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?

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?

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
Clinical use of aspirin?
Antipyretic, analgesic, anti-inflammatory, anti-platelet
26
Aspirin toxicity?
Gastric ulceration, tnnitus. Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding.
27
What is the MOA of clopidogel, ticlopidine, prasugrel, and ticagrelor?
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
Clinical use of ADP receptor inhibitors?
Coronary stenting; decrease incidence or recurrence of thrombotic stroke
29
Toxicity of ADP receptor inhibitors?
Neutropenia; TTP/HUS
30
What are cliostazol and dipyridamole?
PDEIII inhibitors. Increase cAMP in platelets, whihc inhibits platelet aggregation; vasodilators
31
Clinical use of PDEIII inhibitors?
Intermittent claudication, coronary vasodilation, prevention of stroke or TIAs, angina prophylaxis
32
Toxicity of PDEIII inhibitors?
Nausea, headache, facial flushing, hypotension, abdominal pain
33
What are abciximab, eptifibatide, tirofiban?
GP IIb/IIIa inhibitors - prevent platelet aggregation
34
Clinical use of GP IIb/IIIa inhibitors
Unstable angina, PCTA
35
Tox of GPIIb/IIIa inhibitors?
Bleeding, thrombocytopenia