Cardio/Renal--FINAL Flashcards
FDA-Approved cholesterol Drugs for Children
Statins (Atorvastatin, Pravastatin, etc.), Bile Acid Sequestrants, Ezetimibe.
Mechanism of Action - Statins
Inhibit HMG-CoA reductase → Decrease LDL, increase HDL.
Mechanism of Action - Niacin
Reduces hepatic VLDL synthesis, increases HDL.
Mechanism of Action - Bile Acid Sequestrants
Bind bile acids in intestine, increasing LDL clearance.
Mechanism of Action - Ezetimibe
Inhibits cholesterol absorption in small intestine.
Mechanism of Action - Fibrates
Activate PPAR-α to increase lipolysis of triglycerides.
Fenofibrate
Mechanism of Action - Omega-3 Fatty Acids
Reduce hepatic triglyceride production.
First-Line Therapy for Dyslipidemia
Statins (unless contraindicated).
Contraindications of Statins
Liver disease, pregnancy.
Contraindications of Niacin
Peptic ulcers, gout.
Contraindications of Fibrates
Severe kidney/liver disease.
Statin Potency
High: Atorvastatin 40-80 mg, Rosuvastatin 20-40 mg; Moderate: Simvastatin 20-40 mg; Low: Pravastatin 10-20 mg.
Statin Drug Interactions
Gemfibrozil + Statins (myopathy risk); Cyclosporine, Erythromycin (increased toxicity).
Side note: shouldn’t really be taken with PPIs either.
PCSK9 Inhibitors
Name 2
Alirocumab (Praluent), Evolocumab (Repatha)→ Increase LDL clearance, used in familial hypercholesterolemia.
Unfractionated Heparin (UFH) MOA
Enhances antithrombin III → Inhibits thrombin & factor Xa.
UFH Monitoring
aPTT (target 1.5–2.5× normal).
UFH Antidote
Protamine sulfate.
Low-Molecular-Weight Heparins (LMWH)
Enoxaparin, Dalteparin → More predictable, no aPTT monitoring.
Fondaparinux (Arixtra)
Factor Xa inhibitor, no risk of HIT.
Warfarin MOA
Inhibits vitamin K-dependent clotting factors (II, VII, IX, X).
Warfarin Monitoring
INR (target 2.0–3.0; mechanical valves 2.5–3.5).
Warfarin Antidote
Vitamin K, Fresh Frozen Plasma (FFP), PCC (Prothrombin Complex Concentrate containing clotting factors II, VII, IX, and X that are all inhibited by warfarin
Direct Oral Anticoagulants (DOACs)
Dabigatran (Pradaxa, Factor IIa inhibitor); Rivaroxaban, Apixaban (Factor Xa inhibitors).
Reversal Agents for DOACs
Idarucizumab (Pradaxa); Andexanet alfa (Xarelto/Eliquis).
Antiplatelet Agents
Aspirin (COX-1, COX-2 inhibitor),
Clopidogrel/Plavix (P2Y12 inhibitor),
Glycoprotein IIb/IIIa Inhibitors (Tirofiban/Abciximab)
What are the key characteristics of arterial thrombosis?
Platelet-rich clot, forms in medium-sized arteries with atherosclerosis.
What are the key characteristics of venous thrombosis?
Fibrin-rich clot due to stasis or clotting cascade activation.
How does aspirin prevent clot formation?
Irreversibly inhibits COX-1 → Blocks thromboxane A2 → Prevents platelet aggregation.
What are the main uses of aspirin in cardiovascular disease?
Prevention of TIA, MI recurrence, and primary/secondary MI prevention.
Which antiplatelet drug inhibits ADP (P2Y1 and P2Y12) receptors?
Clopidogrel (Plavix), Ticagrelor (Brilinta), Prasugrel (Effient).
What is the role of GP IIb/IIIa inhibitors in clot prevention?
Prevent fibrinogen binding to GP IIb/IIIa receptors → Prevent platelet aggregation.
Which drugs are GP IIb/IIIa inhibitors?
Abciximab, Eptifibatide, Tirofiban.
Abciximab: ReoPro
Eptifibatide: Integrilin
Tirofiban: Aggrastat
What is the mechanism of action of heparin?
Activates antithrombin III → Inhibits thrombin (IIa) and Factor Xa.
What are the uses of unfractionated heparin (UFH)?
DVT, PE, MI, stroke prevention.
How is heparin overdose reversed?
Protamine sulfate (1 mg per 100 U heparin).
What are the advantages of low-molecular-weight heparins (LMWH)?
More predictable effect, longer half-life, no need for aPTT monitoring.
What is an example of an LMWH?
Enoxaparin (Lovenox), Dalteparin (Fragmin).
What is the MOA of warfarin?
Inhibits vitamin K-dependent clotting factors (II, VII, IX, X).
How is warfarin monitored?
INR (target 2.0-3.0; 2.5-3.5 for mechanical valves).
What reverses warfarin overdose?
Vitamin K, Fresh Frozen Plasma (FFP), PCC.
What are Direct Oral Anticoagulants (DOACs)?
Dabigatran (Pradaxa), Rivaroxaban (Xarelto), Apixaban (Eliquis).
What is the mechanism of thrombolytics?
Convert plasminogen to plasmin → Break down fibrin clots.
What are the primary reversal agents for bleeding?
Heparin
Warfarin
Pradaxa
Apixaban (Eliquis)
Protamine sulfate (Heparin),
Vitamin K (Warfarin),
Idarucizumab (Pradaxa),
Andexanet Alfa (Xa inhibitors).
What are the major risk factors for CAD?
Smoking, hypertension, obesity, diabetes, chronic kidney disease, older age.
What are the main components of a lipid profile?
LDL, VLDL, HDL, total cholesterol.
What is the first-line treatment for hyperlipidemia?
Lifestyle modifications (diet, exercise, weight loss).
What are the main classes of lipid-lowering medications?
Statins, Niacin, Fibrates, Bile Acid Sequestrants, Cholesterol Absorption Inhibitors, PCSK9 Inhibitors, Omega-3 Fatty Acids.
What is the mechanism of action of statins?
Inhibit HMG-CoA reductase → Decrease LDL, increase HDL.
Which statins are considered high-potency?
Rosuvastatin (Crestor), Atorvastatin (Lipitor).
What are the major side effects of statins?
Elevated liver enzymes, myopathy, rhabdomyolysis.
Which enzyme system metabolizes most statins?
CYP450 enzymes (except Pravastatin).
How do PCSK9 inhibitors lower LDL?
Inhibit PCSK9, increasing LDL receptor recycling.
How does Niacin affect lipid levels?
Lowers LDL & triglycerides, raises HDL.
What is a common side effect of Niacin?
Flushing (can be reduced by pre-medicating with aspirin).
What is the mechanism of action of fibrates?
Activate PPAR-α, increasing lipoprotein lipase activity.
What is the best drug class for lowering triglycerides?
Fibrates & Omega-3 Fatty Acids.
Which lipid-lowering medication binds bile acids?
Bile Acid Sequestrants (Cholestyramine, Colesevelam).
How does Ezetimibe lower cholesterol?
Inhibits dietary and biliary cholesterol absorption.
Which patients may require combination lipid-lowering therapy?
Those with high ASCVD risk or inadequate response to statins.
What is the most potent combination therapy for LDL reduction?
Statin + PCSK9 Inhibitor.
Which lipid-lowering medicationS should be avoided in severe liver disease?
Statins, Niacin, Fibrates, Ezetimibe.
Which medication is most effective for raising HDL?
Niacin.
What are the risks of combining statins with fibrates?
Increased risk of myopathy and liver toxicity.
What is the main reason statins are used long-term?
To prevent atherosclerosis and reduce cardiovascular risk.
What is the first-line treatment for hypertension in patients with diabetes or CKD?
ACE Inhibitors (e.g., Lisinopril, Enalapril)
Which class of drugs blocks the AT1 receptor to lower blood pressure?
Angiotensin II Receptor Blockers (ARBs, e.g., Losartan, Valsartan) Extra: basically the same MOA as ACEI but does not increase bradykinin levels, CAN NOT be given with an ACE inhibitor
What is a major side effect of ACE inhibitors that does not occur with ARBs?
Cough (due to increased bradykinin)
Which beta-blocker is non-selective and should be avoided in asthma?
Propranolol
Which medication is preferred for treating hypertension in African Americans?
Amlodipine (a dihydropyridine CCB)
Which antihypertensive class is known to cause first-dose orthostatic hypotension?
Alpha Blockers (e.g., Prazosin, Doxazosin), give at bedtime
Which class of diuretics is considered first-line for hypertension?
Thiazide diuretics (e.g., Hydrochlorothiazide, Chlorthalidone)
Which diuretic class works in the ascending loop of Henle and is the most potent?
Loop diuretics (e.g., Furosemide, Torsemide)
Which diuretics block aldosterone and are used in heart failure?
Potassium-sparing diuretics (e.g., hormone blockers: Spironolactone, Eplerenone. & Triamterene)
Which medication class is first-line for reducing mortality in heart failure?
ACE inhibitors or ARBs
Which beta-blockers are used in heart failure?
Carvedilol, Metoprolol succinate, Bisoprolol
What is the MOA of Digoxin?
Inhibits Na+/K+ ATPase, increasing intracellular calcium and contractility, neurohormonal inhibition at low doses decreasing sympathetic activation. EXTRA:+Inotrope, the ONLY one that is NOT associated with a reduction in survival)
What electrolyte imbalance increases Digoxin toxicity? What are the symptoms of toxicity?
Hypokalemia. Sx: Annorexia, nausea, vomiting, blurred or yellowish vision. Extra: DO NOT give with amiodarone, or verapamil as they increase levels.
Which antiarrhythmic drug is associated with pulmonary fibrosis and thyroid dysfunction? Are there other ADE with this drug?
Amiodarone. Other ADE: Hepatotoxicity, Optic neuritis, Blue-gray skin discoloration (permanent), corneal deposits.
What is the drug of choice for acute supraventricular tachycardia (SVT)?
Adenosine
Which Class III antiarrhythmic is the DOC for chemical cardioversion of atrial fibrillation?
Ibutilide
What is the mechanism of action of Warfarin?
Inhibits Vitamin K-dependent clotting factors (II, VII, IX, X)
Which direct oral anticoagulant (DOAC) inhibits Factor Xa?
Rivaroxaban (Xarelto) or Apixaban (Eliquis)
Which antiplatelet drug irreversibly inhibits COX-1 and COX-2?
Aspirin
What is the first-line treatment for high LDL cholesterol?
Statins (e.g., Atorvastatin, Rosuvastatin)
Which lipid-lowering drug can cause flushing?
Niacin
Which drug binds bile acids to reduce cholesterol absorption?
Bile acid sequestrants (e.g., Cholestyramine)
What are the main goals of heart failure treatment?
Alleviate symptoms, slow disease progression, improve survival.
What are the two major types of heart failure?
HFrEF (systolic dysfunction) and HFpEF (diastolic dysfunction).
What is the first-line treatment for HFrEF?
ACE inhibitors (e.g., Lisinopril).
What is the MOA of ACE inhibitors in HF?
Blocks conversion of Angiotensin I to Angiotensin II, reducing preload and afterload.
What is the role of aldosterone receptor antagonists in HF?
Prevents sodium retention, cardiac hypertrophy, and hypokalemia (e.g., Spironolactone, Eplerenone).
Which beta-blockers are used in HFrEF?
Carvedilol, Metoprolol Succinate, Bisoprolol.
What is the primary benefit of beta-blockers in HF?
Reduce HR, inhibit renin release, decrease remodeling and myocardial cell death.
Why should beta-blockers be started at low doses in HF?
To prevent initial worsening of symptoms and allow the heart to adjust.
Which class of diuretics is most commonly used in HF?
Loop diuretics (e.g., Furosemide, Torsemide).
Do diuretics improve survival in HF?
No, they are used for symptom relief only.
What is the MOA of Sacubitril/Valsartan (Entresto)?
Inhibits neprilysin, increasing natriuretic peptides while blocking RAAS activation.
When should Sacubitril/Valsartan (Entresto) replace an ACEI or ARB in HF?
When the patient remains symptomatic despite optimal therapy.
Why must ACEI be stopped 36 hours before starting Entresto?
To prevent an increased risk of angioedema.
What is the MOA of Ivabradine?
Inhibits HCN (Hyperpolarization activated cyclic nucleotide gaged) channels, reducing HR without affecting contractility.
When is Ivabradine used in HF?
For symptomatic patients in NSR with HR >70 bpm on maximum beta-blocker therapy. (HFrEF)
What is a unique side effect of Ivabradine?
Luminous visual changes (phosphenes).
Which vasodilator combination is used in HF, especially in Black patients?
Hydralazine + Isosorbide Dinitrate (BiDil).
What is a rare but serious side effect of Hydralazine?
Drug-induced lupus.
What is the MOA of Digoxin?
Inhibits Na+/K+ ATPase, increasing intracellular Ca++ and contractility.
What electrolyte imbalance increases the risk of Digoxin toxicity?
Hypokalemia.
What is the role of Dobutamine, Dopamine and Milrinone in HF? How do they work?
Used short-term IV for acute decompensated HF. Dopamine & Dobutamine are B adrenerigic agonists causing vasodilation and +inotropic effects. Milrinone is a Phosphodiesterase inhibitor but has the same effect.
What is the MOA of Nesiritide (Natrecor)?
Binds to natriuretic peptide receptors, decreasing preload and afterload. Extra: can worsen renal function as it is renally cleared
When is Nesiritide used in HF?
When IV diuretics are not effective.
What are the two major causes of arrhythmias?
Abnormal automaticity and impulse conduction abnormalities.
What is the most common cause of QT prolongation?
Drugs (e.g., macrolides, antipsychotics, quinolones).
What is the MOA of Class I antiarrhythmics?
Block voltage-sensitive Na+ channels, reducing depolarization.
Which Class IA antiarrhythmic has strong anticholinergic effects?
Disopyramide. Extra: Used to control AF/Afib or alternate for Vent arry. Increases SVR.
Which Class IA antiarrhythmic is used IV for acute atrial and ventricular arrhythmias?
Procainamide.
What is a major side effect of Procainamide?
Drug-induced lupus. RENALLY DOSED. Extra: has ADE of class 3 drug as it is acetylated in liver to make N-acetylprocainamide that functions as a class 3 drug.
Which Class IB antiarrhythmic is used as an alternative to Amiodarone in VT/VF? What is an indicator of toxicity?
Lidocaine. Toxicity: Nystagmus. ADE: Sedation, agitation, confusion, convulsions, slurred speech.
What is the primary use of Mexiletine?
Chronic treatment of ventricular arrhythmias.
Class IB with lidocaine
Which Class IC drug is contraindicated in structural heart disease? Why?
Flecainide. Negative Inotrope with Proarrhythic effects. Extra: Class 1C used moslty for atrial arrhythmias.
Which Class IC antiarrhythmic has weak beta-blocking properties?
Propafenone. CAN cause bronchospasam, do not use in asthmatics.
What is the MOA of Class II antiarrhythmics?
Beta-blockers reduce automaticity and prolong AV conduction.
Which beta-blocker is short-acting and used IV for acute arrhythmias?
Esmolol.
Which Class III antiarrhythmic is the most widely used?
Amiodarone. (K channel blocker)
What are major side effects of Amiodarone?
Pulmonary fibrosis, hepatotoxicity, thyroid dysfunction, corneal deposits.
Which Class III drug is used for chemical cardioversion of atrial flutter?
Ibutilide.
Which Class IV antiarrhythmic is preferred for supraventricular tachycardias?
Verapamil or Diltiazem.
Why should non-dihydropyridine CCBs be avoided in heart failure?
They have negative inotropic effects.
What is the drug of choice for Torsades de Pointes?
Magnesium sulfate.
What are the three types of angina?
Stable angina, unstable angina, and Prinzmetal (variant) angina.
Which medications are first-line for stable angina?
Beta-blockers.
Which type of angina responds best to calcium channel blockers?
Prinzmetal (variant) angina.
Which beta-blockers are cardioselective and preferred for angina?
Metoprolol, Bisoprolol.
Why should beta-blockers be avoided in Prinzmetal angina?
They can worsen vasospasms.
Which calcium channel blocker primarily affects the myocardium?
Verapamil.
Which dihydropyridine CCB is used for angina and has minimal cardiac effects?
Amlodipine.
What is the MOA of nitrates?
Relax vascular smooth muscle, reducing preload and myocardial oxygen demand.
Why should nitrates be avoided with PDE5 inhibitors like Sildenafil?
Severe hypotension can occur.
What is the MOA of Ranolazine?
Inhibits the late Na+ current, improving oxygen supply and demand. Used in angina.
What is a major side effect of Ranolazine?
QT prolongation.
What should we do if the patients SBP is greater than 20mmHg over goal, or the DBP is greater than 10mmHg over goal? (ie 150/90)
Start them on TWO medications at the same time. Meds based on other clinical picture indicators.
What is the drug of choice for elevated blood pressure in patients with: DM, CDK, MI, HF, with at risk of CAD and protinuria?
ACE inhibitor, Lisinopril
Do Beta-Blockers have an effect on cholesterol?
Yes. NON-SELECTIVE beta blockers will decrease HDL and increase triglycerides
What blood pressure medications CAN be used in pregnancy?
Labetalol, Hydralazine, Nifedipine, Methyldopa, thiazide diuretics
Which antihypertensive is associated with gingival hyperplasia?
All of the dihydropyridine calcium channel blockers (Amlodipine, Nifedipine, Nicardipine, Felodipine)
What is the most common antihypertensive drug world wide? What do they do?
Thiazide diuretics (e.g., Hydrochlorothiazide, Chlorthalidone), decrease PVR/SVR with long term use. EXTRA: has a potential cross allergy with SULFA
What is the only diuretic the will INCREASE urine concentration
Thiazide diuretics, must have a GFR>30 to use (except Metolazone) EXTRA: NSAIDS reduce efficacy by reducing renal perfusion.
What is the MOA of loop diuretics?
Block Na and Cl resorption in the kideys even with poor renal function, decreasing PVR, and increasing renal blood flow. (Furosemide, Bumetanide, Torsemide)
What is Eplerenone? Why is it different?
A potassium sparing, hormone diuretic. It is selective to aldosterone receptors therefore does not cause gynecomastia.
What are the uses of potassium sparing diuretics?
Hypokalemia, HF, Resistant HTN, Acne and PCOS
What is Acetazolamide? What is it used for?
A carbonic anhydrase inhibitor. Glaucoma (OA), altitude sickness. Extra: causes mild metabolic acidosis, don’t use in liver patients/cirrhosis as it decreases the release of ammonia.
What would be the concerns using NONdihydropyridine clacium channel blockers in patients with current heart failure?
Negative Inotrope, decreases ventricular contractility and can activate neurohormonal systems. May result in hemodynamic and clinical deterioration and increased risk of CV event.
How do ACEI & ARB affect hemodynamics?
Both decrease preload and afterload
What are the Class I (A,B,C) antiarrhythmic drugs?
Class I Na Channel Blockers. 1A: Quinidine, Procanamide, Disopyramide. 1B: Lidocaine, Mexiletine. 1C: Flecainide, Propafenone
What are the Class II antiarrhythmic drugs?
Beta Blockers: Metoprolol, Esmolol (since it is rapidly metabolized it only has a short duration of action and has no drug-drug interactions)
What are the Class III antiarrhythmic drugs?
K channel blockers: Amiodarone, Dronedarone, Sotalol, Dofetilide, Ibutilide
What medication is an alternative to Amiodarone due to its lack of iodine properties? Are there any contraindications?
Dronedarone. K channel blocker. No thyroid effects, can still cause liver failure. CONTRAINDICATIONS: symtpmatic HF & Permanent AF as they are at increased risk of death.
What is a class III antiarrhythmic that has beta-blocker activity?
Sotalol. One isomer is a BB and the other is K blocker. Maintains NSR but must be started in the hospital due to proarrhythic effects. Renally Dosed.
Why does Dofetilide have to be initiated inpatient?
Proarrhytmic. K channel blocker, pure. Renally excreted, do not use with drugs that inhibit tubular secetion.
What are class IV antiarrhythmic drugs?
Nondihydropyridine Calcium Channel Blockers: Verapamil, Diltiazem.
What class of antiarrhythmic drugs is associated with peripheral edema?
Class IV nondyhydropyridine calcium channel blockers (Verapamil & Diltiazem). MOST effective against artial arrythmias (AF/Afib/SVT) Dose adjustment in LIVER disease. EXTRA: DRUG INTERACTION WITH SIMVASTATIN
What is the drug of choice for digoxin induced arrhythmias?
Magnesium sulfate.
What is the treatment for unstable angina?
Unstable angina is a form of ACS and requires admission and aggressive therapy.
What is the difference between dihydropyridine CCB and nondihydropyridine CCB?
Nondihydropyridine CCB are antiarrhythmics, act primarily in the center of the body decreasing HR and contractility. Dihydropyridine are antihypertnesives, act primarily in the periphery relaxing blood vessles decreasing SVR
