Autonomic Pharmacology Practice Questions

82 multiple-choice questions on Autonomic pharmacology for paramedic and EMT students, from Chapter 13 (Principles of Pharmacology). Read each question, pick your answer, then tap Show answer to check it and read the explanation.

82 practice questions

1. A teenager took a large overdose of pseudoephedrine, a sympathomimetic. Which findings are expected?

   1. A. Tachycardia, hypertension, and diaphoresis
   2. B. Bradycardia, miosis, and salivation
   3. C. Bradycardia, hypotension, and hypoglycemia
   4. D. Hypothermia, dry skin, and slow breathing
   Show answer

   Answer: A. Tachycardia, hypertension, and diaphoresis

   Sympathomimetics mimic sympathetic activity: tachycardia, hypertension, dilated pupils, agitation, hyperthermia, and diaphoresis. Bradycardia, miosis, and salivation are cholinergic; bradycardia, hypotension, and hypoglycemia fit beta-blocker toxicity; and hypothermia with dry skin and slow breathing is not a sympathomimetic picture.

2. Sympatholytic drugs:

   1. A. Mimic sympathetic effects
   2. B. Increase heart rate
   3. C. Stimulate beta receptors
   4. D. Block sympathetic effects
   Show answer

   Answer: D. Block sympathetic effects

   Beta blockers are the common example.

3. Parasympatholytic drugs such as atropine:

   1. A. Stimulate muscarinic receptors, slowing the heart and increasing secretions
   2. B. Block beta receptors, slowing the heart and drying secretions
   3. C. Block muscarinic receptors, raising heart rate and drying secretions
   4. D. Block nicotinic receptors at the neuromuscular junction
   Show answer

   Answer: C. Block muscarinic receptors, raising heart rate and drying secretions

   Anticholinergic is another term for this class. They block acetylcholine at muscarinic receptors.

4. Parasympathomimetic drugs:

   1. A. Mimic acetylcholine, slowing the heart and increasing secretions
   2. B. Block acetylcholine, increasing heart rate and drying secretions
   3. C. Block muscarinic receptors, dilating the pupils and bronchi
   4. D. Mimic norepinephrine, causing bronchodilation and tachycardia
   Show answer

   Answer: A. Mimic acetylcholine, slowing the heart and increasing secretions

   Organophosphate poisoning produces an exaggerated version of these effects.

5. Epinephrine is added to some lidocaine preparations to make local anesthesia last longer. It does this by:

   1. A. Blocking sodium channels along with lidocaine
   2. B. Constricting vessels at the injection site
   3. C. Slowing the liver's metabolism of lidocaine
   4. D. Raising the lipid content of the nerve
   Show answer

   Answer: B. Constricting vessels at the injection site

   Alpha-1 constriction of vessels at the injection site slows blood flow, so lidocaine is carried away more slowly, its effect lasts longer, and peak blood levels are lower. Epinephrine is not blocking sodium channels along with lidocaine, it is not slowing the liver's metabolism of lidocaine, and it is not raising the lipid content of the nerve.

6. Stimulating alpha-2 receptors generally:

   1. A. Directly increases heart rate and contractility
   2. B. Inhibits further norepinephrine release
   3. C. Increases presynaptic norepinephrine release
   4. D. Causes bronchoconstriction in the airways
   Show answer

   Answer: B. Inhibits further norepinephrine release

   Clonidine acts here to lower blood pressure. This acts as a negative feedback brake on sympathetic output.

7. A patient in cardiogenic shock is started on dopamine. His heart rate rises from 110 to 150 and his chest pain worsens. The main mechanism is:

   1. A. Muscarinic blockade at the SA node
   2. B. Beta-1 stimulation raising oxygen demand
   3. C. Dopaminergic dilation of renal vessels
   4. D. Beta-2 constriction of the coronary arteries
   Show answer

   Answer: B. Beta-1 stimulation raising oxygen demand

   Dopamine's beta-1 effect increases heart rate and contractility, raising myocardial oxygen demand; that can worsen ischemia and trigger tachydysrhythmias. Dopamine does not cause muscarinic blockade at the SA node, dopaminergic dilation of renal vessels does not speed the heart, and beta-2 stimulation dilates rather than causes constriction of the coronary arteries.

8. A low-dose epinephrine infusion can lower diastolic blood pressure slightly. This is due to:

   1. A. Alpha-1 constriction of vessels in skin and gut
   2. B. Muscarinic slowing of the heart
   3. C. Beta-2 dilation of skeletal muscle arterioles
   4. D. Beta-1 depression of contractility
   Show answer

   Answer: C. Beta-2 dilation of skeletal muscle arterioles

   At low doses, epinephrine's beta-2 effect dilates skeletal muscle arterioles and lowers diastolic pressure, while beta-1 effects raise systolic pressure and heart rate. Alpha-1 constriction of vessels in skin and gut raises pressure, epinephrine has no muscarinic action to cause slowing of the heart, and beta-1 stimulation increases rather than causes depression of contractility.

9. Dopaminergic receptor stimulation at low doses causes:

   1. A. Increased heart rate and contractility
   2. B. Renal and mesenteric vasodilation
   3. C. Bradycardia from vagal stimulation
   4. D. Generalized peripheral vasoconstriction
   Show answer

   Answer: B. Renal and mesenteric vasodilation

   At higher doses, dopamine's beta and alpha effects dominate. Low-dose dopamine dilates renal, mesenteric, and cerebral vessels.

10. Epinephrine stimulates:

    1. A. Beta-2 receptors only
    2. B. Muscarinic and nicotinic receptors
    3. C. Alpha and beta receptors
    4. D. Alpha-1 receptors only
    Show answer

    Answer: C. Alpha and beta receptors

    That broad action is why it works in anaphylaxis. This produces vasoconstriction, increased cardiac output, and bronchodilation.

11. Norepinephrine acts predominantly on:

    1. A. Dopaminergic receptors in renal vessels
    2. B. Beta-2 receptors, with some alpha activity
    3. C. Alpha receptors, with some beta-1 activity
    4. D. Beta-1 receptors, with little alpha activity
    Show answer

    Answer: C. Alpha receptors, with some beta-1 activity

    It is a first-line vasopressor for septic shock. Its alpha effect produces potent vasoconstriction.

12. A patient taking a beta blocker who becomes hypotensive may:

    1. A. Show a widened pulse pressure and flushing
    2. B. Be unable to mount the expected tachycardia
    3. C. Respond normally to standard epinephrine doses
    4. D. Develop an exaggerated compensatory tachycardia
    Show answer

    Answer: B. Be unable to mount the expected tachycardia

    Glucagon is used for severe beta blocker toxicity.

13. Nicotinic receptors are found at:

    1. A. Smooth muscle of the bronchi and GI tract
    2. B. Cardiac pacemaker cells and exocrine glands
    3. C. Vascular smooth muscle throughout the body
    4. D. Neuromuscular junctions and autonomic ganglia
    Show answer

    Answer: D. Neuromuscular junctions and autonomic ganglia

    Neuromuscular blockers act here.

14. Muscarinic receptor stimulation causes:

    1. A. Tachycardia, dry mouth, and dilated pupils
    2. B. Bradycardia, increased secretions, and miosis
    3. C. Vasoconstriction, hypertension, and mydriasis
    4. D. Bronchodilation, tachycardia, and urinary retention
    Show answer

    Answer: B. Bradycardia, increased secretions, and miosis

    The SLUDGE toxidrome reflects this stimulation. Bronchoconstriction also occurs.

15. Atropine is used in bradycardia because it:

    1. A. Constricts vessels to trigger reflex tachycardia
    2. B. Directly increases calcium entry into pacemaker cells
    3. C. Blocks vagal input, letting heart rate rise
    4. D. Directly stimulates beta-1 receptors at the SA node
    Show answer

    Answer: C. Blocks vagal input, letting heart rate rise

    It is less effective in high-degree blocks below the AV node.

16. Anticholinergic side effects commonly include:

    1. A. Bronchospasm, wheezing, and excessive tearing
    2. B. Diarrhea, urinary incontinence, and profuse sweating
    3. C. Excessive salivation, bradycardia, and pupil constriction
    4. D. Dry mouth, blurred vision, urinary retention, tachycardia
    Show answer

    Answer: D. Dry mouth, blurred vision, urinary retention, tachycardia

    Dry as a bone, blind as a bat, mad as a hatter.

17. The autonomic nervous system consists of the:

    1. A. Sympathetic and parasympathetic divisions
    2. B. Central and peripheral nervous systems
    3. C. Afferent sensory and efferent motor nerves
    4. D. Somatic and central nervous systems
    Show answer

    Answer: A. Sympathetic and parasympathetic divisions

    The ANS regulates involuntary functions through two opposing divisions.

18. The sympathetic division is also called the:

    1. A. Cholinergic system
    2. B. Craniosacral system
    3. C. Rest and digest system
    4. D. Fight or flight system
    Show answer

    Answer: D. Fight or flight system

    Sympathetic activation prepares the body for stress. Craniosacral and cholinergic both describe the parasympathetic division; the sympathetic division is thoracolumbar and mainly adrenergic.

19. The parasympathetic division is also called the:

    1. A. Thoracolumbar system
    2. B. Fight or flight system
    3. C. Rest and digest system
    4. D. Adrenergic system
    Show answer

    Answer: C. Rest and digest system

    Parasympathetic activity promotes digestion and energy conservation. Thoracolumbar is the anatomic name of the sympathetic division.

20. The primary neurotransmitter at sympathetic postganglionic effector sites is:

    1. A. Dopamine
    2. B. Serotonin
    3. C. Norepinephrine
    4. D. Acetylcholine
    Show answer

    Answer: C. Norepinephrine

    Most sympathetic postganglionic neurons release norepinephrine (adrenergic).

21. The neurotransmitter at all autonomic ganglia (both divisions) is:

    1. A. Acetylcholine
    2. B. GABA
    3. C. Epinephrine
    4. D. Norepinephrine
    Show answer

    Answer: A. Acetylcholine

    Preganglionic neurons of both divisions are cholinergic, acting on nicotinic receptors.

22. Parasympathetic postganglionic fibers release:

    1. A. Acetylcholine acting on nicotinic receptors
    2. B. Acetylcholine acting on muscarinic receptors
    3. C. Norepinephrine acting on alpha receptors
    4. D. Epinephrine acting on beta receptors
    Show answer

    Answer: B. Acetylcholine acting on muscarinic receptors

    Muscarinic receptors mediate parasympathetic effects on organs.

23. The vagus nerve (cranial nerve X) carries:

    1. A. Pain fibers from the skin of the chest and abdomen
    2. B. Somatic motor fibers to the diaphragm and chest wall
    3. C. Sympathetic accelerator outflow to the heart
    4. D. Most parasympathetic outflow to the viscera
    Show answer

    Answer: D. Most parasympathetic outflow to the viscera

    Vagal stimulation slows the heart and increases GI activity. It carries most parasympathetic outflow to the thoracic and abdominal organs.

24. Dexmedetomidine produces sedation with little respiratory depression by stimulating:

    1. A. GABA-A receptors
    2. B. Mu opioid receptors
    3. C. Central alpha-2 receptors
    4. D. NMDA-type glutamate receptors
    Show answer

    Answer: C. Central alpha-2 receptors

    Dexmedetomidine is a selective central alpha-2 agonist that reduces sympathetic outflow and produces arousable sedation with little respiratory depression; bradycardia and hypotension are its main side effects. GABA-A receptors are the target of benzodiazepines and propofol, mu opioid receptors of fentanyl, and NMDA-type glutamate receptors of ketamine (which blocks them).

25. Esmolol is sometimes chosen for rate control in a patient with borderline blood pressure mainly because it:

    1. A. Has no effect on blood pressure
    2. B. Blocks alpha receptors instead of beta
    3. C. Is taken orally once a day
    4. D. Wears off within minutes if stopped
    Show answer

    Answer: D. Wears off within minutes if stopped

    Esmolol is a beta-1 selective blocker with a half-life of about 9 minutes, so it wears off within minutes if it is stopped because hypotension develops. It does lower blood pressure, so it is false that it has no effect on blood pressure; it blocks beta-1 rather than alpha receptors; and it is an IV infusion, not a drug taken orally once a day.

26. A COPD patient who uses salmeterol twice daily has acute bronchospasm. Albuterol is given instead of an extra salmeterol dose because salmeterol:

    1. A. Is a beta-1 selective agonist
    2. B. Blocks beta-2 receptors
    3. C. Has a slow onset of action
    4. D. Lasts a shorter time than albuterol
    Show answer

    Answer: C. Has a slow onset of action

    Salmeterol is a long-acting beta-2 agonist whose bronchodilation has a slow onset of action, so it is a maintenance drug, not a rescue drug. It is beta-2 selective, not a beta-1 selective agonist; it stimulates rather than blocks beta-2 receptors; and it lasts about 12 hours, longer than albuterol rather than a shorter time.

27. After naloxone, a fentanyl overdose patient now breathes adequately but stays deeply sedated with bradycardia. The local fentanyl supply is often mixed with xylazine, which is:

    1. A. A long-acting mu agonist reversed by naloxone
    2. B. A benzodiazepine-site agonist
    3. C. An alpha-2 agonist not reversed by naloxone
    4. D. An anticholinergic sedative
    Show answer

    Answer: C. An alpha-2 agonist not reversed by naloxone

    Xylazine is a veterinary sedative that acts as a central alpha-2 agonist, causing sedation, bradycardia, and hypotension that naloxone does not reverse. Titrate naloxone to breathing and support ventilation rather than escalating naloxone for sedation. It is not a long-acting mu agonist reversed by naloxone, not a benzodiazepine-site agonist, and not an anticholinergic sedative.

28. Sepsis guidelines prefer norepinephrine over dopamine as the first vasopressor in septic shock because norepinephrine:

    1. A. Raises pressure through renal dilation instead
    2. B. Is a pure beta-1 agonist
    3. C. Causes fewer dysrhythmias with better outcomes
    4. D. Can be given safely by mouth
    Show answer

    Answer: C. Causes fewer dysrhythmias with better outcomes

    Norepinephrine causes fewer dysrhythmias than dopamine with better outcomes: comparisons found more dysrhythmias with dopamine and a trend toward higher mortality, so the Surviving Sepsis Campaign recommends norepinephrine first. Norepinephrine raises pressure through alpha-1 vasoconstriction, not through renal dilation; it is not a pure beta-1 agonist; and it cannot be given safely by mouth.

29. In cardiac arrest, epinephrine's main benefit comes from which receptor effect?

    1. A. Alpha-1 constriction raising coronary pressure
    2. B. Beta-2 dilation of the small airways in the lungs
    3. C. Beta-1 slowing of AV conduction
    4. D. Muscarinic blockade of vagal tone
    Show answer

    Answer: A. Alpha-1 constriction raising coronary pressure

    During CPR, alpha-1 vasoconstriction raises aortic diastolic pressure, which drives coronary and cerebral perfusion; the 2025 AHA guidelines keep epinephrine 1 mg every 3 to 5 minutes. Beta-2 dilation of the small airways in the lungs is not the goal in arrest, beta-1 stimulation speeds rather than causes slowing of AV conduction, and epinephrine causes no muscarinic blockade of vagal tone.

30. When a norepinephrine infusion is interrupted, its effect fades within a few minutes because norepinephrine is:

    1. A. Rapidly taken up and metabolized
    2. B. Excreted unchanged through the lungs
    3. C. Stored in body fat and released slowly
    4. D. Bound to albumin and inactivated
    Show answer

    Answer: A. Rapidly taken up and metabolized

    Catecholamines are rapidly taken up into nerves and tissues and metabolized by MAO and COMT within minutes, so infusions run continuously by pump and pressure can drop fast if the line is interrupted. Norepinephrine is not excreted unchanged through the lungs, is not stored in body fat and released slowly, and is not bound to albumin and inactivated.

31. Repeated IV doses of ephedrine for hypotension produce smaller and smaller rises in blood pressure. The likely reason is:

    1. A. Its receptors are destroyed by each dose
    2. B. Stored norepinephrine is being depleted
    3. C. An allergy to ephedrine is developing
    4. D. Each dose is cleared faster than the last
    Show answer

    Answer: B. Stored norepinephrine is being depleted

    Ephedrine acts partly indirectly by releasing stored norepinephrine. With repeated doses those stores are depleted and each dose works less well (tachyphylaxis), so a direct agonist such as phenylephrine may be needed. Receptors are not destroyed by each dose, an allergy to ephedrine would not cause a fading effect, and each dose is not cleared faster than the last.

32. In thyroid storm, propranolol is given mainly to:

    1. A. Stop the thyroid gland from releasing its hormone
    2. B. Raise the patient's metabolic rate
    3. C. Blunt tachycardia and other adrenergic effects
    4. D. Stimulate parasympathetic tone directly
    Show answer

    Answer: C. Blunt tachycardia and other adrenergic effects

    Excess thyroid hormone heightens the response to catecholamines; beta blockade is given to blunt tachycardia and other adrenergic effects such as tremor and agitation (propranolol also slightly reduces T4-to-T3 conversion). It does not stop the thyroid gland from releasing its hormone (antithyroid drugs and iodine do that), it lowers rather than raises the metabolic rate's demands on the heart, and it does not stimulate parasympathetic tone directly.

33. Neostigmine reverses a nondepolarizing paralytic such as rocuronium by:

    1. A. Inhibiting acetylcholinesterase
    2. B. Binding rocuronium molecules in plasma
    3. C. Blocking nicotinic receptors on muscle
    4. D. Stimulating beta-1 receptors on muscle
    Show answer

    Answer: A. Inhibiting acetylcholinesterase

    Neostigmine inhibits acetylcholinesterase, so acetylcholine builds up and outcompetes rocuronium at the nicotinic receptor; glycopyrrolate is given with it to block muscarinic effects such as bradycardia. Binding rocuronium molecules in plasma is how sugammadex works, blocking nicotinic receptors on muscle would deepen paralysis, and stimulating beta-1 receptors plays no role at the neuromuscular junction.

34. An 80-year-old wearing a scopolamine patch for motion sickness is confused and flushed, with urinary retention. Besides supportive care, the first step is to:

    1. A. Give atropine to reverse the effect
    2. B. Give naloxone for presumed opioids
    3. C. Give haloperidol for the agitation
    4. D. Remove the patch and monitor
    Show answer

    Answer: D. Remove the patch and monitor

    Scopolamine is an anticholinergic, and older adults are very sensitive to its central effects; remove the patch to stop further absorption and monitor while effects fade over hours. Atropine is also anticholinergic and would worsen toxicity; there is no reason to give naloxone for presumed opioids, as it does not treat anticholinergic delirium; and haloperidol given for the agitation can worsen anticholinergic delirium and heat retention (a benzodiazepine is preferred if sedation is needed).

35. Atropine is used cautiously for bradycardia during an acute MI because a faster heart rate:

    1. A. Raises myocardial oxygen demand
    2. B. Slows AV conduction even further
    3. C. Causes coronary artery spasm
    4. D. Lowers the blood glucose level
    Show answer

    Answer: A. Raises myocardial oxygen demand

    Atropine speeds the heart by blocking vagal tone; during ischemia a faster rate increases myocardial oxygen demand and can extend the infarct or provoke dysrhythmias, so it is reserved for symptomatic bradycardia. Atropine improves rather than slows AV conduction, it does not cause coronary artery spasm, and it does not lower the blood glucose level.

36. A patient with organophosphate poisoning has a heart rate of 128 rather than the expected bradycardia. One explanation is:

    1. A. Muscarinic stimulation of the SA node
    2. B. Beta-receptor blockade caused by the pesticide
    3. C. Nicotinic stimulation of sympathetic ganglia
    4. D. Hypoglycemia from cholinergic excess
    Show answer

    Answer: C. Nicotinic stimulation of sympathetic ganglia

    Excess acetylcholine also stimulates nicotinic receptors at sympathetic ganglia and the adrenal medulla, and hypoxia adds to it, so tachycardia is common and does not rule out organophosphate poisoning; titrate atropine to drying of secretions, not heart rate. Muscarinic stimulation of the SA node causes bradycardia, the pesticide causes no beta-receptor blockade, and hypoglycemia from cholinergic excess is not the mechanism.

37. Anticholinergic poisoning raises body temperature mainly because:

    1. A. Muscarinic stimulation resets the hypothalamus
    2. B. Muscle rigidity generates extra heat
    3. C. Histamine release dilates skin vessels
    4. D. Blocked sweating impairs heat loss
    Show answer

    Answer: D. Blocked sweating impairs heat loss

    Sweat glands are driven by sympathetic fibers that release acetylcholine onto muscarinic receptors; blocked sweating stops evaporative cooling and impairs heat loss, so patients are hot and dry. Anticholinergics block rather than cause muscarinic stimulation of the hypothalamus, severe muscle rigidity that generates heat is typical of neuroleptic malignant syndrome, and histamine release that dilates skin vessels is not the mechanism.

38. A toddler swallowed liquid nicotine from an e-cigarette refill. Which early course is expected?

    1. A. Dry skin, mydriasis, and urinary retention
    2. B. Vomiting and tachycardia, then weakness
    3. C. Bradycardia and hypotension from the outset
    4. D. Deep coma before any vomiting
    Show answer

    Answer: B. Vomiting and tachycardia, then weakness

    Nicotine first stimulates nicotinic receptors at autonomic ganglia and the neuromuscular junction (vomiting, salivation, tachycardia, tremor, seizures), then can block them, causing weakness, bradycardia, and respiratory failure. Dry skin, mydriasis, and urinary retention are anticholinergic. Bradycardia and hypotension belong to the later blocking phase rather than the start, and vomiting is usually an early sign that comes before any decline in consciousness. A small amount of concentrated e-liquid can be fatal to a child.

39. Botulinum toxin causes descending flaccid paralysis by:

    1. A. Blocking nicotinic receptors on muscle cells
    2. B. Inhibiting acetylcholinesterase at the synapse
    3. C. Depolarizing the motor end plate
    4. D. Preventing acetylcholine release
    Show answer

    Answer: D. Preventing acetylcholine release

    Botulinum toxin cleaves the proteins that let acetylcholine vesicles fuse with the nerve membrane, preventing acetylcholine release at the neuromuscular junction and autonomic nerve endings. Blocking nicotinic receptors on muscle cells is how rocuronium works, inhibiting acetylcholinesterase at the synapse is the organophosphate mechanism, and depolarizing the motor end plate is how succinylcholine works.

40. Succinylcholine is a:

    1. A. Nondepolarizing neuromuscular blocker
    2. B. Cholinergic antagonist at muscarinic sites
    3. C. Depolarizing neuromuscular blocker
    4. D. Acetylcholinesterase inhibitor
    Show answer

    Answer: C. Depolarizing neuromuscular blocker

    It depolarizes the motor end plate, causing fasciculations then paralysis.

41. Rocuronium and vecuronium are:

    1. A. Depolarizing (noncompetitive) neuromuscular blockers
    2. B. Anticholinergics acting at muscarinic sites
    3. C. Nondepolarizing (competitive) neuromuscular blockers
    4. D. Short-acting synthetic opioid analgesics
    Show answer

    Answer: C. Nondepolarizing (competitive) neuromuscular blockers

    They compete with acetylcholine at nicotinic receptors.

42. Beta-blocker overdose produces:

    1. A. Bradycardia, hypotension, and hypoglycemia
    2. B. Miosis, salivation, and copious secretions
    3. C. Mydriasis, hyperthermia, and dry flushed skin
    4. D. Tachycardia, hypertension, and hyperglycemia
    Show answer

    Answer: A. Bradycardia, hypotension, and hypoglycemia

    Blocking beta-1 and beta-2 depresses heart and can constrict airways. Hypoglycemia can result because beta blockade impairs glycogenolysis.

43. A selective beta-1 blocker such as metoprolol is preferred in asthma patients because it:

    1. A. Has less beta-2 blockade, reducing bronchospasm risk
    2. B. Directly stimulates beta-2 receptors in the airways
    3. C. Is more potent, so smaller doses spare the lungs
    4. D. Has no effect on heart rate or contractility
    Show answer

    Answer: A. Has less beta-2 blockade, reducing bronchospasm risk

    Cardioselective blockers spare beta-2 receptors at usual doses.

44. Acetylcholinesterase is the enzyme that:

    1. A. Breaks down acetylcholine in the synapse
    2. B. Synthesizes acetylcholine in nerve terminals
    3. C. Breaks down norepinephrine in the synapse
    4. D. Releases acetylcholine from storage vesicles
    Show answer

    Answer: A. Breaks down acetylcholine in the synapse

    Organophosphates inhibit this enzyme, causing cholinergic crisis.

45. Norepinephrine is primarily cleared from the synapse by:

    1. A. Direct renal excretion from the synapse
    2. B. Reuptake into the presynaptic neuron
    3. C. Passive diffusion into the bloodstream alone
    4. D. Breakdown by synaptic acetylcholinesterase
    Show answer

    Answer: B. Reuptake into the presynaptic neuron

    Reuptake inhibition is the mechanism of several drugs (e.g., cocaine, tricyclics). MAO and COMT then metabolize it.

46. An older patient using timolol eye drops for glaucoma has a heart rate of 44. A likely cause is:

    1. A. Muscarinic receptor blockade from the eye drops
    2. B. Systemic absorption of the beta blocker
    3. C. Alpha-1 stimulation of the heart
    4. D. Hypoglycemia caused by the drops
    Show answer

    Answer: B. Systemic absorption of the beta blocker

    Timolol is a nonselective beta blocker; drops drain through the tear duct to the nasal mucosa and are absorbed without first-pass metabolism, causing bradycardia, hypotension, or bronchospasm. Muscarinic receptor blockade from the eye drops would speed the heart, alpha-1 stimulation of the heart does not slow it, and hypoglycemia caused by the drops is not the explanation. Ask about eye drops in the medication history.

47. Vasopressin acts on:

    1. A. Beta-1 receptors, increasing contractility
    2. B. Dopamine receptors, causing renal vasodilation
    3. C. V1 receptors, causing vasoconstriction
    4. D. Alpha-1 receptors, causing vasoconstriction
    Show answer

    Answer: C. V1 receptors, causing vasoconstriction

    Vasopressin is a non-catecholamine vasopressor. Its vasoconstriction is non-adrenergic.

48. Which drug is a selective alpha-1 agonist?

    1. A. Atropine
    2. B. Albuterol
    3. C. Dobutamine
    4. D. Phenylephrine
    Show answer

    Answer: D. Phenylephrine

    Phenylephrine raises BP via pure vasoconstriction.

49. Dobutamine is primarily a:

    1. A. Beta-2 antagonist narrowing airways
    2. B. Alpha-1 agonist increasing vascular tone
    3. C. Muscarinic agonist slowing heart rate
    4. D. Beta-1 agonist increasing contractility
    Show answer

    Answer: D. Beta-1 agonist increasing contractility

    Dobutamine is an inotrope used in cardiogenic shock.

50. Bethanechol, used for urinary retention, is classified as a:

    1. A. Muscarinic agonist
    2. B. Nicotinic antagonist
    3. C. Beta-2 agonist
    4. D. Alpha-1 agonist
    Show answer

    Answer: A. Muscarinic agonist

    Bethanechol stimulates muscarinic receptors, contracting the bladder's detrusor muscle; excess causes cholinergic effects such as bradycardia and salivation. A nicotinic antagonist would cause muscle weakness, a beta-2 agonist relaxes the detrusor, and an alpha-1 agonist tightens the bladder neck; both of those promote retention.

51. Parasympathetic stimulation of the bladder causes:

    1. A. Detrusor relaxation and bladder filling
    2. B. Detrusor contraction and urination
    3. C. Urinary retention and bladder distension
    4. D. Internal sphincter contraction only
    Show answer

    Answer: B. Detrusor contraction and urination

    Anticholinergics cause urinary retention by blocking this.

52. A patient on metoprolol is hypoglycemic but has no tachycardia or tremor. Why?

    1. A. Hypoglycemia does not cause tachycardia
    2. B. Metoprolol directly raises blood glucose
    3. C. Beta blockade masks adrenergic warning signs
    4. D. Metoprolol blocks the cholinergic stress response
    Show answer

    Answer: C. Beta blockade masks adrenergic warning signs

    Tachycardia and tremor are beta-mediated, so beta blockers can mask them; sweating is usually preserved.

53. Sweat glands are innervated by sympathetic fibers that release:

    1. A. Acetylcholine acting on muscarinic receptors
    2. B. Norepinephrine acting on alpha-1 receptors
    3. C. Dopamine acting on dopaminergic receptors
    4. D. Epinephrine acting on beta-2 receptors
    Show answer

    Answer: A. Acetylcholine acting on muscarinic receptors

    This exception explains why anticholinergics cause dry skin and why diaphoresis persists with beta blockade.

54. In organophosphate poisoning, the endpoint for titrating atropine is:

    1. A. Return of normal pupil size and reactivity
    2. B. Heart rate reaching at least 120 per minute
    3. C. Complete resolution of muscle fasciculations
    4. D. Clearing of bronchial secretions
    Show answer

    Answer: D. Clearing of bronchial secretions

    Atropine is titrated to clear pulmonary secretions; pupils and fasciculations are poor endpoints. Drying of secretions makes breathing easier.

55. Atropine does not reverse muscle fasciculations and weakness in organophosphate poisoning because:

    1. A. Atropine acts only on the heart's pacemaker tissue
    2. B. Atropine is too short-acting to reach skeletal muscle
    3. C. Atropine does not block nicotinic receptors
    4. D. The fasciculations are caused by hypoglycemia, not ACh
    Show answer

    Answer: C. Atropine does not block nicotinic receptors

    Atropine is a muscarinic antagonist; pralidoxime addresses the nicotinic effects.

56. Pralidoxime (2-PAM) is used in organophosphate poisoning to:

    1. A. Reactivate the enzyme before the bond ages
    2. B. Block muscarinic receptors to dry secretions
    3. C. Stimulate nicotinic receptors to restore strength
    4. D. Increase acetylcholine release at the synapse
    Show answer

    Answer: A. Reactivate the enzyme before the bond ages

    Pralidoxime removes the organophosphate from the enzyme and must be given early to be effective.

57. Pinpoint pupils in organophosphate poisoning result from:

    1. A. Muscarinic stimulation of the iris sphincter
    2. B. Nicotinic blockade at the ciliary ganglion
    3. C. Alpha-1 stimulation of the iris dilator muscle
    4. D. Beta-2 blockade of the ciliary muscle
    Show answer

    Answer: A. Muscarinic stimulation of the iris sphincter

    Excess acetylcholine contracts the circular (sphincter) muscle of the iris, producing miosis.

58. Physostigmine is avoided in a suspected tricyclic antidepressant overdose mainly because it can:

    1. A. Worsen the patient's anticholinergic delirium
    2. B. Cause severe hyperthermia
    3. C. Speed absorption of the tricyclic
    4. D. Precipitate bradycardia and asystole
    Show answer

    Answer: D. Precipitate bradycardia and asystole

    In tricyclic overdose, sodium channel blockade already slows cardiac conduction, and adding physostigmine's cholinergic effect has been linked to bradycardia and asystole; sodium bicarbonate treats the wide QRS. Physostigmine reverses rather than will worsen the patient's anticholinergic delirium, it does not cause severe hyperthermia, and it does not speed absorption of the tricyclic.

59. A useful finding for distinguishing sympathomimetic (e.g., cocaine) toxicity from anticholinergic toxicity is:

    1. A. Hyperthermia in sympathomimetic toxicity only
    2. B. Moist, diaphoretic skin in sympathomimetic toxicity
    3. C. Tachycardia in anticholinergic toxicity only
    4. D. Dilated pupils in sympathomimetic toxicity only
    Show answer

    Answer: B. Moist, diaphoretic skin in sympathomimetic toxicity

    Both cause mydriasis, tachycardia, and hyperthermia, but anticholinergics block sweating.

60. An IV bolus of phenylephrine may cause:

    1. A. Reflex tachycardia from baroreceptor unloading
    2. B. Reflex bradycardia via baroreceptors
    3. C. Bronchodilation from beta-2 stimulation
    4. D. Hypoglycemia from increased insulin release
    Show answer

    Answer: B. Reflex bradycardia via baroreceptors

    Pure alpha-1 vasoconstriction raises blood pressure, triggering a vagal baroreceptor reflex.

61. In anaphylaxis, epinephrine's alpha-1 effect is beneficial because it produces:

    1. A. Bronchodilation that relieves wheezing and stridor
    2. B. Vasoconstriction that raises BP and reduces edema
    3. C. Increased heart rate and myocardial contractility
    4. D. Direct stabilization of mast cell membranes
    Show answer

    Answer: B. Vasoconstriction that raises BP and reduces edema

    Alpha-1 stimulation causes vasoconstriction, which counters vasodilation and capillary leak, raises blood pressure, and reduces mucosal edema. Bronchodilation is a beta-2 effect, increased heart rate and contractility are beta-1 effects, and reduced mast cell mediator release comes from beta-2 stimulation rather than alpha-1.

62. Isoproterenol is best described as a:

    1. A. Pure alpha-1 agonist with no beta activity
    2. B. Mixed alpha and beta agonist like epinephrine
    3. C. Nonselective beta agonist with no alpha activity
    4. D. Beta-1 selective antagonist with no alpha effect
    Show answer

    Answer: C. Nonselective beta agonist with no alpha activity

    Isoproterenol stimulates beta-1 and beta-2 receptors, raising heart rate and dilating vessels and airways.

63. Labetalol lowers blood pressure by blocking:

    1. A. Only alpha-2 receptors in the brainstem
    2. B. Alpha-1, beta-1, and beta-2 receptors
    3. C. Only beta-1 receptors in the heart
    4. D. L-type calcium channels in vessels
    Show answer

    Answer: B. Alpha-1, beta-1, and beta-2 receptors

    Labetalol combines alpha-1 blockade (vasodilation) with nonselective beta blockade.

64. Propranolol is generally avoided in patients with asthma because it:

    1. A. Blocks beta-2 receptors and can trigger bronchospasm
    2. B. Increases mucus production by stimulating nicotinic receptors
    3. C. Stimulates beta-2 receptors excessively
    4. D. Blocks alpha-1 receptors in the lungs
    Show answer

    Answer: A. Blocks beta-2 receptors and can trigger bronchospasm

    Propranolol is nonselective, so it blocks the beta-2 receptors that keep the airways dilated.

65. Ipratropium relieves bronchospasm in COPD by:

    1. A. Stimulating beta-2 receptors in the airways
    2. B. Stimulating alpha-1 receptors to shrink mucosa
    3. C. Blocking muscarinic receptors in the airways
    4. D. Inhibiting phosphodiesterase in smooth muscle
    Show answer

    Answer: C. Blocking muscarinic receptors in the airways

    Vagal (cholinergic) tone causes much of the bronchoconstriction in COPD, so an anticholinergic helps. This reduces bronchoconstriction and secretions.

66. Atropine is often ineffective for bradycardia caused by third-degree (infranodal) heart block because:

    1. A. The block is below the AV node, beyond vagal influence
    2. B. Atropine stimulates the vagus nerve at high doses
    3. C. Atropine blocks beta-1 receptors in the conduction system
    4. D. Atropine needs 20 minutes to reach the AV node
    Show answer

    Answer: A. The block is below the AV node, beyond vagal influence

    Atropine removes vagal tone at the SA and AV nodes; His-Purkinje blocks need pacing or catecholamines.

67. Atropine may not increase heart rate in a heart transplant recipient because:

    1. A. Antirejection drugs block atropine
    2. B. The transplanted heart lacks beta receptors
    3. C. Transplant patients metabolize atropine instantly
    4. D. The transplanted heart has no vagal innervation
    Show answer

    Answer: D. The transplanted heart has no vagal innervation

    A denervated heart has no vagal tone for atropine to block.

68. Vagal maneuvers can terminate some supraventricular tachycardias by:

    1. A. Increasing sympathetic tone to the atria
    2. B. Blocking calcium channels in the AV node
    3. C. Stimulating beta-1 receptors in the SA node
    4. D. Raising vagal tone at the AV node
    Show answer

    Answer: D. Raising vagal tone at the AV node

    Vagal stimulation releases acetylcholine at the AV node, which can interrupt reentry circuits that pass through it. This slows AV node conduction.

69. Physostigmine can reverse severe anticholinergic delirium because it:

    1. A. Enhances GABA activity at the GABA-A receptor
    2. B. Inhibits acetylcholinesterase in the CNS
    3. C. Blocks nicotinic receptors at the ganglia
    4. D. Blocks muscarinic receptors in the brain
    Show answer

    Answer: B. Inhibits acetylcholinesterase in the CNS

    Raising acetylcholine centrally and peripherally overcomes muscarinic blockade. It is a reversible acetylcholinesterase inhibitor that crosses the blood-brain barrier.

70. Ephedrine is called a mixed-acting sympathomimetic because it:

    1. A. Inhibits both MAO and COMT breakdown enzymes
    2. B. Stimulates both muscarinic and nicotinic receptors
    3. C. Acts directly and releases norepinephrine
    4. D. Blocks both alpha and beta adrenergic receptors
    Show answer

    Answer: C. Acts directly and releases norepinephrine

    It acts both directly on receptors and indirectly by releasing norepinephrine.

71. Cocaine produces sympathomimetic effects mainly by:

    1. A. Blocking reuptake of catecholamines
    2. B. Directly stimulating muscarinic receptors
    3. C. Directly stimulating alpha-1 receptors only
    4. D. Inhibiting acetylcholinesterase in synapses
    Show answer

    Answer: A. Blocking reuptake of catecholamines

    Inhibiting reuptake leaves more catecholamine in the synapse. Cocaine also blocks serotonin reuptake.

72. Amphetamines increase sympathetic activity mainly by:

    1. A. Mimicking acetylcholine at autonomic ganglia
    2. B. Blocking beta receptors on target organs
    3. C. Releasing catecholamines from nerve terminals
    4. D. Inhibiting catecholamine synthesis in neurons
    Show answer

    Answer: C. Releasing catecholamines from nerve terminals

    Amphetamines push norepinephrine and dopamine out of storage vesicles into the synapse.

73. Circulating catecholamines are metabolized mainly by:

    1. A. Monoamine oxidase and COMT
    2. B. Pseudocholinesterase
    3. C. Cytochrome P450 only
    4. D. Acetylcholinesterase
    Show answer

    Answer: A. Monoamine oxidase and COMT

    MAO and COMT inactivate epinephrine, norepinephrine, and dopamine. COMT is catechol-O-methyltransferase.

74. Catecholamines such as epinephrine are not given orally because:

    1. A. They are too large to cross the gut wall
    2. B. Gut and liver enzymes inactivate them
    3. C. They work only after binding plasma albumin
    4. D. They cause immediate vomiting when swallowed
    Show answer

    Answer: B. Gut and liver enzymes inactivate them

    MAO and COMT in the gut wall and liver destroy oral catecholamines.

75. At high infusion rates, dopamine's predominant effect is:

    1. A. Muscarinic mediated bradycardia
    2. B. Alpha-1 mediated vasoconstriction
    3. C. Pure beta-2 mediated bronchodilation
    4. D. Renal and mesenteric vasodilation
    Show answer

    Answer: B. Alpha-1 mediated vasoconstriction

    Dopamine's effects are dose-dependent: dopaminergic at low doses, beta-1 at moderate doses, alpha at high doses.

76. Extravasation of norepinephrine into tissue can cause necrosis because of:

    1. A. Intense local alpha-1 vasoconstriction
    2. B. Direct chemical burn from its acidic pH
    3. C. Histamine release causing local edema
    4. D. Beta-2 mediated local vasodilation
    Show answer

    Answer: A. Intense local alpha-1 vasoconstriction

    Local ischemia results; phentolamine, an alpha blocker, can be infiltrated as an antidote.

77. Terbutaline has been used to slow preterm labor because beta-2 stimulation:

    1. A. Blocks calcium in the cervix
    2. B. Contracts uterine smooth muscle
    3. C. Increases oxytocin release
    4. D. Relaxes uterine smooth muscle
    Show answer

    Answer: D. Relaxes uterine smooth muscle

    Beta-2 agonists relax smooth muscle in both the bronchi and the uterus.

78. Albuterol can be used as an adjunct in hyperkalemia because beta-2 stimulation:

    1. A. Binds potassium in the gut
    2. B. Stabilizes the cardiac membrane
    3. C. Increases renal potassium excretion directly
    4. D. Shifts potassium into cells
    Show answer

    Answer: D. Shifts potassium into cells

    Beta-2 agonists activate Na/K-ATPase, temporarily lowering serum potassium.

79. Preganglionic sympathetic fibers stimulate the adrenal medulla by releasing acetylcholine onto:

    1. A. Beta-1 receptors
    2. B. Muscarinic receptors
    3. C. Alpha-1 receptors
    4. D. Nicotinic receptors
    Show answer

    Answer: D. Nicotinic receptors

    The adrenal medulla works like a sympathetic ganglion and releases epinephrine into the blood.

80. Bradycardia after succinylcholine, especially with repeat doses in children, results from:

    1. A. Blockade of cardiac beta-1 receptors
    2. B. Stimulation of cardiac muscarinic receptors
    3. C. Hypoglycemia from increased insulin release
    4. D. Stimulation of vascular alpha-1 receptors
    Show answer

    Answer: B. Stimulation of cardiac muscarinic receptors

    Succinylcholine resembles acetylcholine and can act on muscarinic receptors; atropine can prevent the bradycardia.

81. A common adverse effect of alpha-1 blockers such as prazosin or tamsulosin is:

    1. A. Bronchospasm from airway alpha-1 blockade
    2. B. Orthostatic hypotension after the first dose
    3. C. Hypertensive crisis from reflex vasoconstriction
    4. D. Bradycardia from additional beta blockade
    Show answer

    Answer: B. Orthostatic hypotension after the first dose

    Blocking alpha-1 vasoconstriction impairs the compensation for standing up.

82. Epinephrine raises blood glucose mainly by:

    1. A. Stimulating muscarinic receptors in the pancreas
    2. B. Increasing intestinal glucose absorption
    3. C. Stimulating hepatic glycogenolysis
    4. D. Increasing insulin release from the pancreas
    Show answer

    Answer: C. Stimulating hepatic glycogenolysis

    Sympathetic stimulation mobilizes glucose for the fight-or-flight response. Hepatic gluconeogenesis also increases.