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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