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Advanced Pharm for Nursing Practice 4

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*REMEMBER THAT A DECR IN blood flow and Na+ content causes the release of Renin   show
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show Aliskiren (Tekturna) is the prototype for Renin Inhibitors  
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show these drugs inhibit renin itself; blocking renin blocks the whole renin-angiotensin-aldosterone mechanism  
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What is the indication for using Aliskiren (Tekturna)?   show
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show they’re best absorbed on empty stomach, they have a ½-life of 24hrs, and once in the bld, it’s not metabolized and is excreted unchanged in the feces  
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What are the SE/ADR of renin inhibitors like aliskiren (Tekturna)?   show
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show *O2 supply: cardiac O2 supply determined by myocardial bld flow. Under resting conditions, t/ heart extracts nearly all O2 delivered to it by the coronary vessels.  
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show stable occlusive: pt is stable w/o exertion; unstable angina: pt is unstable even w/o exertion; vasospastic angina (Prinzmetal’s): variant angina that happens mostly to women under stress (their coronary arteries were NOT occluded)  
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*THE ONLY WAY TO ACCOMMODATE AND INCR IN DEMAND IS TO INCR BLOOD FLOW   show
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What are the main drugs used to treat HTN?   show
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show Nitrates act directly on the smooth muscle cell to release myosin (in t/ actin-myosin contraction) to allow the smooth muscle cell to relax  
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What’s the action of nitrates?   show
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show nitrates are used for t/ tx/prevention of angia pectoris; they can also be used in acute MIs (usually as result of not responding to other drugs). IV nitro is available for acute MI  
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show the main action/prob of nitrates is LARGE 1ST PASS EFFECT; nitrates have short ½-life; if nitrates given sublingually, you bypass 1st pass effect  
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What are the 2 diff thoughts for Nitro admin & angina attacks?   show
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Why call an EMS or 911 if having an angina attack instead of self transport?   show
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What are the SE/ADR of nitrates?   show
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What are warnings about nitrates?   show
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What are the ways to administer nitroglycerin?   show
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show isosorbide mononitrate (ISMO) are drugs very similar to nitrates; it doesn’t have large 1st pass effect, and can be prescribed for 1 or 2x/day to prevent angina attacks  
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show beta-blockers slow the heart rate and decr contractility (inotrope-how strong) which releases workload on heart; beta-blockers do not cause vasodilation  
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What are SE/ADR of beta-blockers?   show
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show DON’T STOP BETA-BLOCKERS ABRUPTLY (remember up regulation)  
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What’s the indication for Ca++ Channel blockers?   show
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show NON-DIHYDROPYRIDINE group (Verapamil), acts on heart to DECR CONTRACTILITY & HEART RATE, Verapamil also has a vasodilating effect; DIHYDROPYRIDINE group (Norvasc) Amlodipine or (Procardia) hv mainly a VASODILATING effect, and no effect on heart  
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*All Ca++ channel blockers decr preload and postload   show
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What is Ranolozine (Ranexa), and what is its indication?   show
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What’s the method of action of ranolozine (Ranexa)?   show
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What are SE/ADR of ranolozine (Ranexa)?   show
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show you want EARLY PERFUSION of coronary vessels, so: O2, heparin, sublingual nitro while prepping IV, and Beta-blocker for tachycardia; tx depends on whether there’s an ST-segment elevation or not  
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What is heart failure?   show
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What happens when there is decr bld flow to tissues?   show
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show the aim of tx in chronic heart failure is to decr sympathetic activity and decr t/ renin-angiotensin-aldosterone systems  
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What’s the drug of choice in chronic heart failure?   show
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show *ONLY ACEIs & beta-blockers are known to improve morbidity and mortality in pts /c heart failure  
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show pts /c CHF hv edema bc of poor cardiac output to kidneys, therefore only loop diuretics (which work with malfunctioning heart) will work in reducing edema; loop diruretics DO NOT IMPROVE MORBIDITY OR MORTALITY  
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How does digoxin work on the heart?   show
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Is heart failure a slow of fast developing process?   show
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Reminders of spironolactone (a K+-sparing diuretic)   show
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show Digoxin (Lanoxin, Digitek)  
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show primary: tx of heart failure if symptoms continue /p use of 1st line drugs; used in atrial fib or flutter bc it blocks AV conduction (allowing heart to not beat sooo fast)  
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Explain how the DIRECT THERAPEUTIC levels of Digoxin work on the heart   show
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Digoxin in a DIRECT way blocks the NA+/K+ ATPase pump which then acts on the Na+/Ca++ pump, incr Ca++ and releasing actin and myosin to contract==INCR CONTRACTILITY   show
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show AT THERAPEUTIC DOSES, T/ MAIN DIRECT EFFECT OF DIGOXIN IS TO INCR CONTRACTILITY  
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Explain how toxic Digoxin levels directly affect the heart: they reduce the resting potential esp in ventricular cells; after a while, ventricles get “itchy” to contract and you’ll see PVCs (premature ventricular contractions),   show
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Explain how INDIRECT EFFECTS OF Digoxin on the heart   show
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show If you slow the heart and pump out more bld to tissues, then that reduces the 911/sympathetic activity  
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show bioavailability of 70%; there are some who metabolize drugs in their gut, they get a larger dose; in elderly, give smaller dose of digoxin  
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What are SE/ADR of Digoxin?   show
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show pt is hungry, nauseated, seeing halos around lights  
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show call physician and make sure if should continue dose  
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XS digoxin = pt death from ventricular fibrillation   show
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What are different Digoxin interactions?   show
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*hypokalemia sensitizes the heart to digitalis w/o changing the bld level   show
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show ACEI decr pre and afterload, so it tends to improve cardiac function; they also stop the remodeling of the heart (*start low and incr as needed; drug may take a couple weeks to show max effect)  
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Aldosterone causes what of the heart? What blocks that?   show
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*Carvedilol (Coreg) ws 1st Beta-blocker approved for tx of mild/moderate HF of ischemic or cardiomyopathic origin in /c digitalis, diuretics, & ACEIs to reduce dz progression   show
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