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AICM High Yield > Hematology (Coagulation Factors) > Flashcards

Hematology (Coagulation Factors) Flashcards

1
Q

what factors need vitamin K

A

9,10,7,2

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2
Q

what factors are the actual clot

A

1-1a

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3
Q

name for factor 1

A

fibrinogen

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4
Q

name for factor 1a

A

fibrin

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5
Q

factors are produced where

A

liver

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6
Q

which factor is made by the endothelial cels of the blood vessels and not the liver

A

factor 8

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7
Q

intrinsic pathway is under the control of what

A

heparin

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8
Q

extrinsic pathway is under the control of what

A

warfarin

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9
Q

what is the process that is used to activate vitamin k

A

gamma carboxylation

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10
Q

what drug inhibits gamma carboxylation (activation of vitamin K)

A

warfarin

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11
Q

what three drugs inhibit factor 10

A

heparin
riveroxaban
apixaban

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12
Q

what are the 3 things made by the endothelial cells to help with keeping the blood vessel vasodialated so that platelets all stay in the middle

A

NO
PGI2
ADP-Dephosphatase

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13
Q

role of heparin sulfate

A

attaches to antithrombin III and then cleaves factors 9,10 and 12

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14
Q

where is antithrombin III made

A

liver

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15
Q

what is lost in nephrotic syndrome and is responsible for the hypercoaguable state

A

antithrombin 3

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16
Q

what inhibits antithrombin 3 causing the patient to be in a hypercoaguable state

A

oral contraception

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17
Q

role of thrombomodulin

A

attaches to 2a and then attaches to protein c and then it cleaves 8a and 5a so that the rest of the coagulation pathway cannot occur and a clot won’t happen

18
Q

role of tPA

A

tPA takes plasminogen from the liver and turns it into plasmin and then it chops 1a (fibrin) into tiny pieces causing it to become a “Fibrin Split Product”

19
Q

4 Thrombolytic Drugs (tPA analogues)

A

Streptokinase
Urokinase
Alteplase
Retaplase

20
Q

risk factor for thrombolytic

A

excessive bleeding

21
Q

what do thrombolytics do

A

they induce the change of plasminogen to plasmin

22
Q

what is the drug that inhibits tPA

A

Aminocarpuic Acid

23
Q

first response to BV damage

A

neurogenic vasoconstriction

24
Q

2nd response to BV damage

A

endothelia release (vasoconstriction)

25
Q

3rd response to BV damage

A

vWF upregualtion

26
Q

GP1b binds to what

A

vWF

27
Q

what happens when Gp1b binds to vWF

A

Cox pathway is stimulated and TXA2 is produced

28
Q

what does thromboxane A2 do

A

causes the degranulation of the alpha and delta cells in the platelets so that ADP can be released

29
Q

what does ADP and ADP receptors on the platelet cells fo

A

causes the up regulation of GPIIb-IIIA

30
Q

what blocks the cox pathway

A

aspirin

31
Q

4 ADP Receptor (platelet) blocker drugs

A

Ticlopidine
Clopidogrel
Prasugrel
Ticagrel

32
Q

3 GPIIb-IIIa receptor inhibitors

A

Abciximab
Epitifibatide
Tirofiban

33
Q

drugs for von wilder brand disease

A

desmopressin
vasopressin
*factor 8

34
Q

Gp1b deficiency is called

A

Bernard Solier

35
Q

GpIIIa deficiency is called

A

Glanzmen Disorder

36
Q

what factor activated factor 13

A

1A

37
Q

WHAT forms mesh work around clot

A

factor 13

38
Q

Drugs that inhibit Factor 10 (3)

A

Heparin
Riveroxaban
Apixaban

39
Q

Direct Thrombin inhibitors

A

Argatroban

Bivalrudin

40
Q

phosphodiesterase 3 inhibitor

A

Cilostazole

AICM High Yield (2 decks)

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