Lippincott Autonomic Drugs

Which of the following is a systemic effect of a muscarinic agonist? A. Reduced heart rate (bradycardia). B. Increased blood pressure. C. Mydriasis (dilation of the pupil). D. Reduced urinary frequency. E. Constipation.

Correct answer = A. A muscarinic agonist binds to and activates muscarinic receptors in the heart, endothelial cells (blood vessels), the gut, and iris sphincter (eye) and urinary bladder wall muscles, in addition to several other tissues. Activation of muscarinic receptors by an agonist causes a reduction in heart rate, constriction of circular muscles in the iris sphincter leading to constriction of the pupil (miosis), increased GI motility (hence, diarrhea, not constipation), and contraction of bladder muscles leading to an increase (not decrease) in urination frequency. In the endothelial cells of blood vessels, muscarinic activation produces release of nitric oxide that causes vasorelaxation and a reduction (not increase) in blood pressure.

Which of the following statements is correct regarding the sympathetic and parasympathetic systems? A. Acetylcholine activates muscarinic receptors. B. Acetylcholine activates adrenergic receptors. C. Norepinephrine activates muscarinic receptors. D. Activation of the sympathetic system causes a drop in blood pressure.

Correct answer = A. Acetylcholine is the neurotransmitter in the cholinergic system, and it activates both muscarinic and nicotinic cholinergic receptors, not adrenergic receptors. Norepinephrine activates adrenergic receptors, not muscarinic receptors. Activation of the sympathetic system causes an increase in blood pressure (not a drop in blood pressure) due to vasoconstriction and stimulation of the heart.

Botulinum toxin blocks the release of acetylcholine from cholinergic nerve terminals. Which of the following is a possible effect of botulinum toxin? A. Skeletal muscle paralysis. B. Improvement of myasthenia gravis symptoms. C. Increased salivation. D. Reduced heart rate.

Correct answer = A. Acetylcholine released by cholinergic neurons acts on nicotinic receptors in the skeletal muscle cells to cause contraction. Therefore, blockade of ACh release causes skeletal muscle paralysis. Myasthenia gravis is an autoimmune disease where antibodies are produced against nicotinic receptors and inactivate nicotinic receptors. A reduction in ACh release therefore worsens (not improves) the symptoms of this condition. Reduction in ACh release by botulinum toxin causes reduction in secretions including saliva (not increase in salivation) causing dry mouth and an increase (not reduction) in heart rate due to reduced vagal activity.

Head and neck irradiation in cancer patients can decrease salivary secretion and cause dry mouth. All of the following drugs or classes of drugs are theoretically useful in improving secretion of saliva in these patients except: A. Muscarinic antagonists. B. Muscarinic agonists. C. Anticholinesterase agents. D. Pilocarpine. E. Neostigmine.

Correct answer = A. Activation of muscarinic receptors in the salivary glands causes secretion of saliva. This can be achieved in theory by using a muscarinic agonist such as pilocarpine or an anticholinesterase agent such as neo- stigmine (increases levels of ACh). Muscarinic antagonists (anticholinergic drugs) will reduce salivary secretion and worsen dry mouth.

All of the following statements regarding central control of autonomic functions are correct except: A. Baroreceptors are pressure sensors located at various cardiovascular sites. B. The parasympathetic system is activated by the CNS in response to a sudden drop in blood pressure. C. The parasympathetic system is activated by the CNS in response to a sudden increase in blood pressure. D. The sympathetic system is activated by the CNS in response to a sudden drop in blood pressure.

Correct answer = B. When there is a sudden drop in blood pressure, the baroreceptors send signals to the brain, and the brain activates the sympathetic system (not the parasympathetic system) to restore blood pressure to normal values.

A 30-year-old male patient was brought to the ER with amphetamine overdose. He presented with high blood pressure and arrhythmia. Which of the following is correct regarding this patient? A. Amphetamine can activate all types of adrenergic receptors. B. β-Blockers are the ideal antidotes for amphetamine poisoning. C. α-Blockers can normalize the blood pressure in this patient. D. Miosis could be a possible symptom of amphetamine poisoning.

Correct answer = A. Amphetamine is an indirect adrenergic agonist that mainly enhances the release of norepinephrine from peripheral sympathetic neurons. Therefore, it activates all types of adrenergic receptors (that is, α and β receptors) and causes an increase in blood pressure. Since both α and β receptors are activated by amphetamine, α-blockers or β-blockers alone cannot relieve the symptoms of amphetamine poisoning. Since amphetamine causes sympathetic activation, it causes mydriasis, not miosis.

Which of the following is correct regarding β-blockers? A. Treatment with β-blockers should not be stopped abruptly. B. Propranolol is a cardioselective β-blocker. C. β-Blockers may cause orthostatic hypotension. D. Cardioselective β-blockers worsen asthma. E. β-Blockers decrease peripheral resistance by causing vasorelaxation.

Correct answer = A. If β-blocker therapy is stopped abruptly, that could cause angina and rebound hypertension. This could be due to the up-regulation of β receptors in the body. β-Blockers do not cause direct vasorelaxation. Therefore, they do not decrease peripheral resistance and are less likely to cause orthostatic hypotension. Propranolol is a nonselective β-blocker (not cardioselective). Cardioselective β-blockers antagonize only β1 receptors and do not worsen asthma as they do not antagonize β2 receptors.

Which of the following is correct regarding neurotransmitters and neurotransmission? A. Neurotransmitters are released from the presynaptic nerve terminals. B. Neurotransmitter release is triggered by the arrival of action potentials in the postsynaptic cell. C. Intracellular calcium levels drop in the neuron before the neurotransmitter is released. D. Serotonin and dopamine are the primary neurotransmitters in the ANS.

Correct answer = A. Neurotransmitters are released from presynaptic neurons, triggered by the arrival of an action potential in the presynaptic neuron (not in the postsynaptic cell). When an action potential arrives in the presynaptic neuron, calcium enters the presynaptic neuron and the calcium levels increase in the neuron before the neurotransmitter is released. The main neurotransmitters in the ANS are norepinephrine and acetylcholine.

Which of the following is correct regarding membrane receptors and signal transduction? A. ANS neurotransmitters bind to membrane receptors on the effector cells, which leads to intracellular events. B. Cholinergic muscarinic receptors are examples of ionotropic receptors. C. Cholinergic nicotinic receptors are examples of metabotropic receptors. D. Metabotropic receptors activate ion channels directly.

Correct answer = A. Neurotransmitters generally bind to the membrane receptors on the postsynaptic effector cells and cause cellular effects. Acetylcholine (ACh) binds to cholinergic muscarinic receptors in the effector cells and activates the second messenger pathway in the effector cells, which in turn causes cellular events. These types of receptors that are coupled to second messenger systems are known as metabotropic receptors. Thus, metabotropic receptors do not directly activate ion channels. ACh also binds to cholinergic nicotinic receptors and activates ion channels on the effector cells directly. These types of receptors that activate ion channels directly are known as ionotropic receptors.

Which of the following is correct regarding ganglion- blocking drugs? A. Blockade of sympathetic ganglia could result in reduced blood pressure. B. Blockade of parasympathetic ganglia could result in reduced heart rate. C. Nicotine is a nondepolarizing ganglion blocker. D. Atropine is a nondepolarizing ganglion blocker.

Correct answer = A. Selective blockade (in theory) of the sympathetic ganglion causes reduction in norepinephrine release and therefore reduction in heart rate and blood pressure. Selective blockade (in theory) of the parasympathetic ganglion causes reduction in ACh release and therefore an increase in heart rate. Receptors at both sympathetic and parasympathetic ganglia are of the nicotinic type. Nicotine is an agonist at nicotinic receptors and produces a depolarizing block in the ganglia. Atropine is a muscarinic antagonist and has no effect on the nicotinic receptors found in the ganglia

Which of the following is correct regarding responses mediated by adrenergic receptors? A. Stimulation of α1 receptors increases blood pressure. B. Stimulation of α receptors reduces blood pressure. C. Stimulation of sympathetic presynaptic α receptors increases norepinephrine release. D. Stimulation of β2 receptors increases heart rate (tachycardia). E. Stimulation of β2 receptors causes bronchoconstriction.

Correct answer = A. Stimulation of α1 receptors, mostly found in the blood vessels, causes vasoconstriction and increase in blood pressure. Stimulation of α2 receptors on the sympathetic presynaptic terminal reduces the release of norepinephrine. β2 receptors are not found in the heart, so activation of β receptors does not affect heart rate. Stimulation of β2 receptors found in the bronchial tissues causes bronchodilation, not bronchoconstriction.

An elderly female who lives in a farm house was brought to the emergency room in serious condition after ingesting a liquid from an unlabeled bottle found near her bed, apparently in a suicide attempt. She presented with diarrhea, frequent urination, convulsions, breathing difficulties, constricted pupils (miosis), and excessive salivation. Which of the following is correct regarding this patient? A. She most likely consumed an organophosphate pesticide. B. The symptoms are consistent with sympathetic activation. C. Her symptoms can be treated using an anticholinesterase agent. D. Her symptoms can be treated using a cholinergic agonist.

Correct answer = A. The symptoms are consistent with that of cholinergic crisis. Since the elderly female lives on a farm and since the symptoms are consistent with that of cholinergic crisis (usually caused by cholinesterase inhibitors), it may be assumed that she has consumed an organophosphate pesticide (irreversible cholinesterase inhibitor). Assuming that the symptoms are caused by organophosphate poisoning, administering an anticholinesterase agent or a cholinergic agonist will worsen the condition. The symptoms are not consistent with that of sympathetic activation, as sympathetic activation will cause symptoms opposite to that of cholinergic crisis seen in this patient.

A patient was administered a neuromuscular blocker (NMB) prior to a surgical procedure to produce skeletal muscle paralysis. This NMB drug affected small, rapidly contracting muscles of the face and eyes first and diaphragm muscles last. The effect of this drug was easily reversed with neostigmine. Which of the following neuromuscular blockers was most likely administered to this patient? A. Rocuronium. B. Succinylcholine. C. Diazepam. D. Tubocurarine.

Correct answer = A. There are two types of NMBs: depolarizing and nondepolarizing NMBs. Depolarizing NMBs are agonists at the nicotinic receptors, whereas nondepolarizing NMBs are antagonists at the nicotinic receptors. Both types of NMBs affect the rapidly contracting muscles (face, eye, etc.) first and diaphragm muscles last. However, cholinesterase inhibitors such as neostigmine increase ACh levels in the NMJ and reverse the effects of nondepolarizing NMBs, but not those of depolarizing NMBs. Therefore, the NMB administered to this patient is most probably rocuronium, which is a nondepolarizing NMB. Tubocurarine is also a nondepolarizing NMB, but it is not used in practice. Succinylcholine is a depolarizing NMB, and diazepam is a benzodiazepine that does not cause paralysis of skeletal muscles.

Which of the following physiological changes could happen when a person is attacked by a grizzly bear? A. Increase in heart rate. B. Increase in lacrimation (tears). C. Constriction of the pupil (miosis). D. Increase in gastric motility.

Correct answer = A. When a person is in the "fight-or-flight" mode, as in the case of a bear attack, the sympathetic system will be activated. Activation of the sympathetic system causes an increase in heart rate and blood pressure and a decrease (not increase) in gastric motility. It also causes dilation (not constriction) of the pupil and inhibition of lacrimation.

Which of the following is correct regarding α-adrenergic blockers? A. α-Adrenergic blockers are used in the treatment of hypotension in anaphylactic shock. B. α-Adrenergic blockers are used in the treatment of benign prostatic hyperplasia (BPH). C. α-Adrenergic blockers may cause bradycardia. D. α-Adrenergic blockers are used in the treatment of asthma. E. α-Adrenergic blockers reduce the frequency of urination.

Correct answer = B. α-Adrenergic blockers are used in the treatment of BPH because of their relaxant effect on prostate smooth muscles. Being antihypertensive agents, they are not useful in treating hypotension in anaphylaxis. α-Adrenergic blockers generally cause reflex tachycardia (not bradycardia) due to the significant drop in blood pressure caused by them. α-Adrenergic blockers have no significant effects on bronchial tissues and are not useful in treating asthma. They increase (not reduce) the frequency of urination by relaxing the internal sphincter of the urinary bladder, which is controlled by α1 receptors.

An asthma patient was given a nonselective β agonist to relieve bronchoconstriction. Which of the following adverse effects would you expect to see in this patient? A. Bradycardia. B. Tachycardia. C. Hypotension (reduction in blood pressure). D. Worsening bronchoconstriction.

Correct answer = B. A nonselective β agonist activates both β1 as well as β2 receptors. β1 activation causes an increase in heart rate (tachycardia), contractility, and subsequent increase in blood pressure. It relieves bronchoconstriction because of the β2 receptor activation.

An elderly man was brought to the emergency room after he ingested a large quantity of carvedilol tablets, a drug that blocks α1, β1, and β2 adrenergic receptors, which mainly mediate the cardiovascular effects of epinephrine and norepinephrine in the body. Which of the following symptoms would you expect in this patient? A. Increased heart rate (tachycardia). B. Reduced heart rate (bradycardia). C. Dilation of the pupil (mydriasis). D. Increased blood pressure.

Correct answer = B. Activation of α1 receptors causes mydriasis, vasoconstriction, and an increase in blood pressure. Activation of β1 receptors increases heart rate, contractility of the heart, and blood pressure. Activation of β2 receptors causes dilation of bronchioles and relaxation of skeletal muscle vessels. Thus, inhibition of these receptors will cause vasorelaxation (α1 blockade), reduction in heart rate (β1 blockade), reduction in contractility of the heart (β1 blockade), reduction in blood pressure, bronchoconstriction (β2 blockade), and constriction of blood vessels supplying skeletal muscles (β2 blockade).

Atropa belladonna is a plant that contains atropine (a muscarinic antagonist). Which of the following drugs or classes of drugs will be useful in treating poisoning with belladonna? A. Malathion. B. Physostigmine. C. Muscarinic antagonists. D. Nicotinic antagonists.

Correct answer = B. Atropine is a competitive muscarinic receptor antagonist that causes anticholinergic effects. Muscarinic agonists or any other drugs that can increase the levels of ACh will be able to counteract the effects of atropine. Thus, anticholinesterases such as malathion and physostigmine can counteract the effects of atropine in theory. However, malathion being an irreversible inhibitor of acetylcholinesterase is not used for systemic treatment in patients. Muscarinic antagonists will worsen the toxicity of atropine. Nicotinic antagonists could worsen the toxicity by acting on parasympathetic ganglionic receptors and thus reducing the release of ACh.

A patient was administered a neuromuscular blocker (NMB) prior to a surgical procedure to produce skeletal muscle paralysis. This NMB drug caused initial skeletal muscle fasciculations before the onset of paralysis. The effect of this drug could not be reversed with neostigmine. Which of the following neuromuscular blockers was most likely administered to this patient? A. Cisatracurium. B. Succinylcholine. C. Diazepam. D. Tubocurarine.

Correct answer = B. Depolarizing NMBs cause muscle fasciculations before causing paralysis, and their effects cannot be reversed using cholinesterase inhibitors such as neostigmine. Nondepolarizing NMBs do not cause muscle fasciculations, and their effects can be reversed using cholinesterase inhibitors. Therefore, the NMB used in this patient is succinylcholine, which is a depolarizing NMB. Cisatracurium and tubocurarine are nondepolarizing NMBs, and diazepam does not cause paralysis of skeletal muscles.

A 50-year-old male was brought to the emergency room after being stung by a hornet. The patient was found to be in anaphylactic shock, and the medical team tried to reverse the bronchoconstriction and hypotension using epinephrine. However, the patient did not fully respond to the epinephrine treatment. The patient's wife mentioned that he is taking a prescription medication for his blood pressure, the name of which she does not remember. Which of the following medications is he most likely taking that could have prevented the effects of epinephrine? A. Doxazosin. B. Propranolol. C. Metoprolol. D. Acebutolol.

Correct answer = B. Epinephrine reverses hypotension by activating β1 receptors and relieves bronchoconstriction by activating β2 receptors in anaphylaxis. Since epinephrine was not effective in reversing hypotension or bronchoconstriction in this patient, it could be assumed that the patient was on a nonselective β-blocker (propranolol). Doxazosin (α1-blocker), metoprolol, or acebutolol (both β1-selective blockers) would not have completely prevented the effects of epinephrine.

If an ophthalmologist wants to dilate the pupils for an eye examination, which of the following drugs/classes of drugs could be theoretically useful? A. Muscarinic receptor activator (agonist). B. Muscarinic receptor inhibitor (antagonist). C. Acetylcholine. D. Pilocarpine. E. Neostigmine.

Correct answer = B. Muscarinic agonists (for example, ACh, pilocarpine) contract the circular smooth muscles in the iris sphincter and constrict the pupil (miosis). Anticholinesterases (for example, neostigmine, physostigmine) also cause miosis by increasing the level of ACh. Muscarinic antagonists, on the other hand, relax the circular smooth muscles in the iris sphincter and cause dilation of the pupil (mydriasis).

Atropine is one of the ingredients in the antidiarrheal combination diphenoxylate/atropine available in the United States. Which of the following effects is produced by atropine that contributes to its antidiarrheal effect? A. Increase in gastrointestinal motility. B. Reduction in gastrointestinal motility. C. Increase in salivation. D. Increase in acid secretion.

Correct answer = B. Muscarinic agonists produce an increase in gastrointestinal motility, salivation, and acid secretion. Atropine is a muscarinic antagonist and therefore causes a reduction in gastrointestinal motility that contributes to its antidiarrheal effect.

Which of the following is correct regarding the neuromuscular blockers (NMBs)? A. Nondepolarizing NMBs are administered orally. B. Cholinesterase inhibitors reduce the effects of nondepolarizing NMBs. C. Nondepolarizing NMBs affect diaphragm muscles first. D. Effects of depolarizing neuromuscular blockers can be reversed using cholinesterase inhibitors.

Correct answer = B. Nondepolarizing NMBs such as cisatracurium and vecuronium are highly polar compounds and are poorly absorbed from the GI tract. Therefore, they are administered parenterally, not orally. Nondepolarizing NMBs are competitive antagonists at nicotinic receptors. Therefore, increasing the levels of ACh at the neuromuscular junction reduces the effects of these agents. Cholinesterase inhibitors increase the levels of ACh at the neuromuscular junction and reduce the effects of nondepolarizing NMBs, but may enhance (not reverse) the effects of depolarizing NMBs. Nondepolarizing NMBs first affect rapidly contracting muscles seen in the face and eyes and affect the diaphragm muscles last.

A β-blocker was prescribed for hypertension in a female asthma patient. After about a week of treatment, the asthma attacks got worse, and the patient was asked to stop taking the β-blocker. Which of the following β-blockers would you suggest as an alternative in this patient that is less likely to worsen her asthma? A. Propranolol. B. Metoprolol. C. Labetalol. D. Carvedilol.

Correct answer = B. The patient was most likely given a nonselective β-blocker (antagonizes both β1 and β2 receptors) that made her asthma worse due to β2 antagonism. An alternative is to prescribe a cardioselective (antagonizes only β1) β-blocker that does not antagonize β2 receptors in the bronchioles. Metoprolol is a cardioselective β-blocker. Propranolol, labetalol, and carvedilol are nonselective β-blockers and could worsen the asthma.

A hypertensive patient was accidentally given an α 2 agonist instead of an α1 blocker. Which of the following is correct in this situation? A. α2 Agonists can increase the release of norepinephrine from sympathetic nerve terminals. B. α Agonists can reduce blood pressure in this 2 patient. C. α2 Agonists can increase blood pressure in this patient. D. α2 Agonists will not affect blood pressure in this patient.

Correct answer = B. α2 Agonists activate α2 receptors located in the presynaptic terminal of sympathetic neurons and cause a reduction in the release of norepinephrine from sympathetic nerve terminals. This leads to a reduction in blood pressure. α2 Agonists such as clonidine and methyl- dopa are therefore used as antihypertensive agents.

Which of the following drugs is commonly used topically in the treatment of glaucoma? A. Atropine. B. Timolol. C. Tropicamide. D. Scopolamine.

Correct answer = B. β-Blockers reduce the formation of aqueous humor in the eye and therefore reduce intraocular pressure, thus relieving glaucoma. Timolol is a nonselective β-blocker that is commonly used topically to treat glaucoma. Atropine, tropicamide, and scopolamine are anticholinergic drugs that might worsen glaucoma.

Which of the following is correct regarding adrenergic neurotransmission? A. Epinephrine is the major neurotransmitter released from sympathetic nerve terminals. B. Norepinephrine is mainly released from the adrenal glands. C. Tricyclic antidepressants and cocaine prevent reuptake of norepinephrine into the nerve terminals. D. Monoamine oxidase (MAO) converts dopamine to norepinephrine in the nerve terminal.

Correct answer = C. Tricyclic antidepressants (TCAs) and cocaine inhibit the transporter protein that prevents the reuptake of norepinephrine into the sympathetic nerve terminals. Norepinephrine, not epinephrine, is the major neurotransmitter released from sympathetic nerve terminals. Epinephrine, not norepinephrine, is mainly released from the adrenal glands. Dopamine is converted to norepinephrine by dopamine β-hydroxylase, not by MAO.

Which of the following drugs would be the most effective anti-motion sickness drug for a person planning to go on a cruise? A. Atropine. B. Tropicamide. C. Scopolamine. D. Darifenacin. E. Tiotropium.

Correct answer = C. All muscarinic antagonists (anticholinergic drugs) listed above are theoretically useful as anti-motion sickness drugs; however, scopolamine is the most effective in preventing motion sickness in practice. Tropicamide mostly has ophthalmic uses, and tiotropium is used for respiratory disorders (COPD). Darifenacin is used for overactive bladder.

A 70-year-old patient was brought to the emergency room with a blood pressure of 76/60 mm Hg, tachycardia, and low cardiac output. He was diagnosed with acute heart failure. Which of the following drugs would be the most appropriate to improve his cardiac function? A. Epinephrine. B. Fenoldopam. C. Dobutamine. D. Isoproterenol.

Correct answer = C. Among the choices, the ideal drug to increase contractility of the heart in acute heart failure is dobutamine, since it is a selective β1-adrenergic agonist. Fenoldopam is a dopamine agonist used to treat severe hypertension. Other drugs are nonselective adrenergic agonists that could cause unwanted side effects.

Which of the following is correct regarding carvedilol? A. Carvedilol is a cardioselective β-blocker. B. Carvedilol is safe for use in asthma patients. C. Carvedilol has α -blocking activity. 1 D. Carvedilol is contraindicated in the treatment of stable chronic heart failure.

Correct answer = C. Carvedilol is a nonselective β-blocker with α1-blocking activity. Since it also blocks β2 receptors in the lungs, carvedilol could exacerbate asthma. Carvedilol is not used in patients with acute exacerbation of heart failure but is used in the treatment of stable, chronic heart failure.

Which of the following adrenergic agonists is commonly present in nasal sprays available over-the-counter (OTC) to treat nasal congestion? A. Clonidine. B. Albuterol. C. Oxymetazoline. D. Dobutamine. E. Norepinephrine.

Correct answer = C. Drugs with selective α1 agonistic activity are commonly used as nasal decongestants because of their ability to cause vasoconstriction in the nasal vessels. Oxymetazoline is an α1 agonist and therefore the preferred drug among the choices as a nasal decongestant. Clonidine is an α2 agonist, albuterol is a β2 agonist, dobutamine is a β1 agonist, and norepinephrine is a nonselective adrenergic agonist.

Which of the following is correct regarding drug interactions with nondepolarizing neuromuscular blockers (NMBs)? A. Desflurane reduces the effects of nondepolarizing NMBs. B. Cholinesterase inhibitors increase the effects of nondepolarizing NMBs. C. Aminoglycosides increase the effects of nondepolarizing NMBs. D. Calcium channel blockers reduce the effects of nondepolarizing NMBs.

Correct answer = C. Halogenated hydrocarbon anesthetics such as desflurane enhance the effects of nondepolarizing NMBs by exerting a stabilization effect at the neuromuscular junction (NMJ). Acetylcholinesterase inhibitors increase the levels of ACh at the NMJ and reduce the effects of nondepolarizing NMBs. Aminoglycoside antibiotics increase the effects of nondepolarizing NMBs by reducing the release of ACh from the cholinergic neurons. Calcium channel blockers increase the effects of nondepolarizing NMBs, possibly by affecting ion transport at the NMJ.

During an ophthalmic surgical procedure, the surgeon wanted to constrict the pupil of the patient using a miotic drug. However, he accidentally used another drug that caused dilation of the pupil (mydriasis) instead. Most likely, which of the following drugs did he use? A. Acetylcholine. B. Pilocarpine. C. Tropicamide. D. Phentolamine. E. Bethanechol.

Correct answer = C. Muscarinic agonists such as ACh, pilocarpine, and bethanechol contract the circular muscles of iris sphincter and cause constriction of the pupil (miosis), whereas muscarinic antagonists such as atropine and tropicamide prevent the contraction of the circular muscles of the iris and cause dilation of the pupil (mydriasis). α-Adrenergic antagonists such as phentolamine relax the radial muscles of the iris and cause miosis.

Sarin is a nerve gas that is an organophosphate cholinesterase inhibitor. Which of the following could be used as an antidote to sarin poisoning? A. Pilocarpine. B. Carbachol. C. Atropine. D. Physostigmine. E. Nicotine.

Correct answer = C. Sarin is an organophosphate cholinesterase inhibitor. It causes an increase in ACh levels in tissues that leads to cholinergic crisis by the activation of muscarinic as well as nicotinic receptors. Most of the symptoms of cholinergic crisis are mediated by muscarinic receptors and, therefore, the muscarinic antagonist atropine is used as an antidote for sarin poisoning. Cholinergic agonists such as pilocarpine, carbachol, physostigmine (indirect agonists), and nicotine will worsen the symptoms of sarin poisoning.

Sarin is a volatile nerve agent that inhibits cholinesterase enzymes. Which of the following symptoms would you expect to see in a patient exposed to sarin? A. Urinary retention. B. Tachycardia. C. Constriction of pupils (miosis). D. Dilation of the pupils (mydriasis). E. Dry mouth.

Correct answer = C. Sarin is an organophosphate nerve gas that inhibits cholinesterase enzymes and increases ACh levels. Therefore, symptoms of cholinergic crisis (increased urination, bradycardia, excessive secretions, constriction of pupils, etc.) should be expected in patients exposed to sarin. Urinary retention, tachycardia, mydriasis, and dry mouth are usually seen with muscarinic antagonists

In Alzheimer's disease, there is a deficiency of cholinergic neuronal function in the brain. Theoretically, which of the following strategies will be useful in treating the symptoms of Alzheimer's disease? A. Inhibiting cholinergic receptors in the brain. B. Inhibiting the release of acetylcholine in the brain. C. Inhibiting the acetylcholinesterase enzyme in the brain. D. Activating the acetylcholinesterase enzyme in the brain.

Correct answer = C. Since there is already a deficiency in brain cholinergic function in Alzheimer's disease, inhibiting cholinergic receptors or inhibiting the release of ACh will worsen the condition. Activating the acetylcholinesterase enzyme will increase the degradation of ACh, which will again worsen the condition. However, inhibiting the acetylcholinesterase enzyme will help to increase the levels of ACh in the brain and thereby help to relieve the symptoms of Alzheimer's disease.

Which of the following is correct regarding ANS? A. Afferent neurons carry signals from the CNS to the effector organs. B. The neurotransmitter at the parasympathetic ganglion is norepinephrine (NE). C. The neurotransmitter at the sympathetic ganglion is acetylcholine (ACh). D. Sympathetic neurons release ACh in the effector organs. E. Parasympathetic neurons release NE in the effector organs.

Correct answer = C. The neurotransmitter at the sympathetic and parasympathetic ganglia is acetylcholine. Sympathetic neurons release NE and parasympathetic neurons release ACh in the effector cells. Afferent neurons carry signals from the periphery to the CNS.

Which of the following statements concerning the parasympathetic nervous system is correct? A. The parasympathetic system uses norepinephrine as a neurotransmitter. B. The parasympathetic system often discharges as a single, functional system. C. The parasympathetic division is involved in accommodation of near vision, movement of food, and urination. D. The postganglionic fibers of the parasympathetic division are long compared to those of the sympathetic nervous system. E. The parasympathetic system controls the secretion of the adrenal medulla.

Correct answer = C. The parasympathetic nervous system maintains essential bodily functions, such as vision, movement of food, and urination. It uses acetylcholine, not norepinephrine, as a neurotransmitter, and it discharges as discrete fibers that are activated separately. The post- ganglionic fibers of the parasympathetic system are short compared to those of the sympathetic division. The adrenal medulla is under the control of the sympathetic system.

A 60-year-old female patient started on a new antihypertensive medication recently. Her blood pressure seems to be under control, but she complains of fatigue, drowsiness, and fainting when she gets up from the bed (orthostatic hypotension). Which of the following drugs is she most likely taking? A. Metoprolol. B. Propranolol. C. Prazosin. D. Clonidine.

Correct answer = C. α-Blockers (prazosin) are more likely to cause orthostatic hypotension compared to β-blockers (metoprolol, propranolol) and α2 agonists (clonidine).

Which of the following changes could theoretically happen in a person when the parasympathetic system is inhibited using a pharmacological agent? A. Reduction in heart rate. B. Constriction of the pupil (miosis). C. Increase in gastric motility. D. Dry mouth (xerostomia). E. Contraction of detrusor muscle in the bladder.

Correct answer = D. Activation of the parasympathetic system causes a reduction in heart rate, constriction of the pupil, an increase in gastric motility and salivation, and contraction of the bladder muscle. Therefore, inhibition of the parasympathetic system causes an increase in heart rate, dilation of the pupil, a decrease in gastric motility, dry mouth, and relaxation of detrusor muscles.

A patient with chronic obstructive pulmonary disease (COPD) was prescribed a β2 agonist for the relief of bronchospasm. However, the patient did not respond to this treatment. Which of the following drugs or classes of drugs would you suggest for this patient as the next option? A. β1 Agonist. B. Muscarinic agonist. C. Physostigmine. D. Ipratropium. E. Phentolamine.

Correct answer = D. Major receptors present in the bronchial tissues are muscarinic and adrenergic-β2 receptors. Muscarinic activation causes bronchoconstriction, and β2 receptor activation causes bronchodilation. Therefore, direct or indirect (physostigmine) muscarinic agonists will worsen bronchospasm. Ipratropium is a muscarinic antagonist that can relax bronchial smooth muscles and relieve bronchospasm in patients who are not responsive to β2 agonists. α1 and β1 receptors are not commonly present in bronchial tissues and, therefore, β1 agonists or α antagonists (phentolamine) do not have any significant effects on bronchospasm

A dentist would like to reduce salivation in a patient in preparation for an oral surgical procedure. Which of the following strategies will be useful in reducing salivation? A. Activate nicotinic receptors in the salivary glands. B. Block nicotinic receptors in the salivary glands. C. Activate muscarinic receptors in the salivary glands. D. Block muscarinic receptors in the salivary glands.

Correct answer = D. Salivary glands contain muscarinic receptors, not nicotinic receptors. Activation of muscarinic receptors in the salivary glands causes secretion of saliva. Blocking muscarinic receptors, using drugs such as atropine, reduces salivary secretions and makes the mouth dry.

Which of the following is correct regarding somatic motor neurons? A. The neurotransmitter at the somatic motor neuron ganglion is acetylcholine. B. The neurotransmitter at the somatic motor neuron ganglion is norepinephrine. C. Somatic motor neurons innervate smooth muscles. D. Somatic motor neurons do not have ganglia. E. Responses in the somatic motor neurons are generally slower than in the autonomic nervous system.

Correct answer = D. Somatic motor neurons innervate skeletal muscles (not smooth muscle) and have no ganglia. Answers A and B are incorrect, since there are no ganglia. Also, the responses in the somatic motor nervous system are faster compared to the responses in the autonomic nervous system due to the lack of ganglia in the former.

A 70-year-old male needs to be treated with an α-blocker for overflow incontinence due to his enlarged prostate. Which of the following drugs would you suggest in this patent that will not affect his blood pressure significantly? A. Prazosin. B. Doxazosin. C. Phentolamine. D. Tamsulosin. E. Terazosin.

Correct answer = D. Tamsulosin is an α1 antagonist that is more selective to the α1 receptor subtype (α1A) present in the prostate and less selective to the α1 receptor subtype (α1B) present in the blood vessels. Therefore, tamsulosin does not affect blood pressure significantly. Prazosin, doxazosin, terazosin, and phentolamine antagonize both these subtypes and cause significant hypotension as a side effect.

Which of the following drugs or classes of drugs will be useful in treating the symptoms of myasthenia gravis? A. Nicotinic antagonists. B. Muscarinic agonists. C. Muscarinic antagonists. D. Anticholinesterase agents.

Correct answer = D. The function of nicotinic receptors in skeletal muscles is diminished in myasthenia gravis due to the development of antibodies to nicotinic receptors in the patient's body (autoimmune disease). Any drug that can increase the levels of ACh in the neuromuscular junction can improve symptoms in myasthenia gravis. Thus, cholinesterase inhibitors help to improve the symptoms of myasthenia gravis. Muscarinic drugs have no role in myasthenia gravis, and nicotinic antagonists will worsen the symptoms.

One of your patients who is hypertensive and gets mild asthma attacks occasionally bought an herbal remedy online to help with his asthma. He is not on any asthma medications currently but is receiving a β1-selective blocker for his hypertension. The herbal remedy seems to relieve his asthma attacks, but his blood pressure seems to increase despite the β-blocker therapy. Which of the following drugs is most likely present in the herbal remedy he is taking? A. Phenylephrine. B. Norepinephrine. C. Dobutamine. D. Ephedrine. E. Salmeterol.

Correct answer = D. Two drugs among the choices that could relieve asthma are ephedrine and salmeterol, as they activate β2 receptors in the bronchioles and cause bronchodilation. However, salmeterol is a selective β2 agonist and should not cause an increase in blood pressure. Ephedrine on the other hand stimulates the release of norepinephrine and acts as a direct agonist at α- and β-adrenergic receptors, thus causing an increase in blood pressure. Phenylephrine (a nonselective α agonist) does not cause bronchodilation. Norepinephrine is a nonselective adrenergic agonist that does not have any stimulatory effects on β2 receptors. Also, norepinephrine is not active when given orally.

All of the following are correct regarding adrenergic receptors; except: A. a1 Receptors are primarily located on the postsynaptic membrane in the effector organs. B. a2 Receptors are primarily located on the presynaptic sympathetic nerve terminals. C. B1 Receptors are found mainly in the heart. D. B2 Receptors are found mainly in adipose tissue.

Correct answer = D. α1 Receptors are located on the post-synaptic membrane in the effector organs such as blood vessels. α2 Receptors are mainly found on the presynaptic sympathetic nerve terminals, where they inhibit the release of norepinephrine when activated. β1 Receptors are found in the heart, in addition to some other tissues, and cause increase in heart rate and contractility when activated. β2 receptors are found in the lungs, in addition to some other tissues, and cause relaxation of bronchial smooth muscles when activated. β3 Receptors are found in adipose tissue and are involved in lipolysis.

A 12-year-old boy who is allergic to peanuts was brought to the emergency room after accidentally consuming peanuts contained in fast food. He is in anaphylactic shock. Which of the following drugs would be most appropriate to treat this patient? A. Norepinephrine. B. Phenylephrine. C. Dobutamine. D. Epinephrine.

Correct answer = D. Norepinephrine has more α agonistic effects and activates mainly α1, α2, and β1 receptors. Epinephrine has more β agonistic effects and activates mainly α1, α2, β1, and β2 receptors. Phenylephrine has predominantly α effects and activates mainly α1 receptors. Dobutamine mainly activates β1 receptors and has no significant effects on β2 receptors. Thus, epinephrine is the drug of choice in anaphylactic shock that can both stimulate the heart (β1 activation) and dilate bronchioles (β2 activation).

Which of the following adrenergic agonists is most likely to cause CNS side effects when administered systemically? A. Epinephrine. B. Norepinephrine. C. Isoproterenol. D. Dopamine. E. Ephedrine

Correct answer = E. Ephedrine is more lipophilic compared to the other drugs listed and therefore is more likely to cross the blood-brain barrier when administered systemically. Therefore, ephedrine is more likely to cause CNS side effects compared to other listed drugs

A new antihypertensive drug was tested in an animal model of hypertension. The drug when given alone reduces blood pressure in the animal. Norepinephrine when given in the presence of this drug did not cause any significant change in blood pressure or heart rate in the animal. The new drug is similar to which of the following drugs in terms of its pharmacological mechanism of action? A. Prazosin. B. Clonidine. C. Propranolol. D. Metoprolol. E. Carvedilol.

Correct answer = E. Norepinephrine activates both α1 and β1 receptors and causes an increase in heart rate and blood pressure. A drug that prevents the increase in blood pressure caused by norepinephrine should be similar to carvedilol that antagonizes both α1 and β1 receptors. Prazosin is an α1 antagonist, clonidine is an α2 agonist, and propranolol and metoprolol are β antagonists, and these drugs cannot completely prevent the cardiovascular effects of norepinephrine.