| Term 
 | Definition 
 
        | 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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        | Term 
 | Definition 
 
        | 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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        | Term 
 | Definition 
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        | Term 
 | Definition 
 
        | Mechanism- inhibits tyrosine hydrooxylase- prevents synthesis of NE and EP used to treat pheochromocytoma
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        | Term 
 | Definition 
 
        | Mechanism- totally block all ganglionic transmission- block nitotinic receptors S.E.- orthostatic hypertension
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        | Term 
 | Definition 
 
        | Mechanism- totally block all ganglionic transmission- block nitotinic receptors S.E.- orthostatic hypertension
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        | Term 
 | Definition 
 
        | 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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        | Term 
 | Definition 
 
        | Mechanism-depletes NE from post ganglionic neurons, does not enter CNS S.E- orthostatic hypertension
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        | Term 
 | Definition 
 
        | Mechanism- alpha 1 blocker block effect of NE on end organ receptor
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        | Term 
 | Definition 
 
        | Mechanism- alpha 1 blocker block effect of NE on end organ receptor
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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- alpha 1 blocker block effect of NE on end organ receptor
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        | Term 
 | Definition 
 
        | 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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        | Term 
 | Definition 
 
        | 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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        | Term 
 | Definition 
 
        | 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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        | Term 
 | Definition 
 
        | Mechanism- Beta 1 blocker doesn't enter CNS
 S.E.- fatigue and bradycardia
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        | Term 
 | Definition 
 
        | Mechanism- Beta 1 blocker doesn't enter CNS
 S.E.- fatigue and bradycardia
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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- Beta 1 blocker doesn't enter CNS
 S.E.- fatigue and bradycardia
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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- Beta 1 blocker that also increases NO and causes vasodilation |  | 
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        | Term 
 | Definition 
 
        | Mechanism- combined alpha and beta blocker |  | 
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        | Term 
 | Definition 
 
        | Mechansim- combined alpha and beta blocker |  | 
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        | Term 
 | Definition 
 
        | Mechanism- blocks angiotension receptor S.E.- fetal abnormalities
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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- blocks angiotension receptor S.E.- fetal abnormalities
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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- blocks angiotension receptor S.E.- fetal abnormalities
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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- blocks angiotension receptor S.E.- fetal abnormalities
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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- blocks angiotension receptor S.E.- fetal abnormalities
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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- blocks angiotension receptor S.E.- fetal abnormalities
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        | Term 
 | Definition 
 
        | 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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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- acts directly on smooth muscle opens K+ channels
 S.E.- dec. insulin secretion
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        | Term 
 | Definition 
 
        | Mechanism- acts directly on smooth muscle inc. cGMP
 S.E. can cause loupous like symptoms in slow accelators
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        | Term 
 | Definition 
 
        | 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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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- Calcium channel blocker- causes vasodilation by dec. Ca2+ uptake into smooth muscle vasculature |  | 
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        | Term 
 | Definition 
 
        | Mechanism- Calcium channel blocker- causes vasodilation by dec. Ca2+ uptake into smooth muscle vasculature |  | 
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        | Term 
 | Definition 
 
        | Mechanism- Calcium channel blocker- causes vasodilation by dec. Ca2+ uptake into smooth muscle vasculature |  | 
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        | Term 
 | 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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        |  | 
        
        | Term 
 | 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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        |  | 
        
        | Term 
 | 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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        |  | 
        
        | Term 
 | 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
 |  | 
        |  | 
        
        | Term 
 | 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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        |  | 
        
        | Term 
 | Definition 
 
        | Mechanism- direct inhibitor of renin S.E.- dry cough, fetal abnormalities
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        | Term 
 | Definition 
 
        | Mechanism-acts directly on dopamine receptors in muscle given IV for hypertensive emergencies
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