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*REMEMBER THAT A DECR IN blood flow and Na+ content causes the release of Renin
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What is the prototype for Renin Inhibitors?
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Cardio Drugs 4
Advanced Pharm for Nursing Practice 4
| Question | Answer |
|---|---|
| *REMEMBER THAT A DECR IN blood flow and Na+ content causes the release of Renin | *REMEMBER THAT A DECR IN blood flow and Na+ content causes the release of Renin |
| What is the prototype for Renin Inhibitors? | Aliskiren (Tekturna) is the prototype for Renin Inhibitors |
| What the method of action of renin inhibitors? | these drugs inhibit renin itself; blocking renin blocks the whole renin-angiotensin-aldosterone mechanism |
| What is the indication for using Aliskiren (Tekturna)? | the renin inhibitors like Aliskiren Tekturna are used PO x1/day for HTN (HBP) |
| What are the pharmacokinetics of aliskiren (Tekturna)? | 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 |
| What are the SE/ADR of renin inhibitors like aliskiren (Tekturna)? | the side effects of renin inhibitors is 1% rash, 2% diarrhea |
| *O2 supply: cardiac O2 supply determined by myocardial bld flow. Under resting conditions, the heart extracts nearly all O2 delivered to it by the coronary vessels. | *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. |
| What are the 3 different types of angina? | 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) |
| *THE ONLY WAY TO ACCOMMODATE AND INCR IN DEMAND IS TO INCR BLOOD FLOW | *THE ONLY WAY TO ACCOMMODATE AND INCR IN DEMAND IS TO INCR BLOOD FLOW |
| What are the main drugs used to treat HTN? | Nitrates (Nitroglycerin) are the main drugs used to treat HTN |
| What’s the method of action of nitrates? | Nitrates act directly on the smooth muscle cell to release myosin (in t/ actin-myosin contraction) to allow the smooth muscle cell to relax |
| What’s the action of nitrates? | /c nitrates, relaxation of smooth muscle cell results in vasodilation. /c preload, you decr t/ amt of bld coming in heart (which was stretching the muscle). You decr wk on damaged part of heart and dilate other bld vessels not involved in angina |
| What’s the indication for nitrates? | 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 |
| What are the pharmacokinetics of nitroglycerin? | 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 |
| What are the 2 diff thoughts for Nitro admin & angina attacks? | 1-Traditional) place nitro tablet sublingual max x3/ q 5min, /p 2nd placemt, call EMS or 911. 2-Amer Col of Cardiology) take max 2 nitro tabs sublingual q5 min, if no improvmt /p 1st one, call EMS/911 |
| Why call an EMS or 911 if having an angina attack instead of self transport? | b/c EMS usually generate bttr assistance than self transport |
| What are the SE/ADR of nitrates? | since nitrates cause vasodilation, may hv postural hypotension, might get palpitations, tachycardia, dizziness, headache |
| What are warnings about nitrates? | nitrate tolerance builds up fast, so have NITRATE FREE PERIODS EVERYDAY of 10-12hrs (unless pt only taking nitrates for acute attacks); nitrates are volatile & should be kept in glass bottle /c screw cap –anything else will make it ineffective |
| What are the ways to administer nitroglycerin? | emergency (usually acute MI): IV, acute attack: sublingual tablet/oral spray; capsule tablets for prevention maintenance /c nitrate free period & CCB used @ night; patch: place on hairless torso /c daily site change and nitrate free period |
| What is a drug very similar to nitrates? | 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 |
| What’s the method of action of beta adrenergic antagonists? | beta-blockers slow the heart rate and decr contractility (inotrope-how strong) which releases workload on heart; beta-blockers do not cause vasodilation |
| What are SE/ADR of beta-blockers? | bradycardia; at first it was contraindicated in thos with diminished cardiac output, until they realized that actualy slowing the heart gave it enough time to refill with O2 rich blood during diastole |
| What’s a serious Beta-blcoker warning? | DON’T STOP BETA-BLOCKERS ABRUPTLY (remember up regulation) |
| What’s the indication for Ca++ Channel blockers? | CCBs are useful in vasospastic (Prenzmetal’s) angina b/c they cause VASODILATION |
| What are the 2 groups of CCBs and what are their actions? | 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 |
| *All Ca++ channel blockers decr preload and postload | *All Ca++ channel blockers decr preload and postload |
| What is Ranolozine (Ranexa), and what is its indication? | Ranexa is an anti-anginal med for the tx of chronic angina in pts who don’t respond to other agents; it’s used in combo with amlodipine, Beta-blockers, or nitrates and given 2x/day |
| What’s the method of action of ranolozine (Ranexa)? | the MOA is unknown, though it seems to wrk like a metabolic modulator and seems to improve exercise duration |
| What are SE/ADR of ranolozine (Ranexa)? | dizziness, HA, constipation; main worry is RANEXA PROLONGS Q-T INTERVAL, so it’s contraindicated /c other Q-T interval drugs |
| What’s the plan of action with acute myocardial infarctions/ acute coronary syndrome? | 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 |
| What is heart failure? | heart failure is a serious progressive disorder characterized by: ventricular dysfunction, decr cardiac output, insufficient bld flow to tissues, ultimately leading to fluid retention (not enough bld to kidneys) |
| What happens when there is decr bld flow to tissues? | Compensatory Responses /c Sympathetic NS causing: vasoconstriction mostly in skin & splanchnic area, incr hrt rate & strength of contraction (if poss); this sets of renin-angiotensin-aldosterone sys (which could be vry dangerous to damaged hrt) |
| In heart failure, the aim of tx is what? | the aim of tx in chronic heart failure is to decr sympathetic activity and decr t/ renin-angiotensin-aldosterone systems |
| What’s the drug of choice in chronic heart failure? | ACETs are the drug of choice in chronic heart failure (beta-blockers are also liked bc it slows down hrt enough for it to refill /c O2 rich bld) |
| *ONLY ACEIs & beta-blockers are known to improve morbidity and mortality in pts /c heart failure | *ONLY ACEIs & beta-blockers are known to improve morbidity and mortality in pts /c heart failure |
| Most pts with CHF hv edema and need which kind of diuretic? Why? | 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 |
| How does digoxin work on the heart? | Digoxin slows the heart and incr contractility (inotrope), making the heart a better pump (IT DOES NOT improve mortality) |
| Is heart failure a slow of fast developing process? | heart dz is a very SLOW developing process |
| Reminders of spironolactone (a K+-sparing diuretic) | /c the renin-angiotensin-aldosterone sys release, aldosterone tends to cause remodeling of the heart; spironolactone is a relatively poor diuretic, but it DOES BLOCK ALDOSTERONE and blocks heart remodeling, so some list it as step 1 drug |
| What is digitalis glycoside, and what are the trade names? | Digoxin (Lanoxin, Digitek) |
| What’s the clinical use of digoxin? | 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) |
| Explain how the DIRECT THERAPEUTIC levels of Digoxin work on the heart | therapeutic levels of 0.5-0.8nanograms/mL will act on the Na+/K+ -ATPase pump. (/c lower serum K+, there’s less K+ to pump into cell so hv decr pump action. Digoxin works by blocking Na+/K+ pump, there’s risk of dysrrhthmias |
| 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 | Digoxin in a DIRECT way blocks t/ NA+/K+ ATPase pump which then acts on t/ Na+/Ca++ pump, incr Ca++ and releasing actin and myosin to contract==INCR CONTRACTILITY |
| AT THERAPEUTIC DOSES, THE MAIN DIRECT EFFECT OF DIGOXIN IS TO INCR CONTRACTILITY | AT THERAPEUTIC DOSES, T/ MAIN DIRECT EFFECT OF DIGOXIN IS TO INCR CONTRACTILITY |
| 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), | this leads to 2 PVCs in a row (bigeminy), and then 3 PVCs (trigeminy), & then ventricular fib. If treating sinus fib, need to use larger doses of digoxin |
| Explain how INDIRECT EFFECTS OF Digoxin on the heart | Digoxin stimulates the vagus nerve which slows the heart at therapeutic doses bc there’s a reflex induced decr sympathetic tone associated /c improvement in circulation (vagus thinks bld pressure too high) |
| If you slow the heart and pump out more bld to tissues, then that reduces the 911/sympathetic activity | If you slow the heart and pump out more bld to tissues, then that reduces the 911/sympathetic activity |
| What are the pharmacokinetics of Digoxin? | bioavailability of 70%; there are some who metabolize drugs in their gut, they get a larger dose; in elderly, give smaller dose of digoxin |
| What are SE/ADR of Digoxin? | digoxin-caused cardiac arrhythmias due to pt also on diuretic --> hypokalemia –OR- pt has decr renal function & digoxin dose too big & causing cardiac dysrhythmias (from toxicity) |
| What are early signs of digoxin toxicity? | pt is hungry, nauseated, seeing halos around lights |
| If on Digoxin & pts hrt rate goes below 60bpm, what should you do? | call physician and make sure if should continue dose |
| XS digoxin = pt death from ventricular fibrillation | XS digoxin = pt death from ventricular fibrillation |
| What are different Digoxin interactions? | quinidine, verapamil, & amiodarone are enzyme & p-glycoprotein inhibitors, so could raise digoxin toxicity |
| *hypokalemia sensitizes the heart to digitalis w/o changing the bld level | *hypokalemia sensitizes the heart to digitalis w/o changing the bld level |
| Why are ACEIs the drug of choice for the heart? | 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) |
| Aldosterone causes what of the heart? What blocks that? | aldosterone causes remodeling of the heart; aldactone blocks that |
| *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 | *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 |
Created by:
Fukanwa
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