Antiadrenergic Drugs Practice Questions Flashcards
Which of the following drugs is a partial agonist at beta-1 and beta-2 receptors? Labetalol Atenolol Propranolol Esmolol
Labetalol
Which of the following drugs is a selective beta-1 antagonist that is used to treat patients after myocardial infarction? Carvedilol Propranolol Pindolol Metoprolol
Metoprolol
Which of following drugs is a non-selective beta blocker that can also block potassium channels? Timolol Sotalol Propranolol Atenolol
Sotalol
Which of following drugs is used to treat symptoms caused by prostatic hyperplasia? Dobutamine Timolol Tamsulosin Isoproterenol
Tamsulosin
Blockade of alpha-1 receptors decreases contraction of prostate smooth muscle. This helps to prevent urinary obstruction caused by an enlarged prostate.
Tamsulosin is an alpha-1 antagonist.
None of the other drugs are alpha-1 antagonists.
Which of the following drugs is administered perioperatively to treat hypertension and tachycardia because it has a very short half-life? Esmolol Phenoxybenzamine Tamsulosin Propranolol
Esmolol
Esmolol is a selective beta-1 antagonist with a very short half life that is used to treat the conditions described.
Phenoxybenzamine is an irreversible alpha antagonist. It has a very long half-life and is used to treat patients with pheochromocytoma.
Tamsulosin is an alpha-1 antagonist used to treat symptoms of BPH.
Propranolol does not have a short half-life.
Which of the following is a pharmacological effect of alpha-1 receptor antagonists?
Reversal of norepinephrine-induced blood pressure increase
Reversal of epinephrine-induced blood pressure increase
Reversal of isoproterenol-induced tachycardia
Relaxation of bladder external sphincter
Reversal of epinephrine-induced blood pressure increase
Epinephrine activates alpha-1 receptors so causing vasoconstriction, and beta-2 receptors, so causing vasodilation. Alpha-1 receptor mediated vasoconstriction and the epinephrine-induced increased stroke volume cause an increase in mean blood pressure. By blocking alpha-1 receptors the beta-2 mediated vasodilating activity of epinephrine is unopposed and blood pressure falls.
A) The hypertensive effect of norepinephrine is decreased, but not reversed because norepinephrine has no vasodilating activity (it does not activate beta-2 receptors).
C) Isoproterenol is an agonist at beta-1 and beta-2 receptors. Vasodilation of skeletal muscle due to beta-2 receptors will cause a baroreceptor mediated increase in heart rate. The addition of an alpha-1 antagonist will cause further vasodilation which will lead to increase in reflex tachycardia.
D) The external sphincter is a voluntary muscle, an alpha-1 antagonist would have no effect.
Which of the following is the most likely adverse effect of chronic treatment with selective alpha-1 blockers? Hypertension Bradycardia Digital vasospasm Sodium and water retention Urinary retention
Sodium and water retention
A chronic treatment with selective alpha-1 blockers may cause hypotension. This hypotension usually elicits compensatory effects namely Na+ retention and expansion of blood volume.
A) Hypotension, not hypertension, is a likely adverse effects of alpha-1 blockers.
B) By causing hypotension these drugs tend to cause reflex tachycardia, not bradycardia.
C) Alpha-1 blockers cause peripheral vasodilation, so digital vasospasm is quite unlikely.
E) Alpha-1 blockers relax the internal sphincter of the bladder ,so urinary retention is unlikely
In an experimental animal model, acute prazosin pretreatment will most effectively counteract which of the following drug-induced effects?
Isoproterenol-induced tachycardia
Nicotine-induced sweating
Dopamine-induced increase in renal blood flow
Phenylephrine-induced hypertension
Phenylephrine-induced hypertension
Prazosin is a selective alpha-1 blocker and therefore will most effectively counteract the effect of a selective alpha-1 agonist like phenylephrine.
A) Isoproterenol induces tachycardia by activating beta-1 and beta-2 receptors. The blockade of alpha-1 receptors cannot antagonize this effect.
B) Nicotine induces sweating by activating Nn receptors in ganglia which in turn increases sympathetic firing. However the sympathetic fibers innervating sweat glands are cholinergic and therefore, the blockade of alpha-1 receptors cannot antagonize this effect.
C) Dopamine increases renal blood flow by activating D1 receptors. By blocking alpha-1 receptors prazosin can also increases renal blood flow.
An IV injection of norepinephrine was given to a laboratory animal before and after the administration of a new drug X, and the mean blood pressure was recorded. The results are depicted in the figure below. Which of the following drugs does Drug X most closely resemble?
Albuterol Cocaine Labetalol Phenylephrine Propranolol Dopamine
Labetalol
The blood pressure depends on cardiac output and total peripheral resistance according to the formula: BP = SV x HR x TPR. In order to completely abolish the action of norepinephrine the drug must antagonize the increased stoke volume (mediated by the activation of beta receptors) and the increased total peripheral resistance (mediated by the activation of alpha-1 receptors). Therefore the drug must have both alpha and beta blocking activity, like labetalol.
Answers (A, B, D, E and F) do not block alpha and beta beta receptors.
Which of the following is a metabolic effect of non-selective beta blockers?
Enhancement of insulin-induced hypoglycemia Increased lipolysis Increased renin release Increased hepatic glycogenolysis Increased HDL
Enhancement of insulin-induced hypoglycemia
Gluconeogenesis and glycogenolysis are beta-2 mediated effects. By blocking these effects non-selective beta-blockers can enhance hypoglycemia induced by insulin (or other hypoglycemic drugs) in diabetic patients.
C) Renin release can be stimulated by the activation of beta-1 receptors in the juxtaglomerular cells of macula densa. All beta-blockers decrease, not increase, renin release.
B) Beta blockers actually decrease lipolysis and usually reduce the release of free fatty acid from adipose tissue.
D, E) Beta blockers actually decrease hepatic gluconeogenesis and plasma levels of HDL.
In an experimental animal model, an acute propranolol pretreatment will most effectively counteract which of the following drug-induced effects?
Isoproterenol-induced hyperglycemia
Nicotine-induced decrease in skin blood flow
Norepinephrine-induced reflex bradycardia
Phenylephrine-induced mydriasis
Isoproterenol-induced hyperglycemia
Isoproterenol-induced hyperglycemia is mainly due to beta-2 receptor mediated gluconeogenesis and glycogenolysis, and therefore it can be effectively counteracted by propranolol, which block beta-2 receptors. All the other listed actions cannot be antagonized by propranolol because they are not mediated by activation of beta receptors.
B) Nicotine-induced activation of Nn receptors in ganglia increases the firing of postganglionic sympathetic nerves, which in turn cause skin vasoconstriction by activating alpha-1 receptors
C) Norepinephrine-induced reflex bradycardia is mediated by the activation of M2 cardiac receptors.
D) Phenylephrine-induced mydriasis is mediated by the activation of alpha-1 receptors
Which of the following pairs of autonomic drugs is a correct receptor agonist-antagonist match?
Isoproterenol - prazosin Epinephrine - labetalol Phenylephrine - atropine Albuterol - Atenolol Nicotine - dopamine Norepinephrine - clonidine
Epinephrine - labetalol
Epinephrine activates alpha-1, alpha-2, beta-1 and beta-2 receptors. Labetalol is able to block all these receptors. Therefore it will be able to antagonize all the effects of epinephrine.
A, C, D, E, F) All these drug pairs act on different receptors and therefore are not a receptor agonist-antagonist match.
A 74-year-old man reports to his physician that he has trouble when urinating. He reports a weak stream that stops and starts. The man was diagnosed with benign prostatic hyperplasia. He has congestive heart failure and surgical ablation of the prostate was contraindicated. A drug suitable for the treatment of the patient's impaired bladder emptying was prescribed. Which of the following molecular actions most likely mediated the therapeutic effect of the drug in the patient's disease? Beta-2 adrenoceptor blockade Beta-2 adrenoceptor activation Alpha-2 adrenoceptor activation Alpha-1 adrenoceptor blockade M3 muscarinic receptor activation
Alpha-1 adrenoceptor blockade
Selective alpha-1 blockers (like prazosin, tamsulosin etc.) are the drugs of choice for the treatment of impaired bladder emptying in prostatic hyperplasia. By blocking alpha-1 receptors these drugs relax the prostate capsule and the internal sphincter of the bladder (which have plentiful alpha-1 receptors), so allowing a better urine flow.
A, B) Beta receptors are not significantly involved in the regulation of the internal sphincter of the bladder.
C) Even if activation of alpha-2 receptors would cause a decrease of norepinephrine release, the action is too weak to be clinically significant.
E) Activation of M3 receptors would cause a contraction of the detrusor muscle of the bladder, which would increase the urgency to void without improving voiding because of the urethral compression due to prostate hyperplasia.
Phenoxybenzamine was given IM to a dog during a lab experiment. One hour later the dog received norepinephrine IM and some effects of that drug were recorded. Which of the following expected drug-induced effects was most likely prevented by phenoxybenzamine pretreatment? Dilation of skeletal muscle vessels Increased heart rate Bronchodilation Decreased insulin secretion
Decreased insulin secretion
Phenoxybenzamine blocks irreversibly alpha-1 and alpha-2 receptors. Activation of alpha-2 receptors in pancreas decreases insulin secretion. By blocking alpha-2 receptors phenoxybenzamine counteracts this effect.
(A, B and C) All these actions are due to activation of beta receptors and therefore are not blocked by phenoxybenzamine
A 41-year-old man complained to his physician of painful prolonged erection and impaired ejaculation during intercourse. Two week earlier he had been diagnosed with chronic bacterial prostatitis and had started an appropriate therapy. Which of the following drugs most likely caused the patient's symptoms? Prazosin Propranolol Phenoxybenzamine Metyrosine Phenylephrine Ephedrine
Prazosin
Chronic bacterial prostatitis is usually caused by sequestered urinary pathogens (Escherichia, Klebsiella, Proteus) that antibiotics have not eradicated. When symptoms of urinary obstruction are present due to the inflamed prostate, alpha adrenergic blockers may be indicated. Painful erection and impaired ejaculation are typical adverse effects of adrenergic blockers. Ejaculation is controlled by alpha-1 receptors and the vasodilation due to alpha-1 receptor blockade could result in prolonged erection.
B, C, D, E, F) These drugs are not used in case of urinary obstruction and do not cause the symptoms reported by the patient
