Beta-adrenergic antagonists US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Beta-adrenergic antagonists. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Beta-adrenergic antagonists US Medical PG Question 1: A 39-year-old woman is brought to the emergency department 30 minutes after her husband found her unconscious on the living room floor. She does not report having experienced light-headedness, nausea, sweating, or visual disturbance before losing consciousness. Three weeks ago, she was diagnosed with open-angle glaucoma and began treatment with an antiglaucoma drug in the form of eye drops. She last used the eye drops 1 hour ago. Examination shows pupils of normal size that are reactive to light. An ECG shows sinus bradycardia. This patient is most likely undergoing treatment with which of the following drugs?
- A. Brimonidine
- B. Dorzolamide
- C. Latanoprost
- D. Pilocarpine
- E. Timolol (Correct Answer)
Beta-adrenergic antagonists Explanation: ***Timolol***
- **Timolol** is a **non-selective beta-blocker** used to treat open-angle glaucoma by reducing aqueous humor production
- Can be **systemically absorbed** from eye drops, causing cardiac side effects including **bradycardia, hypotension, and syncope**
- The patient's presentation of **sudden unconsciousness without prodromal symptoms** plus **sinus bradycardia** is classic for beta-blocker toxicity
- Systemic absorption is enhanced with frequent dosing and can occur even with topical ophthalmic use
*Brimonidine*
- **Brimonidine** is an **alpha-2 adrenergic agonist** that reduces aqueous humor production and increases uveoscleral outflow
- Systemic absorption can cause CNS depression, fatigue, and hypotension, but **bradycardia is not a prominent feature**
- Would not typically present with syncope as the primary manifestation
*Dorzolamide*
- **Dorzolamide** is a **carbonic anhydrase inhibitor** that reduces aqueous humor production
- Systemic side effects include metabolic acidosis and electrolyte disturbances with chronic use
- **Not associated with significant bradycardia or acute syncope**
*Latanoprost*
- **Latanoprost** is a **prostaglandin F2-alpha analog** that increases uveoscleral outflow to lower intraocular pressure
- Side effects are primarily local (iris pigmentation, eyelash growth, conjunctival hyperemia)
- Has **minimal systemic absorption** and would not cause bradycardia or syncope
*Pilocarpine*
- **Pilocarpine** is a **muscarinic cholinergic agonist** that causes miosis and increases trabecular outflow
- Can cause cholinergic side effects including bradycardia, but typically accompanied by **miosis, salivation, lacrimation, nausea, and sweating**
- Patient has **normal-sized reactive pupils** and no cholinergic symptoms, ruling this out
Beta-adrenergic antagonists US Medical PG Question 2: A 55-year-old man comes to the physician because of episodic retrosternal chest pain and shortness of breath for the past 6 months. His symptoms occur when he takes long walks or climbs stairs but resolve promptly with rest. He has a history of chronic obstructive pulmonary disease, for which he takes ipratropium bromide. His pulse is 81/min and blood pressure is 153/82 mm Hg. Physical examination shows mild expiratory wheezing over both lungs. Additional treatment with a beta blocker is considered. Which of the following agents should be avoided in this patient?
- A. Betaxolol
- B. Esmolol
- C. Bisoprolol
- D. Atenolol
- E. Labetalol (Correct Answer)
Beta-adrenergic antagonists Explanation: ***Labetalol***
- **Labetalol** is a **non-selective beta-blocker** with additional **alpha-1 blocking activity**.
- Its **non-selective beta-blocking** effects can exacerbate **bronchoconstriction** in patients with **COPD**, leading to worsening respiratory symptoms.
*Betaxolol*
- **Betaxolol** is a **beta-1 selective blocker (cardioselective)**, meaning it primarily targets the heart.
- While no beta-blocker is entirely safe in **COPD**, cardioselective agents are generally preferred due to their reduced risk of **bronchospasm**.
*Esmolol*
- **Esmolol** is an **ultra-short-acting**, **beta-1 selective blocker** often used for acute cardiac conditions.
- Its **cardioselective nature** and rapid metabolism make it relatively safer in patients with **COPD** compared to non-selective agents.
*Bisoprolol*
- **Bisoprolol** is a **highly beta-1 selective blocker** commonly used for chronic cardiac conditions.
- Its high **cardioselectivity** minimizes its impact on **bronchial beta-2 receptors**, making it a safer option for patients with **COPD**.
*Atenolol*
- **Atenolol** is a **beta-1 selective blocker** used for conditions like hypertension and angina.
- Like other cardioselective beta-blockers, it has a lower risk of causing **bronchoconstriction** in patients with **COPD** compared to non-selective agents.
Beta-adrenergic antagonists US Medical PG Question 3: A 55-year-old man comes to the physician because of intermittent palpitations that occur when he is stressed, exercising, or when he drinks alcohol. Physical examination shows an irregularly irregular pulse. An ECG shows irregular QRS complexes without any discrete P waves. Pharmacotherapy with carvedilol is initiated for his condition. Compared to treatment with propranolol, which of the following adverse effects is most likely?
- A. Bradycardia
- B. Bronchospasm
- C. Hyperkalemia
- D. Hypotension (Correct Answer)
- E. Hyperglycemia
Beta-adrenergic antagonists Explanation: ***Hypotension***
- **Carvedilol** is a non-selective beta-blocker with additional **alpha-1 adrenergic receptor blocking activity**, which leads to peripheral vasodilation and a greater potential for **hypotension** compared to propranolol (a pure beta-blocker).
- The **alpha-1 blockade** causes a reduction in peripheral vascular resistance, leading to a more pronounced decrease in blood pressure.
*Bradycardia*
- Both carvedilol and propranolol are beta-blockers and can cause **bradycardia** by reducing heart rate.
- However, the question asks for an adverse effect **more likely** with carvedilol compared to propranolol, and while both can cause bradycardia, carvedilol's additional alpha-blocking activity makes hypotension more distinguishing.
*Bronchospasm*
- Both carvedilol and propranolol are **non-selective beta-blockers** (blocking both beta-1 and beta-2 receptors) and can cause **bronchospasm** by blocking beta-2 receptors in the bronchi.
- Therefore, this adverse effect is common to both and not more likely with carvedilol specifically in comparison to propranolol.
*Hyperkalemia*
- Neither carvedilol nor propranolol is directly associated with causing **hyperkalemia** as a primary adverse effect.
- Beta-blockers can sometimes lead to minor shifts in potassium, but it's not a common or more significant side effect compared to others listed.
*Hyperglycemia*
- **Non-selective beta-blockers** like propranolol can impair the recovery from **hypoglycemia** and mask its symptoms.
- While beta-blockers can have some metabolic effects, **hyperglycemia** is not a generally recognized or more prominent adverse effect of carvedilol compared to propranolol.
Beta-adrenergic antagonists US Medical PG Question 4: A 50-year-old man with a history of atrial fibrillation presents to his cardiologist’s office for a follow-up visit. He recently started treatment with an anti-arrhythmic drug to prevent future recurrences and reports that he has been feeling well and has no complaints. The physical examination shows that the arrhythmia appears to have resolved; however, there is now mild bradycardia. In addition, the electrocardiogram recording shows a slight prolongation of the PR and QT intervals. Which of the following drugs was most likely used to treat this patient?
- A. Metoprolol
- B. Sotalol (Correct Answer)
- C. Propranolol
- D. Verapamil
- E. Carvedilol
Beta-adrenergic antagonists Explanation: ***Sotalol***
- **Sotalol** is a **beta-blocker** and a **Class III antiarrhythmic** drug, meaning it blocks potassium channels.
- This dual action explains the **bradycardia** (beta-blockade) and the **prolongation of the PR and QT intervals** (potassium channel blockade), which are characteristic side effects.
*Metoprolol*
- **Metoprolol** is a **selective beta-1 blocker** (Class II antiarrhythmic) that would cause **bradycardia** and **PR prolongation**, but it does not typically prolong the **QT interval**.
- It primarily affects the heart rate and AV nodal conduction without significant potassium channel blocking properties.
*Propranolol*
- **Propranolol** is a **non-selective beta-blocker** (Class II antiarrhythmic) that would cause **bradycardia** and **PR prolongation**.
- Similar to metoprolol, it does not typically prolong the **QT interval**.
*Verapamil*
- **Verapamil** is a **non-dihydropyridine calcium channel blocker** (Class IV antiarrhythmic) that causes **bradycardia** and **PR prolongation**.
- However, it does not prolong the **QT interval**; instead, it can sometimes shorten it.
*Carvedilol*
- **Carvedilol** is a **non-selective beta-blocker** with **alpha-1 blocking properties** (Class II antiarrhythmic), leading to **bradycardia** and **PR prolongation**.
- It does not have effects on potassium channels that would lead to **QT prolongation**.
Beta-adrenergic antagonists US Medical PG Question 5: A 70-year-old male presents for an annual exam. His past medical history is notable for shortness of breath when he sleeps, and upon exertion. Recently he has experienced dyspnea and lower extremity edema that seems to be worsening. Both of these symptoms have resolved since he was started on several medications and instructed to weigh himself daily. Which of the following is most likely a component of his medical management?
- A. Lidocaine
- B. Verapamil
- C. Carvedilol (Correct Answer)
- D. Aspirin
- E. Ibutilide
Beta-adrenergic antagonists Explanation: ***Carvedilol***
- The patient exhibits classic symptoms of **heart failure**, such as **dyspnea on exertion**, **orthopnea** (shortness of breath when he sleeps), and **lower extremity edema**.
- **Beta-blockers** like carvedilol are essential for managing **chronic heart failure** by reducing myocardial oxygen demand and improving cardiac function.
*Lidocaine*
- **Lidocaine** is primarily an **antiarrhythmic drug** used for acute treatment of **ventricular arrhythmias**, not for chronic heart failure management.
- It works by blocking sodium channels and has no direct benefit in addressing the underlying pathophysiology of heart failure.
*Verapamil*
- **Verapamil** is a **non-dihydropyridine calcium channel blocker** typically used for hypertension, angina, and supraventricular tachyarrhythmias.
- It can have **negative inotropic effects**, which are generally contraindicated or used with extreme caution in patients with **systolic heart failure** due to its potential to worsen cardiac function.
*Aspirin*
- **Aspirin** is an **antiplatelet agent** used for primary or secondary prevention of **atherosclerotic cardiovascular disease** (e.g., in patients with coronary artery disease).
- It does not directly manage the symptoms or pathophysiology of **heart failure** unless there is a coexisting ischemic etiology.
*Ibutilide*
- **Ibutilide** is an **antiarrhythmic drug** specifically used for the rapid conversion of **atrial flutter and atrial fibrillation** of recent onset to sinus rhythm.
- It is not a medication used for the long-term management of **heart failure** symptoms described in the patient.
Beta-adrenergic antagonists US Medical PG Question 6: A 77-year-old woman with congestive heart failure is admitted to the hospital for evaluation prior to cardiac transplantation. During her stay at the hospital, the physician prescribes a drug to improve cardiac contractility. The drug works by selectively inhibiting an isoenzyme that is responsible for the degradation of cyclic adenosine monophosphate. Which of the following is the most likely adverse effect of this drug?
- A. Hyperkalemia
- B. QT interval prolongation
- C. Hyperglycemia
- D. Bronchospasm
- E. Hypotension (Correct Answer)
Beta-adrenergic antagonists Explanation: ***Hypotension***
- The drug described is likely a **phosphodiesterase-3 inhibitor** (e.g., milrinone), which increases cyclic AMP in cardiac myocytes and vascular smooth muscle cells.
- Increased **cyclic AMP** in vascular smooth muscle leads to **vasodilation**, causing a drop in systemic vascular resistance and subsequently **hypotension**.
*Hyperkalemia*
- **Hyperkalemia** is not a characteristic adverse effect of phosphodiesterase inhibitors. It is associated with drugs like **ACE inhibitors**, **ARBs**, or **aldosterone antagonists**.
- These drugs primarily affect the **renin-angiotensin-aldosterone system** or potassium excretion.
*QT interval prolongation*
- While some **phosphodiesterase inhibitors** can cause **QT prolongation**, it is not the *most likely* adverse effect compared to hypotension, especially in a patient with heart failure.
- Furthermore, **QT prolongation** is a more prominent concern with drugs like **antiarrhythmics** (e.g., amiodarone, sotalol) or certain **antibiotics** (e.g., macrolides).
*Hyperglycemia*
- **Hyperglycemia** is typically associated with drugs that interfere with **insulin secretion** or **insulin sensitivity**, such as **corticosteroids** or some **atypical antipsychotics**.
- Phosphodiesterase inhibitors do not directly cause significant **glucose disturbances**.
*Bronchospasm*
- **Bronchospasm** is a common side effect of **beta-blockers** due to their antagonism of beta-2 adrenergic receptors in the airways.
- Phosphodiesterase inhibitors, by increasing **cyclic AMP**, would theoretically cause **bronchodilation**, not bronchospasm.
Beta-adrenergic antagonists US Medical PG Question 7: Match the following:
Column A:
a. Beta 1
b. Beta 2
c. Beta 3
Column B:
1. Mirabegron
2. Betaxolol
3. Salbutamol
- A. a-2, b-3 ,c-1 (Correct Answer)
- B. a-2, b-1, c-3
- C. a-3, b-2, c-1
- D. a-3, b-1, c-2
Beta-adrenergic antagonists Explanation: ***a-2, b-3, c-1***
- This pairing correctly matches **Betaxolol** with **Beta 1 selective** antagonism, **Salbutamol** with **Beta 2 selective** agonism, and **Mirabegron** with **Beta 3 selective** agonism.
- **Betaxolol** is a beta-1 selective adrenergic receptor antagonist, primarily used in ophthalmology to reduce intraocular pressure and as an antihypertensive. **Salbutamol** is a selective beta-2 adrenergic agonist used as a bronchodilator in asthma and COPD, causing relaxation of bronchial smooth muscle. **Mirabegron** is a selective beta-3 adrenergic agonist used to treat overactive bladder by relaxing the detrusor muscle.
*a-2, b-1, c-3*
- This option incorrectly assigns **Mirabegron** to Beta 2. Mirabegron is a **Beta 3 selective agonist**.
- It also incorrectly assigns **Salbutamol** to Beta 3. Salbutamol is a **Beta 2 selective agonist**.
*a-3, b-2, c-1*
- This option incorrectly assigns **Salbutamol** to Beta 1. Salbutamol is a **Beta 2 selective agonist**.
- It also incorrectly assigns **Betaxolol** to Beta 2. Betaxolol is a **Beta 1 selective antagonist**.
*a-3, b-1, c-2*
- This option incorrectly assigns **Salbutamol** to Beta 1 and **Betaxolol** to Beta 3.
- **Salbutamol** is a Beta 2 selective agonist, and **Betaxolol** is a Beta 1 selective antagonist.
Beta-adrenergic antagonists US Medical PG Question 8: A 53-year-old man presents to the office for a routine examination. The medical history is significant for diabetes mellitus, for which he is taking metformin. The medical records show blood pressure readings from three separate visits to fall in the 130–160 mm Hg range for systolic and 90–100 mm Hg range for diastolic. Prazosin is prescribed. Which of the following are effects of this drug?
- A. Vasodilation, decreased heart rate, bronchial constriction
- B. Vasodilation, increased peristalsis, bronchial dilation
- C. Vasoconstriction, bladder sphincter constriction, mydriasis
- D. Vasoconstriction, increase in AV conduction rate, bronchial dilation
- E. Vasodilation, bladder sphincter relaxation (Correct Answer)
Beta-adrenergic antagonists Explanation: ***Vasodilation, bladder sphincter relaxation***
- **Prazosin** is an **alpha-1 adrenergic receptor antagonist**, which blocks the effects of norepinephrine on vascular smooth muscle, leading to **vasodilation** and decreased blood pressure.
- Blocking alpha-1 receptors in the bladder neck and prostate causes **bladder sphincter relaxation**, which can improve urine flow and is also useful in benign prostatic hyperplasia (BPH).
- These are the two primary clinically relevant effects of alpha-1 blockade with prazosin.
*Vasodilation, decreased heart rate, bronchial constriction*
- While prazosin causes **vasodilation**, it does not typically decrease heart rate directly; alpha-1 blockade can lead to **reflex tachycardia** due to decreased blood pressure.
- Prazosin has no significant effect on bronchial smooth muscle and does not cause **bronchial constriction**; bronchial effects are primarily mediated by beta-2 receptors or muscarinic (M3) receptors.
*Vasodilation, increased peristalsis, bronchial dilation*
- Prazosin does cause **vasodilation** but does not directly cause **increased peristalsis**; gastrointestinal motility is mainly regulated by the autonomic nervous system via muscarinic receptors and the enteric nervous system.
- Prazosin does not cause **bronchial dilation**; this effect is mediated by beta-2 adrenergic receptor stimulation.
*Vasoconstriction, bladder sphincter constriction, mydriasis*
- Prazosin is an alpha-1 antagonist, meaning it *blocks* **vasoconstriction** and instead causes vasodilation.
- Similarly, it causes **bladder sphincter relaxation**, not constriction.
- Prazosin has minimal effects on pupil size; mydriasis would be caused by alpha-1 agonists or muscarinic antagonists, not alpha-1 antagonists.
*Vasoconstriction, increase in AV conduction rate, bronchial dilation*
- Prazosin causes **vasodilation**, not vasoconstriction.
- It does not significantly affect **AV conduction rate** or directly cause **bronchial dilation**.
Beta-adrenergic antagonists US Medical PG Question 9: A 73-year-old man presents to his primary care physician with chest pain. He noticed the pain after walking several blocks, and the pain is relieved by sitting. On exam, he has a BP 155/89 mmHg, HR 79 bpm, and T 98.9 F. The physician refers the patient to a cardiologist and offers prescriptions for carvedilol and nitroglycerin. Which of the following describes the mechanism or effects of each of these medications, respectively?
- A. Increased contractility; Decreased endothelial nitric oxide
- B. Decreased cAMP; Increased cGMP (Correct Answer)
- C. Increased cAMP; Increased cAMP
- D. Decreased cGMP; Increased venous resistance
- E. Increased heart rate; Decreased arterial resistance
Beta-adrenergic antagonists Explanation: ***Decreased cAMP; Increased cGMP***
- **Carvedilol** is a beta-blocker that *blocks β1 and β2 adrenergic receptors*, leading to a **decrease in intracellular cAMP**, which in turn reduces heart rate, contractility, and blood pressure.
- **Nitroglycerin** acts by releasing **nitric oxide**, which activates **guanylate cyclase** to convert GTP to **cGMP**, leading to smooth muscle relaxation and vasodilation.
*Increased contractility; Decreased endothelial nitric oxide*
- **Carvedilol** (a beta-blocker) causes a **decrease in contractility**, not an increase, by blocking beta-adrenergic receptors.
- **Nitroglycerin** works by **increasing** the production of nitric oxide, not decreasing it.
*Increased cAMP; Increased cAMP*
- **Carvedilol** (a beta-blocker) functions by **decreasing** cAMP, not increasing it.
- While other agents might increase cAMP, this is not the mechanism for nitroglycerin.
*Decreased cGMP; Increased venous resistance*
- **Nitroglycerin** works by **increasing cGMP**, which promotes vasodilation, rather than decreasing it.
- Nitroglycerin causes **decreased venous resistance** (venous dilation) to reduce preload, not increased resistance.
*Increased heart rate; Decreased arterial resistance*
- **Carvedilol** (a beta-blocker) primarily **decreases heart rate**, not increases it.
- While nitroglycerin does cause some arterial dilation, its primary effect at therapeutic doses is **venous dilation** to reduce preload, not just decreased arterial resistance.
Beta-adrenergic antagonists US Medical PG Question 10: A 56 year old female comes to the ED complaining of moderate right eye pain, headache, and acute onset of blurry vision, which she describes as colored halos around lights. She was watching a movie at home with her husband about an hour ago when the pain began. On physical exam of her right eye, her pupil is mid-dilated and unresponsive to light. Her right eyeball is firm to pressure. Intraocular pressure (IOP) measured with tonometer is elevated at 36mmHg. Which of the following is the most appropriate emergency treatment?
- A. Laser peripheral iridotomy
- B. Epinephrine ophthalmic solution
- C. Anti-cholinergic ophthalmic solution
- D. NSAID ophthalmic solution
- E. Timolol ophthalmic solution (Correct Answer)
Beta-adrenergic antagonists Explanation: ***Timolol ophthalmic solution***
- The patient presents with symptoms and signs consistent with **acute angle-closure glaucoma** (AAGC), including acute eye pain, headache, colored halos, mid-dilated non-reactive pupil, firm eyeball, and elevated IOP. **Timolol** is a **beta-blocker** that reduces aqueous humor production, thereby lowering intraocular pressure.
- Emergency treatment for AAGC focuses on rapidly lowering IOP to prevent permanent vision loss, often involving a combination of topical medications like beta-blockers (e.g., timolol), **alpha-agonists**, and **carbonic anhydrase inhibitors**, along with systemic agents if needed.
*Laser peripheral iridotomy*
- This is a definitive treatment for AAGC, creating an opening in the iris to equalize pressure between the anterior and posterior chambers; however, it is typically performed **after initial medical management** has reduced the IOP.
- While it addresses the underlying anatomical cause, it is not the immediate first-line emergency treatment to acutely lower a critically high IOP.
*Epinephrine ophthalmic solution*
- Epinephrine can cause **pupil dilation (mydriasis)**, which can further exacerbate angle closure in AAGC by pushing the iris into the angle.
- Therefore, it is **contraindicated** in acute angle-closure glaucoma.
*Anti-cholinergic ophthalmic solution*
- Anti-cholinergic agents like atropine cause **pupil dilation (mydriasis)** and relaxation of the ciliary muscle, pulling the iris posteriorly and potentially worsening angle closure.
- These are **contraindicated** in acute angle-closure glaucoma as they can worsen the condition by further narrowing the anterior chamber angle.
*NSAID ophthalmic solution*
- NSAID ophthalmic solutions are primarily used to treat **ocular inflammation** and **pain** in conditions such as postoperative inflammation or allergic conjunctivitis.
- They do not directly lower intraocular pressure and are therefore not an appropriate emergency treatment for acute angle-closure glaucoma.
More Beta-adrenergic antagonists US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
