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Pharmacology
Phar 512 Drugs
| Question | Answer |
|---|---|
| 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
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