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Pharmacotherapy Preview Program (P3) Module 3 Hypertension Antiarrhythmics Brandon Dyson, PharmD, BCPS Diuretics • Thiazides – HCTZ • K sparing – Triamterene, amiloride A. B. C. D. • Loop – Furosemide, bumetanide, torsemide • Aldosterone antagonist – Spironolactone, eplerenone E. F. G. H. I. J. MOA: Na channel blockade in collecting duct, increased K reabsorption MOA: inhibit Na-K-CL cotransporter in loop of Henle MOA: competitive antagonism of Na-Cl transporter in distal tubule MOA: competitive antagonist at aldosterone receptor; inhibits mineralcorticoid receptors Less effective if CrCl <30 Often used with HCTZ Alleviate congestive sxs of HF AE: dose related ototoxicity, ↓ Mg, ↓ Ca, “sulfa” allergy AE: hypokalemia AE: hyperkalemia Case Study: HTN Reducing Sympathetic Tone You start a hypertensive patient with asthma on low dose Metoprolol (Lopressor). • Why did you pick this drug from the others in its class? What are other drugs in this class? • What important patient education would you provide? • What drug would be a good choice for someone with HTN and BPH? HTN: Case Study A 35 y/o obese, hypertensive female comes to see you because she is newly pregnant, and her OB was not sure whether she should keep taking her Propranolol. You would best counsel the patient by saying: A. Your OB is an incompetent idiot. You should stop the Propranolol, start Methyldopa (Aldomet) and find a new OB B. Your OB is an incompetent idiot. Continue the Propranolol, follow up monthly with me during pregnancy and find a new OB. C. I’m glad your OB referred you to me for your BP management. Stop the Propranolol, start Methyldopa and follow up with me in 1-2 weeks for BP check. D. I’m glad your OB referred you to me for your BP management. Continue the Propranolol and follow up monthly with me during your pregnancy. HTN: Case Study Cont’d • How would you counsel the patient on Methyldopa? • What is the MOA, clinical uses and it’s advantages? • What is another centrally acting antihypertensive drug? Renin-Angiotensin Pathway A. ACE, ACEIs B. Renin; direct renin inhibitors C. Angiotensin II receptors; ARBs D. Aldosterone; aldosterone antagonists HTN: Renin-Angiotensin Modulation ACEI ARB Lisinopril, captopril, ramipril, enalapril, fosinopril, quinapril, benazepril • MOA Losartan, valsartan, candesartan, irbesartan, telmisartan, eprosartan • MOA • Clinical Use • Clinical Use • AE’s/CI’s • AE’s/CI’s Direct Renin Inhibitor: Aliskiren (Tekturna) HTN: Calcium Channel Blockers Dihydropyridine Non-Dihydropyrdine Amlodipine, felodipine, nifedipine ER, nicardipine, nimodipine Verapamil, diltiazem • MOA • MOA • Clinical Use • Clinical Use • AE’s/CI’s • AE’s/CI’s Drugs & Potassium Effects Hypokalemia Hyperkalemia A. B. C. D. E. F. G. H. I. J. HCTZ Spironolactone Furosemide (Lasix) Aliskiren (Tekturna) Lisinopril Nifedipine Verapamil Losartan Metoprolol Diltiazem HTN: Vasodilators Nitroprusside Hydralazine Fenoldopam Minoxidil A. Stimulates NO formation in endothelial cells arteriole dilation B. Used for alopecia as well as HTN C. K+ channel openers D. Gives off NO arteriovenous dilation in smooth muscle E. Active metabolite can cause hypotensive effects for 24 hrs despite short t 1/2 F. Renal and hepatic insufficiency risk of cyanide toxicity G. D1 stimulation diuresis, natriuresis H. Adverse effect – SLE I. Rapid first-pass metabolism J. Available parenteral form K. Used in HTN urgency/emergency Case Study: HTN A 55 y/o WM with type II DM comes into your free clinic with c/o constant headaches and BP of 160/100. He stopped taking medications several years ago because he couldn’t afford it. • What would be his BP goal and the best initial medication regimen for his HTN based on JNC8 recommendations? • What labs would you want to monitor? • How would you counsel him about lifestyle changes? Case Study Cont’d The patient comes back 2 weeks later. Labs show normal BUN/creatinine, LDL>100. His BP is 148/90, and he has developed a dry, hacking cough. • What is a likely cause for the cough? • How would you change his medication regimen? Cardiac Conduction ECG ERP Class 1 Antiarrhythmics – Na+ Channels Class Ia Procainamide, Quinidine, Disopyramide Class Ib Lidocaine, Mexilitine Class Ic Flecainide, Propafenone, Moricizine, Encainide A. Decreases conduction velocity B. Shortens repolarization and QT interval C. Prolongs repolarization D. Prolongs QT risk for TdP E. Most potent Na channel blockade – depressive and proarrhythmic effects F. Used for ventricular arrhythmias, not effective for SVT G. Anticholinergic effects H. AEs are primarily neurological Class II Antiarrhythmics – Beta receptors • This class is also known as Beta Blockers • This class has a (+/-) _________ inotropic effect. • They slow SA node firing and conduction through the AV node Class III Antiarrhythmics – K+ Channels • Sotalol, Amiodarone, and Dronedarone also have B-blocking action. • Dofetilide and Ibutilide can cause Torsades de pointes and pts must be monitored closely in a hospitalized setting. • Dronedarone is similar in structure to amiodarone. • Amiodarone has several CYP450 drug interactions including with warfarin. Case Study: AFib You have a patient being treated for atrial fibrillation by his cardiologist who comes into your office complaining that his skin is turning blue. • What drug is he likely taking that might cause this? • How does this drug work? • What monitoring/tests should be done while taking this drug? Class IV Antiarrhythmics – Ca++ Channels • Affect depolarization via blockade of Calcium Channel causing slowed SA node firing and slowed conduction through the AV node • The __________ (nonDHP/DHP) CCB’s are primarily used, such as __________ and __________. • These drugs cannot be used to treat Ventricular arrhythmias. • Major AEs include bradycardia, excessive AV blockade, heart failure, hypotension and constipation. Which of the following delay cardiac cell repolarization (prolong QT), thus increasing the risk of TdP? A. B. C. D. E. F. G. Quinidine Procainamide Lidocaine Ibutilide Sotalol Dofetilide Mexilitine