

A

converts fibrinogen to fibrin

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19
Q

what makes prothrombin and firbrinogen

A

liver

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20
Q

what does plasmin do?

A

clot contraction

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21
Q

why are arterial clots called white clots?

A

trap mostly platelets

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22
Q

why are venous clots called red clots?

A

trap mostly RBCs and fibrin

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23
Q

what are the 4 major events of hemostasis

A

vasoconstriction, platelet actions, fibrin clot formation, fibrinolysis

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24
Q

what does TPA do?

A

activate fibrinolysis by activating plasmin

25
Q

what is primary hemostasis?

A

platelet plug formation

26
Q

what is secondary hemostasis?

A

fibrin clot formation

27
Q

what do alpha granules in platelets release?

A

fibrinogen
factor V
factor VIII

28
Q

how do platelets bind to each other?

A

bind through the GP IIB/IIIA and fibrinogen

29
Q

what do dense granules release?

A

Ca
ADP
serotonin

30
Q

how does aspirin block platelet aggregation?

A

blocks Cox 1 so TXA2 release

31
Q

how does vorapaxar block platelet aggregation

A

blocks thrombin receptor PAR

32
Q

how does abciximab, tirofiban, eptifibitide block platelet aggregation

A

block IIB/IIIA receptor

33
Q

how does clopidogrel block platelet aggregation?

A

blocks ADP receptor

34
Q

what two proteins block coagulatin?

A

protein C and S

35
Q

where are the Vitamin K dependent CFs made?

A

liver

36
Q

which CFs need vitamin K?

A

Prothrombin
VII
IX
X

37
Q

what is the key step in Vitamin K cycle?

A

carboxylation of glutamic residues

38
Q

what coagulation study looks at the extrinsic coagulation cascade?

A

PT/INR

39
Q

what coagulation study looks at the intrinsic coagulation cascade?

A

aPTT

40
Q

prothrombinase complex consists of?

A

X + Va + Ca -> thrombin

41
Q

extrinsic tenase complex composed of?

A

VIIa via VII and Ca

42
Q

intrinsic tenase complex composed of?

A

IX a + VIII

43
Q

what inhibits initiation of secondary hemostasis?

A

TFP1

44
Q

what initiates secondary hemostasis amplification?

A

thrombin

45
Q

what do the extrinsic and intrinsic tenases ultimately do?

A

activate factor X

46
Q

amplification stage of secondary hemostais leads to?

A

thrombin burst

47
Q

what inhibits fibrinolysis naturally/

A

PAI & alpha 2 antiplasmin

48
Q

what activates protein C?

A

thrombomodulin

49
Q

what does protein C inhibit?

A

Factors V and VIII

50
Q

what drug can inhibit the extrinsic pathway?

A

vitamin K antagonist like coumadin

51
Q

what pathway does heparin block?

A

intrinsic

52
Q

what are the 4 types of inherited thrombophilias?

A

factor V leiden mutations
protein C def
protein S def
antithrombin def.

53
Q

how does factor V leiden mutation cause thrombosis?

A

protein C cant inactivate factor V -> inc. thrombin -> inc. fibrin

54
Q

most common congenital thrombophilia?

A

factor V leiden

AD on Chr 1

55
Q

when can antithrombin III def. be acquired?

A

with nephrotic syndrome

56
Q

antiphospholipid antibody syndrome characterized by?

A

thromboembolic event (by act. coag cascade)
pregnancy related complications
thrombocytopenia

57
Q

how does the autoantibody to apolipoprotein H lead to thrombosis?

A

block protein C and protein S

58
Q

what is the most common acquired blood protein defects?

A

lupus anticoagulant/antiphospholipid antibody

Final HEME (6 decks)

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