Drugs Flashcards

1
Q

Warfarin (2)

A

1) Phytonadione 2) Mephyton

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2
Q

Indirect Thrombin Inhibitors (4)

A

1) Warfarin (Coumadin) 2) UF/ HMW heparin 3) LMW Heparin (Lovenix) 4) Fondaparinux (Arixtra)

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3
Q

Direct Thrombin Inhibitors (3)

A

1) Lepirudin (Refludon) 2) Argatroban 3) Bivalirudin (Angiomax)

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4
Q

Warfarin -MOA

A

Inhibits Vitamin-K dependent factors II, VII, IX, X (and Protein C & Protein S) via inhibition of Vitamin-K Epoxide Reductase

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5
Q

Warfarin -Monitoring

A

PT (and INR)

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6
Q

Lepirudin -(trade name) -Drug Class -Use

A

(Refludan); synthetic form of hirudin, -Class = DTI -Use: Alternative anticoagulant/ therapy for HIT patients

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7
Q

Lepirudin -Monitoring (2) (why?)

A

1) aPTT 2) Renal f(x) Why: -VERY antigenic -RENAL clearance (biggest difference between the similar drug, Argatroban=hepatic clearance)

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8
Q

Bivalirudin -(trade name) -Drug Class -Use -Monitoring

A

(Angiomax) -Class = DTI -Use: anticoagulant for HIT patients (expensive) -Monitoring = ECT (but ACT is commonly used)

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9
Q

Argatroban -Drug Class -Monitoring -Clearance?

A

Class = DTI -Monitoring = aPTT

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10
Q

UF Heparin (aka) -MOA (2)

A

aka HMWH (5,000-30,000 Da) - potentiates AT-III (>1000x) interaction with: 1) Thrombin 2) Factor Xa

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11
Q

LMWH -MOA -T1/2

A

-potentiates AT-III interaction with “Factor Xa” only -T1/2: 3-7 hrs (much longer than UF)

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12
Q

ASA -MOA (2)

A

Blocks platelet aggregation via: 1) inactivation of COX-1: -inhibits platelet ADP release -inhibits TXA2 & PGE2 synthesis from Arachadonic Acid 2) modifies COX-2: -production of “lipoxins”

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13
Q

Thienopyidines (3)

A

1) Ticlopidine (Ticlid) 2) Clopidogrel (Plavix) 3) Prasugrel (Effient)

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14
Q

Ticlopidine -(trade name) -Black Box Warning (3)

A

(Ticlid) = Thienopydine Black Box: 1) Aplastic Anemia 2) Neutropenia 3) Thrombotic Thrombocytopenia Purpura

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15
Q

Clopidogrel -(trade name) -Drug Class

A

(Plavix) Thienopydines

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16
Q

Prasugrel -(trade name) -Drug Class

A

(Effient) Thienopydines

17
Q

Thienopydines -MOA (diff. from ASA)

A

Blocks “ADP-mediated” platelet aggregation which blocks platelet receptors GPIIb/IIIa

18
Q

ASA -Dose for complete platelet inactivation

A

approx. 160mg = complete platelet inactivation

19
Q

ASA -Side Effects (3)

A

1) Bleeding 2) GI (gastric ulcers) 3) Kidney damage (interstitial nephritis)

20
Q

GP IIb/IIIa Blockers (3)

A

1) Abciximab (Repro) 2) Eptifibatide (Integrilin) 3) Tirofiban (Aggrastat)

21
Q

Dipyridamole -(trade name) & Drug Class -MOA

A

(Persantine) = Platelet Inhibitor blocks cAMP which ultimately inhibits TXA2 synthesis (w/ NO effect on PG)

22
Q

Platelet Inhibitors 1) 2a) 2b) 3)

A

1) Dipyridamole (Persantine) 2a) Dextran 70 (Macrodex) 2b) Dextran 40 (Rheomacrodex) 3) Hespan

23
Q

Dextrans (2) -MOA -Max Dose

A

1) Dextran 70 (Macrodex) - Plt. inhibitor 2) Dextran 40 (Rheomacrodex) - Plt. inhibitor -Decreases Factors V, VIII and IX functionality -MAX DOSE = 2g/kg (20 ml/kg)

24
Q

Hespan -MOA -Max Dose

A

-Platelet Inhibitor (glucose polymer) -significantly reduces Factor VIII; results in elevated aPTT -MAX DOSE = 20 ml/kg

25
Q

Thrombolytics (4)

A

1) Alteplase/ tPA (Activase) 2) Reteplase (Retavase) 3) Streptokinase (Streptase) 4) Urokinase (Kinlytic)

26
Q

Streptokinase -(trade name) -MOA

A

(Streptase) = Thrombolytic -attaches to plasminogen and converts it to plasmin; also destroys Fibrinogen, FV, FVII

27
Q

Antithrombin III -2 synthetic forms and sources

A

1) Thrombate - made from pooled human plasma 2) Atryn - genetically modified goat milk