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Antihypertensives

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