Direct acting sympathomimetics – Terbutaline MCQs With Answer

Direct acting sympathomimetics – Terbutaline MCQs With Answer

Terbutaline is a selective beta-2 adrenergic agonist widely covered in B. Pharm pharmacology for its bronchodilator and tocolytic properties. This concise guide reviews terbutaline’s mechanism of action, receptor selectivity, pharmacokinetics, clinical uses, adverse effects, monitoring parameters and drug interactions. B. Pharm students will benefit from focused questions on intracellular signaling (cAMP), therapeutic formulations, contraindications, and comparative aspects versus other beta-2 agonists. Emphasis is placed on safety issues such as tachycardia, tremor, hypokalemia and precautions in pregnancy and cardiac disease. Practical MCQs will strengthen clinical reasoning and exam readiness. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. Which receptor subtype does terbutaline primarily stimulate?

• Alpha-1 adrenergic receptor
• Beta-1 adrenergic receptor
• Beta-2 adrenergic receptor
• Muscarinic M3 receptor

Correct Answer: Beta-2 adrenergic receptor

Q2. The primary intracellular effect of beta-2 receptor activation by terbutaline is:

• Decrease in intracellular cAMP via Gi protein
• Increase in intracellular cAMP via Gs protein
• Increase in intracellular IP3 and DAG via Gq protein
• Activation of tyrosine kinase cascade

Correct Answer: Increase in intracellular cAMP via Gs protein

Q3. Terbutaline produces bronchodilation mainly by:

• Blocking muscarinic receptors on bronchial smooth muscle
• Relaxation of bronchial smooth muscle through increased cAMP
• Inhibition of leukotriene synthesis
• Stimulating histamine release from mast cells

Correct Answer: Relaxation of bronchial smooth muscle through increased cAMP

Q4. Which of the following is a common adverse effect of terbutaline?

• Bradycardia
• Hypotension with flaccid muscles
• Tremor and palpitations
• Severe sedation

Correct Answer: Tremor and palpitations

Q5. Terbutaline can cause hypokalemia by which mechanism?

• Renal potassium wasting via aldosterone secretion
• Cellular shift of potassium into cells via stimulation of Na+/K+ ATPase
• Direct destruction of skeletal muscle releasing potassium
• Inhibition of intestinal potassium absorption

Correct Answer: Cellular shift of potassium into cells via stimulation of Na+/K+ ATPase

Q6. Which clinical use of terbutaline is considered off-label or used with caution?

• Acute bronchospasm in asthma
• Tocolysis to inhibit preterm labor
• Maintenance therapy for COPD exclusively
• Treatment of nasal congestion

Correct Answer: Tocolysis to inhibit preterm labor

Q7. Compared to catecholamines like epinephrine, terbutaline is more suitable for oral use because:

• It is a catechol and resists metabolism by COMT
• It is non-catechol and less susceptible to COMT degradation
• It has higher affinity for alpha receptors
• It is primarily renally excreted unchanged

Correct Answer: It is non-catechol and less susceptible to COMT degradation

Q8. Which formulation(s) is terbutaline commonly available in?

• Inhalation (nebulizer/MDI) and subcutaneous injection
• Only as a transdermal patch
• Intrathecal infusion only
• Topical cream for bronchial use

Correct Answer: Inhalation (nebulizer/MDI) and subcutaneous injection

Q9. Which patient history is a relative contraindication for terbutaline use?

• Well-controlled seasonal allergies
• History of tachyarrhythmias or ischemic heart disease
• Chronic constipation
• Mild osteoarthritis

Correct Answer: History of tachyarrhythmias or ischemic heart disease

Q10. The tachycardia seen with terbutaline is primarily due to:

• Pure reflex vagal stimulation
• Direct beta-1 stimulation and reflex sympathetic activation
• Inhibition of cardiac sodium channels
• Excessive parasympathetic activity

Correct Answer: Direct beta-1 stimulation and reflex sympathetic activation

Q11. Which monitoring parameter is important during systemic terbutaline therapy?

• Serum potassium levels
• Serum bilirubin levels only
• Urine creatinine exclusively
• Cerebrospinal fluid glucose

Correct Answer: Serum potassium levels

Q12. Co-administration of terbutaline with a nonselective beta-blocker will likely result in:

• Enhanced bronchodilation
• Reduced bronchodilatory effect of terbutaline
• Unchanged therapeutic response
• Immediate allergic reaction

Correct Answer: Reduced bronchodilatory effect of terbutaline

Q13. Which molecular feature contributes to terbutaline’s beta-2 selectivity?

• Tertiary butyl substitution on the amino group
• Catechol hydroxyl groups at 3,4 positions
• Long hydrophobic steroid backbone
• Presence of a bulky aromatic ring fused to catechol

Correct Answer: Tertiary butyl substitution on the amino group

Q14. Terbutaline’s bronchodilatory effect is mediated by which second messenger pathway?

• cGMP increase via guanylate cyclase
• cAMP increase via adenylyl cyclase
• Inositol triphosphate (IP3) release
• Direct calcium channel blockade

Correct Answer: cAMP increase via adenylyl cyclase

Q15. In acute severe bronchospasm, an advantage of terbutaline over salbutamol (albuterol) is:

• Complete lack of cardiac effects even in high doses
• Availability as a subcutaneous injection for rapid administration
• Longer half-life with no need for repeat dosing for weeks
• Potent anticholinergic action

Correct Answer: Availability as a subcutaneous injection for rapid administration

Q16. Which metabolic effect can terbutaline produce in susceptible patients?

• Hypoglycemia via increased insulin release
• Hyperglycemia via increased glycogenolysis and gluconeogenesis
• Severe lactic acidosis invariably
• Reduced hepatic gluconeogenesis

Correct Answer: Hyperglycemia via increased glycogenolysis and gluconeogenesis

Q17. A pharmacist counseling a patient on inhaled terbutaline should advise that tremor is due to:

• CNS GABA receptor blockade
• Beta-2 stimulation of skeletal muscle causing increased neuromuscular excitability
• Direct muscle fiber necrosis
• Dehydration from inhaler propellants

Correct Answer: Beta-2 stimulation of skeletal muscle causing increased neuromuscular excitability

Q18. Terbutaline’s effectiveness is reduced in patients who use which chronic medication?

• Topical nasal decongestants only
• Nonselective beta-adrenergic blockers such as propranolol
• Proton pump inhibitors
• Topical antifungal agents

Correct Answer: Nonselective beta-adrenergic blockers such as propranolol

Q19. The risk of pulmonary edema during tocolysis with terbutaline is increased by:

• Concurrent use of intravenous fluids and beta-agonist therapy
• Strict fluid restriction during therapy
• Administration of terbutaline via inhalation only
• Low maternal blood pressure

Correct Answer: Concurrent use of intravenous fluids and beta-agonist therapy

Q20. Which statement about terbutaline pharmacokinetics is most accurate?

• It is rapidly metabolized by catechol-O-methyltransferase (COMT)
• It has oral activity because it is not a catechol and resists COMT degradation
• It is only effective when given intravenously
• It is eliminated exclusively via biliary excretion

Correct Answer: It has oral activity because it is not a catechol and resists COMT degradation

Q21. Terbutaline’s tocolytic effect is due to relaxation of uterine smooth muscle via:

• Inhibition of prostaglandin synthesis
• Activation of beta-2 receptors and increased cAMP in myometrial cells
• Estrogen receptor antagonism
• Direct blockade of oxytocin receptors

Correct Answer: Activation of beta-2 receptors and increased cAMP in myometrial cells

Q22. Which laboratory abnormality is most commonly associated with acute high-dose terbutaline use?

• Hyperkalemia
• Hypokalemia
• Marked leukopenia
• Elevated amylase only

Correct Answer: Hypokalemia

Q23. Terbutaline should be used cautiously in patients with hyperthyroidism because:

• Hyperthyroid patients have decreased beta-receptor sensitivity
• They are more susceptible to tachyarrhythmias from beta-agonists
• Tertiary butyl groups interact with thyroid hormone
• It causes profound hypothyroidism when combined with antithyroid drugs

Correct Answer: They are more susceptible to tachyarrhythmias from beta-agonists

Q24. Which drug interaction increases the risk of cardiac arrhythmias with terbutaline?

• Concurrent use of inhaled corticosteroids only
• Use with digitalis glycosides or certain antiarrhythmics
• Concurrent multivitamin supplements
• Topical antifungal therapy

Correct Answer: Use with digitalis glycosides or certain antiarrhythmics

Q25. In the setting of hypokalemia induced by terbutaline, the immediate mechanism is best described as:

• Renal excretion enhanced by increased aldosterone only
• Shift of potassium into cells mediated by beta-2 receptor stimulation
• Gastrointestinal loss due to terbutaline-induced diarrhea
• Bone deposition of potassium

Correct Answer: Shift of potassium into cells mediated by beta-2 receptor stimulation

Q26. A laboratory pharmacology question: activation of beta-2 receptors by terbutaline in bronchial smooth muscle leads to which ion change?

• Increased intracellular calcium promoting contraction
• Decreased intracellular calcium causing relaxation
• Increased intracellular sodium causing depolarization
• Direct chloride influx to hyperpolarize cells

Correct Answer: Decreased intracellular calcium causing relaxation

Q27. Which adverse effect might be mistaken for worsening asthma after terbutaline administration?

• Beta-2 mediated tremor misinterpreted as bronchospasm
• Terbutaline-induced cough causing airway obstruction
• Immediate allergic anaphylaxis only
• Exacerbation of fever

Correct Answer: Beta-2 mediated tremor misinterpreted as bronchospasm

Q28. Which statement about terbutaline vs. salmeterol is correct?

• Terbutaline is a long-acting beta-2 agonist while salmeterol is short-acting
• Salmeterol is long-acting; terbutaline is used for short-term relief
• Both are irreversible beta-2 antagonists
• Neither drug has bronchodilator activity

Correct Answer: Salmeterol is long-acting; terbutaline is used for short-term relief

Q29. Which monitoring is essential when terbutaline is given intravenously for acute therapy?

• Continuous fetal heart rate monitoring only
• Continuous maternal cardiac monitoring and electrolytes
• Weekly complete blood counts only
• No monitoring is required for IV terbutaline

Correct Answer: Continuous maternal cardiac monitoring and electrolytes

Q30. A mechanism-based MCQ: terbutaline reduces bronchial hyperresponsiveness by:

• Promoting mucous hypersecretion to trap irritants
• Inhibiting mediator release from mast cells via increased intracellular cAMP
• Stimulating vagal reflexes to dilate airways
• Blocking histamine H1 receptors directly

Correct Answer: Inhibiting mediator release from mast cells via increased intracellular cAMP

Q31. Which statement is true about tolerance (tachyphylaxis) to beta-2 agonists like terbutaline?

• Tachyphylaxis cannot occur with beta-2 agonists
• Repeated use may lead to receptor downregulation and reduced responsiveness
• Tolerance leads to permanent receptor loss that is irreversible
• Tachyphylaxis is only due to placebo effect

Correct Answer: Repeated use may lead to receptor downregulation and reduced responsiveness

Q32. In emergency treatment of bronchospasm, an advantage of terbutaline SC injection is:

• Slower onset than oral tablets
• Rapid systemic absorption when inhalation is not possible
• Permanent bronchodilation after one dose
• Absence of any systemic side effects

Correct Answer: Rapid systemic absorption when inhalation is not possible

Q33. Which electrolyte should be monitored and corrected when starting high-dose terbutaline?

• Magnesium only
• Potassium
• Calcium only
• Phosphate exclusively

Correct Answer: Potassium

Q34. Why are beta-2 agonists like terbutaline sometimes avoided in diabetic patients?

• They cause profound hypoglycemia
• They can increase blood glucose and interfere with glycemic control
• They neutralize insulin in the bloodstream
• They cause permanent pancreatic beta-cell destruction

Correct Answer: They can increase blood glucose and interfere with glycemic control

Q35. Which feature distinguishes direct-acting sympathomimetics like terbutaline from indirect-acting agents?

• Direct-acting drugs stimulate adrenergic receptors directly; indirect agents increase endogenous catecholamine release
• Direct agents block adrenergic receptors while indirect agents activate them
• Direct agents have no clinical use
• Indirect agents are always safer

Correct Answer: Direct-acting drugs stimulate adrenergic receptors directly; indirect agents increase endogenous catecholamine release

Q36. Terbutaline’s bronchodilatory effects are reduced in the presence of which electrolyte disturbance?

• Hyperkalemia
• Hypokalemia
• Hyponatremia
• Hypermagnesemia

Correct Answer: Hypokalemia

Q37. Which adverse maternal effect is associated with prolonged terbutaline use for tocolysis?

• Severe bradycardia and syncope only
• Potential for pulmonary edema and cardiovascular events
• Renal failure in all cases
• Complete reversal of labor without risks

Correct Answer: Potential for pulmonary edema and cardiovascular events

Q38. What is the primary reason terbutaline has less short-term metabolic inactivation than epinephrine?

• Terbutaline is a catechol and rapidly metabolized
• Terbutaline lacks catechol hydroxyl groups and resists COMT metabolism
• Terbutaline is a peptide and degraded slowly
• Terbutaline is bound irreversibly to receptors

Correct Answer: Terbutaline lacks catechol hydroxyl groups and resists COMT metabolism

Q39. Which statement about neonatal exposure to maternal terbutaline is correct?

• No neonatal effects are possible because terbutaline does not cross the placenta
• Neonatal hypoglycemia and tachycardia may occur with significant maternal exposure
• Terbutaline causes permanent neural defects in all cases
• Terbutaline leads to immediate neonatal hypertension in every delivery

Correct Answer: Neonatal hypoglycemia and tachycardia may occur with significant maternal exposure

Q40. Which of the following is a reason to avoid combining terbutaline with monoamine oxidase inhibitors (MAOIs)?

• MAOIs will completely block terbutaline’s bronchodilator effect
• Concomitant use may potentiate cardiovascular adverse effects
• MAOIs convert terbutaline into inactive metabolites
• There is no interaction between beta-2 agonists and MAOIs

Correct Answer: Concomitant use may potentiate cardiovascular adverse effects

Q41. For a pharmacology exam: the site of action for terbutaline in producing bronchodilation is primarily:

• Bronchial gland mucosa
• Bronchial smooth muscle cells
• Pulmonary alveolar type II cells
• Tracheal cartilage

Correct Answer: Bronchial smooth muscle cells

Q42. Which clinical scenario would most likely require caution or dose adjustment for terbutaline?

• Young healthy adult with seasonal asthma only
• Patient with uncontrolled hypertension and recent myocardial infarction
• Patient using topical emollients for dry skin
• Patient with mild osteopenia

Correct Answer: Patient with uncontrolled hypertension and recent myocardial infarction

Q43. Which of these best describes a pharmacodynamic interaction with terbutaline?

• Loop diuretics increasing terbutaline oral bioavailability
• Beta-blockers antagonizing terbutaline’s effect at beta receptors
• Antacids accelerating terbutaline hepatic clearance
• Vitamin supplements chemically inactivating terbutaline

Correct Answer: Beta-blockers antagonizing terbutaline’s effect at beta receptors

Q44. In teaching mechanisms, which enzyme is directly stimulated downstream of beta-2 receptor activation?

• Adenylyl cyclase, increasing cAMP production
• Phospholipase C, increasing IP3
• Tyrosine hydroxylase for catecholamine synthesis
• Acetylcholinesterase in synaptic cleft

Correct Answer: Adenylyl cyclase, increasing cAMP production

Q45. Which symptom would most likely prompt discontinuation of terbutaline therapy in a pregnant patient?

• Mild transient headache after inhalation
• Acute chest pain and shortness of breath suggesting cardiopulmonary compromise
• Occasional mild hand tremor without functional impairment
• Minor nasal dryness

Correct Answer: Acute chest pain and shortness of breath suggesting cardiopulmonary compromise

Q46. Which property makes terbutaline useful in acute asthma management?

• Slow onset of action by all routes
• Rapid bronchodilation when given inhaled or subcutaneous
• Total absence of systemic absorption after SC injection
• Primary action as an antimuscarinic agent

Correct Answer: Rapid bronchodilation when given inhaled or subcutaneous

Q47. Which adverse metabolic change can occur with excessive terbutaline use in children?

• Persistent hypoglycemia leading to seizures
• Hyperglycemia and potential lactic acidosis in severe overdose
• Profound hyponatremia only
• Severe iron deficiency anemia

Correct Answer: Hyperglycemia and potential lactic acidosis in severe overdose

Q48. Which patient education point is correct for inhaled terbutaline MDI use?

• Rinse mouth after use to prevent systemic absorption
• Use as needed for acute relief and follow device-specific instructions
• Terbutaline should be swallowed immediately after inhalation
• Store inhaler in a freezer at all times

Correct Answer: Use as needed for acute relief and follow device-specific instructions

Q49. Which best describes terbutaline’s role in COPD management?

• Mainstay long-term controller as monotherapy in all COPD patients
• Short-acting bronchodilator option for symptom relief in COPD and asthma
• It cures COPD by reversing emphysematous changes
• It is contraindicated in COPD

Correct Answer: Short-acting bronchodilator option for symptom relief in COPD and asthma

Q50. For exam preparation: which pharmacological principle explains why terbutaline’s effects may wane with frequent use?

• Drug-induced receptor upregulation increasing sensitivity
• Receptor desensitization and downregulation leading to decreased response
• Permanent increase in receptor number causing overdose
• Increased renal elimination converting drug to inactive metabolites

Correct Answer: Receptor desensitization and downregulation leading to decreased response

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.

Mail- Sachin@pharmacyfreak.com