Week 7 Flashcards

1
Q

action of clotting factor

A

prothrombin to thrombin

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2
Q

effect of thrombin

A

fibrinogen to fibrin (insoluble keeps clot)

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3
Q

waht is a platelets action

A

adhere to each other to form a clot paltelets red blood cesll held together by fibrin

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4
Q

What is in dense granules of platelet

A

small molecules driving activating)

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5
Q

waht is in alpha granules of platelets

A

contain secreted prtteins such as clotting factors and PDGF-

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6
Q

thrombopoeisis pathway

A

Hemocytoblast- stem cells
Promegakaryocyte
Megakaryocyte- release platelets

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7
Q

what is thrombocytosis and what this does

A

high platelet count

unwanted clotting- occlusion and ischemia

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8
Q

what causes thrombocytosis

A

splenectomy, after hemorrhage, myloproliferative disorders such as CML

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9
Q

what is Thrombocytopenia

A

paltelets below 150,000 mm3

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10
Q

waht causes Thrombocytopenia

A

Idiopathic thrombocytopenis perpura (ITP)
Bleeding disorder in which immune system destroys platelets
Leukemia, infections

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11
Q

what causes platelet aggregation

A

Fibers of collagen not usually exposed to the bloodstream but damage such as atherosclerosis causes collagen to be exposed and recognized by
GP1b complex recognizes VMF then GPVI is activated so granules are released

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12
Q

aggregates released by platelets

A

Thromboxane A2 (TXA2) and ADP

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13
Q

action of clopidogril

A

inhibits ADP binding with P2Y12- so the level of cAMP increases in the patlet which inhibits it – prevents unwanted clotting

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14
Q

where is clopidogril metabolised

A

liver to active metabolites

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15
Q

what is clopidogril

A

Oral anti-platelet- often used to treat coronary artery disease, reduce risk of stroke

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16
Q

what causes low bioaviability of clopidorgil

A

85% iof drug is immediately eliminated by esterases

17
Q

waht happens toa ctive metabolites

A

15% enters 2-OXO-clopidogrel and then second step to ctive metabolite

18
Q

limitations of clopidorgril

A

Low efficiency-
Reliance on hepative processing casues interindividual variability
compelx determination

19
Q

gene involved in metabolizing clopdogril

A

CYP2C19

20
Q

alternatives to clopidogrel

A

Prasugrel- simimpler convertion- faster action and elss resistance as not reliant upon hepatic system
Ticagrelor- no conversion/ faster action
Cangrelor- no conversion/ less resistance

21
Q

poor metaboliser of clopidogrel

A

not likely to receive full benefit- increased risk for heart attack (3%)

22
Q

intermediate metaboliser of clopidogrel

A

may not receive fill benefit- possible increased risk for ehart attacka dn stroke (20%)

23
Q

extensive metaboliser of clopidogrel

A

expected to benefit from standard clopidogrel dose (38%)

24
Q

ultra rapid metaboliser of clopidogrel

A

expected to process medication more quick;y- possible increased benefit possible increased risk for bleeding (32%)

25
Q

Drugs effecting clopidogrel

A

NSAIDS- GI bleeding

proton pump inhibitors - less liely to prevent clots