1. A 71-year-old man with hypertension (on lisinopril 10 mg daily, BP 148/88 mmHg above goal) and BPH (IPSS [International Prostate Symptom Score] 18, peak urinary flow 9 mL/s) presents for medication management. Which of the following most accurately identifies the best single alpha-1 blocker choice to simultaneously address both conditions?

• A) Silodosin -- its extreme alpha-1A selectivity produces maximal BPH relief with no cardiovascular effects; since silodosin has no blood pressure effect, a separate second antihypertensive agent would also be needed.
• B) Tamsulosin -- the ALLHAT trial established tamsulosin as the preferred agent for combined BPH and hypertension because its low cardiovascular impact makes it safer; tamsulosin should be added with the expectation of significant additional blood pressure lowering.
• C) Phentolamine -- its nonselective alpha-1 and alpha-2 blockade provides both BPH symptom relief and the most potent antihypertensive effect among all alpha blockers.
• D) Doxazosin or terazosin -- the non-uroselective, long-acting selective alpha-1 blockers -- are the most appropriate choice for this patient who has both inadequately controlled hypertension and symptomatic BPH; their non-subtype-selective alpha-1 blockade produces meaningful blood pressure reduction (alpha-1B vasodilation in systemic vessels) in addition to BPH symptom relief (alpha-1A/D relaxation in the lower urinary tract), addressing both conditions with a single agent; uroselective agents (tamsulosin, silodosin) would address BPH but provide much less blood pressure benefit, requiring a separate additional antihypertensive agent to meet blood pressure goals; doxazosin XR or terazosin are appropriate with counseling about first-dose phenomenon, PDE5 inhibitor interaction, and use as add-on rather than monotherapy replacement for the lisinopril given ALLHAT heart failure data.

2. During laparoscopic adrenalectomy for a pheochromocytoma in a patient preoperatively prepared with phenoxybenzamine 30 mg twice daily and propranolol 40 mg twice daily, surgical manipulation of the adrenal gland causes BP to rise from 142/88 to 236/148 mmHg and HR to 112 bpm. The anesthesiologist administers phentolamine 2 mg IV with partial response; two minutes later BP spikes again to 242/152 mmHg. Which of the following most accurately identifies the mechanism and appropriate immediate management?

• A) The surge is caused by inadequate preoperative propranolol dosing -- the heart rate of 112 bpm confirms beta-1 excess; immediate management is IV propranolol 1-2 mg boluses; alpha-1 blockade is adequate and does not need to be augmented.
• B) The intraoperative surge results from mechanical pressure on the tumor releasing a massive catecholamine bolus that exceeds the basal secretion rate; even with adequate preoperative phenoxybenzamine blockade, some alpha-1 receptors are newly synthesized after the preoperative preparation period and are available for catecholamine-mediated vasoconstriction; additionally, the catecholamine surge activates cardiac beta-1 receptors contributing to the BP elevation; the immediate management is additional IV phentolamine (2-5 mg boluses titrated to target systolic 120-140 mmHg) with sodium nitroprusside infusion (0.25-0.5 mcg/kg/min) for sustained control between boluses; the anesthesiologist should request brief pauses in tumor manipulation during pharmacological management.
• C) The intraoperative surge is a false emergency from a faulty arterial line transducer; mechanical pressure on the adrenal gland can compress the vena cava triggering a Cushing reflex; the appropriate management is to confirm the reading with a cuff blood pressure before administering any antihypertensive medications.
• D) The immediate management is labetalol 20 mg IV because its combined alpha-1 and beta blockade addresses both the vasoconstriction and the tachycardia; phentolamine should be avoided because its presynaptic alpha-2 blockade would further disinhibit NE release from the tumor.

3. A 68-year-old man on tamsulosin 0.4 mg daily for BPH is referred by his urologist to an ophthalmologist for evaluation of progressive bilateral cataracts. The referring note does not mention tamsulosin. The ophthalmologist schedules the patient for standard phacoemulsification using a routine surgical protocol. Which of the following most accurately identifies what communication failure has occurred and what the consequence could be?

• A) The failure to inform the ophthalmologist of tamsulosin use is a clinically significant medication reconciliation error; the ophthalmologist is planning a routine surgical protocol without knowledge of the patient's alpha-1 blocker history; without this information, the ophthalmologist will not plan for IFIS -- the flaccid iris that billows and prolapses toward the phacoemulsification incision, the progressive intraoperative miosis despite mydriatic agents, and the potential iris prolapse that characterize IFIS; if IFIS occurs without preparation, the ophthalmologist may lack the iris expansion devices (iris hooks, Malyugin ring) and intracameral pharmacological tools (phenylephrine) on the surgical table; the potential consequences include iris trauma, posterior capsule rupture, retained lens fragments, and increased overall surgical morbidity; the standard of care requires that any prior or current alpha-1 blocker use be communicated to the ophthalmologist in the referral regardless of when the drug was last taken, so that appropriate surgical planning can occur preoperatively rather than reactively.
• B) The failure to disclose tamsulosin is not clinically significant because IFIS only occurs in patients currently taking tamsulosin at the time of surgery; since a simple phone call to the patient before surgery to ask about current medications would identify active tamsulosin use, the routine preoperative medication review is sufficient; the referral note does not need to specifically mention tamsulosin.
• C) The failure to disclose tamsulosin is clinically significant but the consequence is limited to a slightly higher rate of intraoperative pupillary miosis; the ophthalmologist can manage this with a higher dose of intracameral phenylephrine; iris prolapse and posterior capsule rupture are theoretical risks not confirmed in prospective randomized controlled trials.
• D) The failure to disclose tamsulosin is clinically significant only if the patient is currently taking tamsulosin; if the patient stopped tamsulosin at any time before surgery, the IFIS risk is eliminated and the referral omission is not consequential.

4. A 34-year-old combat veteran with PTSD presents to the VA mental health clinic with severe combat-related nightmares occurring almost nightly and daytime hyperarousal. He has failed two SSRI trials and psychotherapy. His blood pressure is 128/78 mmHg. His psychiatrist considers prazosin for nightmares. Which of the following most accurately describes the initiation protocol and monitoring required?

• A) Prazosin should be initiated at a standard antihypertensive dose (2 mg twice daily) because the central noradrenergic target requires achieving minimum plasma concentrations consistent with antihypertensive dosing; lower doses are subtherapeutic for the CNS indication.
• B) Prazosin should be avoided in this patient because his blood pressure of 128/78 mmHg is at the low end of normal; adding prazosin would reduce his blood pressure into the hypotensive range; patients with pre-treatment systolic BP below 130 mmHg are not candidates for prazosin PTSD therapy as established by the exclusion criteria in the Raskind et al. trials.
• C) Prazosin for PTSD nightmares should be initiated at a very low dose (1 mg at bedtime) and titrated slowly upward every 1-2 weeks based on nightmare response and blood pressure tolerance; the titration often proceeds to 3-15 mg at bedtime based on individual response; the primary adverse effect requiring monitoring is orthostatic hypotension -- the patient should be instructed to rise slowly from bed in the morning; baseline standing and supine blood pressure should be recorded; the dose should be taken at bedtime to exploit the recumbent position during peak drug effect and to target the drug's maximum alpha-1 blockade to the hours of REM-predominant sleep when nightmares most commonly occur; blood pressure should be checked at each visit, particularly supine-to-standing measurements; the patient should be informed that morning dizziness on rising is the primary symptom to report.
• D) Prazosin should be initiated at 1 mg at bedtime and the dose should not be increased beyond 2 mg because higher doses produce an unacceptable risk of morning orthostatic syncope; the prescribing information for prazosin specifically caps the PTSD indication at 2 mg based on the Raskind trial protocols.

5. A 62-year-old man with BPH and erectile dysfunction presents asking about starting sildenafil. He is currently taking tamsulosin 0.4 mg every morning. His cardiologist has cleared him for sexual activity. His blood pressure today is 136/84 mmHg. Which of the following most accurately describes the hemodynamic risk of adding sildenafil and the management strategy to minimize it?

• A) Sildenafil is absolutely contraindicated with tamsulosin at any dose; the FDA has issued a black-box warning prohibiting the concurrent use of any PDE5 inhibitor with any alpha-1 blocker; the patient must switch from tamsulosin to finasteride before sildenafil can be prescribed.
• B) Sildenafil is safe to start at the standard 50 mg dose without any modification when combined with tamsulosin because tamsulosin's uroSelectivity means it has no clinically meaningful effect on systemic blood pressure; the hemodynamic interaction only applies to non-uroselective alpha-1 blockers; tamsulosin can be combined with any PDE5 inhibitor at standard doses without hemodynamic precautions.
• C) The hemodynamic risk from sildenafil plus tamsulosin is entirely eliminated if tamsulosin is taken in the morning and sildenafil is taken in the evening; because tamsulosin's half-life is 9-13 hours, taking sildenafil 12 or more hours after the morning tamsulosin dose ensures there is no pharmacodynamic overlap and the patient can take sildenafil at bedtime with no hemodynamic precautions.
• D) The interaction between tamsulosin and sildenafil is pharmacokinetic rather than pharmacodynamic -- tamsulosin inhibits CYP3A4, the primary enzyme metabolizing sildenafil; the resulting 3-5 fold increase in sildenafil plasma concentrations produces the clinically observed hypotension; the management strategy is to reduce the sildenafil dose to 12.5 mg.
• E) The hemodynamic interaction between tamsulosin and sildenafil is a real class effect pharmacodynamic interaction driven by additive vasodilation from two independent mechanisms -- tamsulosin's alpha-1 receptor blockade on vascular smooth muscle (reducing NE-mediated vasoconstriction) and sildenafil's PDE5 inhibition (increasing cGMP, relaxing vascular smooth muscle through the NO pathway) -- that together can produce clinically significant orthostatic hypotension particularly within 2-6 hours after sildenafil ingestion; although tamsulosin's uroSelectivity makes this interaction less severe than with non-uroselective agents, it is not eliminated; management strategy: start sildenafil at the lowest available dose (25 mg rather than 50 mg); counsel the patient to avoid sudden postural changes within the first several hours after taking sildenafil; separate doses by 4-6 hours where possible; ensure adequate hydration; monitor blood pressure at follow-up and adjust sildenafil dose accordingly.

6. A 54-year-old woman undergoes successful laparoscopic right adrenalectomy for a 3.8 cm pheochromocytoma with markedly elevated preoperative plasma free metanephrines. She had no prior history of hypertension before tumor discovery. On postoperative day 3, her blood pressure is 118/72 mmHg. She asks the endocrinologist whether she will need blood pressure medications long-term. Which of the following most accurately describes the expected post-resection blood pressure trajectory?

• A) This patient will definitely require lifelong antihypertensive therapy because pheochromocytoma irreversibly damages the vascular endothelium and renal arterioles during the years of catecholamine excess; the structural vascular changes are permanent and independent of catecholamine levels; she should be started immediately on long-term amlodipine.
• B) In a patient without prior hypertension whose elevated blood pressure was directly caused by pheochromocytoma catecholamine excess, successful tumor resection usually normalizes blood pressure within 1-4 weeks as circulating catecholamine levels fall precipitously, phenoxybenzamine-mediated alpha-1 blockade progressively wanes as new adrenergic receptor protein is synthesized, and postsynaptic adrenergic receptors that were downregulated from chronic catecholamine excess begin to upregulate back toward normal density; however, approximately 25-50% of patients have residual hypertension 1-3 months post-resection from either underlying essential hypertension, structural vascular changes from chronic hypertension, or incomplete tumor resection; management: discontinue antihypertensives and monitor blood pressure closely over the first 1-4 weeks post-resection rather than prescribing long-term medication empirically; perform biochemical surveillance (plasma free metanephrines) at 2-6 weeks post-resection to confirm biochemical cure; if hypertension persists at 4-6 weeks post-resection with confirmed biochemical normalization, begin standard antihypertensive therapy at that time.
• C) This patient's blood pressure will remain elevated postoperatively despite successful tumor removal because phenoxybenzamine irreversible receptor blockade persists for 3-6 months after the last dose; after the blockade wears off at 3-6 months, blood pressure will rise to reflect the patient's underlying vascular status; the endocrinologist should wait 3-6 months before making any determination about long-term antihypertensive need.
• D) Blood pressure normalization after pheochromocytoma resection is guaranteed in all patients because the hypertension is entirely driven by excess catecholamine-mediated alpha-1 receptor activation; once catecholamines are removed and phenoxybenzamine blockade wanes, there is no remaining mechanism for hypertension; this patient will never require blood pressure medication.