Acute respiratory distress syndrome US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Acute respiratory distress syndrome. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Acute respiratory distress syndrome US Medical PG Question 1: A previously healthy 35-year-old woman is brought into the emergency department after being found unresponsive by her husband. Her husband finds an empty bottle of diazepam tablets in her pocket. She is stuporous. At the hospital, her blood pressure is 90/40 mm Hg, the pulse is 58/min, and the respirations are 6/min. The examination of the pupils shows normal size and reactivity to light. Deep tendon reflexes are 1+ bilaterally. Babinski sign is absent. All 4 extremities are hypotonic. The patient is intubated and taken to the critical care unit for mechanical ventilation and treatment. Regarding the prevention of pneumonia in this patient, which of the following strategies is most likely to achieve this goal?
- A. Nasogastric tube insertion
- B. Daily evaluation for ventilator weaning
- C. Subglottic drainage of secretions (Correct Answer)
- D. Oropharynx and gut antibacterial decontamination
- E. Prone positioning during mechanical ventilation
Acute respiratory distress syndrome Explanation: ***Subglottic drainage of secretions***
- This is a highly effective strategy to prevent **ventilator-associated pneumonia (VAP)** by continuously removing secretions that pool above the endotracheal tube cuff before they can be aspirated.
- Endotracheal tubes with a **subglottic secretion drainage port** reduce VAP incidence by preventing microaspiration of contaminated oropharyngeal secretions into the lower respiratory tract.
- This is a **specific mechanical intervention** that directly addresses one of the key pathogenic mechanisms of VAP.
*Nasogastric tube insertion*
- While an NG tube may be needed for feeding or gastric decompression, it does not directly prevent VAP and may **increase aspiration risk** by compromising the lower esophageal sphincter.
- NG tubes can promote gastroesophageal reflux and provide a conduit for bacterial migration.
*Daily evaluation for ventilator weaning*
- This is also a **critical component of VAP prevention** as part of the ventilator bundle, since reducing duration of mechanical ventilation is the most effective overall strategy to prevent VAP.
- However, in this question asking for a strategy to prevent pneumonia in an intubated patient, subglottic drainage is the more specific technical intervention, whereas daily weaning assessment is a broader protocol that reduces exposure time.
- Both strategies are important; subglottic drainage addresses the "how" of prevention during intubation, while weaning protocols address the "duration" of risk exposure.
*Oropharynx and gut antibacterial decontamination*
- Selective digestive decontamination (SDD) aims to reduce bacterial colonization, but evidence for routine use is mixed and raises concerns about **antimicrobial resistance**.
- Not universally recommended as a primary VAP prevention strategy in most guidelines.
*Prone positioning during mechanical ventilation*
- **Prone positioning** is primarily indicated for improving oxygenation in **Acute Respiratory Distress Syndrome (ARDS)**, not for VAP prevention.
- While it may improve secretion drainage, it is not a standard VAP prevention measure and carries its own risks and logistical challenges.
Acute respiratory distress syndrome US Medical PG Question 2: A 63-year-old man with alpha-1-antitrypsin deficiency is brought to the emergency department 1 hour after his daughter found him unresponsive. Despite appropriate care, the patient dies. At autopsy, examination of the lungs shows enlargement of the airspaces in the respiratory bronchioles and alveoli. Enzymatic activity of which of the following cells is the most likely cause of these findings?
- A. Alveolar macrophages (Correct Answer)
- B. Ciliated bronchiolar epithelial cells
- C. Elastic fibers in alveolar septa
- D. Type I pneumocytes
- E. Alveolar septal cells
Acute respiratory distress syndrome Explanation: ***Alveolar macrophages***
- In **alpha-1-antitrypsin deficiency**, alveolar macrophages (and neutrophils) release **elastase**, which is normally inhibited by alpha-1-antitrypsin.
- Unchecked elastase activity from alveolar macrophages leads to the **destruction of elastic fibers** in the alveolar walls, causing emphysema with characteristic **panacinar** distribution (worse in lower lobes).
- This results in enlargement of airspaces distal to terminal bronchioles.
*Ciliated bronchiolar epithelial cells*
- These cells are primarily involved in **mucociliary clearance** and do not produce proteolytic enzymes that degrade elastic tissue.
- Their dysfunction would lead to impaired mucus clearance and increased susceptibility to infections, but not emphysema.
*Elastic fibers in alveolar septa*
- Elastic fibers are **extracellular matrix components**, not cells.
- While their destruction is the pathological mechanism of emphysema, they do not have enzymatic activity.
*Type I pneumocytes*
- **Type I pneumocytes** form the structural lining of the alveoli and are primarily involved in gas exchange.
- They do not produce elastase or other proteolytic enzymes responsible for tissue destruction in emphysema.
*Alveolar septal cells*
- This term broadly refers to structural cells including Type I and Type II pneumocytes.
- While these cells may be damaged secondarily in emphysema, they do not produce the elastase responsible for elastic fiber destruction.
Acute respiratory distress syndrome US Medical PG Question 3: A 72-year-old man with coronary artery disease comes to the emergency department because of chest pain and shortness of breath for the past 3 hours. Troponin levels are elevated and an ECG shows ST-elevations in the precordial leads. Revascularization with percutaneous coronary intervention is performed, and a stent is successfully placed in the left anterior descending artery. Two days later, he complains of worsening shortness of breath. Pulse oximetry on 3L of nasal cannula shows an oxygen saturation of 89%. An x-ray of the chest shows distended pulmonary veins, small horizontal lines at the lung bases, and blunting of the costophrenic angles bilaterally. Which of the following findings would be most likely on a ventilation-perfusion scan of this patient?
- A. Matched ventilation and perfusion bilaterally
- B. Normal ventilation with multiple, bilateral perfusion defects
- C. Normal perfusion with bilateral ventilation defects (Correct Answer)
- D. Normal perfusion with decreased ventilation at the right base
- E. Increased apical ventilation with normal perfusion bilaterally
Acute respiratory distress syndrome Explanation: ***Normal perfusion with bilateral ventilation defects***
- The patient's presentation with **worsening shortness of breath** after an acute coronary event, along with chest x-ray findings of **distended pulmonary veins, Kerley B lines (small horizontal lines at the lung bases), and blunting of the costophrenic angles**, is highly suggestive of **pulmonary edema** due to heart failure.
- In pulmonary edema, the alveoli fill with fluid, impeding gas exchange. This leads to **impaired ventilation** in the affected areas, while **pulmonary blood flow (perfusion) remains intact**. This results in **ventilation-perfusion (V/Q) mismatch** with impaired ventilation.
*Matched ventilation and perfusion bilaterally*
- This pattern would indicate a **normal ventilation-perfusion scan**, which is inconsistent with the patient's severe shortness of breath, hypoxemia, and radiographic signs of pulmonary edema.
- A matched V/Q scan suggests **healthy lung function** and gas exchange.
*Normal ventilation with multiple, bilateral perfusion defects*
- This pattern is characteristic of **pulmonary embolism**, where blood clots obstruct pulmonary arteries, leading to areas of the lung being ventilated but not perfused.
- The clinical picture and chest x-ray findings in this patient are not consistent with pulmonary embolism.
*Normal perfusion with decreased ventilation at the right base*
- While a focal ventilation defect could occur, the patient's symptoms and chest x-ray findings (distended pulmonary veins, Kerley B lines, bilateral blunting of costophrenic angles) suggest **generalized rather than localized pulmonary edema**.
- This option describes a unilateral and focal issue, whereas heart failure typically causes bilateral findings.
*Increased apical ventilation with normal perfusion bilaterally*
- This finding is not typical in any common pulmonary pathology. Increased apical ventilation is not a characteristic of pulmonary edema or other V/Q mismatch disorders.
- This scenario does not align with the patient's symptoms or imaging findings.
Acute respiratory distress syndrome US Medical PG Question 4: A neonate suffering from neonatal respiratory distress syndrome is given supplemental oxygen. Which of the following is a possible consequence of oxygen therapy in this patient?
- A. Anosmia
- B. Atelectasis
- C. Atopy
- D. Blindness (Correct Answer)
- E. Cardiac anomalies
Acute respiratory distress syndrome Explanation: ***Blindness***
- High concentrations of supplemental oxygen in neonates, particularly premature infants, can lead to **retinopathy of prematurity (ROP)**.
- ROP involves abnormal growth of blood vessels in the retina, which can detach the retina and result in **permanent blindness**.
*Anosmia*
- **Anosmia** is the loss of the sense of smell, typically caused by nasal polyps, head trauma, or certain viral infections.
- It is **not a recognized complication** of oxygen therapy in neonates.
*Atelectasis*
- **Atelectasis** refers to the collapse of lung tissue, which can be caused by bronchial obstruction or hypoventilation.
- While underlying respiratory distress syndrome can predispose to atelectasis, oxygen therapy itself typically aims to improve ventilation and **does not directly cause atelectasis**.
*Atopy*
- **Atopy** is a genetic predisposition to developing allergic diseases such as asthma, eczema, and allergic rhinitis.
- It is **unrelated to oxygen therapy** and is determined by genetic factors and environmental exposures.
*Cardiac anomalies*
- **Cardiac anomalies** (congenital heart defects) are structural problems in the heart present at birth, resulting from abnormal fetal development.
- They are **not a consequence of oxygen therapy** given postpartum; oxygen therapy may be used to manage their symptoms.
Acute respiratory distress syndrome US Medical PG Question 5: An 83-year-old man is being seen in the hospital for confusion. The patient was admitted 4 days ago for pneumonia. He has been improving on ceftriaxone and azithromycin. Then 2 nights ago he had an episode of confusion. He was unsure where he was and attempted to leave. He was calmed down by nurses with redirection. He had a chest radiograph that was stable from admission, a normal EKG, and a normal urinalysis. This morning he was alert and oriented. Then this evening he became confused and agitated again. The patient has a history of benign prostatic hyperplasia, severe dementia, and osteoarthritis. He takes tamsulosin in addition to the newly started antibiotics. Upon physical examination, the patient is alert but orientated only to name. He tries to get up, falls back onto the bed, and grabs his right knee. He states, “I need to get to work. My boss is waiting, but my knee hurts.” He tries to walk again, threatens the nurse who stops him, and throws a plate at the wall. In addition to reorientation, which of the following is the next best step in management?
- A. Morphine
- B. Lorazepam
- C. Haloperidol (Correct Answer)
- D. Rivastigmine
- E. Physical restraints
Acute respiratory distress syndrome Explanation: ***Haloperidol***
- The patient exhibits **delirium** with acute agitation, threatening behavior, and violent actions (throwing objects), representing an **imminent safety risk** to himself and staff.
- After **non-pharmacological interventions** (reorientation) have failed, **low-dose haloperidol** is appropriate for managing **severe agitation** in delirium when there is risk of harm.
- While antipsychotics have an FDA black box warning for increased mortality in elderly patients with dementia and recent evidence questions their efficacy in delirium, they remain indicated for **acute agitation with safety concerns** as a short-term intervention.
- Haloperidol is preferred over atypical antipsychotics in acute hospital settings due to availability in parenteral forms and lower anticholinergic burden.
*Morphine*
- While the patient mentions knee pain (likely from osteoarthritis), his **primary issue** is acute agitation and delirium, not pain management.
- **Opioids** can worsen delirium and confusion in elderly patients through anticholinergic effects and sedation.
- Pain should be addressed, but not as the primary intervention for violent, agitated behavior.
*Lorazepam*
- **Benzodiazepines** are generally **contraindicated in delirium** as they worsen confusion, increase fall risk, and can cause paradoxical agitation in elderly patients.
- The **only exceptions** are delirium from alcohol or benzodiazepine withdrawal, or seizures—none of which apply to this patient.
- Lorazepam would likely exacerbate rather than improve this patient's mental status.
*Rivastigmine*
- **Rivastigmine** is an acetylcholinesterase inhibitor for chronic management of **dementia symptoms**, not acute delirium.
- It has **no role** in managing acute behavioral disturbances and takes weeks to show any effect.
- Studies have not shown benefit of cholinesterase inhibitors in preventing or treating delirium.
*Physical restraints*
- Physical restraints should be used only as a **last resort** when pharmacological and non-pharmacological interventions have failed and there is immediate, serious risk of harm.
- Restraints can **increase agitation**, cause injuries, lead to delirium worsening, and are associated with increased morbidity and mortality.
- They do not address the underlying cause and should be avoided when other options are available.
Acute respiratory distress syndrome US Medical PG Question 6: A 2500-g (5-lb 8-oz) female newborn delivered at 37 weeks' gestation develops rapid breathing, grunting, and subcostal retractions shortly after birth. Despite appropriate lifesaving measures, the newborn dies 2 hours later. Autopsy shows bilateral renal agenesis. Which of the following is the most likely underlying cause of this newborn's respiratory distress?
- A. Displacement of intestines into the pleural cavity
- B. Injury to the diaphragmatic innervation
- C. Collapse of the supraglottic airway
- D. Decreased amniotic fluid ingestion
- E. Pulmonary hypoplasia (Correct Answer)
Acute respiratory distress syndrome Explanation: ***Pulmonary hypoplasia***
- **Bilateral renal agenesis** (Potter sequence) leads to severely reduced or absent fetal urine production, causing **oligohydramnios**.
- **Oligohydramnios** prevents normal lung development, resulting in **pulmonary hypoplasia**, which is the primary cause of respiratory distress and death in these newborns.
*Displacement of intestines into the pleural cavity*
- This describes a **congenital diaphragmatic hernia**, which can cause respiratory distress due to lung compression.
- However, the autopsy finding of **bilateral renal agenesis** points to Potter sequence as the underlying cause, not a diaphragmatic hernia.
*Injury to the diaphragmatic innervation*
- Injury to the phrenic nerve (diaphragmatic innervation) can lead to **diaphragmatic paralysis** and respiratory distress.
- This is not directly related to **bilateral renal agenesis** or the characteristic findings of Potter sequence.
*Collapse of the supraglottic airway*
- This describes conditions like **laryngomalacia** or other upper airway obstructions.
- While these can cause respiratory distress, they are not typically linked to **bilateral renal agenesis** or the systemic consequences of **oligohydramnios**.
*Decreased amniotic fluid ingestion*
- Fetal swallowing of amniotic fluid is important for gastrointestinal development and recycling of fluid.
- However, decreased ingestion primarily affects **gastrointestinal maturation** and amniotic fluid volume (if there is a swallowing problem), not directly lung development in the way oligohydramnios from renal agenesis does.
Acute respiratory distress syndrome US Medical PG Question 7: A 52-year-old woman presents to the emergency room complaining of chest pain. She reports a 4-hour history of dull substernal pain radiating to her jaw. Her history is notable for hypertension, diabetes mellitus, and alcohol abuse. She has a 30 pack-year smoking history and takes lisinopril and metformin but has an allergy to aspirin. Her temperature is 99.1°F (37.3°C), blood pressure is 150/90 mmHg, pulse is 120/min, and respirations are 22/min. Physical examination reveals a diaphoretic and distressed woman. An electrocardiogram reveals ST elevations in leads I, aVL, and V5-6. She is admitted with plans for immediate transport to the catheterization lab for stent placement. What is the mechanism of the next medication that should be given to this patient?
- A. Cyclooxygenase activator
- B. ADP receptor inhibitor (Correct Answer)
- C. Phosphodiesterase activator
- D. Thrombin inhibitor
- E. Vitamin K epoxide reductase inhibitor
Acute respiratory distress syndrome Explanation: ***ADP receptor inhibitor***
- This patient is experiencing an **ST-elevation myocardial infarction (STEMI)** as evidenced by ST elevations in leads I, aVL, and V5-6 (lateral wall infarction)
- **Dual antiplatelet therapy** is the standard of care for STEMI, typically consisting of aspirin plus a P2Y12 inhibitor (ADP receptor inhibitor)
- Since this patient has an **aspirin allergy**, an ADP receptor inhibitor such as **clopidogrel, ticagrelor, or prasugrel** becomes the critical next antiplatelet medication
- These agents **irreversibly or reversibly block the P2Y12 receptor** on platelets, preventing ADP-mediated platelet activation and aggregation
- This is essential for preventing further thrombotic complications during and after percutaneous coronary intervention (PCI)
*Cyclooxygenase activator*
- No cyclooxygenase activator exists in clinical practice for cardiovascular disease
- Aspirin works as a **cyclooxygenase inhibitor**, blocking COX-1 to prevent thromboxane A2 synthesis, but the patient is allergic to aspirin
- "Activating" cyclooxygenase would promote platelet aggregation, which is counterproductive in acute MI
*Phosphodiesterase activator*
- Phosphodiesterase activation would decrease cAMP/cGMP levels, which is not therapeutically beneficial
- **Phosphodiesterase inhibitors** (such as cilostazol or dipyridamole) can have antiplatelet effects by increasing cAMP, but they are not first-line agents for acute STEMI
- An activator would have the opposite and undesirable effect
*Thrombin inhibitor*
- Thrombin inhibitors (e.g., **bivalirudin, heparin**) are anticoagulants that prevent conversion of fibrinogen to fibrin
- While **anticoagulation is important in STEMI management**, it is used as adjunctive therapy alongside antiplatelet agents
- Given the aspirin allergy, the immediate priority is **antiplatelet therapy with an ADP receptor inhibitor**
- Anticoagulation would typically be given concurrently but is not "the next" critical medication in this specific context
*Vitamin K epoxide reductase inhibitor*
- Warfarin is a vitamin K epoxide reductase inhibitor used for chronic anticoagulation
- It has a **slow onset of action** (days) and is inappropriate for acute STEMI management
- It is used for long-term anticoagulation in conditions like atrial fibrillation or mechanical heart valves, not for acute coronary syndromes requiring rapid platelet inhibition
Acute respiratory distress syndrome US Medical PG Question 8: A 35-year-old woman who was recently ill with an upper respiratory infection presents to the emergency department with weakness in her lower limbs and difficulty breathing. Her symptoms began with a burning sensation in her toes along with numbness. She claims that the weakness has been getting worse over the last few days and now involving her arms and face. Currently, she is unable to get up from the chair without some assistance. Her temperature is 37.0°C (98.6°F), the blood pressure is 145/89 mm Hg, the heart rate is 99/min, the respiratory rate is 12/min, and the oxygen saturation is 95% on room air. On physical examination, she has diminished breath sounds on auscultation of bilateral lung fields with noticeably poor inspiratory effort. Palpation of the lower abdomen reveals a palpable bladder. Strength is 3 out of 5 symmetrically in the lower extremities bilaterally. The sensation is intact. What is the most likely diagnosis?
- A. Guillain-Barré syndrome (Correct Answer)
- B. Adrenoleukodystrophy
- C. Myasthenia Gravis
- D. Multiple sclerosis
- E. Acute disseminated encephalomyelitis
Acute respiratory distress syndrome Explanation: ***Guillain-Barré syndrome***
- The patient presents with **ascending paralysis** (weakness starting in lower limbs and progressing upwards to arms and face) following an **upper respiratory infection**, which is a classic presentation of GBS.
- The presence of **respiratory compromise** (difficulty breathing, diminished breath sounds, poor inspiratory effort), **dysautonomia** (palpable bladder due to urinary retention), and the pattern of **symmetrical weakness with intact sensation** are characteristic features of GBS.
- GBS typically presents with areflexia and shows albumino-cytologic dissociation on CSF analysis (elevated protein with normal cell count).
*Adrenoleukodystrophy*
- This is a rare, **X-linked genetic disorder** that primarily affects white matter in the brain and spinal cord, typically presenting in childhood with neurological deficits, not an acute ascending paralysis after an infection.
- It involves demyelination and adrenal insufficiency, which are not suggested by the acute onset and progressive neurological symptoms described.
*Myasthenia Gravis*
- Myasthenia gravis typically presents with **fluctuating muscle weakness** that worsens with activity and improves with rest, often affecting ocular and bulbar muscles first.
- The progression of weakness in this case is constant and ascending, not fluctuating, and there is no mention of characteristic findings like ptosis or diplopia.
*Multiple sclerosis*
- MS is characterized by **demyelinating lesions** in the central nervous system, leading to neurological symptoms that are often **disseminated in space and time**, meaning they affect different parts of the body at different times.
- While it can cause weakness, the acute onset of rapidly progressive, ascending, symmetrical paralysis following an infection is not typical for MS; MS symptoms are usually more insidious or relapsing-remitting.
*Acute disseminated encephalomyelitis*
- ADEM is an **acute inflammatory demyelinating disease** of the central nervous system that typically follows an infection or vaccination, but it usually presents with **encephalopathy** (altered mental status), multifocal neurological deficits, and often affects the brain and spinal cord diffusely.
- While it can cause weakness, the prominent ascending paralysis, intact sensation, and lack of encephalopathy make GBS a more fitting diagnosis.
Acute respiratory distress syndrome US Medical PG Question 9: A 42-year-old man is referred for an endocrinology consult because of decreased triiodothyronine (T3) hormone levels. He presented to the emergency department 1 week prior to this consultation with pneumonia and was admitted to a medicine service for management of his infection. He has since recovered from his infection after intravenous antibiotic administration. He currently has no symptoms and denies feeling cold or lethargic. A panel of laboratory tests are obtained with the following results:
Thyroid-stimulating hormone: 4.7 µU/mL
Thyroxine (T4): 6 µg/dL
Triiodothyronine (T3): 68 ng/dL
Which of the following additional findings would most likely also be seen in this patient?
- A. Increased free T3 concentration
- B. Increased reverse T3 concentration (Correct Answer)
- C. Decreased free T3 concentration
- D. Normal free and reverse T3 concentration
- E. Decreased reverse T3 concentration
Acute respiratory distress syndrome Explanation: ***Increased reverse T3 concentration***
- The patient's presentation including recent severe illness (pneumonia), normal TSH, slightly low T4, and low T3, with no symptoms of hypothyroidism, is classic for **euthyroid sick syndrome** (also known as non-thyroidal illness syndrome).
- In euthyroid sick syndrome, there is a characteristic increase in the peripheral conversion of T4 to **inactive reverse T3 (rT3)** rather than to active T3, due to altered deiodinase activity (decreased type 1 deiodinase and increased type 3 deiodinase).
- **Elevated rT3 is the most specific finding** that distinguishes euthyroid sick syndrome from primary hypothyroidism.
*Increased free T3 concentration*
- This would contradict the initial finding of **decreased total T3** and the typical pattern of euthyroid sick syndrome, where free T3 is usually decreased or low-normal.
- An increased free T3 level would suggest **hyperthyroidism**, which is inconsistent with the patient's clinical picture and other lab values.
*Decreased free T3 concentration*
- While free T3 would indeed be decreased in euthyroid sick syndrome along with total T3, this finding is **less specific** than elevated reverse T3.
- Decreased free T3 can be seen in **primary hypothyroidism, central hypothyroidism, and euthyroid sick syndrome**, making it less diagnostically useful.
- The question asks for the "most likely" additional finding, and **elevated reverse T3 is the hallmark biochemical marker** that best characterizes euthyroid sick syndrome and differentiates it from true hypothyroidism.
*Normal free and reverse T3 concentration*
- This would be inconsistent with the primary finding of **decreased T3** and the clinical context of recent severe illness, which almost invariably alters thyroid hormone metabolism.
- Normal levels would imply that the initial T3 finding was an anomaly or that the patient does not have euthyroid sick syndrome.
*Decreased reverse T3 concentration*
- A decreased reverse T3 concentration is typically seen in conditions like **hyperthyroidism** or during recovery phases of severe illness, not during the acute phase where rT3 is elevated.
- This finding would contradict the metabolic adaptations seen in **euthyroid sick syndrome**, where T4 is preferentially converted to rT3 (via type 3 deiodinase) to conserve energy during critical illness.
Acute respiratory distress syndrome US Medical PG Question 10: A 73-year-old man presents to the outpatient clinic complaining of chest pain with exertion. He states that resting for a few minutes usually resolves the chest pain. Currently, he takes 81 mg of aspirin daily. He has a blood pressure of 127/85 mm Hg and heart rate of 75/min. Physical examination reveals regular heart sounds and clear lung sounds bilateral. Which medication regimen below should be added?
- A. Metoprolol and a statin daily. Sublingual nitroglycerin as needed. (Correct Answer)
- B. Clopidogrel and amlodipine daily. Sublingual nitroglycerin as needed.
- C. Amlodipine and a statin daily. Sublingual nitroglycerin as needed.
- D. Amlodipine daily. Sublingual nitroglycerin as needed.
- E. Metoprolol and ranolazine daily. Sublingual nitroglycerin as needed.
Acute respiratory distress syndrome Explanation: ***Metoprolol and a statin daily. Sublingual nitroglycerin as needed.***
- This patient presents with symptoms consistent with **stable angina** (**chest pain with exertion, relieved by rest**). The recommended medical therapy includes **antiplatelet agents** (aspirin, already prescribed), **beta-blockers** (metoprolol) for symptom control and improved survival post-MI, and **high-intensity statins** for lipid management and plaque stabilization. **Sublingual nitroglycerin** is crucial for acute symptom relief.
- Beta-blockers like metoprolol decrease myocardial **oxygen demand** by reducing heart rate and contractility, effectively treating angina. Statins are essential for **atherosclerosis management**.
*Clopidogrel and amlodipine daily. Sublingual nitroglycerin as needed.*
- While clopidogrel is an **antiplatelet agent**, aspirin is typically the first-line choice for stable angina unless there's an intolerance or compelling reason for dual antiplatelet therapy (e.g., recent stent placement), which is not indicated here.
- Amlodipine, a **calcium channel blocker**, can be used for angina but is usually a second-line agent if beta-blockers are contraindicated or insufficient; it doesn't offer the mortality benefit seen with beta-blockers post-MI.
*Amlodipine and a statin daily. Sublingual nitroglycerin as needed.*
- This regimen includes a **statin** and sublingual nitroglycerin, which are appropriate. However, it uses amlodipine instead of a beta-blocker, which is generally the preferred initial therapy for angina due to its benefits in reducing myocardial oxygen demand and improving outcomes, especially in patients with a history of MI or heart failure.
- Beta-blockers provide superior **mortality reduction benefits** in patients with coronary artery disease compared to calcium channel blockers.
*Amlodipine daily. Sublingual nitroglycerin as needed.*
- This option misses two critical components of comprehensive treatment for stable angina: a **statin** for lipid management and plaque stabilization, and a **beta-blocker** for primary symptom control and long-term cardiac protection.
- Relying solely on amlodipine and sublingual nitroglycerin would leave the patient incompletely treated for their underlying **coronary artery disease**.
*Metoprolol and ranolazine daily. Sublingual nitroglycerin as needed.*
- This option lacks a **statin**, which is a cornerstone of therapy for stable angina to manage atherosclerosis.
- While metoprolol is appropriate and ranolazine can be used as an add-on therapy for refractory angina, it's not typically a first-line agent and doesn't replace the need for a statin.
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