Direct acting sympathomimetics – Dopamine MCQs With Answer

Direct acting sympathomimetics – Dopamine MCQs With Answer offer B. Pharm students a focused review of dopamine’s pharmacology, receptor selectivity, dose-dependent cardiovascular and renal effects, metabolism (MAO/COMT), transporters (DAT), and clinical applications in shock and heart failure. This concise, exam-oriented introduction emphasizes mechanism of action at D1/D2, beta and alpha receptors, pharmacokinetics, adverse effects, drug interactions (MAOIs, tricyclics), and monitoring parameters. Questions are tailored to strengthen understanding of molecular signaling (cAMP), therapeutic dosing, and comparisons with selective D1 agonists like fenoldopam. The MCQs below will deepen conceptual and applied knowledge for B. Pharm exam preparation. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. What is the predominant effect of low-dose intravenous dopamine (0.5–2 µg/kg/min) on renal vasculature?

• Dilation via D1 receptor-mediated increase in cAMP
• Constriction via alpha1 receptor activation
• Increased contractility via beta1 receptor activation
• Vasodilation via nitric oxide release

Correct Answer: Dilation via D1 receptor-mediated increase in cAMP

Q2. Which receptor subtype is primarily responsible for dopamine’s presynaptic inhibition of norepinephrine release?

• D1 receptor on vascular smooth muscle
• D2 receptor on sympathetic nerve terminals
• Beta2 receptor on skeletal muscle
• Alpha2 receptor on presynaptic terminals

Correct Answer: D2 receptor on sympathetic nerve terminals

Q3. Dopamine’s dose-dependent effects include beta1 stimulation at intermediate doses. Which clinical effect corresponds to beta1 activation?

• Increased renal blood flow
• Increased heart rate and contractility
• Systemic vasoconstriction and increased afterload
• Bronchodilation

Correct Answer: Increased heart rate and contractility

Q4. Which enzymes are primarily responsible for dopamine metabolism when administered intravenously?

• CYP3A4 and CYP2D6
• Monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)
• Aldehyde dehydrogenase and alcohol dehydrogenase
• Acetylcholinesterase and butyrylcholinesterase

Correct Answer: Monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)

Q5. Which statement best describes dopamine’s ability to cross the blood-brain barrier (BBB)?

• Dopamine freely crosses the BBB via passive diffusion
• Dopamine requires active transport across the BBB and crosses readily
• Dopamine does not cross the BBB effectively; L-DOPA is used for CNS delivery
• Dopamine crosses the BBB only at high infusion rates

Correct Answer: Dopamine does not cross the BBB effectively; L-DOPA is used for CNS delivery

Q6. Fenoldopam is often compared to dopamine. What is the primary pharmacologic distinction of fenoldopam?

• Nonselective adrenergic agonist affecting alpha and beta receptors
• Selective D1 receptor agonist causing arterial vasodilation
• Selective D2 antagonist used for antipsychotic effects
• MAO inhibitor that increases endogenous dopamine

Correct Answer: Selective D1 receptor agonist causing arterial vasodilation

Q7. At high doses (>10 µg/kg/min), which effect predominates with dopamine infusion?

• Renal vasodilation via D1 receptors
• Beta2-mediated bronchodilation
• Alpha1-mediated vasoconstriction increasing systemic vascular resistance
• Pure D2-mediated decrease in norepinephrine release

Correct Answer: Alpha1-mediated vasoconstriction increasing systemic vascular resistance

Q8. Which transporter is primarily responsible for dopamine reuptake into presynaptic neurons?

• SERT (serotonin transporter)
• DAT (dopamine transporter)
• NET (norepinephrine transporter)
• OATP (organic anion transporting polypeptide)

Correct Answer: DAT (dopamine transporter)

Q9. Dopamine stimulates renin release. Which receptor mediates this effect?

• Renal D1 receptor causing increased renin secretion
• Beta1 receptor on juxtaglomerular cells increasing renin release
• Alpha2 receptor inhibiting renin secretion
• D2 receptor decreasing renin release

Correct Answer: Beta1 receptor on juxtaglomerular cells increasing renin release

Q10. Which adverse effect is most commonly associated with dopamine infusion in critically ill patients?

• Severe hypoglycemia
• Arrhythmias and tachycardia
• Prolonged QT interval due to potassium channels
• Profound bronchospasm

Correct Answer: Arrhythmias and tachycardia

Q11. Which pharmacokinetic property of dopamine necessitates continuous IV infusion rather than bolus dosing?

• Highly protein bound with long half-life
• Very short plasma half-life (about 1–2 minutes) due to rapid metabolism
• Large volume of distribution requiring loading dose
• Oral bioavailability close to zero because of gut absorption

Correct Answer: Very short plasma half-life (about 1–2 minutes) due to rapid metabolism

Q12. In comparison to dobutamine, dopamine’s unique advantage at low doses is primarily:

• Greater beta1 selectivity improving inotropy without chronotropy
• Renal vasodilation via D1 receptors increasing urine output
• Oral administration for chronic outpatient use
• Longer half-life allowing intermittent bolus dosing

Correct Answer: Renal vasodilation via D1 receptors increasing urine output

Q13. Which clinical scenario is a traditional indication for dopamine infusion?

• Chronic management of hypertension in outpatient setting
• Acute cardiogenic shock with low cardiac output and renal hypoperfusion
• Mild asthma exacerbation requiring bronchodilation
• Parkinson’s disease as primary therapy

Correct Answer: Acute cardiogenic shock with low cardiac output and renal hypoperfusion

Q14. Dopamine’s action on vascular D1 receptors involves which intracellular signaling pathway?

• Activation of phospholipase C and increased IP3/DAG
• Gs protein activation leading to increased cAMP
• Gi protein activation decreasing cAMP
• Activation of tyrosine kinase receptors

Correct Answer: Gs protein activation leading to increased cAMP

Q15. Which drug interaction increases the risk of exaggerated hypertensive response when given with dopamine?

• Concurrent MAO inhibitor therapy
• Concurrent ACE inhibitor therapy
• Concurrent beta-blocker therapy
• Concurrent diuretic therapy

Correct Answer: Concurrent MAO inhibitor therapy

Q16. Which laboratory parameter would most directly reflect improved renal perfusion after low-dose dopamine?

• Decrease in serum creatinine and increased urine output
• Decrease in serum sodium concentration
• Increase in blood urea nitrogen without urine change
• Drop in serum potassium due to intracellular shift

Correct Answer: Decrease in serum creatinine and increased urine output

Q17. Dopamine’s effect on systemic vascular resistance (SVR) is dose-dependent. What happens to SVR at intermediate doses?

• Marked decrease due to predominant D1 activation
• Increase due to beta1-mediated vasoconstriction
• Variable effect; may stay near baseline due to mixed beta1 and mild alpha1 effects
• Profound increase due to strong alpha1 stimulation

Correct Answer: Variable effect; may stay near baseline due to mixed beta1 and mild alpha1 effects

Q18. Which statement about dopamine receptors is correct?

• D1-like receptors (D1, D5) are Gi-coupled and reduce cAMP
• D2-like receptors (D2, D3, D4) are Gs-coupled and increase cAMP
• D1-like receptors are Gs-coupled and increase cAMP; D2-like receptors are Gi-coupled and inhibit cAMP
• All dopamine receptors are ion channels mediating fast synaptic responses

Correct Answer: D1-like receptors are Gs-coupled and increase cAMP; D2-like receptors are Gi-coupled and inhibit cAMP

Q19. Which clinical monitoring is most critical during dopamine infusion?

• Blood pressure, heart rate, and urine output
• Liver enzymes every hour
• Serum magnesium concentration continuously
• Pulmonary function tests daily

Correct Answer: Blood pressure, heart rate, and urine output

Q20. Which structural precursor is converted into dopamine in catecholamine biosynthesis?

• Tryptophan
• Tyrosine → L-DOPA
• Histidine
• Phenylalanine → Serotonin

Correct Answer: Tyrosine → L-DOPA

Q21. Which statement regarding dopamine and heart rate is true?

• Low-dose dopamine consistently reduces heart rate via vagal stimulation
• Intermediate doses increase heart rate due to beta1 stimulation and reflex mechanisms
• High-dose dopamine always reduces heart rate due to baroreceptor activation
• Dopamine has no effect on heart rate at any dose

Correct Answer: Intermediate doses increase heart rate due to beta1 stimulation and reflex mechanisms

Q22. Which of the following is a contraindication to using dopamine?

• Hypotension from septic shock needing vasopressors
• Pheochromocytoma due to risk of excessive vasoconstriction
• Bradycardia with low cardiac output
• Acute renal failure where renal perfusion is desired

Correct Answer: Pheochromocytoma due to risk of excessive vasoconstriction

Q23. Which effect distinguishes D2 receptor activation from D1 activation?

• D2 activation increases cAMP in vascular smooth muscle
• D2 activation leads to inhibition of neurotransmitter release via Gi coupling
• D2 activation causes potent arterial vasodilation via Gs
• D2 activation increases intracellular Ca2+ through IP3

Correct Answer: D2 activation leads to inhibition of neurotransmitter release via Gi coupling

Q24. A patient on MAOI therapy receives dopamine. What is the expected interaction?

• MAOIs have no effect on exogenous catecholamines
• Enhanced and prolonged pressor response with risk of hypertensive crisis
• Complete antagonism of dopamine’s effects
• Conversion of dopamine into inactive metabolites more rapidly

Correct Answer: Enhanced and prolonged pressor response with risk of hypertensive crisis

Q25. Which formulation and route are appropriate for clinical dopamine administration?

• Oral tablets for chronic outpatient use
• Continuous intravenous infusion due to rapid metabolism
• Intramuscular injection for emergency bolus dosing
• Transdermal patch for gradual release

Correct Answer: Continuous intravenous infusion due to rapid metabolism

Q26. Which lab change could indicate dopamine-induced tissue ischemia from excessive vasoconstriction?

• Rising lactate and worsening metabolic acidosis
• Decreasing creatine kinase levels
• Hypoglycemia without other signs
• Lowered white blood cell count

Correct Answer: Rising lactate and worsening metabolic acidosis

Q27. Dopamine’s action on D1 receptors in the kidney primarily affects which part of renal microcirculation?

• Constriction of efferent arterioles only
• Dilation of renal afferent arterioles and increased renal blood flow
• Constriction of renal veins causing congestion
• No effect on renal microcirculation

Correct Answer: Dilation of renal afferent arterioles and increased renal blood flow

Q28. Which statement about dopamine and oxygen demand is correct?

• Dopamine decreases myocardial oxygen demand in all doses
• Beta1 stimulation by dopamine increases myocardial oxygen consumption
• D1 activation increases myocardial oxygen consumption more than beta1
• Dopamine has no effect on myocardial oxygen consumption

Correct Answer: Beta1 stimulation by dopamine increases myocardial oxygen consumption

Q29. When comparing dopamine to norepinephrine, which is true regarding receptor activity?

• Dopamine has the same pure alpha1 agonist profile as norepinephrine
• Norepinephrine has greater alpha1-mediated vasoconstriction and less renal D1 activity than dopamine
• Norepinephrine selectively activates D1 receptors more than dopamine
• Dopamine and norepinephrine have identical effects at all doses

Correct Answer: Norepinephrine has greater alpha1-mediated vasoconstriction and less renal D1 activity than dopamine

Q30. Which adverse metabolic effect can dopamine produce at therapeutic doses?

• Hyperkalemia due to cellular potassium release
• Hyperglycemia due to glycogenolysis and beta-adrenergic effects
• Severe hyponatremia from antidiuretic hormone release
• Marked hypocalcemia due to chelation

Correct Answer: Hyperglycemia due to glycogenolysis and beta-adrenergic effects

Q31. Which receptor-mediated mechanism explains dopamine-induced increase in cardiac output?

• D1-mediated chronotropy via direct sinoatrial stimulation
• Beta1-mediated positive inotropy and chronotropy
• D2-mediated myocardial relaxation
• Alpha2-mediated increase in vagal tone

Correct Answer: Beta1-mediated positive inotropy and chronotropy

Q32. In drug preparation, dopamine solutions are often protected from light. Why?

• Dopamine is light-stable and requires no special handling
• Dopamine is photosensitive and can degrade when exposed to light
• Light exposure increases potency and should be promoted
• Light causes dopamine to polymerize into active metabolites

Correct Answer: Dopamine is photosensitive and can degrade when exposed to light

Q33. Which monitoring parameter helps detect early tachyarrhythmia during dopamine therapy?

• Continuous ECG monitoring
• Daily chest X-ray
• Serum troponin every 12 hours
• Pulmonary function testing hourly

Correct Answer: Continuous ECG monitoring

Q34. Which statement reflects dopamine’s interaction with beta-blockers?

• Beta-blockers enhance dopamine’s renal vasodilatory effect
• Beta-blockers may blunt dopamine’s beta1-mediated inotropic effects, unmasking alpha effects at higher doses
• Beta-blockers convert dopamine into norepinephrine
• Beta-blockers have no influence on dopamine pharmacodynamics

Correct Answer: Beta-blockers may blunt dopamine’s beta1-mediated inotropic effects, unmasking alpha effects at higher doses

Q35. Which condition would most likely reduce dopamine’s effectiveness due to receptor downregulation?

• Short-term single low-dose infusion
• Prolonged continuous high-dose catecholamine therapy causing receptor desensitization
• Concurrent fenoldopam infusion
• Administration of dopamine only at night

Correct Answer: Prolonged continuous high-dose catecholamine therapy causing receptor desensitization

Q36. Which pharmacologic agent is a selective D1 receptor agonist used for hypertensive emergencies with renal protection?

• Fenoldopam
• Dobutamine
• Clonidine
• Methylphenidate

Correct Answer: Fenoldopam

Q37. In the setting of septic shock, why has dopamine fallen out of favor compared to norepinephrine?

• Dopamine causes less tachycardia than norepinephrine
• Dopamine is associated with higher arrhythmia risk and inconsistent benefit in mortality
• Dopamine is more effective at reversing sepsis-related hypotension
• Dopamine is an oral agent unsuitable for ICU use

Correct Answer: Dopamine is associated with higher arrhythmia risk and inconsistent benefit in mortality

Q38. Which pharmacodynamic property explains dopamine’s short onset and offset of action?

• High lipid solubility leading to slow equilibration
• Rapid enzymatic degradation by MAO and COMT in plasma and tissues
• Extensive enterohepatic recycling prolonging action
• Depot storage in adipose tissue releasing drug slowly

Correct Answer: Rapid enzymatic degradation by MAO and COMT in plasma and tissues

Q39. Which hemodynamic effect would indicate that a patient has moved from low-dose to higher-dose dopamine infusion?

• Increased urine output without heart rate change
• Onset of systemic vasoconstriction and rising blood pressure with potential tachycardia
• Profound bradycardia with hypotension
• Persistent vasodilation and decreased systemic vascular resistance

Correct Answer: Onset of systemic vasoconstriction and rising blood pressure with potential tachycardia

Q40. Which receptor family does D1 belong to and what is its primary second messenger?

• D1 is ionotropic and uses IP3 as second messenger
• D1 is a G-protein-coupled receptor (Gs) that increases cAMP
• D1 is a tyrosine kinase receptor that increases MAPK only
• D1 is Gi-coupled and decreases cAMP

Correct Answer: D1 is a G-protein-coupled receptor (Gs) that increases cAMP

Q41. Which clinical sign would most suggest excessive alpha1 stimulation from high-dose dopamine?

• Profuse sweating and miosis
• Cool, pale extremities with diminished peripheral pulses
• Flushed warm extremities and hypotension
• Sustained hypoglycemia unresponsive to glucose

Correct Answer: Cool, pale extremities with diminished peripheral pulses

Q42. Dopamine’s D2 receptor activation in the CNS influences which function relevant to pharmacology students?

• Peripheral vasoconstriction exclusively
• Modulation of neurotransmitter release and motor control
• Direct stimulation of skeletal muscle contraction
• Inhibition of gastric acid secretion only

Correct Answer: Modulation of neurotransmitter release and motor control

Q43. Which statement about synthetic modifications of dopamine to produce longer-acting agents is true?

• Adding an extra hydroxyl group prevents COMT metabolism completely
• Structural changes can increase receptor selectivity and resistance to MAO/COMT metabolism
• All dopamine analogs are less selective and shorter acting
• Modification always increases central nervous system penetration

Correct Answer: Structural changes can increase receptor selectivity and resistance to MAO/COMT metabolism

Q44. What effect does dopamine have on pulmonary vascular resistance at therapeutic doses?

• Marked increase due to alpha1 activity at low doses
• Variable; beta1 effect may increase cardiac output but pulmonary effects depend on dose
• Exclusive pulmonary vasodilation mediated by D1 receptors in the lung
• Complete blockage of pulmonary vasoconstriction irrespective of dose

Correct Answer: Variable; beta1 effect may increase cardiac output but pulmonary effects depend on dose

Q45. In a patient with acute renal failure, what is the current evidence-based view on using low-dose dopamine for renal protection?

• Strong evidence supports routine use to prevent or treat ARF
• Routine low-dose dopamine is not recommended for renal protection due to lack of benefit
• It is the first-line therapy for all renal impairment cases
• It should be used in all ICU patients prophylactically

Correct Answer: Routine low-dose dopamine is not recommended for renal protection due to lack of benefit

Q46. Which monitoring parameter is LEAST useful when titrating dopamine for hemodynamic support?

• Urine output
• Continuous invasive arterial blood pressure
• Electrocardiogram for arrhythmias
• Serum total cholesterol

Correct Answer: Serum total cholesterol

Q47. Which cellular effect is expected when dopamine activates D1 receptors on renal tubular cells?

• Inhibition of adenylate cyclase and decreased cAMP
• Activation of adenylate cyclase and increased cAMP leading to natriuresis
• Opening of voltage-gated sodium channels causing sodium retention
• Stimulation of aldosterone release directly from renal tubules

Correct Answer: Activation of adenylate cyclase and increased cAMP leading to natriuresis

Q48. Which patient factor would increase the risk of dopamine-induced tachyarrhythmias?

• Concurrent beta-blocker therapy
• Underlying ischemic heart disease and high-dose catecholamine exposure
• Renal impairment alone without cardiac disease
• Young healthy athlete on low-dose dopamine

Correct Answer: Underlying ischemic heart disease and high-dose catecholamine exposure

Q49. Which statement about peripheral vs central dopamine receptors is correct for therapeutic dopamine infusion?

• Infused dopamine primarily activates peripheral receptors because it poorly crosses the BBB
• IV dopamine mainly activates central receptors due to excellent CNS penetration
• Peripheral and central receptor activation are identical after infusion
• Dopamine selectively activates only central D2 receptors when given IV

Correct Answer: Infused dopamine primarily activates peripheral receptors because it poorly crosses the BBB

Q50. For exam-level pharmacology, which best summarizes why dopamine is classified as a direct-acting sympathomimetic?

• It increases catecholamine release indirectly by blocking reuptake
• It directly stimulates adrenergic and dopaminergic receptors to mimic sympathetic activity
• It acts only through enhancing endogenous serotonin
• It binds exclusively to muscarinic receptors producing parasympathetic effects

Correct Answer: It directly stimulates adrenergic and dopaminergic receptors to mimic sympathetic activity

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

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