Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Antihypertensives
| Question | Answer |
|---|---|
| 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
Popular Pharmacology sets