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Haematology > Drugs used in Coagulation Disorders > Flashcards

Drugs used in Coagulation Disorders Flashcards

1
Q

Drugs used in clotting/bleeding disorders fall into two categories

A
  1. drugs used to decrease clotting or dissolve clots already present
  2. drugs used to increase clotting in patients at risk of a bleed
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2
Q

Anticoagulants are used for

A
  1. acute MI
  2. A-fib
  3. Ischemic stroke
  4. DVT
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3
Q

anticoag drugs and thromoboylitic drugs are effective againt

A

arterial and venous thrombi

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4
Q

antiplatelet drugs are used against

A

arterial thrombi only

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5
Q

List the categories of anticoagulants

A

heparins, direct thrombin inhibitors, direct Xa inhibitor, warfarin

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6
Q

name the thrombolytics

A

urokinase, TPA derivatives

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7
Q

name the antiplatlet drugs

A

aspirin, glycoprotein IIb/IIIa inh., ADP inihibitors, pde uptake inhibitors

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8
Q

dosage route of heparin

A

parenterally (IV or subQ)

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9
Q

dosage route of coumadin

A

oral

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10
Q

dosage route of thrombin/X inh

A

parenteral or oral

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11
Q

antidote to heparin

A

protamine

works well on unfract. hep, partially on LMWH and not at all on Fondaparinux

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12
Q

Advantages of LMWH

A

*more specific for ATIII and not II
greater F
longer duration
lower chance of HIT

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13
Q

example of a LMWH

A

enoxaparin sodium

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14
Q

heparin like products are measure

A

by APTT

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15
Q

APPT used to measure

A

effect of heparin and direct thrombin inhibitors

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16
Q

Antithrombin II inactivates

A

thrombin, X, 9, 11

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17
Q

Heparin MOA

A

increases ATIII’s activity by 1000 fold

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18
Q

GPIIb/IIIa is activated by

A

platelet release of ADP, TXA2, and serotonin–> cause upreg of GP2b3a on platelet surface

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19
Q

How does HIT happen

A

more common with unfractionated heparin–> IgG ab to PF4-Heparin complex–> results in marked thrombocytopenia

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20
Q

will APTT measure LMWH

A

no

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21
Q

Can heparin be used in pregnancy

A

yes–> does not cross placenta

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22
Q

Fondaparinux

A

mimics the bioactive pentasaccharide on heparin–> same effects, given sub Q once a day

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23
Q

onset of heparin

A

instant (minutes)

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24
Q

excretion of heparin

A

renal

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25
Q

choice anticoag during pregnancy

A

heparin

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26
Q

site of action for heparin

A

blood

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27
Q

site of action for coumadin

A

liver

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28
Q

onset of coumadin

A

slow–> days 10 mg 5 mg 5 mg–> then recheck INR–> decide what to do from there

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29
Q

protein C inhibits

A

factors 5 and 8

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30
Q

cleaved by thrombin

A

1, 5, 8, 11, 13

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31
Q

common uses of heaprin

A

ACUTE

PE, MI, DVT

32
Q

prolonged use of unfractionated heparin is associated with

A

osteoporosis

33
Q

inibited by heparin

A

11, 8, 5, *accoriding to the book

34
Q

inhibited by coumadin

A

2, 7, 9, 10 c, s

35
Q

Direct thrombin inhibitors

administered parenterally

A

Lepuridin
Desirudin
bivalirudin
argotroban

36
Q

direct thrombin inhibitors

administered orally

A

Dabigatran

37
Q

MOA of Lepuridin

A

bind simulatenously to the acitve site of thrombin and thrombin substrates

38
Q

MOA of Argatroban

A

binds only the thrombin active site

39
Q

reversal agents for dorect thrombin inhibitors and direct Xa inhibitors

A

none

40
Q

Direct thrombin inhibitor that can also inhibit platelets

A

Bivalirudin

41
Q

how do you monitor coumadin

A

PT–> turn it into INR

42
Q

INR range for someone who needs coumadin

A

2-3

43
Q

INR range for someone with persistent dvt

A

2.5-3.5

44
Q

antidote for coumadin toxicity

A

vitamin K, FFP, prothombin complexes

45
Q

MOAS for coumadin

A

inhibits Vitamin K epoxide reductase preventing Vit K from being replenished and therefore GAMMA carboxylation cannot occur for factors 2, 7, 9, 10 C or S

46
Q

Direct Xa inhibitors

A

rivaroxaban

apixaban

47
Q

do Direct Xa or Direct thrombin inhibitors require monitoring

A

no

48
Q

preferred anticoagulant in pt.s with HIT

A

direct thrombin inhibitors

49
Q

Rivaroxaban indication

A

pt.s undergoing hip/knee replacement and prevention of stroke for Afib pt.’s

50
Q

Warfarin in the circulation

A

99% bound

*anything that causes it to come unbound will have a major impact

51
Q

Warfarin broekn down in the liver by

A

CYP2C9

52
Q

can coumadin be used in pregnant women

A

no

53
Q

necrosis due to warfarin toxicity is due to

A

acute deficiency of factor C

54
Q

inducers of CYP–> causing low coumadin and therefore hypercoaguability

A

rifampin, phenytoin, and barbituates

55
Q

inhibitors of CYP causing warfarin to be too low–> blled risk

A

SSRI’s, cimetidine

56
Q

explain INR

A

inr= patients test PT/ standard PT (12-13)

57
Q

high INR=

A

pt is more anticoagulated than a “normal” person and at a risk for bleed *their pt is long=slow clot

58
Q

low INR=

A

pt is hypercoagulated and at a risk thrombus

*their pt time is quick=fast clotter)

59
Q

Thrombolytic agents

A

T-PA (alteplase)

streptokinase (protein made by streptococci)

60
Q

Thrombolytic enzymes MOA’s

A

catalyze the cleavage of plasminogen to plasmin so it can cleave fibrin and free serum fibrinogen–> dissolving and preventing a clot

61
Q

seletivity of TPa

A

only cleaves plasminogen when bound to fibrin (but selectivity is less than you would hope for)

62
Q

streptokinase MOA

A

does not cleave plasminogen directly–>forms a complex with plasminogen and causes it to undergo conf. change where it is cleaved rapidly by normal TPA

63
Q

does streptokinase show selectivity for fibrin

A

no

64
Q

most important indication of thrombolytic agents

A

as an alternative to percuatenous coronary angioplasty in emergency tx of coronary artery thrombosis with 6 hours

  • also Stroke if within 3 hours
  • also severe PE
65
Q

name the antiplasmin drugs

A

tranexamic acid and aminocaproic acid

66
Q

side effect specific to streptokinase

A

those with prevoius infection to the bacteria may have ab’s specific for the drug–> immune response

67
Q

major adverse event you’re concerned with about thrombolytic agents

A

cerebral hemorrhage and bleeding

68
Q

how does PGI2 (prostacylin) inihibit platelet aggregation

A

increases cAMP which dereases free calcium levels–> this will inihibit platelet aggregation

69
Q

Antipletelet drugs include

A
  1. aspirin and other NSADS (not tyelenol)
  2. GP2b3a inh, abciximab, tirofiban,
  3. ADP antagonists (clopidogrel)
  4. Phosphodiesterase inh. (dipyramidole)
70
Q

dipyramidole MOA

A

prolong the platelet inhibiting action of cAMP by inhibiting phosphodesterase (which breaks down cAMP)–> Ca2+ stays low and pletelets dont aggregate

  • increases cGMP levels–> a vasodilator
  • inhibit the uptake of Adenosine–> increase plasma concentration of adenosine
71
Q

Drug used to treat vitamin K deffieiency

A

phytonadione

72
Q

most important agents to treat hemophillia A/B

A

FFP, and factor 8 (A), 9 (B)

73
Q

increases plasma concentration of vWF

A

desmopressin and factor 8

74
Q

when do you use desmopressin

A

hemophilia A or to prepare pt.’s non vW disease for elective surgery

75
Q

antiplasmin agents do what

A

increas clotting for the prevention of acute bleeding apirsodes in patients with hemophillia and others with high risk of bleeding disorders

76
Q

name he antiplasmin meds

A

aminocaproic acid and tranexamic acid

Haematology (7 decks)

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