Board-Style Questions
Eight questions. Cover the choices. Read the last line. Hunt the clue.
Question 1
A 72-year-old man on tamsulosin develops anaphylaxis in the ER. You administer epinephrine 0.3 mg IM.
His BP drops from 90/60 to 65/35. HR is 130. Which receptor mechanism best explains this response?
- A. Excess b1 stimulation causing tachycardia-induced hypotension
- B. Blocked a1 allows unopposed b2-mediated vasodilation
- C. Anaphylaxis causes release of histamine that degrades epinephrine
- D. Tamsulosin blocks b1 receptors, reducing cardiac output
- E. a2 receptors are stimulated, increasing NE release and causing vasodilation
Correct: B
Tempting to pick tachycardia (B1-driven) or mast cell release as the BP mechanism: the patient got epinephrine and things got worse, so something counteracted the epi. The trap is that tamsulosin removed the alpha-1 vasoconstriction component of epinephrine while leaving B2 vasodilation unopposed. Think of epinephrine as a two-engine plane: the alpha-1 engine provides lift (vasoconstriction, raises BP) and the B2 engine provides drag (skeletal muscle vasodilation). Tamsulosin disables the lift engine. The plane (BP) descends despite the pilot adding throttle (epinephrine). Tamsulosin blocks a1 receptors in vascular smooth muscle. Normally Epi raises BP via a1 (vasoconstriction) despite b2 vasodilation. With a1 blocked, the b2 effect (skeletal muscle vasodilation) is unopposed. Cardiac output goes up (b1 intact), but systemic vascular resistance falls. Net: BP drops. This is the Epi reversal phenomenon.
A: Good instinct, tachycardia is present, but it's b1-driven and doesn't cause hypotension on its own here. The problem is the vascular side, not rate.
C: You know how histamine works in anaphylaxis: it causes direct vasodilation and bronchoconstriction, but it does not enzymatically degrade epinephrine.
D: Tamsulosin is selective for a1, not b1. It does not touch cardiac beta receptors at therapeutic doses.
E: a2 blockade would increase NE, not decrease BP through vasodilation.
Break it down: Epi reversal = a1 blocked + b2 unopposed. Rescue: phenylephrine (pure a1) or NE (strong a1/b1, minimal b2).
Question 2
A surgeon plans resection of a pheochromocytoma. The patient is placed on propranolol first due to tachycardia and palpitations.
Two days later, during a routine exam, BP is 230/135. What is the most likely cause?
- A. Propranolol is metabolized too quickly and lost its effect
- B. Tumor manipulation released a large catecholamine surge
- C. Beta blockade without prior alpha blockade allows unopposed a1 vasoconstriction
- D. Propranolol directly stimulates a2 autoreceptors, increasing NE
- E. Renal artery stenosis unmasked by the propranolol
Correct: C
Tempting to think the beta-blocker just failed to work on the tumor: propranolol is potent, so maybe the pheo just overpowered it. The trap is that propranolol actively made things worse by removing B2 vasodilation (the one partial brake on alpha-driven vasoconstriction). Think of the pheo as a fire hose on full pressure with only one hand partially covering the nozzle (B2 vasodilation). Propranolol pulled that hand away, leaving the full alpha-1 pressure blast uncovered. The pheo still produces NE and Epi continuously. Propranolol blocks b2-mediated vasodilation (the only thing partially counteracting the a1 constriction). Without b2 dilation and with all that NE hitting unopposed a1 receptors: severe hypertensive crisis. Alpha blockade MUST precede beta blockade in pheo management.
A: Good instinct, propranolol has a short half-life (3-6 hrs), but that's not the mechanism here. Two days in, it's still active.
B: Tumor manipulation is an intraoperative concern. This patient has not had surgery yet.
D: Propranolol does not directly affect alpha receptors or autoreceptors.
E: No prior renal disease suggested, and propranolol does not typically unmask RAS.
Break it down: Pheo protocol = alpha first (phenoxybenzamine 10-14 days), then beta. Reverse the order = hypertensive crisis.
Question 3
A 64-year-old man on tamsulosin for BPH is scheduled for cataract surgery. His ophthalmologist is notified preoperatively.
During phacoemulsification, the iris suddenly billows toward the wound and begins to prolapse.
What is the mechanism of this complication?
- A. Tamsulosin blocks b2 receptors in ciliary muscle, reducing aqueous outflow
- B. Tamsulosin blocks a1A receptors in iris dilator muscle, causing flaccidity during surgery
- C. Tamsulosin increases iris sphincter tone via muscarinic blockade
- D. Prior mydriatic use with tamsulosin produces paradoxical miosis
- E. Tamsulosin blocks a2 receptors in the iris, causing uncontrolled pupil dilation
Correct: B
Tempting to blame ciliary muscle B2 blockade since tamsulosin is a selective alpha-blocker and the ciliary muscle is involved in accommodation. The trap is that the iris dilator specifically uses alpha-1A receptors for its tone, and tamsulosin blocks exactly that receptor even weeks after the drug is stopped. Think of the iris dilator muscle as a tent kept taut by alpha-1A ropes: tamsulosin cuts the ropes. The tent collapses inward during surgery. The iris dilator muscle contains a1A adrenergic receptors. Tamsulosin (uroselective a1A blocker) relaxes this muscle even weeks after stopping the drug. During phacoemulsification, the iris lacks normal tone, billows into the surgical wound, constricts despite dilating drops, and prolapses. This is Intraoperative Floppy Iris Syndrome (IFIS).
A: Tamsulosin acts on a1A, not b2. The ciliary muscle is not relevant here.
C: Tamsulosin has no muscarinic activity. Cholinergic blockade would dilate, not constrict.
D: Mydriatics and tamsulosin don't combine to cause paradoxical miosis specifically.
E: Tamsulosin is selective for a1A, not a2. a2 blockade would increase NE and could affect pupil size differently.
Break it down: IFIS = a1A block in iris dilator. Warn surgeon before any cataract case in a patient on tamsulosin (or silodosin).
Question 4
A 45-year-old woman on phenelzine (MAOI) for depression eats aged cheese at a party.
Minutes later she has a BP of 220/130 and a severe headache. Which agent is most appropriate for acute management?
- A. Prazosin PO
- B. Phenoxybenzamine IV
- C. Phentolamine IV
- D. Clonidine PO
- E. Labetalol IV
Correct: C
Tempting to pick prazosin (also an alpha blocker) or phenoxybenzamine (irreversible alpha blocker): both are alpha-1 blockers and fit the mechanism. The trap is that an acute hypertensive emergency needs titratable IV therapy, not oral or irreversible agents. Think of managing a hypertensive crisis like adjusting a dimmer switch: you need a precise, fast, reversible control. Prazosin is a light switch (oral, slow), phenoxybenzamine is a broken dimmer that you cannot turn back up if BP drops too low. Phentolamine is the properly functioning IV dimmer. MAOI-tyramine crisis: tyramine is normally degraded by gut/liver MAO. With MAO blocked, tyramine enters systemic circulation, enters sympathetic terminals, displaces NE, and floods a1 receptors. Hypertensive crisis. Treatment: phentolamine IV (reversible non-selective alpha blocker, titratable, 15-30 min duration). Blocks the a1-mediated vasoconstriction.
A: Good instinct since prazosin is an a1 blocker, but it's oral and slow. This is a hypertensive emergency requiring IV titratable therapy.
B: Phenoxybenzamine is irreversible with a very long duration (24+ hours). You cannot easily reverse it if BP drops too low. Not appropriate for acute management.
D: Clonidine is an a2 agonist (decreases NE release). It can help chronic hypertension but is too slow and unpredictable for this emergency.
E: You know how labetalol works: it's a + b block. In a pure NE-driven crisis, adding beta blockade without adequate alpha coverage can worsen vasoconstriction. Phentolamine is safer here.
Break it down: MAOI + tyramine = flood of NE at a1. Phentolamine IV = titratable non-selective a-block. Phenoxybenzamine is for pre-op pheo, not acute crises.
Question 5
A 52-year-old man starts prazosin for hypertension. Three hours after the first dose at bedtime, he collapses while walking to the bathroom.
BP lying: 125/80. BP standing: 78/50. What is the mechanism of this event?
- A. Prazosin blocks b1 receptors, reducing cardiac output acutely
- B. a1 blockade prevents reflex vasoconstriction when standing, causing orthostatic hypotension
- C. Prazosin activates a2 autoreceptors, reducing NE release at the synapse
- D. Excessive b2 stimulation by endogenous Epi causes vasodilation
- E. Prazosin causes bradycardia that reduces cerebral perfusion pressure
Correct: B
Tempting to pick B1 blockade: the heart slows when you stand (reflex tachycardia is absent) so it seems like a cardiac mechanism. The trap is that prazosin is a pure alpha-1 blocker with no B1 activity. Think of the standing vasoconstriction reflex as a counterweight system in an elevator: when you rise (stand), the counterweight (alpha-1-mediated vasoconstriction) keeps the car from dropping. Prazosin removes the counterweight. Without it, the blood (car) drops into the legs (basement) the moment you stand. First-dose phenomenon: when prazosin blocks a1 receptors acutely, the normal postural reflex (sympathetic-mediated vasoconstriction upon standing) is blunted. Blood pools in the legs. Cardiac output cannot immediately compensate. Result: orthostatic hypotension and syncope. Particularly severe on the first dose before tachyphylaxis develops.
A: Prazosin is selective for a1 only. It does not block b1 receptors. Cardiac output is not directly reduced.
C: Prazosin is a postsynaptic a1 blocker. It does not activate presynaptic a2 autoreceptors.
D: There is no reason for excess endogenous Epi in this scenario, and b2 vasodilation is not the mechanism here.
E: Prazosin does not typically cause bradycardia. If anything, reflex tachycardia occurs as BP falls.
Break it down: First-dose prazosin = a1 block abolishes standing vasoconstriction reflex. Fix: start at 1 mg at bedtime, titrate slowly.
Question 6
A 58-year-old man with hypertension and BPH is asking about a drug that can treat both conditions with one pill.
Which agent is the best choice?
- A. Tamsulosin
- B. Doxazosin
- C. Phenoxybenzamine
- D. Clonidine
- E. Silodosin
Correct: B
Tempting to pick tamsulosin: it is the most commonly prescribed alpha-blocker for BPH and it works well for the urinary symptoms. The trap is that tamsulosin is uroselective (alpha-1A dominant) and has minimal systemic blood pressure effect, so it will not treat hypertension. Think of uroselective agents as a key that only opens the prostate door but not the vascular door: one problem solved. Non-uroselective agents (doxazosin, terazosin) are master keys that open both doors simultaneously. Doxazosin (or terazosin) blocks a1 receptors non-selectively: vessels AND the prostate/bladder neck. One drug, two problems solved. The uroselective agents (tamsulosin, silodosin) block mostly a1A in the prostate and have minimal effect on systemic blood pressure, making them useless for hypertension.
A: Tamsulosin is uroselective (a1A dominant). Excellent for BPH but will not adequately control blood pressure.
C: Phenoxybenzamine is irreversible and reserved for pheochromocytoma prep. Using it for BPH and HTN would be dangerous long-term.
D: Clonidine is a central a2 agonist. It lowers BP but has no role in BPH management.
E: Silodosin is even more uroselective than tamsulosin. Same issue as A.
Break it down: BPH + HTN combo = non-uroselective a1 blocker (doxazosin or terazosin). Uroselective agents only handle the plumbing, not the pressure.
Question 7
A 34-year-old woman is 22 weeks pregnant and has a blood pressure of 158/100. She has no prior history of hypertension.
Which antihypertensive agent is most appropriate at this time?
- A. Lisinopril (ACE inhibitor)
- B. Metoprolol (beta-1 blocker)
- C. Methyldopa (central a2 agonist)
- D. Clonidine
- E. Doxazosin
Correct: C
Tempting to pick a beta-blocker (well-tolerated in pregnancy) or labetalol (alpha + beta): both are used in pregnant patients. The trap is that methyldopa has decades of fetal safety data that no other agent matches. Think of drug safety in pregnancy like a courtroom evidence standard: methyldopa has the most case files, the most follow-up data, and the most favorable rulings. ACE inhibitors are convicted felons (absolute contraindication). Beta-blockers have shorter records. Methyldopa is the established precedent. Methyldopa is the drug of choice for hypertension in pregnancy. It has the longest safety track record, with decades of data showing no fetal harm. The mechanism: central a2 agonist in the brainstem, reduces sympathetic outflow, lowers BP without dangerous vasoconstriction.
A: ACE inhibitors are CONTRAINDICATED in pregnancy (teratogenic: renal agenesis, oligohydramnios, skull ossification defects in 2nd/3rd trimester). This is an absolute contraindication.
B: Beta-blockers in pregnancy are sometimes used but are not first-line. Associated with intrauterine growth restriction. Not the best choice here.
D: Clonidine is also a central a2 agonist but lacks the long safety record methyldopa has in pregnancy.
E: Doxazosin has insufficient safety data in pregnancy. Not first-line.
Break it down: HTN in pregnancy = methyldopa first. Know this cold. ACE inhibitors are CONTRAINDICATED (teratogenic). Boards LOVES testing this distinction.
Question 8
A 29-year-old woman on heroin is admitted for detoxification. She is restless with a heart rate of 108, blood pressure of 162/98, gooseflesh, and yawning.
Which drug best addresses the adrenergic symptoms of opioid withdrawal?
- A. Prazosin
- B. Clonidine
- C. Methadone
- D. Naloxone
- E. Phenoxybenzamine
Correct: B
Tempting to pick methadone: it treats opioid withdrawal by substituting a long-acting opioid, which is a valid strategy. The trap is that the question asks about the mechanism of the ADRENERGIC symptoms (tachycardia, hypertension, piloerection, sweating), not opioid craving. Think of opioid withdrawal as a fire alarm triggered by the locus coeruleus firing massively: clonidine acts as the master alarm shutoff at the central alpha-2 autoreceptor, turning off the entire norepinephrine cascade from the source. Methadone replaces the opioid substrate but doesn't touch the adrenergic fire alarm. Clonidine is a central a2 agonist. In opioid withdrawal, the locus coeruleus fires massively, flooding the system with norepinephrine and causing all the adrenergic fireworks: tachycardia, hypertension, piloerection (gooseflesh), sweating, yawning. Clonidine stimulates central a2 autoreceptors, slams the brakes on NE release, and blunts those symptoms. It does not treat the opioid craving itself, but it makes withdrawal survivable.
A: Prazosin is a postsynaptic a1 blocker. It would lower peripheral vascular resistance but would not address the central adrenergic storm driving the withdrawal symptoms. Think of it like mopping the floor with the tap still running.
C: Methadone treats withdrawal by substituting a long-acting opioid agonist. It works through opioid receptors, not adrenergic receptors. A different mechanism entirely.
D: Naloxone PRECIPITATES opioid withdrawal by blocking opioid receptors acutely. You would make things much worse.
E: Phenoxybenzamine blocks a1 and a2 peripherally and irreversibly. Using it for withdrawal would cause massive hypotension. Wrong target.
Break it down: Opioid withdrawal adrenergic storm = clonidine (central a2 agonist). It turns off the NE tap at the source. Naloxone precipitates withdrawal. Know both directions.
