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Antihypertensives

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Question
Answer
Prevelance of cardiovascular disease   33% without or 66% with perhypertensives  
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Effects of htn   kidney failure, stroke, heart failure, or any end organ failure  
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secondary htn   from underlying curable disease; primary hyperaldosteronism, renal vascular stenosis, pheochromocytoma; can be cured  
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essential htn   unknown cause; lifestyle contributions - obesity, sedentary, diet high in Na and fat; only controlled but no cure; goal is control of htn  
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Risk factors of primary htn   older male, AA women before and after menopause, menopausal women  
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Normal bp   Less than 80 dbp Less than 120 sbp  
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prehypertension   80-89 dbp 120-139 sbp  
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stage 1   90-99 dbp 140-159 sbp  
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stage 2   greater than or equal to 100 dbp greater than or equal to 160 sbp  
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Risk doubles with each   20mmHg increase sbp 10mmHg increase dbp  
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Goal bp   different based on patient population  
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goal if tolerated   <140/<90  
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goal in diabetics   <130/<80  
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goal in cardiac failure   <130/<85  
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goal in renal failure   <130/<85  
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goal in renal failure with proteinuria >1.0 g/24hr   <125/<75  
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bp reduction of 2mmHg =   reduces risk up to 10% in stroke and 7% in CHD  
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normal bmi   less than 25 kg/m2  
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DASH eating plan Dietary approach to stop htn   reduces bp 8-14mmHg  
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Dietary intake suggestions   decrease alcohol; increase fruit, mg2, k, ca, vegetables, whole grains, fish, nuts, poultry  
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DASH restrictions   Low salt, low fat dairy, reduced red meat, sugar, fat, and choleserol  
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Systems affecting blood pressure   Volume, CNS, PNS, renal, cardiac, adrenal, vasodilators, vasoconstrictors  
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Mean arterial pressure =   CO x TPR  
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Cardiac output =   stroke volume x heart rate  
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TPR =   vascular structure + vascular tone + blood volume  
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Baroreflex   Aortic depressor nerve in aortic arch and carotid tells brain either to release or not release NE based on blood pressure  
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Renal mechanisms   secretion of renin in glomerulous and the formation of angiotensin II  
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Non-renal mechanisms   Baroreflex and hormone system (NO vs endothelium)  
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Malignant hypertension cycle    
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Classification of htn drugs   diuretics, agents affecting adrenergic function, vasodilators, RAAS agents  
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Thiazides   work on descending loop where 67% of water reabsorption takes place; lose potassium  
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Loop diuretics   potassium wasting; work on ascending loop and renal tubule  
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Potassium sparing   want to combing these with thiazides to not only increase water excretion but also prevent some of the potassium loss from the thiazides  
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Agents affecting adrenergic function   reserpine, guanethedine, guanadrel; prevent release of NE to vasculature or heart  
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Reserpine   Depletes neurotransmitter in nerve endings by flushing NE out of intraneuronal vesicles and replacing it with itself which is released instead  
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Reserpine effects   Depresses sympathetic function peripherally and centrally; decrease HR, contractility, PVR; depression, insomnia, nightmares, diarrhea, cramps, orthostatic hypotension, dry mouth, impotence  
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Guanethedine   Depletes NE from nerve vesicles peripherally only and not centrally but still have orthostatic hypotension  
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Guanadrel   Depletes NE from nerve vesicles peripherally; less orthostatic hypotension, diarrhea, and impotence than guanethadine  
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Prazosin   A1 blocker used in combination with diuretic and B-blocker; good for lipid profile  
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1st dose phenomenon   first time you take A1 blocker it drops blood pressure severely; patient should take half dose for first week  
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Prazosin adverse effects   1st dose phenomenon, fluid retention, dizziness, headache  
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Non-selective beta blockers   b1 and b2  
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Intrinsic beta blocker   block betas but stimulate alphas; maintain some sympathetic tone  
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cardio-selective beta blockers   b1 blocker  
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effects of blocking b1   decrease renin release, contractility, and heart rate  
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beta blocker risks   asthma, a/v block if taking calcium channel blockers  
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Propranolol   b1 and b2 blocker  
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Labetolol   b1 and b2 blocker; a1 activator; can be given IV  
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A2 receptor location   presynaptic terminals; part of negative feedback mechanism; a2 is located peripherally on vasculature  
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A2 presynaptic effects   NE binds to them and inhibits future NE release  
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Clonidine   A2 agonist; work on presynaptic receptors; can cause rebound hypertension when you stop taking it suddenly (opposite of first dose phenomenon); limited use because of sedation and CNS effects  
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Calcium channel blockers   reduce intracellular calcium concentration-relaxing arteriolar smooth muscle-reducing PVR  
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Potassium channel openers   hyperpolarize the heart-increasing refractory period and reducing heart rate; hyperpolarize smooth muscle cells in vessels preventing contraction; reflex tach, Na and fluid retention  
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Direct acting vasodilators   Nitric oxide donors  
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2 groups of calcium channel blockers   phenylalkylamines and benzothiazepines-block vasculature and heart-no reflex tach but promote fluid retention; dihydropyridines-block vascular calcium channels  
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Nifedipine   dihydropyridine; main side effect is reflex tachycardia  
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Verapamil   phenylalkylamine; ccb on vasculature and heart; no reflex tach  
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Diltiazem   benzothiazepine; ccb on vasculature and heart; no reflex tach  
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Minoxidil   K channel opener; hirsutism (hair growth) is side effect  
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Diazoxide IV   K channel opener; for hypertensive emergency  
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Pinacidil   K channel opener  
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Sodium nitroprusside   Nitric oxide donor; direct acting vasodilator; side effect is cyanide poisoning and reflex tachycardia; used for hypertensive emergency  
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Hydralazine   direct acting vasodilator; reflex tachycardia  
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2 types of agents affecting RAS   angiotension converting enzyme inhibitors; angiotensin II receptor blockers  
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Captopril   ACE inhibitor  
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Enalapril   ACE inhibitor  
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Lisinopril   ACE inhibitor  
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Losartan   Ang II receptor blocker  
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Valsartan   Ang II receptor blocker  
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Irbesartan   Ang II receptor blocker  
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Ramipril   ACE inhibitor  
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Aliskiren   Renin inhibitor; dont have to remember this one  
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Clinically important consequence of htn   Damages large and small vessels, leads to left-ventricular hypertrophy, and end organ damage  
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First medications tried for hypertension   diuretics  
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How does RAS work?   Kidney releases renin-converts angiotensinogen from liver into angio I (inactive)-converted in lung by ACE to angio II (vasoconstrictor) increases sympathetic drive, Na reabsorption, aldosterone release, vasopressin (ADH) release  
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3 ways to block angiotensin II   block renin secretion; block conversion of ang I to ang II; block ang II receptor  
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effects of ACE   converts ang I to ang II; breaks down bradykinin (too much makes you cough)  
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side effects of ACE inhibitor   dry cough due to accumulation of bradykinin; hyperkalemia  
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side effects of ARBs   hyperkalemia because of reduced aldosterone; but no cough because ACE is still free to break down bradykinin  
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effects of renin inhibitors   binds to renin and blocks its activity so there is no conversion of angiotensinogen to ang I  
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side effects of renin inhibitors   hyperkalemia; hypotension; fluid retention (angiodema)  
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