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Mechanism- works on alpha 2 site to prevent NE release- dec. sympathetic output prodrug- active when metabolized S.E.- depression, drowsiness, impaired ejaculation |
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Mechanism- works on alpha 2 site to prevent NE release- dec. sympathetic output S.E.- depression, drowsiness, impaired ejaculation sudden withdrawl can cause hypertensive emergency unlisted uses- help with opiate withdrawal, fibromyalgia, insomnia |
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Mechanism- inhibits tyrosine hydrooxylase- prevents synthesis of NE and EP used to treat pheochromocytoma |
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Mechanism- totally block all ganglionic transmission- block nitotinic receptors S.E.- orthostatic hypertension |
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Mechanism- totally block all ganglionic transmission- block nitotinic receptors S.E.- orthostatic hypertension |
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Mechanism-prevents encorporation of NE into vesicles, depletion of NE- also works on CNS S.E.- depression (suicides), drowsiness, diarrhea, impaired ejaculation |
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Mechanism-depletes NE from post ganglionic neurons, does not enter CNS S.E- orthostatic hypertension |
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Mechanism- alpha 1 blocker block effect of NE on end organ receptor |
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Mechanism- alpha 1 blocker block effect of NE on end organ receptor |
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Mechanism- alpha 1 blocker block effect of NE on end organ receptor |
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Mechanism- alpha 1 blocker used for treatment of benign prostatic hypertophy (BPH) S.E.-first dose effect- fast orthostatic hypotension, can be avoided by taking at night before sleep |
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Mechanism- alpha 1 blocker used for treatment of benign prostatic hypertophy (BPH) S.E.-first dose effect- fast orthostatic hypotension, can be avoided by taking at night before sleep |
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Mechanism- blocks all Beta receptors blocks B1 on heart and slows heart down gets into CNS S.E.- depression, fatigue, can cause asthma because it prevents dialation of bronchiole |
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Mechanism- Beta 1 blocker doesn't enter CNS S.E.- fatigue and bradycardia |
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Mechanism- Beta 1 blocker doesn't enter CNS S.E.- fatigue and bradycardia |
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Mechanism- Beta 1 blocker doesn't enter CNS S.E.- fatigue and bradycardia |
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Mechanism- Beta 1 blocker that also increases NO and causes vasodilation |
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Mechanism- combined alpha and beta blocker |
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Mechansim- combined alpha and beta blocker |
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Mechanism- blocks angiotension receptor S.E.- fetal abnormalities |
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Mechanism- blocks angiotension receptor S.E.- fetal abnormalities |
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Mechanism- blocks angiotension receptor S.E.- fetal abnormalities |
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Mechanism- blocks angiotension receptor S.E.- fetal abnormalities |
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Mechanism- blocks angiotension receptor S.E.- fetal abnormalities |
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Mechanism- blocks angiotension receptor S.E.- fetal abnormalities |
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Mechanism- acts directly on smooth muscle and opens K+ channels S.E.- causes hair growth- hypertrichosis used to treat edema, pericardial effusion |
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Mechanism- acts directly on smooth muscle opens K+ channels S.E.- dec. insulin secretion |
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Mechanism- acts directly on smooth muscle inc. cGMP S.E. can cause loupous like symptoms in slow accelators |
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Mechanism- acts directly on smooth muscle inc. cGMP- acts on all vasculature and is given IV and acts in seconds S.E.- degrades into cyanide so must be made on the spot is the drug of choice for hypertensive emergencies |
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Mechanism- Calcium channel blocker- causes vasodilation by dec. Ca2+ uptake into smooth muscle vasculature |
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Mechanism- Calcium channel blocker- causes vasodilation by dec. Ca2+ uptake into smooth muscle vasculature |
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Mechanism- Calcium channel blocker- causes vasodilation by dec. Ca2+ uptake into smooth muscle vasculature |
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Mechanism-inhibits formation of angiotensin by inhibiting angiogensin converting enzyme (ACE) which converts angiotensin I into angiotenin II- also prevents breakdown of bradykinin because ACE breaks down bradykinin S.E.- dry cough that doesn't respond to meds, fetal abnormalities |
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Mechanism-inhibits formation of angiotensin by inhibiting angiogensin converting enzyme (ACE) which converts angiotensin I into angiotenin II- also prevents breakdown of bradykinin because ACE breaks down bradykinin S.E.- dry cough that doesn't respond to meds, fetal abnormalities |
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Mechanism-inhibits formation of angiotensin by inhibiting angiogensin converting enzyme (ACE) which converts angiotensin I into angiotenin II- also prevents breakdown of bradykinin because ACE breaks down bradykinin S.E.- dry cough that doesn't respond to meds, fetal abnormalities |
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Mechanism-inhibits formation of angiotensin by inhibiting angiogensin converting enzyme (ACE) which converts angiotensin I into angiotenin II- also prevents breakdown of bradykinin because ACE breaks down bradykinin S.E.- dry cough that doesn't respond to meds, fetal abnormalities |
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Definition
Mechanism-inhibits formation of angiotensin by inhibiting angiogensin converting enzyme (ACE) which converts angiotensin I into angiotenin II- also prevents breakdown of bradykinin because ACE breaks down bradykinin S.E.- dry cough that doesn't respond to meds, fetal abnormalities |
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Mechanism- direct inhibitor of renin S.E.- dry cough, fetal abnormalities |
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Mechanism-acts directly on dopamine receptors in muscle given IV for hypertensive emergencies |
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