Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Pulmonology (COPD, asthma, interstitial lung disease). These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 1: A 35-year-old pregnant woman at 24 weeks gestation with moderate persistent asthma presents with worsening symptoms over 3 days. She has been using albuterol 6-8 times daily. She discontinued her ICS/LABA inhaler when she learned she was pregnant due to concerns about fetal safety. Current medications include prenatal vitamins only. Vital signs: respiratory rate 24/min, oxygen saturation 94% on room air, heart rate 98/min. Peak flow is 60% of her personal best. Fetal heart monitoring is reassuring. Synthesizing the management approach that balances maternal asthma control and fetal safety, what is the most appropriate treatment plan?
- A. Continue albuterol only until delivery to minimize fetal medication exposure
- B. Start oral prednisone and continue albuterol only
- C. Restart ICS/LABA, give oral prednisone burst, close monitoring (Correct Answer)
- D. Give IM corticosteroids and restart ICS after delivery
- E. Hospitalize for IV corticosteroids and continuous monitoring
Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Restart ICS/LABA, give oral prednisone burst, close monitoring***
- For a patient with **moderate persistent asthma** experiencing an exacerbation, an **oral corticosteroid burst** is necessary to reduce inflammation, while **ICS/LABA** must be resumed to provide long-term control.
- Maintaining maternal asthma control is vital for preventing **fetal hypoxia**; the risks of uncontrolled asthma to the fetus far outweigh the potential risks of these medications.
*Continue albuterol only until delivery to minimize fetal medication exposure*
- Relying solely on a **SABA** for persistent asthma is dangerous and increases the risk of **preterm birth**, **low birth weight**, and maternal respiratory failure.
- **Suboptimal control** of asthma during pregnancy is more harmful to the fetus than the medications used to manage it.
*Hospitalize for IV corticosteroids and continuous monitoring*
- The patient’s oxygen saturation (94%) and **peak flow (60%)** indicate a moderate exacerbation that can typically be managed in the **outpatient setting** with close follow-up.
- Hospitalization is reserved for those with **severe respiratory distress**, failed outpatient therapy, or signs of **fetal compromise**.
*Start oral prednisone and continue albuterol only*
- While prednisone clears the acute flare, failing to restart maintenance **controller therapy** (ICS/LABA) will likely lead to another exacerbation as soon as the steroid burst ends.
- Chronic airway inflammation in **moderate persistent asthma** requires daily preventive treatment, not just episodic rescue medication.
*Give IM corticosteroids and restart ICS after delivery*
- **IM corticosteroids** are not the standard of care for acute asthma flares; **oral prednisone** is preferred for its predictable absorption and efficacy.
- Delaying the resumption of controller therapy until **after delivery** leaves the mother and fetus at high risk during the remainder of the pregnancy.
Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 2: A 56-year-old woman presents with 6 months of progressive dyspnea. She has no occupational exposures or smoking history. HRCT shows bilateral peripheral and basal predominant reticular opacities with honeycombing and minimal ground-glass opacities. No significant mediastinal lymphadenopathy. PFTs show FVC 62% predicted, FEV1/FVC 0.84, DLCO 52% predicted. She was started on prednisone 40 mg daily by another physician 3 weeks ago with minimal improvement. Surgical lung biopsy shows usual interstitial pneumonia pattern with fibroblastic foci and temporal heterogeneity. Evaluate the most appropriate management modification.
- A. Discontinue prednisone, start nintedanib (Correct Answer)
- B. Increase prednisone dose to 60 mg daily
- C. Continue prednisone and add azathioprine
- D. Continue prednisone and add N-acetylcysteine
- E. Continue prednisone and add mycophenolate
Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Discontinue prednisone, start nintedanib***
- The patient's clinical and radiological findings, combined with a **usual interstitial pneumonia (UIP) pattern** on biopsy, confirm a diagnosis of **Idiopathic Pulmonary Fibrosis (IPF)**.
- **Corticosteroids** are not indicated for IPF; clinical trials like **PANTHER-IPF** demonstrated that they increase mortality and hospitalization compared to placebo.
*Continue prednisone and add azathioprine*
- The combination of **prednisone and azathioprine** was shown to be harmful in the **PANTHER-IPF trial**, increasing the risk of death and hospitalization.
- This pharmacological approach is no longer recommended for patients with a confirmed diagnosis of **Idiopathic Pulmonary Fibrosis**.
*Continue prednisone and add mycophenolate*
- While **mycophenolate** is used for **connective tissue disease-associated ILD** or **NSIP**, it has no proven efficacy in treating the **UIP pattern** of IPF.
- Maintaining **corticosteroids** in IPF patients provides no benefit and exposes the patient to unnecessary side effects like **hyperglycemia** and **osteoporosis**.
*Increase prednisone dose to 60 mg daily*
- Escalating **steroid doses** does not reverse the **fibroblastic foci** seen in IPF and may lead to serious complications such as **peptic ulcer disease** or **infections**.
- High-dose steroids are rarely useful in IPF unless there is a specific suspected **acute exacerbation**, and even then, evidence is weak.
*Continue prednisone and add N-acetylcysteine*
- **N-acetylcysteine (NAC)** as a monotherapy or in combination with steroids/azathioprine was found to be ineffective for IPF in the **PANTHER-IPF trial**.
- Continuing **prednisone** while adding NAC fails to address the need for **antifibrotic therapy** and maintains the risk of steroid-induced morbidity.
Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 3: A 68-year-old man with COPD (FEV1 38% predicted) presents with his third exacerbation in 4 months despite LAMA/LABA/ICS therapy. Each exacerbation has required oral antibiotics and prednisone. He quit smoking 2 years ago. Blood eosinophil count is 80 cells/μL. Sputum cultures from previous exacerbations grew Haemophilus influenzae twice and Moraxella catarrhalis once. He remains symptomatic with mMRC dyspnea score of 3. Evaluating strategies to reduce future exacerbations, what intervention would provide the most benefit?
- A. Switch to LAMA/LABA and discontinue ICS
- B. Add N-acetylcysteine 600 mg twice daily
- C. Add roflumilast to current regimen
- D. Increase ICS to high dose
- E. Add azithromycin 250 mg three times weekly (Correct Answer)
Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Add azithromycin 250 mg three times weekly***
- In patients with **COPD** who experience frequent exacerbations despite **triple therapy** (LAMA/LABA/ICS), the addition of a **long-term macrolide** like azithromycin is recommended to reduce exacerbation frequency.
- This strategy is particularly effective in **former smokers** and patients with low **blood eosinophil counts** (<100 cells/µL), as seen in this clinical scenario.
*Add roflumilast to current regimen*
- **Roflumilast** is a PDE4 inhibitor targeted at patients with **chronic bronchitis** and FEV1 <50%, but it is often associated with significant **gastrointestinal side effects** and weight loss.
- While it can reduce exacerbations, **azithromycin** is preferred in former smokers and those already on triple therapy with persistent infectious-type exacerbations.
*Switch to LAMA/LABA and discontinue ICS*
- Discontinuing **Inhaled Corticosteroids (ICS)** in a patient already experiencing frequent exacerbations is likely to increase the risk of further **respiratory decompensation**.
- This patient's FEV1 is very low (**38% predicted**), making him a high-risk candidate who generally requires the anti-inflammatory benefits of ICS despite a low eosinophil count.
*Add N-acetylcysteine 600 mg twice daily*
- **N-acetylcysteine** is a mucolytic that may reduce exacerbations in specific subsets of patients with **chronic bronchitis**, but the evidence of benefit is less robust than that for **macrolide therapy**.
- It does not address the underlying bacterial colonization or recurrent infection risk as effectively as **azithromycin** in high-risk COPD patients.
*Increase ICS to high dose*
- Increasing the dose of **Inhaled Corticosteroids** provides diminishing returns and significantly increases the risk of side effects, most notably **pneumonia**.
- Given the patient's low **blood eosinophil count** (80 cells/µL), he is unlikely to derive significant additional benefit from escalating steroid therapy.
Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 4: A 42-year-old woman with severe asthma on high-dose ICS/LABA has had 4 hospitalizations in the past year despite good adherence. Her pre-bronchodilator FEV1 is 65% predicted, improving to 78% post-bronchodilator. Laboratory studies show peripheral eosinophil count of 420 cells/μL, total IgE 180 IU/mL. She has no history of nasal polyps. Skin testing is positive for dust mites and cat dander, but she has no pets and uses allergen-proof bedding. Analyzing this case, which biologic therapy is most appropriate?
- A. Mepolizumab (anti-IL-5) (Correct Answer)
- B. Benralizumab (anti-IL-5Rα)
- C. Omalizumab (anti-IgE)
- D. Tezepelumab (anti-TSLP)
- E. Dupilumab (anti-IL-4Rα)
Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Mepolizumab (anti-IL-5)***
- This patient has **severe eosinophilic asthma**, characterized by a peripheral blood **eosinophil count ≥150 cells/μL** (hers is 420 cells/μL) and frequent exacerbations despite high-dose therapy.
- **Mepolizumab** is a humanized monoclonal antibody against **IL-5** that reduces eosinophil recruitment and maturation, effectively decreasing the rate of **asthma exacerbations**.
*Omalizumab (anti-IgE)*
- While she has an elevated **total IgE** and positive skin tests, her primary symptoms do not focus on clear **allergen-triggered** episodes that would make this the primary choice over eosinophil-targeted therapy.
- **Omalizumab** is less effective than IL-5 inhibitors in patients where the **peripheral eosinophil count** is markedly elevated (e.g., >300-400 cells/μL).
*Dupilumab (anti-IL-4Rα)*
- **Dupilumab** blocks **IL-4 and IL-13** signaling and is highly effective in eosinophilic asthma and those with a high **fractional exhaled nitric oxide (FeNO)**.
- It is clinically prioritized for patients with comorbid **nasal polyps** or **atopic dermatitis**, neither of which are present in this patient's history.
*Benralizumab (anti-IL-5Rα)*
- **Benralizumab** targets the **alpha subunit of the IL-5 receptor**, leading to the near-complete depletion of eosinophils via **antibody-dependent cell-mediated cytotoxicity (ADCC)**.
- While a valid option, **Mepolizumab** is the classic first-line representative for IL-5 inhibition in standardized testing unless specific rapid depletion or dosing intervals are being tested.
*Tezepelumab (anti-TSLP)*
- **Tezepelumab** is an anti-thymic stromal lymphopoietin (**TSLP**) monoclonal antibody that acts high up in the inflammatory cascade, making it suitable for **non-eosinophilic (Th2-low)** asthma.
- Because this patient has a clear **eosinophilic phenotype** (420 cells/μL), more targeted therapies like IL-5 inhibitors are typically selected first.
Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 5: A 48-year-old woman presents with 8 months of progressive dyspnea and dry cough. She works as a dental technician. Exam reveals bibasilar fine crackles. HRCT shows bilateral lower lobe reticular opacities with honeycombing and traction bronchiectasis. Pulmonary function tests show FVC 58% predicted, FEV1/FVC ratio 0.82, DLCO 48% predicted. Bronchoalveolar lavage shows lymphocytosis with CD4/CD8 ratio of 0.8. Transbronchial biopsy is non-diagnostic. Analyzing the pattern of findings, what is the most likely diagnosis?
- A. Idiopathic pulmonary fibrosis
- B. Sarcoidosis
- C. Chronic hypersensitivity pneumonitis (Correct Answer)
- D. Cryptogenic organizing pneumonia
- E. Nonspecific interstitial pneumonia
Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Chronic hypersensitivity pneumonitis***
- This diagnosis is supported by the patient's occupation as a **dental technician** (exposure to dusts/chemicals) and a **BAL lymphocytosis** with a **CD4/CD8 ratio < 1.0 (0.8)**.
- Chronic HP often mimics a **UIP pattern** with honeycombing and traction bronchiectasis, but the history of exposure and BAL findings point away from idiopathic causes.
*Idiopathic pulmonary fibrosis*
- While the HRCT shows a **UIP pattern** (honeycombing, reticulation), IPF is a diagnosis of exclusion and typically does not present with **significant BAL lymphocytosis**.
- The CD4/CD8 ratio in IPF is usually normal or increased, whereas this patient has a decreased ratio suggesting an **extrinsic allergic** or inflammatory process.
*Nonspecific interstitial pneumonia*
- NSIP characteristically shows **ground-glass opacities** and **subpleural sparing**, which are not the dominant features in this case.
- Although it is associated with a restrictive pattern, the presence of **honeycombing** is much more common in UIP/Chronic HP than in NSIP.
*Sarcoidosis*
- Sarcoidosis usually presents with a **high CD4/CD8 ratio (>3.5)** in the BAL fluid, whereas this patient has a low ratio.
- Imaging would typically show **hilar lymphadenopathy** and nodules in a **perilymphatic distribution** (upper/middle zones) rather than lower lobe honeycombing.
*Cryptogenic organizing pneumonia*
- COP typically presents with a more subacute onset and shows **patchy, subpleural, or peribronchovascular consolidations** rather than honeycombing.
- It is highly **steroid-responsive** and lacks the severe fibrotic architectural distortion (traction bronchiectasis) seen on this patient's HRCT.
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