Science Quiz / Antihypertensive Drugs

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Can you name the Antihypertensive Drugs?

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HintDrugClass fo Drug
Unknown target; decreases TPR by relaxing arterioles; vasodilation is followed by reflex tachycardia, increased contractility and increased rennin secretionVasodilator
Blocks Ang I-Ang II conversion in endothelial cells of the lung, leading to natriuresis, decreased TPR, decreased aldosterone, and increased Na excretion; can cause fetotoxicityACE Inhibitor
Opens K channels on SM; decreases TPR by relaxing arterioles; side effects include rapid drop in TPR, hypertrichosis, tachycardia, and fluid retentionVasodilator
Converted to a false transmitter in CNS neurons; acts centrally to decrease SNS activity, and reduces CO, HR, rennin release and TPROther
Opens K channels on SM; decreases TPR by relaxing arterioles; side effects include rapid drop in TPR, and pronounced tachycardia, hyperglycemia, and hypertrichosisVasodilator
Reduces SNS and PNS activity, decreasing TPR and CO; side effects include paralytic ileus, bladder dysfunction, constipation, postural hypotension, blurred vision, and dry mouthGanglionic Blocker
Decreases Co, HR, contractility, CNS outflow, and rennin release; side effects include bronchospasm, bradycardia, renal vasoconstriction, depression, bad dreams, and fatigueOther
Inhibits the synthesis of catecholamines by tyrosine hydroxylase; good for management of pheochromocytomaAdrenergic Neuronal Blocker
Blocks AT1 receptors to induce vasodilation; also increases Na and water excretion; side effects include 1st dose hypotension, hyperkalemia, hepatic dysfunction, and fetotoxicityAngiotensin Receptor Antagonist
Beta blocker with intrinsic sympathomimetic activityBeta Blocker
HintDrugClass fo Drug
Directly activates presynaptic alpha2-AR receptors; decreases SNS activity, no reflex, and reduces CO, HR, rennin release, and TPRAlpha2-AR Agonist
Cardiosolective beta blockerBeta Blocker
Directly inhibits the protease activity of renin; causes vasodilation and natriuresis; side effects include 1st dose hypotension, hyperkalemia, angiodema, and fetotoxicityRenin Inhibitor
Red blood cells metabolize it into NO, which induces vascular SM relaxation in both arteries and veins; decreases TPR, but also venous poolingVasodilator
Alpha and beta blockerBeta Blocker
Non-Selective beta blockerBeta Blocker
Inhibits L-type Ca channels in the heart and vasculature, reducing contraction; this leads to lower contractility and CO in the heart, and reduced vasoconstriction and TPRCa Channel Blocker
Blocks peripheral postjunctional adrenergic receptors that cause contraction of vascular SM, decreases TPR and causes reflex increase in HRAlpha1-AR Antagonist
Replaces NE in secretory vesicles; does not cross blood-brain barrier, so no CNS effectsAdrenergic Neuronal Blocker
Depletes CNS and peripheral NE and 5-HT as well as adrenal catecholamines by interfering with storage vesicles; least desirable antihypertensive, but is cheap and effectiveAdrenergic Neuronal Blocker

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