Pharm Angina, Antiarrythmics, Antiplates, Anticoagulants Quiz

What do class I antiarrhythmics block?

Sodium channels; they slow conduction through cardiac muscle.

What do class II antiarrhythmics block?

Beta receptors; they slow heart rate and AV nodal conduction.

What do class III antiarrhythmics block?

Potassium channels; they delay repolarization and prolong the refractory period.

What do class IV antiarrhythmics block?

Calcium channels; verapamil and diltiazem slow AV nodal conduction.

What mnemonic remembers antiarrhythmic classes I-IV?

Some Block Potassium Channels: Sodium, Beta, Potassium, Calcium.

Which drugs are class IA antiarrhythmics?

Quinidine, procainamide, and disopyramide.

What is quinidine's mechanism?

Blocks sodium channels to slow conduction and potassium channels to delay repolarization.

Which antiarrhythmic causes cinchonism?

Quinidine. Think tinnitus, headache, and dizziness; also cardiotoxicity and an interaction with digoxin.

Which antiarrhythmic causes a lupus-like syndrome?

Procainamide. Its boxed warning highlighted in the lecture is blood dyscrasias.

What is the lecture's boxed warning for disopyramide?

Increased mortality; reserved for ventricular arrhythmias when other medications fail.

What class is mexiletine, and what does it treat?

Class IB sodium channel blocker; accelerates repolarization and treats symptomatic ventricular arrhythmias.

What are mexiletine's adverse effects and boxed warning in the lecture?

GI and neurologic effects; increased mortality in non-life-threatening arrhythmias.

Which drugs are class IC antiarrhythmics?

Flecainide and propafenone; markedly slow conduction according to the overview slide.

What major risks does the lecture emphasize for flecainide?

Serious adverse effects; increased mortality and heart failure in certain populations.

Which class IC drug also has beta-blocking activity?

Propafenone; caution with heart failure, AV block, and asthma. Boxed warning: proarrhythmic actions.

Which beta blockers are listed as class II antiarrhythmics?

Metoprolol, propranolol, acebutolol, and esmolol.

Which class II drug can cause adverse immunologic reactions?

Acebutolol.

What are amiodarone's boxed warnings highlighted in the lecture?

Pulmonary toxicity and liver toxicity.

What other amiodarone toxicities should you recognize?

Thyroid, cardiac, ophthalmic, and dermatologic toxicity; many drug interactions.

Why can amiodarone toxicity persist after the drug is stopped?

It is highly lipid soluble; toxicity may continue for weeks to months. It is metabolized by CYP3A4.

How does dronedarone compare with amiodarone?

Less toxic but less effective. Lecture boxed warning: increased death risk in severe heart failure.

Which antiarrhythmic belongs to both class II and class III?

Sotalol: beta blockade plus potassium channel blockade.

Which two class III drugs have torsades de pointes boxed warnings in the lecture?

Sotalol and dofetilide; avoid interacting QT-prolonging drugs.

What organ impairment especially matters for dofetilide?

Renal impairment increases its half-life/exposure. Verapamil is an important interaction.

What are verapamil and diltiazem's major adverse effects?

Bradycardia, AV block, heart failure, hypotension, peripheral edema, and constipation.

Which combinations can excessively slow AV nodal conduction?

Verapamil or diltiazem with beta blockers or digoxin.

What does digoxin do to cardiac conduction?

Decreases AV nodal conduction and SA node automaticity. Cardiotoxicity is a major concern; caution with diuretics.

Which drug does the lecture identify for converting acute supraventricular tachycardia?

IV adenosine; it decreases AV nodal conduction and increases AV nodal refractoriness.

Which drug treats torsades de pointes?

IV magnesium sulfate. The lecture also lists it for digoxin-induced arrhythmias; oral magnesium is ineffective for treating acute arrhythmias.

What causes stable angina, and what drug class is emphasized first?

Fixed atherosclerotic narrowing with increased oxygen demand; beta blockers reduce heart rate and contractility.

What causes unstable angina, and what treatment groups are needed?

Plaque rupture plus thrombus; anti-ischemic drugs plus antiplatelets and anticoagulants.

What causes variant (Prinzmetal) angina, and what treats it?

Coronary vasospasm; calcium channel blockers with or without nitrates. Avoid beta blockers, especially nonselective agents.

How does nitroglycerin relieve stable angina?

Venodilation reduces ventricular filling/preload, lowering cardiac oxygen demand.

How does nitroglycerin help variant angina?

Relaxes coronary artery spasm, increasing oxygen supply.

What are nitroglycerin's common adverse effects?

Headache, orthostatic hypotension, flushing, and reflex tachycardia.

What dangerous interaction must you remember for nitrates?

PDE-5 inhibitors such as sildenafil can cause profound, potentially fatal hypotension.

Why is a nitrate-free interval used?

Tolerance develops rapidly; an interval without nitrate helps prevent tolerance.

How do dihydropyridine calcium channel blockers help angina?

Amlodipine, nifedipine, and felodipine dilate arteries to lower afterload; also relieve coronary spasm.

What adverse effect strongly suggests a dihydropyridine calcium channel blocker?

Peripheral edema; also headache, flushing, and hypotension.

Which calcium channel blockers should be avoided in heart failure with reduced ejection fraction?

Verapamil and diltiazem because they decrease cardiac contractility.

What is ranolazine's antianginal mechanism and major risk?

Late sodium-current inhibition; major risk is QT prolongation. Little effect on heart rate or blood pressure.

What should be avoided with ranolazine according to the lecture?

Preexisting QT prolongation, other QT-prolonging drugs, hepatic impairment, and interacting CYP3A4 inhibitors.

How do antiplatelets, anticoagulants, and thrombolytics differ?

Antiplatelets reduce platelet aggregation; anticoagulants reduce fibrin formation; thrombolytics break down existing clots.

What is aspirin's antiplatelet mechanism?

Irreversible COX inhibition reduces thromboxane A2 formation; the effect lasts for the platelet's lifetime.

What are aspirin's major adverse effects and pediatric warning?

Bleeding, GI irritation, and hypersensitivity; Reye syndrome risk with viral illness in children and teenagers.

How do P2Y12 inhibitors reduce platelet aggregation?

Block ADP signaling at P2Y12 receptors, preventing downstream activation of GP IIb/IIIa.

Which P2Y12 inhibitors are irreversible, and which are reversible?

Irreversible: clopidogrel and prasugrel. Reversible: ticagrelor and cangrelor.

What is clopidogrel's boxed warning in the lecture?

Reduced antiplatelet effect in CYP2C19 poor metabolizers because clopidogrel requires activation as a prodrug.

Why is omeprazole a problem with clopidogrel?

It inhibits CYP2C19 and can reduce clopidogrel activation and antiplatelet effect.

What is prasugrel's key contraindication and boxed warning?

History of stroke or transient ischemic attack; serious bleeding risk.

Which antiplatelet can cause dyspnea and bradyarrhythmias?

Ticagrelor. Evaluate other causes of new dyspnea rather than automatically attributing it to the drug.

What drug interactions are emphasized for ticagrelor?

Strong CYP3A inhibitors/inducers; it can increase simvastatin, lovastatin, and digoxin concentrations.

What boxed warnings does the lecture list for ticagrelor?

Bleeding risk; reduced effectiveness with higher maintenance aspirin doses. No dosing memorization included in this set.

What distinguishes cangrelor from the other P2Y12 inhibitors?

IV administration, reversible inhibition, and very rapid onset/offset. Give clopidogrel or prasugrel after the infusion ends.

What do eptifibatide and tirofiban block?

GP IIb/IIIa receptors, preventing fibrinogen binding and platelet aggregation.

What are the major risks of eptifibatide and tirofiban?

Bleeding and thrombocytopenia; renal clearance matters. Eptifibatide is contraindicated in dialysis-dependent kidney failure.

What is cilostazol's mechanism and major contraindication?

PDE-3 inhibition increases cAMP, reducing platelet aggregation and causing vasodilation. Contraindicated in heart failure.

What should be monitored with antiplatelet therapy?

CBC, bleeding, renal/liver function, and duration of therapy. Other antithrombotics and NSAIDs increase bleeding risk.

How does unfractionated heparin work, and what monitors it?

Enhances antithrombin, inhibiting thrombin and factor Xa; monitor aPTT or anti-Xa.

What is enoxaparin, and what organ function matters?

Low-molecular-weight heparin acting through antithrombin, predominantly against Xa. Renal impairment increases exposure; selected patients need anti-Xa monitoring.

What is HIT, and can enoxaparin replace heparin in HIT?

Heparin-induced thrombocytopenia: low platelets with thrombosis risk. No—avoid both heparin and enoxaparin.

Which alternative anticoagulants for HIT are listed in the lecture?

Bivalirudin, argatroban, and fondaparinux.

What are the four components of the HIT 4T score?

Thrombocytopenia, timing of platelet fall, thrombosis, and other causes of thrombocytopenia.

How do bivalirudin and argatroban work?

IV direct thrombin inhibitors; inhibit free and fibrin-bound thrombin. Used in HIT and coronary intervention.

How do bivalirudin and argatroban differ in organ considerations?

Bivalirudin: renal impairment prolongs effect. Argatroban: hepatic metabolism; liver impairment prolongs effect. Both can falsely elevate INR.

Which oral anticoagulant directly inhibits thrombin?

Dabigatran; it is a prodrug, renal function matters, and it is dialyzable.

Why should dabigatran capsules not be opened?

Opening the capsule substantially increases absorption and exposure.

Which oral anticoagulants directly inhibit factor Xa?

Apixaban and rivaroxaban; edoxaban is also listed in the lecture overview.

What interactions reduce apixaban and rivaroxaban effectiveness?

Strong P-glycoprotein/CYP3A inducers such as phenytoin and carbamazepine reduce drug exposure.

What is fondaparinux's mechanism and major organ warning?

Indirect selective factor Xa inhibition through antithrombin; avoid severe renal impairment.

What is warfarin's mechanism?

Blocks vitamin K recycling, reducing synthesis of active factors II, VII, IX, X and proteins C and S.

What test monitors warfarin, and why is its onset slow?

PT/INR; existing clotting factors must disappear before its full effect develops.

What are warfarin's major warning and contraindication?

Boxed warning: major or fatal bleeding. Contraindicated in pregnancy; tissue necrosis is an important adverse effect.

Which drugs increase INR during warfarin therapy?

Amiodarone and antimicrobials such as trimethoprim-sulfamethoxazole, metronidazole, and fluconazole.

Which factors decrease INR during warfarin therapy?

Rifampin, carbamazepine, and increased vitamin K intake; the slides also list smoking.

What oral anticoagulant is selected in the lecture case involving phenytoin?

Warfarin; phenytoin can reduce direct oral anticoagulant exposure.

What two boxed warnings are shared by dabigatran, apixaban, and rivaroxaban in the slides?

Premature discontinuation increases thrombosis risk; spinal/epidural hematomas may occur with neuraxial anesthesia or spinal puncture.

Which agent reverses heparin and partially reverses enoxaparin?

Protamine. Its boxed warning is hypersensitivity reactions; hypotension and bradycardia can occur.

Which agent specifically reverses dabigatran?

Idarucizumab (Praxbind), an antibody fragment that binds dabigatran.

How do phytonadione and PCC differ in warfarin reversal?

Phytonadione is vitamin K and restores liver factor synthesis more slowly; PCC directly supplies factors II, VII, IX, and X for rapid reversal.

What is PCC's boxed warning and important HIT contraindication?

Thromboembolic complications. The lecture products contain heparin and are contraindicated in HIT.

What reversal option for direct Xa inhibitors is listed in the lecture?

PCC, off-label.

How do alteplase and tenecteplase dissolve clots?

Convert plasminogen to plasmin, which breaks down fibrin. Major risk: serious bleeding, including intracranial hemorrhage.

How does tenecteplase differ from alteplase?

More fibrin-specific and longer acting; can be administered as a single IV bolus.

What key history question comes first in the lecture's stroke-thrombolysis case?

Ask whether the patient takes an oral anticoagulant and when the last dose was taken; blood pressure and other eligibility criteria also matter.

What major concerns can prevent thrombolytic treatment?

Intracranial bleeding, recent brain injury/surgery, severe coagulopathy, and recent anticoagulant exposure; eligibility depends on the clinical setting.

How do tranexamic acid and aminocaproic acid work?

Antifibrinolytics: prevent plasminogen binding/activation and preserve fibrin by reducing clot breakdown.

What major contraindication is listed for tranexamic acid and aminocaproic acid?

An active thromboembolic process; CNS adverse effects can include seizures.