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EOB - Blood Cardio > Heme Pharm > Flashcards

Heme Pharm Flashcards

1
Q

MOA of heparin?

A

Binds to antithrombin, enhancing activity (reducing thrombin and Factor Xa activity)

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2
Q

Clinical use of heparin?

A

Immediate anticoagulation for PE, ACS, MI, DVT. PREGNANCY

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3
Q

How do you test for heparin tox?

A

PTT

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4
Q

Toxicity of heparin?

A

Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions.

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5
Q

Antidote to heparin?

A

Protamine sulfate

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6
Q

What is LMW heparin?

A

Heparins that act more on Xa and havd better bioavailability and longer half life. Can be administered without lab monitoring; not easily reversible.

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7
Q

Examples of LMW Heparin?

A

Enoxaparin, dalteparin

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8
Q

What is HIT?

A

Heparin-induced thrombocytopenia - development of IgG antibodies against heparin bound to PF4. Immune complex activates platelets - thrombosis and thrombocytopenia

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9
Q

What are argatroban and bivalirudin?

A

Direct thrombin inhibitors. Use instead of heparin for anticoagulating pts with HIT

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10
Q

What is the MOA of warfarin?

A

Blocks Vitamin K epoxide reductase, preventing synthesis of II, VII, IX, and X as well as protein C and S

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11
Q

How to check for warfarin tox?

A

PT

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12
Q

Clinical use of heparin?

A

Chronic anticoagulation - STEMI, VTE, and prevention of stroke in a-fib. NOT FOR PREGNANT WOMEN.

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13
Q

Warfarin toxicity?

A

Bleeding, teratogenic, skin necrosis, drug-drug interactions

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14
Q

Antidote of warfarin?

A

Vitamin K or fresh frozen plasma if severe

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15
Q

What are apixaban and ravaroxaban?

A

Direct factor Xa inhibitors

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16
Q

What are Xa inhibitors used for?

A

Treatment and prophylaxis of DVT and PE, a-fib stroke prophylaxis

17
Q

How is heparin administered?

A

IV

18
Q

What are alteplase, reteplase, and tenecteplase?

A

Thrombolytics

19
Q

MOA of thrombolytics?

A

Aids conversion of plasminogen to plasmin; Increases both PT and PTT.

20
Q

Clinical use of thrombolytics?

A

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

21
Q

Toxicity of thrombolytics?

A

Bleeding

22
Q

Antidote to thrombolytics?

A

Aminocaproic acid

23
Q

Aspirin MOA?

A

Irreversible inhibition of COX (both 1 and 2) enzyme by covalent acetylation. Lasts until new platelets are produced.

24
Q

Effects of aspirin?

A

Increased BT, decreased TXA2 and prostaglandins. NO effect on PT or PTT

25
Q

Clinical use of aspirin?

A

Antipyretic, analgesic, anti-inflammatory, anti-platelet

26
Q

Aspirin toxicity?

A

Gastric ulceration, tnnitus. Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding.

27
Q

What is the MOA of clopidogel, ticlopidine, prasugrel, and ticagrelor?

A

ADP receptor inhibitors - prevent platelet aggregation by blocking ADP receptors on platelet surfaces. Inhibition of fibrinogen binding by preventing GP IIb/IIIa from binding fibrinogen.

28
Q

Clinical use of ADP receptor inhibitors?

A

Coronary stenting; decrease incidence or recurrence of thrombotic stroke

29
Q

Toxicity of ADP receptor inhibitors?

A

Neutropenia; TTP/HUS

30
Q

What are cliostazol and dipyridamole?

A

PDEIII inhibitors. Increase cAMP in platelets, whihc inhibits platelet aggregation; vasodilators

31
Q

Clinical use of PDEIII inhibitors?

A

Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs, angina prophylaxis

32
Q

Toxicity of PDEIII inhibitors?

A

Nausea, headache, facial flushing, hypotension, abdominal pain

33
Q

What are abciximab, eptifibatide, tirofiban?

A

GP IIb/IIIa inhibitors - prevent platelet aggregation

34
Q

Clinical use of GP IIb/IIIa inhibitors

A

Unstable angina, PCTA

35
Q

Tox of GPIIb/IIIa inhibitors?

A

Bleeding, thrombocytopenia

EOB - Blood Cardio (5 decks)

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