Alpha-Adrenergic Antagonists (α-Blockers)

Name: Alpha-Adrenergic Antagonists (α-Blockers) — Autonomics pharmacology
Creator: LearnDrugs

High-yield Verified · Oct 2026

Block α1 receptors (Gq → IP3/DAG → calcium → smooth-muscle contraction) in vessels and the prostate — and, with phentolamine and phenoxybenzamine, the α2 receptors whose loss releases more norepinephrine onto β receptors. Metyrosine is the odd one out: it stops catecholamines being made.

Nursing view → administration, monitoring and patient teaching

Compare: Autonomic receptors compared — muscarinic, nicotinic, adrenergic and dopamine →

Compare: α-blockers compared — selectivity, uses and adverse effects →

Drugs

phentolamine OraVerse, Ryzumvi

phenoxybenzamine —

tamsulosin —

alfuzosin Uroxatral

silodosin —

metyrosine Demser

Mechanism

Block α-adrenergic receptors. Phentolamine (reversible) and phenoxybenzamine (irreversible, covalent) block both α1 and α2: vasodilation and lower vascular resistance, with reflex and α2-mediated tachycardia. Tamsulosin, silodosin (α1A-preferring) and alfuzosin block α1 receptors in the prostate, prostatic capsule, prostatic urethra and bladder neck, relaxing smooth muscle and improving urine flow. Metyrosine is not a receptor blocker: it inhibits tyrosine hydroxylase, the rate-limiting step of catecholamine synthesis.

α1 is Gq, α2 is Gi

Adrenergic receptors are G-protein-coupled. α1 receptors couple to Gq: phospholipase C forms IP3 and DAG, and intracellular calcium rises, so smooth muscle contracts. Most α1 receptors lie on vascular smooth muscle, where catecholamines cause vasoconstriction and raise blood pressure and peripheral resistance; norepinephrine has a higher affinity for them than epinephrine. α1 receptors are also abundant in the prostate, prostatic capsule, prostatic urethra and bladder neck, where they set smooth-muscle tone.

α2 receptors couple to Gi: adenylate cyclase is inactivated and intracellular cAMP falls. On peripheral nerve endings they inhibit norepinephrine release when activated — a negative-feedback brake on the sympathetic terminal. (Agonist signalling at α and β receptors is covered on the Cardiovascular vasopressors page.)

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α1 raises calcium through Gq; α2 lowers cAMP through Gi and brakes norepinephrine release.

Nonselective, α1-selective and uroselective

Nonselective blockers (phentolamine, phenoxybenzamine) block α1 and α2. Blocking α1 dilates vessels, but blocking α2 removes the brake, so more norepinephrine is released; the spillover stimulates β receptors and causes tachycardia and tremulousness, and it can counteract the vasodilation. They work best when sympathetic activity is high, as in pheochromocytoma.

α1-selective blockers (the "-osin" drugs) leave the α2 brake intact, so they cause less reflex tachycardia than nonselective agents. The antihypertensive ones — prazosin, doxazosin, terazosin — are second-line for hypertension because of orthostatic hypotension (Cardiovascular › Other Antihypertensives).

Uroselective blockers aim at the prostate. At least three α1 subtypes exist (α1A, α1B, α1D), distributed differently between tissues, and about 70% of the α1 receptors in the human prostate are α1A. Tamsulosin is selective for prostatic α1 receptors, silodosin binds α1A with high affinity, and alfuzosin is a selective post-synaptic α1 antagonist at the prostate and bladder; for BPH they have relatively minimal orthostatic effects. Tamsulosin, alfuzosin and silodosin are not indicated for hypertension.

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Which receptors each group blocks — and what follows.

Phenoxybenzamine binds for good

Phenoxybenzamine is a nonselective, irreversible antagonist: it bonds covalently to a component of the α receptor, most likely a cysteine residue, producing a long-lasting noncompetitive blockade. After an IV dose its half-life is about 24 hours, effects persist for at least 3 to 4 days, and daily dosing is cumulative for nearly a week. It lowers both supine and erect blood pressure and has no effect on the parasympathetic system.

Phentolamine, by contrast, is a reversible α-blocker of relatively short duration (IV half-life about 19 minutes). It also has direct, though less marked, positive inotropic and chronotropic and vasodilator effects. Phentolamine eye drops show the reversibility at a single tissue: they bind α1 receptors on the iris dilator, shrinking the pupil without affecting the ciliary muscle, and so reverse drug-induced mydriasis.

Pheochromocytoma: block the receptors, then the heart — or the synthesis

Tumor catecholamines constrict vessels, so the patient is hypertensive yet volume-contracted. An α-blocker started 10 to 14 days before surgery controls pressure and allows the volume to be restored: α1 and α2 blockade relaxes arterioles and venous capacitance vessels. Normal blood pressure with mild orthostasis shows the blockade is adequate.

A β-blocker is never started first. Blocking β receptors before α leaves circulating catecholamines acting unopposed at α receptors — a hypertensive crisis, with a sharp rise in afterload and myocardial oxygen demand. Once α-blockade is established, esmolol or metoprolol may be titrated for heart rate. Labetalol is not preferred: intravenously its α:β ratio is about 1:7, a preference for β that risks unopposed α stimulation.

Metyrosine works one step earlier. It inhibits tyrosine hydroxylase, which converts tyrosine to DOPA — the first and rate-limiting step of catecholamine synthesis — and in pheochromocytoma it has cut catecholamine biosynthesis by about 35% to 80%. The biochemical effect peaks in 2 to 3 days and wears off 3 to 4 days after stopping. It is an adjunct, notably for malignant or unresectable tumors, and does not remove the danger of hypertensive crises during tumor manipulation.

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Three places to intervene in pheochromocytoma — and the order that matters.

Comparing the drugs

Receptor profile and use

Drug	Target	Binding	Main use
Phentolamine	α1 + α2 (nonselective)	Reversible; short-acting	Pheochromocytoma hypertensive episodes; norepinephrine extravasation
Phenoxybenzamine	α1 + α2 (nonselective)	Irreversible (covalent); long-acting	Preoperative pheochromocytoma
Tamsulosin	α1, selective for the prostate (≈ 70% of prostatic α1 are α1A)	—	BPH (not for hypertension)
Alfuzosin	Selective post-synaptic α1 (prostate, bladder base and neck)	—	BPH (not for hypertension)
Silodosin	α1, high affinity for α1A	—	BPH (not for hypertension)
Metyrosine	No receptor — tyrosine hydroxylase	Enzyme inhibition	Pheochromocytoma (adjunct; malignant or unresectable)

— = binding mode not stated in the listed sources.

Pharmacokinetics at a glance

Drug	Absorption	Elimination	Half-life
Phentolamine	IV or IM	About 13% unchanged in urine (IV)	About 19 min (IV)
Phenoxybenzamine	20–30% of an oral dose absorbed in active form	Liver; 10% unchanged in urine	About 24 h (IV); effects 3–4 days
Tamsulosin	Over 90% (fasting); food lowers exposure	CYP3A4 and CYP2D6; under 10% unchanged in urine	Apparent 9–13 h (14–15 h in patients)
Alfuzosin	49% (fed); 50% lower fasting	CYP3A4; 11% unchanged in urine; inactive metabolites	About 10 h
Silodosin	About 32%	Glucuronidation (UGT2B7), alcohol/aldehyde dehydrogenase, CYP3A4; P-gp substrate	About 13 h (active glucuronide about 24 h)
Metyrosine	Well absorbed	53–88% unchanged in urine	3–3.7 h

Label values. The uroselective agents are highly protein-bound (tamsulosin 94–99%, silodosin about 97%, alfuzosin 82–90%).

Pharmacokinetics

CYP3A4 — the shared liability — tamsulosin, alfuzosin, silodosin: All three are metabolized by CYP3A4. Ketoconazole raised tamsulosin AUC 2.8-fold and silodosin exposure 3.2-fold, which is why strong CYP3A4 inhibitors are contraindicated with alfuzosin and silodosin and are not combined with tamsulosin. The moderate inhibitor diltiazem raised alfuzosin AUC about 1.3-fold.
Food — tamsulosin, alfuzosin: Tamsulosin taken fasting gives about 30% more AUC and 40–70% higher peaks than after food, which is why it is taken after the same meal each day; alfuzosin absorption is 50% lower fasting, so it is taken with food.
Glucuronidation and P-gp — silodosin: Its main metabolite, the glucuronide KMD-3213G formed by UGT2B7, is active in vitro, has a half-life of about 24 hours and reaches about four times the parent’s exposure. Silodosin is a P-gp substrate, so strong P-gp inhibitors (e.g. cyclosporine) are not recommended, and UGT2B7 inhibitors (probenecid, valproic acid, fluconazole) may raise exposure.
Kidney and liver — silodosin, alfuzosin: In moderate renal impairment, total silodosin AUC was 3.2-fold higher and its half-life doubled. Alfuzosin is extensively metabolized by the liver, with only 11% excreted unchanged, and is contraindicated in moderate or severe hepatic impairment.
Age — tamsulosin: Intrinsic clearance falls with age, giving about 40% higher tamsulosin exposure in older men.
Duration of blockade — phenoxybenzamine, phentolamine: Phenoxybenzamine’s irreversible blockade outlasts the drug: effects persist 3–4 days after an IV dose and build up over about a week of daily dosing. Phentolamine’s half-life in blood is about 19 minutes, so its block is short.
Renal excretion and the urine test — metyrosine: Metyrosine is excreted largely unchanged in urine (53–88%), where it can crystallize; less than 1% appears as catechol metabolites, but these are enough to interfere with routine urinary catecholamine assays.

Pharmacogenomics

CYP2D6 tamsulosin

Paroxetine, a strong CYP2D6 inhibitor, raised tamsulosin AUC 1.6-fold, and a similar increase is expected in CYP2D6 poor metabolizers (about 7% of Caucasians and 2% of African Americans). Because poor metabolizers cannot be readily identified, and adding a strong CYP3A4 inhibitor could raise exposure much further, tamsulosin is not used with strong CYP3A4 inhibitors; the label also advises caution in known poor metabolizers. The FDA Table of Pharmacogenomic Biomarkers lists CYP2D6 for tamsulosin.

Uses & drug choice

Phentolamine to prevent or control hypertensive episodes in pheochromocytoma before and during surgery, and for the phentolamine blocking test
Phentolamine injected locally to prevent or treat dermal necrosis and sloughing after norepinephrine extravasation
Phenoxybenzamine to control episodes of hypertension and sweating in pheochromocytoma
Metyrosine in pheochromocytoma to prepare for surgery, when surgery is contraindicated, and for chronic treatment of malignant pheochromocytoma
Tamsulosin, alfuzosin and silodosin for the signs and symptoms of benign prostatic hyperplasia, not for hypertension
Phentolamine as OraVerse to reverse lip and tongue anesthesia after a dental injection, and as Ryzumvi eye drops to reverse drug-induced pupil dilation

Preparing a patient with pheochromocytoma for surgery → Phenoxybenzamine started 10–14 days before surgery (selective α1 blockers are alternatives)

It is long-acting and irreversible, giving steady blockade while volume is restored. Prazosin, terazosin or doxazosin may also be used and cause less reflex tachycardia, because α2 inhibition is left intact.

A hypertensive surge during pheochromocytoma surgery, or norepinephrine extravasation → Phentolamine

It is a reversible, short-acting α-blocker given IV or IM to prevent or control hypertensive episodes during preparation and excision, and infiltrated locally to prevent or treat dermal necrosis after norepinephrine extravasation.

Tachycardia in pheochromocytoma → Add a β-blocker (e.g. esmolol, metoprolol) only after α-blockade — not labetalol

β-blockade first leaves α stimulation unopposed and can cause a hypertensive crisis. Labetalol’s IV α:β ratio of about 1:7 favors β blockade and can worsen hypertension.

Malignant or unresectable pheochromocytoma → Metyrosine (adjunct)

It inhibits tyrosine hydroxylase, the rate-limiting enzyme of catecholamine synthesis, so the tumor makes less catecholamine — useful where removing the tumor is not possible.

Symptomatic BPH → A uroselective α1-blocker — tamsulosin, alfuzosin or silodosin

They relax the dynamic (smooth-muscle) component of outlet obstruction within days and have relatively minimal orthostatic effects, so they are first-line for BPH; prazosin, doxazosin and terazosin work but are not preferred because of their adverse effects. Rule out prostate cancer first.

A man due for cataract surgery who needs BPH treatment → Do not start tamsulosin before the surgery; tell the ophthalmologist about any α1-blocker

Floppy iris syndrome is most often linked to tamsulosin, can occur even after the drug is stopped, and starting tamsulosin when cataract or glaucoma surgery is scheduled is not recommended.

Adverse effects

Common

Orthostatic hypotension, dizziness, nasal congestion, headache, tachycardia (nonselective agents), abnormal or retrograde ejaculation, fatigue.

Serious — orthostatic hypotension and syncope

Postural hypotension with dizziness, and possible syncope — especially when starting, and in older patients.

Serious — myocardial infarction, cerebrovascular spasm (phentolamine)

Myocardial infarction, cerebrovascular spasm and occlusion have followed phentolamine, usually with marked hypotension; tachycardia and arrhythmias also occur.

Serious — priapism (tamsulosin, alfuzosin)

Rarely, a persistent painful erection unrelated to sexual activity.

Intraoperative floppy iris syndrome (tamsulosin, alfuzosin, silodosin)

During cataract surgery the iris may billow and prolapse and the pupil constrict despite dilating drops — even in patients who stopped the drug weeks to months earlier.

Serious — angina, QT prolongation (alfuzosin)

Stop alfuzosin if angina appears or worsens; use caution with QT prolongation or QT-prolonging drugs.

Metyrosine · sedation, extrapyramidal signs, crystalluria

Moderate to severe sedation in almost all patients; drooling, speech difficulty and tremor in about 10%; diarrhea; crystals in the urine.

Phenoxybenzamine · carcinoma reports with long-term use

Cases of carcinoma have been reported after long-term treatment, so long-term use is not recommended.

Orthostatic and first-dose hypotension, syncope, falls: Blocking arterial α1 receptors relaxes vascular smooth muscle, and venous capacitance vessels relax too, so pressure falls most on standing and with the first doses; older patients are most affected.
Tachycardia and tremulousness (nonselective agents): α2 blockade removes the brake on norepinephrine release, and the spillover stimulates β receptors; the fall in vascular tone also triggers a baroreceptor-mediated reflex tachycardia. Selective α1 blockers leave α2 intact and cause less of it.
Nasal congestion, miosis, inhibited or retrograde ejaculation: These are evidence of adrenergic blockade and vary with its degree: blocking α1 on the iris dilator lets the pupil narrow, and α-blockers decrease semen volume and inhibit seminal emission.
Myocardial infarction and cerebrovascular events (phentolamine): They have usually occurred in association with marked hypotensive episodes.
Intraoperative floppy iris syndrome: Pupil dilation relies on α1 receptors of the iris dilator muscle; long-term α-blockade may cause dysfunction or atrophy of that muscle, so the iris fails to dilate, billows and prolapses during cataract surgery — sometimes long after the drug is stopped.
Metyrosine sedation and extrapyramidal signs; crystalluria: Metyrosine lowers catecholamine synthesis; the label notes that this inhibition can be expected to potentiate the extrapyramidal effects of phenothiazines and haloperidol. Crystalluria follows from its renal excretion: most of a dose leaves unchanged in urine, where it can crystallize as needles or rods.

Toxicity & antidote

Overdose is the blockade taken too far: postural hypotension with dizziness or fainting, tachycardia, vomiting, lethargy and shock with phenoxybenzamine; arrhythmias, tachycardia, hypotension and possibly shock with phentolamine. There is no specific antidote.

Epinephrine is contraindicated. It stimulates both α and β receptors; with α receptors blocked, the net effect is vasodilation and blood pressure falls further (“epinephrine reversal”). Usual pressors are not effective against phenoxybenzamine’s irreversible block, but levarterenol, which stimulates mainly α receptors, can overcome it in sufficient dose. Patients are kept supine (after phenoxybenzamine, possibly for 24 hours or more), given fluids, and vasopressors as a last resort.

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With α receptors blocked, epinephrine’s net effect is vasodilation.

Interactions

Phenoxybenzamine or phentolamine + epinephrine

With α receptors blocked, epinephrine’s β effects dominate — an exaggerated fall in blood pressure and tachycardia (“epinephrine reversal”). Epinephrine is not used to treat their hypotension.

Tamsulosin, alfuzosin or silodosin + strong CYP3A4 inhibitors (ketoconazole, itraconazole, ritonavir, clarithromycin)

Raise their blood levels — contraindicated with alfuzosin and silodosin, and not to be combined with tamsulosin; tamsulosin also needs caution with CYP2D6 inhibitors (e.g. paroxetine) and in CYP2D6 poor metabolizers.

Tamsulosin, alfuzosin or silodosin + PDE5 inhibitors, antihypertensives or nitrates

Both are vasodilators — risk of symptomatic hypotension; use with caution.

Tamsulosin, alfuzosin or silodosin + another α-blocker

Should not be combined — additive α-blockade.

Tamsulosin + warfarin

The label advises caution with the combination.

Metyrosine + alcohol or other CNS depressants

Additive sedation.

Metyrosine + phenothiazines or haloperidol

Their extrapyramidal effects can be potentiated by the inhibition of catecholamine synthesis.

Phentolamine + cardiac glycosides

Tachycardia and arrhythmias can occur with phentolamine; when possible, cardiac glycosides are deferred until the rhythm returns to normal.

Contraindications

Phentolamine injection with myocardial infarction (current or past), coronary insufficiency, angina or other evidence of coronary artery disease — Labeled contraindication — phentolamine-associated hypotension has been followed by myocardial infarction.
Phenoxybenzamine where a fall in blood pressure may be undesirable — Labeled contraindication — its long-lasting α-blockade lowers both supine and erect blood pressure.
Alfuzosin with moderate or severe hepatic impairment (Child-Pugh B or C), or with potent CYP3A4 inhibitors (ketoconazole, itraconazole, ritonavir) — Labeled contraindications — alfuzosin blood levels are increased.
Silodosin with severe renal impairment (CrCl < 30 mL/min), severe hepatic impairment (Child-Pugh ≥ 10), or strong CYP3A4 inhibitors — Labeled contraindications — ketoconazole raised silodosin exposure about 3-fold, and moderate renal impairment alone tripled its levels.
Tamsulosin with strong CYP3A4 inhibitors (e.g. ketoconazole); serious sulfa allergy use caution — The label says not to combine it with strong CYP3A4 inhibitors and advises caution in serious sulfa allergy — warnings, not listed contraindications.
Phenoxybenzamine or phentolamine with marked cerebral arteriosclerosis, renal damage, or a respiratory infection; phenoxybenzamine with marked coronary arteriosclerosis (for phentolamine injection, coronary artery disease is a listed contraindication) use caution — Cautions on the phenoxybenzamine label and in StatPearls for the nonselective agents; adrenergic blockade may also aggravate the symptoms of a respiratory infection.
Phenoxybenzamine or phentolamine while breastfeeding use caution — StatPearls calls breastfeeding a contraindication for both; their labels ask for a decision between stopping nursing and stopping the drug, without listing it as a contraindication.

High-yield

Irreversible, covalent, nonselective α-blocker given for 10–14 days before pheochromocytoma surgery Phenoxybenzamine

Reversible, short-acting IV α-blocker; norepinephrine extravasation Phentolamine

Inhibits tyrosine hydroxylase, the rate-limiting step of catecholamine synthesis Metyrosine

Billowing iris and progressive miosis during cataract surgery in a man on BPH treatment Floppy iris syndrome — tamsulosin most often

Blood pressure falls further when epinephrine is given to an α-blocked patient Epinephrine reversal (net vasodilation once α is blocked)

α1 receptor second messenger Gq → phospholipase C → IP3 + DAG → ↑ Ca²⁺

α2 receptor second messenger and role on the nerve ending Gi → ↓ cAMP; inhibits norepinephrine release

Subtype making up about 70% of prostatic α1 receptors α1A

Most common side effect is an orgasm with reduced or no semen Silodosin (retrograde ejaculation)

α-blocker contraindicated in moderate or severe hepatic impairment and with potent CYP3A4 inhibitors Alfuzosin

A before B, like the alphabet

A — α-blockade first (phenoxybenzamine for 10–14 days) in pheochromocytoma
B — β-blocker only after α-blockade is established; β first leaves α unopposed → hypertensive crisis

Labetalol does not shortcut the rule: intravenously it blocks β about seven times more than α.

Phenoxy-BENZ-amine BONDS

BONDS — binds covalently (irreversibly) to the α receptor
So its effects last for days and build up over about a week of dosing

Phentolamine is the reversible, short-acting counterpart.

Practice questions

Q1A 42-year-old woman with episodic headaches, sweating and palpitations has a pheochromocytoma on imaging. Before adrenalectomy she is given an oral drug for two weeks; her blood pressure normalizes with mild orthostasis, and the effect lasts for days after the last dose.

The drug’s prolonged action is best explained by:

A.Inhibition of tyrosine hydroxylase
B.Competitive, reversible blockade of α1 receptors only
C.An active metabolite with a long half-life
D.Covalent, irreversible binding to α1 and α2 receptors
E.Blockade of β1 receptors in the heart

Show answer

D. Covalent, irreversible binding to α1 and α2 receptors — Phenoxybenzamine is a nonselective, irreversible α-blocker that bonds covalently to the receptor, most likely at a cysteine residue. Its effects persist for 3 to 4 days after an IV dose and build up over about a week. Tyrosine hydroxylase inhibition is metyrosine; reversible blockade is phentolamine; β-blockade would be dangerous before α-blockade.

Q2A 50-year-old man with pheochromocytoma is started on propranolol for palpitations before any other drug. Within an hour his blood pressure rises to 240/130 mm Hg.

Which mechanism explains the hypertensive crisis?

A.Unopposed catecholamine stimulation of α receptors after β blockade
B.Direct α1 agonism by propranolol
C.Inhibition of norepinephrine reuptake
D.Release of catecholamines by propranolol from the tumor
E.Blockade of α2 receptors on nerve endings

Show answer

A. Unopposed catecholamine stimulation of α receptors after β blockade — A β-blocker should never be started before α-blockade: with β receptors blocked, circulating catecholamines act unopposed on α receptors and can precipitate a hypertensive crisis, raising afterload and myocardial oxygen demand. Once α-blockade is established, a β-blocker such as esmolol or metoprolol may be titrated for heart rate. Propranolol itself is a nonselective β-blocker with no other autonomic nervous system activity: it does not stimulate or block α receptors, or alter catecholamine reuptake or release — the catecholamines come from the tumor.

Q3A 68-year-old man takes tamsulosin for BPH. During cataract surgery the iris billows with the irrigation currents and the pupil keeps constricting despite dilating drops.

Which receptor action best explains this complication?

A.Muscarinic blockade of the iris sphincter
B.α1 blockade affecting the iris dilator muscle
C.α2 blockade at the ciliary body
D.Nicotinic blockade at the extraocular muscles
E.β2 blockade of ciliary epithelium

Show answer

B. α1 blockade affecting the iris dilator muscle — The radial iris dilator is activated by α1 receptors; long-term α1 blockade may cause dysfunction or atrophy of that muscle, so the pupil cannot dilate adequately and the iris billows and prolapses — intraoperative floppy iris syndrome. It is most commonly associated with tamsulosin and can occur even after the drug has been stopped. Tamsulosin is an α1-adrenoceptor blocker selective for prostatic α1 receptors, so the complication comes from α1 blockade of the dilator, not from muscarinic, nicotinic, α2 or β2 effects.

Q4A patient on phenoxybenzamine becomes severely hypotensive. A colleague proposes an epinephrine infusion.

What is expected if epinephrine is given?

A.Pressure rises promptly through α1 receptors
B.No effect, because all adrenergic receptors are blocked
C.Pressure falls further because its β effects are unopposed and the net effect is vasodilation
D.Bradycardia through α2 stimulation
E.Pressure rises, but only after 3–4 days

Show answer

C. Pressure falls further because its β effects are unopposed and the net effect is vasodilation — Epinephrine stimulates both α and β receptors. With α receptors blocked by phenoxybenzamine, the net effect is vasodilation and a further drop in blood pressure — epinephrine reversal — so epinephrine is contraindicated. Levarterenol, which stimulates mainly α receptors, can overcome the block in sufficient dose.

Q5A 66-year-old man with BPH takes tamsulosin. He is found to be a CYP2D6 poor metabolizer and is about to start ketoconazole for a fungal infection.

Why is this combination a concern?

A.Ketoconazole blocks tamsulosin’s binding to α1A receptors
B.Ketoconazole raises urinary excretion of unchanged tamsulosin
C.Tamsulosin induces CYP3A4 and lowers ketoconazole levels
D.Tamsulosin is cleared mainly by glucuronidation, which ketoconazole blocks
E.With CYP2D6 already deficient, inhibiting CYP3A4 removes the other main route and tamsulosin exposure can rise substantially

Show answer

E. With CYP2D6 already deficient, inhibiting CYP3A4 removes the other main route and tamsulosin exposure can rise substantially — Tamsulosin is extensively metabolized, mainly by CYP3A4 and CYP2D6. Ketoconazole raised tamsulosin AUC 2.8-fold, and CYP2D6 poor metabolizers already have higher exposure; because poor metabolizers cannot be readily identified and the combination could raise exposure substantially, tamsulosin is not used with strong CYP3A4 inhibitors.

More in the Autonomics question bank →

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Educational summary for medical students. Always verify against current prescribing information and guidelines. Not medical advice.