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7# Adrenergic Ag & Antag
1. Activation of α1-adrenergic receptors produces which primary effect?
Vasoconstriction
Bronchodilation
Decreased insulin release
Lipolysis
Explanation:
α1 stimulation causes vasoconstriction, mydriasis, bladder sphincter contraction, and piloerection.
2. Which receptor activation leads to decreased sympathetic outflow centrally?
α1
β1
α2
β2
Explanation:
α2 receptors inhibit NE release presynaptically and reduce central sympathetic tone.
3. Phenylephrine causes mydriasis without cycloplegia because it:
Blocks muscarinic receptors
Stimulates α1 receptors in radial muscle
Stimulates β2 receptors
Paralyzes ciliary muscle
Explanation:
α1 stimulation contracts the radial muscle, dilating the pupil without affecting accommodation.
4. Sudden withdrawal of clonidine may cause:
Severe hypotension
Bradycardia
Respiratory depression
Rebound hypertension
Explanation:
Abrupt clonidine withdrawal removes α2 inhibition, causing sympathetic overactivity.
5. Dobutamine is most useful in:
Cardiogenic shock
Asthma
Anaphylaxis
Hypertension
Explanation:
Dobutamine is a β1 agonist that increases cardiac contractility and heart rate.
6. Tremor and hypokalemia are adverse effects of:
β1 agonists
α1 agonists
β2 agonists
α2 agonists
Explanation:
β2 agonists drive potassium into cells and stimulate skeletal muscle tremor.
7. Why can catecholamines NOT be taken orally?
Low receptor affinity
Rapid metabolism by MAO and COMT
High protein binding
Poor renal excretion
Explanation:
Catecholamines are rapidly inactivated by MAO and COMT enzymes.
8. Drug of choice for anaphylactic shock is:
Norepinephrine
Isoproterenol
Dopamine
Epinephrine
Explanation:
Epinephrine reverses hypotension (α1), bronchoconstriction (β2), and mast cell mediator release.
9. Low-dose dopamine primarily causes:
Renal vasodilation
Vasoconstriction
Bradycardia
Bronchoconstriction
Explanation:
Low-dose dopamine stimulates D1 receptors, improving renal and cerebral blood flow.
10. Which drug increases NE release from presynaptic terminals?
Cocaine
Propranolol
Amphetamine
Phenoxybenzamine
Explanation:
Amphetamine is an indirect sympathomimetic that enhances NE release.
11. Cocaine produces sympathomimetic effects mainly by:
Stimulating β receptors
Inhibiting NE and dopamine reuptake
Inhibiting MAO
Stimulating α2 receptors
Explanation:
Cocaine blocks reuptake transporters, increasing synaptic catecholamines.
12. Prazosin improves symptoms of BPH by:
Reducing prostate size
Blocking β receptors
Reducing testosterone
Relaxing bladder neck smooth muscle
Explanation:
α1 blockade relaxes smooth muscle in the prostate and bladder neck.
13. First-dose syncope is a known adverse effect of:
Prazosin
Metoprolol
Clonidine
Epinephrine
Explanation:
Sudden vasodilation from α1 blockade can cause postural hypotension and syncope.
14. Nonselective beta blockers are CONTRAINDICATED in:
Hypertension
Migraine
Asthma
Anxiety
Explanation:
β2 blockade can precipitate life-threatening bronchoconstriction.
15. Propranolol causes nightmares because it:
Stimulates α receptors
Crosses the blood–brain barrier
Blocks dopamine receptors
Activates serotonin receptors
Explanation:
High lipid solubility allows propranolol to penetrate the CNS.
16. Best beta blocker for pregnancy-induced hypertensive crisis is:
Propranolol
Metoprolol
Nebivolol
Labetalol
Explanation:
Labetalol blocks β and α1 receptors with minimal placental transfer.
17. Which beta blocker causes vasodilation via nitric oxide release?
Nebivolol
Atenolol
Propranolol
Sotalol
Explanation:
Nebivolol stimulates endothelial NO release in addition to β1 blockade.
18. Abrupt withdrawal of beta blockers may cause:
Hypotension
Bradycardia
Rebound angina and sudden death
Respiratory depression
Explanation:
Upregulation of β receptors leads to exaggerated sympathetic responses.
19. Beta blocker overdose with severe bradycardia is treated initially with:
Epinephrine
Atropine and glucagon
Calcium gluconate
Naloxone
Explanation:
Glucagon increases cAMP independently of β receptors; atropine treats bradycardia.
20. Beta blockers mask hypoglycemia in diabetics EXCEPT:
Tremor
Palpitations
Anxiety
Sweating
Explanation:
Sweating is mediated by muscarinic receptors and is NOT blocked by β blockers.