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Pharm - Coagulation Disorders Flashcards

(108 cards)

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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
PDE inhibitor MOA
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
26
Sweatman quote about Dipyridamole
"It is uninteresting w/ regards to adverse effects"
27
GpIIb/IIIa inhibitors route of admin
Abciximab, Eptifibatide, Tirofiban --> IV
28
Abciximab
Fab fragment of chimeric monoclonal Ab --> NONCOMPETITIVE (causes steric hindrance, conformational change) of GpIIb/IIIa site
29
Abciximab reversible or irreversible
irreversible - protracted duration up to 2 weeks
30
Reactions seen to these GpIIb/IIIa antagonists
Abciximab, Eptifibatide, Tirofiban --> anaphylactic reactions
31
adv effect seen with Abciximab
thrombocytopenia --> numan anti-chimeric Ab formation to abciximab
32
PAR-1 antagonist route of admin
Vorapaxar --> oral
33
Vorapaxar half life / reversibility
technically reversible --> but t1/2 = 8 days --> effectively irreversible
34
Vorapaxar persistence
up to 4 weeks --> Holding a dose will do NOTHING to correct bleeding or reduce risk
35
PAR-1 antagonist metabolism/elimination
Vorapaxar --> hepatic metabolism (3A4) - fecal elimination
36
Herbal Product Interactions w/ antiplatelet drugs
Ginkgo Biloba - antiplatelet properties garlic - antiplatelet properties ginger - inhibits TxA synthetase, a platelet aggregation inducer
37
indirect thrombin inhibitors (anticoagulant drugs)
Heparin
38
Heparin antidote
protamine sulfate
39
direct thrombin inhibitors (anticoagulant drugs)
Dabigatran (Bivalirudin, Lepirudin)
40
Factor Xa inhibitors (anticoagulant drugs)
Enoxaparin, Apixaban, Rivaroxaban (Fondaparinux)
41
inhibitor of clotting factor synthesis (anticoagulant drug)
Warfarin
42
Warfarin antidotes
prothrombin complex, Phytonadione vit K1
43
Heparin route of admin
IV
44
Heparin structure
glycosaminoglycan - chains of alternating D-glucosamine and uronic acid
45
what does Heparin bind
binds ATIII (Antithrombin) (and also thrombin, form ternary complex)
46
Heparin MOA
causes conformational change in Antithrombin (ATIII) accelerates ability of ATIII to inactivate thrombin, factor Xa, and factor IXa
47
which clotting factor is least sensitive to action of Heparin
thrombin
48
what is the structure of what is going on when heparin is indirectly inhibiting thrombin?
ternary complex --> heparin/ATIII complex binds to thrombin
49
How is the MOA of heparin on Factor Xa different?
inactivation of factor Xa does not require heparin/ATIII complex (I think he means it does not require "ternary complex" formation)
50
low molecular weight heparin
enoxaparin
51
enoxaparin MOA
catalyzes inhibition of factor Xa by ATIII
52
enoxaparin cannot do...
cannot accelerate inactivation of thrombin by ATIII (not long enough to form ternary complex)
53
major adv effects of heparin
bleeding, THROMBOCYTOPENIA - immune mediated (HIT - heparin induced thrombocytopenia)
54
what are you worried about with the LMWH
NOT thrombocytopenia --> much lower risk of thrombocytpenia w/ LMWH
55
other possible adv effect w/ both unfractionated hep and LMWH
anaphylactic reactions --> derived from animal products, may be antigenic
56
Monitoring Heparin drug dosing
aPTT
57
Monitoring LMWH
(enoxaparin) - lower impact on aPTT test, instead use Factor Xa assay
58
can you give Hep for outpatient?
No
59
antidote for Heparin
Protamine
60
what is the antidote for Hep derived from?
Protamine is derived from fish sperm
61
who do you need to be careful of with protamine
ppl with a fish hypersensitivity --> b/c it is derived from fish sperm
62
which enantiomer of Warfarin is more potent
S
63
route of admin for Warfarin
oral --> can give outpatient
64
warfarin MOA
inhibits hepatic synthesis of vit K dependent coagulation factors II, VII, IX, and X, and proteins C and S
65
What specifically does warfarin act on
the C1 subunit of the vit K epoxide reductase (VKORC1) enzyme -- is a genetic variable
66
result of warfarin therapy
depletion of reduced form of vit K --> limits gamma-carboxylation of vit K dependent coag proteins
67
what does warfarin onset depend on?
persistence of individual cofactors already formed
68
Which factors deplete first/quickest
Protein C and S, which are anticoagulant - this necessitates bridging therapy
69
bridgin therapy with Warfarin
must co-admin Heparin to prevent initial hypercoagulable state caused by warfarin depleting protein C and S
70
Monitoring clinical activity of warfarin
PT assay
71
Pharmacokinetic issues with warfarin
CYP2C9 inhibitors or inducers affect levels of active s-warfarin --> Cimetidine (OTC) inhibitor CYP activity, bleed into urine
72
Pharmacogenetics of warfarin
CYP2C9 and VKROC1 --> variability in pt response --> African Americans may have 2C9 allele not currently tested for
73
Heparin vs Warfarin - which has a longer duration of actioin?
Warfarin - chronic duration, on the order of days
74
site and speed of action for hep and warfarin
hep - blood, rapid | warfarin - liver, slow
75
Hep v Warfarin - teratogenecity
warfarin - cannot use during pregnancy | heparin = "happy" during pregnancy
76
Apixaban, Rivaroxaban MOA
bind to and directly inhibit factor Xa --> thrombin inhibition
77
do Apixaban and Rivaroxaban require ATIII?
no
78
clinical utility of direct factor Xa inhibitors
Apixaban, Rivaroxaban --> tx and prophylaxis of DVT and PE, stroke prophylaxis
79
Apixaban, Rivaroxaban route of admin
oral
80
toxicity of Apixaban, Rivaroxaban
Bleeding --> no reversal agent available
81
Fondaparinux MOA
bind to ATIII which inhibits factor Xa (indirectly), --> thrombin inhibition
82
Fondaparinux route of admin
IV or SC
83
clinical utility of indirect factor Xa inhibitors
Fondaparinux - tx and prophylaxis of DVT and PE; stroke prophylaxis
84
Fondaparinux toxicity
bleeding --> no reversal agent available
85
Dabigatran, Bivalirudin, Lepirudin MOA
bind to and directly inhibit both free and clot-bound thrombin
86
Route of Admin for Dabigatran
oral (other direct thrombin inhibitors are IV)
87
Dabigatran toxicity
bleeding; no reversal agent
88
Apixaban, Rivaroxaban pharmacokinetics
metabolized through Cyp, potential drug-drug interactions
89
Dabigatran ADME shit
can interact w/ P-gp inhibitors or inducers
90
Warfarin antagonists
Phytonadione; Vit K1 | Prothrombin complex concentrate (PCC)
91
Phytonadione vit K1 MOA
identical to natural K vitamins
92
Phytonadione clinical utility
prophylaxis or tx of hemorrhage, hemorrhagic diseases of newborn, hypoprothrombinemia, nutritional supplementation and vit K deficiency
93
Prothrombin complex concentrate componenets
factors II, VII, IX, and X - antithrombotic proteins C and S
94
plasminogen activators (thrombolytic drugs)
Alteplase, t-PA (Reteplase, Tenecteplase, streptokinase)
95
inhibitors of fibrinolysis (thrombolytic drugs)
aminocaproic acid
96
Alteplase (and derivatives) MOA
specific in activating fibrin-bound plasminogen
97
streptokinase MOA
has no specificity for fibrin-bound plasminogen --> has the ability to activate both free and fibrin-bound forms
98
activation of circulating plasminogen results..
generation of activated plasmin that overwhelms alpha2-antiplasmin -
99
what can unopposed plasmin in circulation do
trigger a systemic lytic state
100
drugs that are products of recombinant genetic technology
drugs ending in "-plase"
101
use of thrombolytics
early MI, early ischemic stroke, direct thrombolysis of severe PE
102
thrombolytics adverse events
bleeding - internal, intacranial, retroperitoneal, GI, GU, respiratory
103
Aminocaproic Acid
antifibrinolytic drug - use for hemorrhage and hyperfibrinolysis
104
aminocaproic acid MOA
blocks conversion of plasminogen to plasmin
105
aminocaproic acid metabolism and elimination
hepatic metabolism, hepatic/renal elimination
106
Aminocaproic acid adv effects
short term adversity to CV system, especially when IV
107
aminocaproic acid contraindicated
DIC or active intracascular clotting w/out concurrent use of heparin
108
aminocaproic acid - monitor cardiac patients
hypotension and bradycardia may occur if you slam the IV

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