Heme Drugs Flashcards Preview

Step Nuggets > Heme Drugs > Flashcards

Flashcards in Heme Drugs Deck (14):
1

Heparin

cofactor for activation of antithrombin -> decreases thrombin and factor Xa
use: immediate anticoagulation for PE, ACS, DVT...
acts on the intrinsic pathway (PTT)
used as anticoag during pregnancy
tox: bleeding, thrombocytopenia (HIT), osteoporosis

2

Heparin toxicity reversal

Protamine sulfate

3

Argatroban, bivalirudin

derived from leeches
inhibit thrombin directly
used instead of heparin with HIT

4

Warfarin - Mechanism

interferes with gamma-carboxylation of Vitamin K dependent factors (2,7,9,10,C,S)
metabolized by P450 - common interactions
increases PT (extrinsic pathway)

5

Warfarin - Use

chronic anticoagulation after MI, in AFib
follow PT/INR
crosses placenta, teratogen, so no use in pregnancy

6

Warfarin - Toxicity

bleeding, teratogenic, skin/tissue necrosis, common with P450 interactions
reversal: give Vitamin K or FFP

7

Apixaban, Rivaroxaban

direct factor Xa inhibitors
anticoagulation
doesn't require constant monitoring
tox: bleeding, no reversal agent available

8

Thrombolytics, tPA, rPA

increase conversion of plasminogen to plasmin
recall: plasmin cleaves thrombin and fibrin clots
increases PT and PTT, no effect on platelets
use: early MI or stroke, severe PE
tox: bleeding, contraindicated in active bleeding or recent surgery;

9

Thrombolytic toxicity treatment

FFP to restore factors
aminocaproic acid

10

Aspirin

irreversibly inhibits COX (both 1 and 2) by aceytlation
effects last until new platelets are produced
increases BT, decreases TXA2 and prostagladins; no effects on PT or PTT
use: antipyretic, analgesic, anti-inflammatory, antiplatelet

11

Aspirin Toxicity

Gastric ulceration and bleeding, tinnitus, analgesic nephropathy
Reye syndrome in children with viral illness
initially causes respiratory alkalosis, then a superimposed metabolic acidosis

12

Clopedigrel, have -grel- in the name somewhere, and ticlopidine

ADP receptor inhibitors
block platelet aggregation by blocking ADP receptors, thus inhibiting fibrinogen binding by blocking surface expression of Gp IIb/IIIa
use: ACS, coronary stenting
tox: neutropenia with ticlopidine; TTP or HUS

13

Cilostazol, dipyridamole

phosphodiesterase III inhibitor, increases cAMP in platelets and inhibiting aggregation; also vasodilators
use: claudication, stroke/TIA prevention, angina prophylaxis
tox: nausea, headache, flushing, hypotension, abdominal pain

14

Abciximab, eptifibatide, tirofiban

Gp IIb/IIIa inhibitors
bind to activated Gp IIb/IIIa on platelets, preventing aggregation
use: unstable angina, during angioplasty