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HEME > Pharm - Coagulation Disorders > Flashcards

Pharm - Coagulation Disorders Flashcards

1
Q

COX inhibitors (antiplatelet drugs)

A

Aspirin (Ibuprofen)

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2
Q

ADP P2Y12 inhibitors (Antiplatelet drugs)

A

Clopidogrel, Ticlopidine, (Prasugrel)

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3
Q

Phosphodiesterase Inhibitors (Antiplatelet drugs)

A

Dipyridamole (Boner Pills)

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4
Q

GpIIb/IIIa inhibitors (antiplatelet drugs)

A

Abciximab, Eptifibatide (Tirofiban)

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5
Q

PAR-1 inhibitors (Antiplatelet drugs)

A

Vorapaxar

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6
Q

Aspirin MOA

A

irreversible COX-1 inhibitor, reduces TxA2 production, reduces platelet aggregation

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7
Q

P2Y12 receptor antagonists MOA

A

Clopidogrel, Ticlopidine, Prasugrel –> block effect of ADP at receptor, inhibit platelet function/activation/aggregation

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8
Q

GpIIb/IIIa antagonists MOA

A

Abciximab, Eptifibatide, Tirofiban –> block binding of fibrinogen to activated platelet receptor

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9
Q

PDE inhibitor MOA

A

Dipyridamole –> inhibits the catalysis of cAMP and cGMP –> elevated cAMP levels inhibit platelet function

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10
Q

PAR-1 antagonist MOA

A

Vorapaxar –> block thrombin-induced platelet aggregation

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11
Q

Major adv effects of platelet inhibitors

A

bleeding

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12
Q

Contraindications to use of platelet inhibitors

A

pts w/ conditions pre-disposing them to bleeding –> PMH of active pathological bleeding, trauma, surgery,

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13
Q

Aspirin and Ibuprofen - both act on COX - which one is irreversible? (and other one is reversible)

A

Aspirin = irreversible (ibuprofen = reversible)

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14
Q

What effect does aspirin have on the PT or PTT?

A

none

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15
Q

Why does aspirin have specificity for the platelet? (B/c endothelial cells have COX also)

A

platelets are anucleat –> have no ability to recover from COX inhibition, b/c cannot synthesize more. Endothelial cells can regenerate COX

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16
Q

What do endothelial cells COX produce, why is it impt?

A

PGI2, it inhibits platelet action

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17
Q

What does the dose/response profile for aspirin look like compared to the dose/risk profile? (Idk how to ask this question)

A

there is no additional clinical effect w/ increased dose, only increase risk

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18
Q

Adverse effects of aspirin

A

GI related, they are dose dependent –> severely toxic in high doses (suicide), hepatic and renal toxicity

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19
Q

contraindications for aspirin use

A

previous hx of aspirin-induced bronchospasm

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20
Q

what happens when ADP binds the P2Y12 receptor on platelet surface

A

inhibition of adenylyl cyclase –> lower levels of cAMP, platelets have less inhibition

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21
Q

P2Y12 inhibitors - reversible or irreversible

A

Clopidogrel, Ticlopidine, Prasugrel –> irreversible

–> persistence of effect ~10 days

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22
Q

black box warning for Clopidogrel

A

poor Cyp2C9 metabolizers –> at risk for reduced response, genetic tests available

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23
Q

black box warning for Ticlopidine

A

second line tx due to life threatening hematologic toxicities –> agranulocytosis, neutropenia, thrombocytopenia, TTP, anemia

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24
Q

route of excretion for the P2Y12 inhibitors

A

Clopidogrel, Ticlopidine, Prasugrel –> hepatic/renal elimination

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25
Q

PDE inhibitor MOA

A

Dipyridamole –> induce elevations in cAMP –> block release of AA from membrane phospholipids, reduce TxA2 –> less inhibition of platelets
also, stimulates release PGI2 (prostacyclin) which induces adenylate cyclase, thus raising cAMP levels , inhibit platelet aggregation even more

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26
Q

Sweatman quote about Dipyridamole

A

“It is uninteresting w/ regards to adverse effects”

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27
Q

GpIIb/IIIa inhibitors route of admin

A

Abciximab, Eptifibatide, Tirofiban –> IV

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28
Q

Abciximab

A

Fab fragment of chimeric monoclonal Ab –> NONCOMPETITIVE (causes steric hindrance, conformational change) of GpIIb/IIIa site

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29
Q

Abciximab reversible or irreversible

A

irreversible - protracted duration up to 2 weeks

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30
Q

Reactions seen to these GpIIb/IIIa antagonists

A

Abciximab, Eptifibatide, Tirofiban –> anaphylactic reactions

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31
Q

adv effect seen with Abciximab

A

thrombocytopenia –> numan anti-chimeric Ab formation to abciximab

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32
Q

PAR-1 antagonist route of admin

A

Vorapaxar –> oral

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33
Q

Vorapaxar half life / reversibility

A

technically reversible –> but t1/2 = 8 days –> effectively irreversible

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34
Q

Vorapaxar persistence

A

up to 4 weeks –> Holding a dose will do NOTHING to correct bleeding or reduce risk

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35
Q

PAR-1 antagonist metabolism/elimination

A

Vorapaxar –> hepatic metabolism (3A4) - fecal elimination

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36
Q

Herbal Product Interactions w/ antiplatelet drugs

A

Ginkgo Biloba - antiplatelet properties
garlic - antiplatelet properties
ginger - inhibits TxA synthetase, a platelet aggregation inducer

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37
Q

indirect thrombin inhibitors (anticoagulant drugs)

A

Heparin

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38
Q

Heparin antidote

A

protamine sulfate

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39
Q

direct thrombin inhibitors (anticoagulant drugs)

A

Dabigatran (Bivalirudin, Lepirudin)

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40
Q

Factor Xa inhibitors (anticoagulant drugs)

A

Enoxaparin, Apixaban, Rivaroxaban (Fondaparinux)

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41
Q

inhibitor of clotting factor synthesis (anticoagulant drug)

A

Warfarin

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42
Q

Warfarin antidotes

A

prothrombin complex, Phytonadione vit K1

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43
Q

Heparin route of admin

A

IV

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44
Q

Heparin structure

A

glycosaminoglycan - chains of alternating D-glucosamine and uronic acid

45
Q

what does Heparin bind

A

binds ATIII (Antithrombin) (and also thrombin, form ternary complex)

46
Q

Heparin MOA

A

causes conformational change in Antithrombin (ATIII) accelerates ability of ATIII to inactivate thrombin, factor Xa, and factor IXa

47
Q

which clotting factor is least sensitive to action of Heparin

A

thrombin

48
Q

what is the structure of what is going on when heparin is indirectly inhibiting thrombin?

A

ternary complex –> heparin/ATIII complex binds to thrombin

49
Q

How is the MOA of heparin on Factor Xa different?

A

inactivation of factor Xa does not require heparin/ATIII complex (I think he means it does not require “ternary complex” formation)

50
Q

low molecular weight heparin

A

enoxaparin

51
Q

enoxaparin MOA

A

catalyzes inhibition of factor Xa by ATIII

52
Q

enoxaparin cannot do…

A

cannot accelerate inactivation of thrombin by ATIII (not long enough to form ternary complex)

53
Q

major adv effects of heparin

A

bleeding, THROMBOCYTOPENIA - immune mediated (HIT - heparin induced thrombocytopenia)

54
Q

what are you worried about with the LMWH

A

NOT thrombocytopenia –> much lower risk of thrombocytpenia w/ LMWH

55
Q

other possible adv effect w/ both unfractionated hep and LMWH

A

anaphylactic reactions –> derived from animal products, may be antigenic

56
Q

Monitoring Heparin drug dosing

A

aPTT

57
Q

Monitoring LMWH

A

(enoxaparin) - lower impact on aPTT test, instead use Factor Xa assay

58
Q

can you give Hep for outpatient?

A

No

59
Q

antidote for Heparin

A

Protamine

60
Q

what is the antidote for Hep derived from?

A

Protamine is derived from fish sperm

61
Q

who do you need to be careful of with protamine

A

ppl with a fish hypersensitivity –> b/c it is derived from fish sperm

62
Q

which enantiomer of Warfarin is more potent

A

S

63
Q

route of admin for Warfarin

A

oral –> can give outpatient

64
Q

warfarin MOA

A

inhibits hepatic synthesis of vit K dependent coagulation factors II, VII, IX, and X, and proteins C and S

65
Q

What specifically does warfarin act on

A

the C1 subunit of the vit K epoxide reductase (VKORC1) enzyme – is a genetic variable

66
Q

result of warfarin therapy

A

depletion of reduced form of vit K –> limits gamma-carboxylation of vit K dependent coag proteins

67
Q

what does warfarin onset depend on?

A

persistence of individual cofactors already formed

68
Q

Which factors deplete first/quickest

A

Protein C and S, which are anticoagulant - this necessitates bridging therapy

69
Q

bridgin therapy with Warfarin

A

must co-admin Heparin to prevent initial hypercoagulable state caused by warfarin depleting protein C and S

70
Q

Monitoring clinical activity of warfarin

A

PT assay

71
Q

Pharmacokinetic issues with warfarin

A

CYP2C9 inhibitors or inducers affect levels of active s-warfarin –> Cimetidine (OTC) inhibitor CYP activity, bleed into urine

72
Q

Pharmacogenetics of warfarin

A

CYP2C9 and VKROC1 –> variability in pt response –> African Americans may have 2C9 allele not currently tested for

73
Q

Heparin vs Warfarin - which has a longer duration of actioin?

A

Warfarin - chronic duration, on the order of days

74
Q

site and speed of action for hep and warfarin

A

hep - blood, rapid

warfarin - liver, slow

75
Q

Hep v Warfarin - teratogenecity

A

warfarin - cannot use during pregnancy

heparin = “happy” during pregnancy

76
Q

Apixaban, Rivaroxaban MOA

A

bind to and directly inhibit factor Xa –> thrombin inhibition

77
Q

do Apixaban and Rivaroxaban require ATIII?

A

no

78
Q

clinical utility of direct factor Xa inhibitors

A

Apixaban, Rivaroxaban –> tx and prophylaxis of DVT and PE, stroke prophylaxis

79
Q

Apixaban, Rivaroxaban route of admin

A

oral

80
Q

toxicity of Apixaban, Rivaroxaban

A

Bleeding –> no reversal agent available

81
Q

Fondaparinux MOA

A

bind to ATIII which inhibits factor Xa (indirectly), –> thrombin inhibition

82
Q

Fondaparinux route of admin

A

IV or SC

83
Q

clinical utility of indirect factor Xa inhibitors

A

Fondaparinux - tx and prophylaxis of DVT and PE; stroke prophylaxis

84
Q

Fondaparinux toxicity

A

bleeding –> no reversal agent available

85
Q

Dabigatran, Bivalirudin, Lepirudin MOA

A

bind to and directly inhibit both free and clot-bound thrombin

86
Q

Route of Admin for Dabigatran

A

oral (other direct thrombin inhibitors are IV)

87
Q

Dabigatran toxicity

A

bleeding; no reversal agent

88
Q

Apixaban, Rivaroxaban pharmacokinetics

A

metabolized through Cyp, potential drug-drug interactions

89
Q

Dabigatran ADME shit

A

can interact w/ P-gp inhibitors or inducers

90
Q

Warfarin antagonists

A

Phytonadione; Vit K1

Prothrombin complex concentrate (PCC)

91
Q

Phytonadione vit K1 MOA

A

identical to natural K vitamins

92
Q

Phytonadione clinical utility

A

prophylaxis or tx of hemorrhage, hemorrhagic diseases of newborn, hypoprothrombinemia, nutritional supplementation and vit K deficiency

93
Q

Prothrombin complex concentrate componenets

A

factors II, VII, IX, and X - antithrombotic proteins C and S

94
Q

plasminogen activators (thrombolytic drugs)

A

Alteplase, t-PA (Reteplase, Tenecteplase, streptokinase)

95
Q

inhibitors of fibrinolysis (thrombolytic drugs)

A

aminocaproic acid

96
Q

Alteplase (and derivatives) MOA

A

specific in activating fibrin-bound plasminogen

97
Q

streptokinase MOA

A

has no specificity for fibrin-bound plasminogen –> has the ability to activate both free and fibrin-bound forms

98
Q

activation of circulating plasminogen results..

A

generation of activated plasmin that overwhelms alpha2-antiplasmin -

99
Q

what can unopposed plasmin in circulation do

A

trigger a systemic lytic state

100
Q

drugs that are products of recombinant genetic technology

A

drugs ending in “-plase”

101
Q

use of thrombolytics

A

early MI, early ischemic stroke, direct thrombolysis of severe PE

102
Q

thrombolytics adverse events

A

bleeding - internal, intacranial, retroperitoneal, GI, GU, respiratory

103
Q

Aminocaproic Acid

A

antifibrinolytic drug - use for hemorrhage and hyperfibrinolysis

104
Q

aminocaproic acid MOA

A

blocks conversion of plasminogen to plasmin

105
Q

aminocaproic acid metabolism and elimination

A

hepatic metabolism, hepatic/renal elimination

106
Q

Aminocaproic acid adv effects

A

short term adversity to CV system, especially when IV

107
Q

aminocaproic acid contraindicated

A

DIC or active intracascular clotting w/out concurrent use of heparin

108
Q

aminocaproic acid - monitor cardiac patients

A

hypotension and bradycardia may occur if you slam the IV

HEME (12 decks)

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