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Pharmacology

Phar 512 Drugs

QuestionAnswer
UFH Antithrombotic, Potentiates the action of AT III, inactivates factors IIa and Xa
LMWH antithrombotic, potentiates the action of AT III, inhibits factor Xa and IIa; 25-50% of molecules have 18 saccharide units, hepatic metabolism
Factor Xa Inhibitors (oral) antithrombotic, binds directly to Xa
Direct thrombin inhibitors antithrombotic, inhibits factor II only; CAN get to clot-bound thrombin
warfarin antithrombotic, inhibits vit k epoxide reductase, which decreases the gamma-carboxylation of vit k dependent clotting factors
Needed to bind thrombin AND Xa >18 saccharide glycosaminoglycans
aPTT (activated partial thromboplastin time) measures the efficacy of intrinsic and common pathways
ACT activated clotting time
Needed to inhibit Xa (UFH) unique pentasaccharide
Does UFH cross the breast milk or placenta? No
UFH ADEs Bleeding, osteoporosis, thrombocytopenia, overdose
Benefits of UFH cheap, effective, easily reversible, can use in pregnancy
Limitations of UFH variable coagulant response, intensive monitoring, risk of HIT
HIT Type 1 -not immune mediated, mild/moderate decrease in platelet count, not clinically significant, usually occurs within 2 days, count returns to normal with continued heparin use. More common than HIT type 2
HIT Type 2 sever drop in platelet count, immune mediated reaction, clinically significant, usually occurs within 4-10 days, stop heparin to return to normal
HIT pathophysiology 1. PF4 complexes with heparin 2. conformation change that is highly antigenic 3. IgG and igM are formed 4. bind to heparin-PF4 complex 5. activated platelets clot
HIT complications new thrombosis, skin necrosis, venous thrombosis, arterial thrombosis. death
4T Score Thromocytopenia, Timing, THrombosis, oTher causes (score 0-3 low, 6-8 high)
When to monitor Anti-Xa activity for LMWH obesity, pregnancy, poor renal function
LMWH ADEs bleeding, HIT
LMWH benefits no monitoring, DOC pregnancy, less incidence of major bleed vs. UFH, less incidence of HIT
LMWH limitations not completely reversible, renally excreted, renal adjustments needed in renal dysfunction
Enoxaparin LMWH
Dalteparin LMWH
Tinzaparin LMWH
Fondaparinux potentiates the action of AT III, indirect inhibitor of factor Xa; Hepatic metabolism
Fondaparinux indications DVT px, VTE tx, ACS
Fondaparinux dosing >100 kg = 10mg SQ d; 50-100kg = 7.5mg SQ d; <50kg= 5 mg SQ d
Fondaparinux Contraincications CrCl<30 mL/min
Rivaroxaban Factor Xa inhibitor
Rivaroxaban indications Stroke PX in NVAF, DVT px, VTE tx
Rivaroxaban warnings hemorrhage in pregnancy; avoid with mod-severe hepatic impairment; renal dosing, CYP3A4
Apixaban Factor Xa inhibitor
Apixaban indications Stroke Px, DVT Px, VTE Tx
Edoxaban Factor Xa inhibitor
Edoxaban indications Stroke Px in NVAF, VTE tx
Edoxaban warnings do not use for NVAF in patients with CrCl > 95 ml/min; renal dosing
Which Xa inhibitor is not used for Px in NVAF? fondaparinux
Which Xa inhibitor is not used for DVT px in hip/knee surgery? edoxaban
Edoxaban contraindications CrCl<15
Rivaroxaban contraindications VTE px/tx CrCl < 30, NVAF CrCl < 15
Apixaban reduced dosing Scr more than or equal to 1.5
Xa inhibitors ADEs bleeding, HIT, (rivaroxaban: increased LFTs, muscle cramps/spasms)
Xa inhibitors benefits almost no incidence of HIT, no lab monitoring
Xa inhibitors limitations most are contraindicated in renal dysfunction
Lepirudin direct thrombin inhibitor, IV, increases INR
Bivalrudin direct thrombin inhibitor, IV
Argatroban direct thrombin inhibitor, IV, increases INR, hepatic clearance
Dabigatran direct thrombin inhibitor, oral, increases INR
Reversal agent for DTIs NONE
Dabigatran renal dosing CrCl 15-30 = 75 mg po BID
Dabigatran indications Stroke Px in NVAF, DVT Px, VTE tx
Dabigatran warnings high rate of GI upset, increase incidence of MI, NO Reversal agent, need to start 5-10 days parenteral tx first
Dabigatran C/I patients with mechanical heart valves, Incrased thromboembolic events
Monitroing for bivalirudin ACT
monitoring for argatroban aPTT
monitoring for lepiruduin aPTT
DTI ADEs Bleeding, MI
Factors inhibited by warfarin II, VII, IX, X; decreases protein C and protein S
Does warfarin inhibit existing clotting factors? no, so we need a warfarin bridge in therapy
Warfarin monitoring PT; measures activity of II, VI, VII and X
INR Patients PT/normal mean PT (to the ISI power)
normal therapeutic range for INR 2.0 to 3.0 most indications
therapeutic INR index for prosthetic mechanical heart valves 2.5 to 3.5
higher INR means increased anticoagulation, bleeding
lower INR means decreased anticoagulation, clotting
INR frequency Daily for initiation, then q 2-3 days, then weekly until stable; monthly until 3 therapeutic INRs are achieved then q 12 weeks
how often should a patient with stable INR be monitored? every 12 weeks
Warfarin maintenance doses are ________ proportional to weight and ________ proportional to age directly, indirectly
Warfarin ADEs bleeding, skin necrosis, minor GI irritation
Warfarin drug interactions Several CYP enzymes, CYP2C9 is the most concerning
Warfarin dietary considerations consistent vit k intake, chronic alcohol drinking = increased clearance of warfarin, bing drinking = decrased metabolism of warfarin; smoking incrases metabolism of warfarin
Warfarin reversal agent phytonadione
Warfarin resistance stored vit K can be used even when warfarin is blocking the vit K epoxide reductase
suggestions for INR that is increased rapid reversal: PCC, prolonged effect: vitamin K
Aspirin antiplatelet, MOA: irreversibly inhibits COX in platelets, decreases thromboxane A2 and prostaglandin in life of the platelet (7-10 days)
Aspirin ADEs bleeding, GI (dose related) i.e. bleeds
ADP receptor antagonists MOA: inhibits P2Y12 receptors on platelets and prevents ADP from binding and activating platelets; takes 4-7 days to reach steady state
Ticlopidine ADP receptor antagonist; limited use due to severe neutropenia
Clopidogrel ADP receptor antagonist; binds irreversibly to P2Y12 receptor on platelets; prodrug CYP enzymes
Prasugrel ADP receptor antagonist; prodrug, binds irreversibly to P2Y12
Prasugrel indication ACS
Prasugrel advantages more rapid onset of action, 10x more potent
prasugrel C/I any history of stroke or TIA, active or recent pleeding;
prasugrel dose adjustments reduction for age > 75, if <60kg, decrase dose to 5 mg d
Ticagrelor ADP receptor antagonist; binds REVERSIBLY to the P2Y12 receptor
Ticagrelor indications ACS, stent thrombosis recution
Ticagrelor BBW Aspirin dose may be 325 mg for one dose, then must be <100 mg daily if combined with tacagrelor
Cangrelor ADP receptor antagonist: ATP analog, binds selectively to P2Y12 receptor and blocks ADP; suppresses platelets within 2 minutes
Cangrelor indications PCI
ADP receptor antagonists ADEs bleeding (thrombocytopenia), discomfort, elevated LFTS, dyspnea (ticagrelor and cangrelor)
Glycoprotein IIB/IIIA inhibitors MOA: blocks GP IIb/IIIa receptors and prevents fibrinogen binding; all IV drugs
GP IIB/III A indications PCI
Abciximab GP IIB/IIIa inhibitor
Eptifabatide GP IIB/IIIa inhibitor
Tirofiban GP IIB/IIIa inhibitor
GP IIB/IIIa inhibitor ADEs bleeding, thrmobocytopenia, antibody formation (abciximab only)
GP IIB/IIIa inhibitor C/Is Any H/O hemorrhagic stroke, suspected aoritc dissection, severe uncontrolled HTN, H/O cerebrovascular accident in last 2 years, thrombocytopenia, on warfarin with INR > 2, recent surgery or trauma (within last 12 weeks)
eptifibatide dosage adjustments decrease dose if CrCl <50, C/I in dialysis
tirofiban dosage adjustments decrase dose if CrCl < 30
fibrinolytics facilitate the conversion of plasminogen to plasmin
Alteplase recombinant form of tPA
Reteplase Recombinant plasminogen activator, Renal metabolism
Fibrinolytic inducations use to quickly dissolve clots in patients having: ischemic stroke, ACS, VTE
Fibrinolytic ADEs bleeding, thrombocytopenia,
Streptokinase ADE antibody formation
Fibrinolytic C/Is pregancny, active PUD, prolonged CPR (>10 min), h/0 hemorrhagic stroke, h/0 cerebrovascular accident in last 2 years, recent surery or head trauma (within last 12 weeks), severe uncontrolled hypertension, suspected aortic dissection, on warfarin INR >2
Bleeding- what to do 1. stop the anticoagulant, 2. give blood prodcuts, 3. administer a reversl agent
Bleeding- what to moitor H & H, decrased BP, blood in urine/stool, aPTT, INR, etc.
NO reversal agents for Factor Xa inhibitors, DTIs, antiplatelets
Protamine used for UFH and LMWH reversal to some extend
phytonadione vit k, used for warfarin reversal
aminocaprioc acid used for fibrinolytic reversal, keeps plassminogen from getting activated, mainly used in cardiac bypass surger
indarucizumab used to reverse the effects of dabigatran
HIT tx 1. discontinue heparin, 2. direct thrombin inhibitor (argatroban) 3. warfarin (start once platelet count is >150)
Created by: Bmiller01