Hypertension
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| What class of drugs deplete sodium stores and decreases blood volume? | Diuretics
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| Which thiazide diuretic can be used with GFR less than 30 mL/min? | Metolazone (thiazide-like)
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| Why is metolazone advantageous over loop diuretics? | More mild diuresis
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| Which loop diuretic is the most potent? | Bumetanide
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| Which loop diuretic has the longer duration of action? | Torsemide
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| What is ethacrynic acid? | Loop diuretic
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| What is eplerenone? | aldosterone receptor antagonist
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| What is amiloride? | sodium channel blocker
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| What medication(s) are centrally acting agents/vasomotor center? | methyldopa, clonidine
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| What is the MOA of centrally acting sympathoplegic agents? | Bind to presynaptic alpha-2 receptors and decrease NE release/decrease outflow to vasculature
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| Does methyldopa have CNS ADE? | yes (sedation, mental lassitude, decreased concentration)
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| Which drug binds to the imidazoline receptor? | clonidine
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| Which medications have withdrawal symptoms? | Clonidine, beta-blockers
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| When is clonidine CI? | depression patients
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| What is trimethaphan? | ganglion-blocking agent
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| What is the MOA of ganglion blocking agents? | blocks nicotinic cholinoreceptors on postganglionic neurons (decrease sympathetic outflow)
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| What are guanethidine and reserpine? | adrenergic neuron-blocking agents/sympathetic nerve terminals
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| What amino acid is the precursor for NE? | tyrosine
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| What is the MOA of reserpine? | prevents dopamine from entering vessicles
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| What is the MOA of guanethidine? | prevents release of NE and depletes NE in vessicles via anesthesia of sodium conduction channels
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| Does reserpine or guanethidine act peripherally but not centrally? | guanethidine
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| Does reserpine or guanethidine irreversibly block uptake and storage of amines? | reserpine
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| Which medication has EPS symptoms? | reserpine
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| Why does reserpine act centrally and peripherally? | lippophilicity
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| Where do beta-blockers work in the kidney? | Beta-1 receptors on granular cells of JG apparatus
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| Where do beta-blockers work in the body? | Heart, brain, kidney (JG cells), presynaptic adrenergic neurons
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| What drug is the prototype of non-selective beta blockers? | propranolol
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| What are the indicators of beta-blockers in patients? | resting bradycardia, smaller rise in BP in exercise
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| What drug is the prototype of cardioselective beta blockers? | metoprolol
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| What drug is the prototype of long half life beta blockers? | atenolol
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| How is atenolol excreted? | renally
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| Which beta-blocker(s) have intrinsic sympathomimetic activity? (partial agonists) | pindolol, acebutolol
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| Which drug is the prototype for mixed adrenergic antagonists? | labetolol
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| What is the beta:alpa antagonist ration for labetolol? | 3:1
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| Which drug is the prototype for short half life beta blockers? | esmolol
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| What is the MOA of alpha-adrenoreceptor antagonists? | block alpha-1 receptors and dilate arterioles and venules
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| When are alpha-adrenoreceptor antagonists most effective? | In combo with diuretic or beta-blocker
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| What do beta-blockers prevent? | reflex tachycardia
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| What is a common ADE with alpha-adrenoreceptor antagonists? | first dose syncope
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| What drug is the prototype for alpa-1 blockers? | prazosin
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| Which alpha-adrenoreceptor antagonist is an irreversible blocker? | phenoxybenzamine
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| Which drug has no MOA? | Hydralazine
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| Which vasodilator dilates arterioles but not veins? | hydralazine, minoxidil, diazoxide
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| Which vasodilator can have fast and slow metabolizers? | hydralazine
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| Which medication can have a lupus-erythematosus-like syndrome ADE? | hydralazine
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| What is minoxidil? | vasodilator
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| What is the MOA of minoxidil? | opens K+ channels of smooth muscle (stabilizes membranes)
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| Which vasodilator is used for hypertensive emergencies? | Sodium nitroprusside, diazoxide, fenoldopam
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| Which vasodilator activates gyanylyl cyclase? | Sodium nitroprusside
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| Which vasodilator dilates both arterioles and veins? | Sodium nitroprusside
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| What is the "antidote" of cyanide accumulation? | sodium thiosulfate==> thiocyanate is still toxic
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| Which vasodilator causes sodium natriuresis? | fenoldopam
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| When should fenoldopam be avoided? | glaucoma patients
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| What is the MOA of calcium channel blockers? | decrease sodium influx into arteriolar smooth muscle celsls
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| What are the prototypes for DHP CCBs? | amlodipine, felodipine, and nifedipine
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| What are the prototypes for non-DHP CCBs? | verapamil and diltiazem
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| Which CCB's work on cardiac muscle and vasculature? | non-DHPs
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| What class of medicine activates the kallikrein-kinin system? | ACE inhibitors
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| What is the MOA of ARBs? | Competitive antagonists at the AT1 receptor
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| What three responses does Angiotensin II cause besides ADH, thirst, and vasoconstriction? | rapid pressor response, slow pressor response, and vascular and cardiac hypertrophy and remodeling
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| What type of response is increased aldosterone release? | slow pressor response
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| What type of response is increased afterload and vessel wall tension? | cardiac remodeling
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| What are the prototypes for ACE inhibitors? | captopril, enalapril, and lisinopril
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| Chronic use of what class of drugs causes increased transient plasma angiotensin II levels? | ARBs
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| Which drug class has antiproliferative and antiremodeling effects> | ARBs
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| What is the prototype for ARB/AT1 receptor blocker? | losartan
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| Which drug is a renin inhibitor? | aliskiren
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