Pulmonology (COPD, asthma, interstitial lung disease)

Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 1: A 65-year-old man comes to the physician because of a 10-month history of progressive shortness of breath and a cough productive of a small amount of white phlegm. Bilateral end-expiratory wheezing is heard on auscultation of the chest. Pulmonary function tests show total lung capacity that is 108% of predicted, an FEV1 that is 56% of predicted, and an FEV1:FVC ratio of 62%. Which of the following interventions is most likely to slow the decline in FEV1 in this patient?

• A. Salmeterol therapy
• B. Fluticasone therapy
• C. Smoking cessation (Correct Answer)
• D. Alpha-1 antitrypsin therapy
• E. Breathing exercises

Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Smoking cessation*** - This patient's symptoms (progressive shortness of breath, cough, end-expiratory wheezing) and PFT results (reduced FEV1, reduced FEV1:FVC ratio, normal TLC) are highly suggestive of **COPD**, which is primarily caused by smoking. - **Smoking cessation** is the only intervention clearly shown to slow the rate of FEV1 decline in patients with COPD, thereby improving long-term prognosis. *Salmeterol therapy* - **Salmeterol** is a long-acting beta-agonist (LABA) that provides bronchodilation and symptom relief in COPD. - While it improves symptoms and quality of life, it does **not alter the natural history of the disease** or slow the decline in FEV1. *Fluticasone therapy* - **Fluticasone** is an inhaled corticosteroid (ICS) used in COPD, often in combination with LABAs, particularly for patients with frequent exacerbations. - ICS therapy can reduce exacerbations but does **not slow the FEV1 decline** in COPD and may increase the risk of pneumonia. *Alpha-1 antitrypsin therapy* - **Alpha-1 antitrypsin deficiency** is a genetic cause of emphysema, typically presenting at a younger age or with a strong family history. This patient's history does not directly point to this diagnosis. - While augmentation therapy with alpha-1 antitrypsin can slow lung function decline in genetically deficient individuals, it is **ineffective for typical smoking-induced COPD**. *Breathing exercises* - **Breathing exercises**, such as pursed-lip breathing, are components of pulmonary rehabilitation programs. - They can improve symptoms, exercise tolerance, and quality of life but do **not impact the underlying disease progression** or FEV1 decline in COPD.

Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 2: A 40-year-old man comes to the physician because of a 2-year history of gradually worsening shortness of breath. He smoked half a pack of cigarettes daily for 10 years but stopped 8 years ago. His pulse is 72/min, blood pressure is 135/75 mm Hg, and respirations are 20/min. Examination shows an increased anteroposterior diameter of the chest. Diminished breath sounds are heard on auscultation of the chest. An x-ray of the chest shows widened intercostal spaces, a flattened diaphragm, and bilateral hyperlucency of the lung bases. This patient's condition puts him at greatest risk for which of the following conditions?

• A. Antineutrophil cytoplasmic antibody-positive vasculitis
• B. Bronchiolitis obliterans
• C. IgA nephropathy
• D. Bronchogenic carcinoma (Correct Answer)
• E. Hepatocellular carcinoma

Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Bronchogenic carcinoma*** - The patient's presentation with **shortness of breath**, history of **smoking**, and chest X-ray findings (increased AP diameter, flattened diaphragm, hyperlucency) are highly suggestive of **emphysema**, a strong risk factor for bronchogenic carcinoma. - While he stopped smoking 8 years ago, his past smoking history significantly increases his lifetime risk for lung cancer, and emphysema itself is an independent risk factor for malignancies. *Antineutrophil cytoplasmic antibody-positive vasculitis* - This condition involves systemic inflammation of blood vessels, often affecting the **lungs and kidneys**, but there are no clinical or radiological findings suggestive of vasculitis here. - There is no mention of symptoms like **hematuria**, **rash**, or other systemic inflammatory signs that would point towards ANCA-positive vasculitis. *Bronchiolitis obliterans* - This is a rare, severe obstructive lung disease often caused by toxic inhalant exposure (e.g., **sulfur mustard**, **diacetyl**) or as a complication of **lung transplantation** or **rheumatoid arthritis**, none of which are indicated in this patient. - While it can cause shortness of breath, the characteristic imaging findings in this patient (hyperlucency, flattened diaphragm) are more indicative of **emphysema**, not bronchiolitis obliterans. *IgA nephropathy* - This is a **primary glomerulonephritis** characterized by IgA deposits in the glomeruli, leading to **hematuria** and **proteinuria**, and is not related to the patient's respiratory symptoms or imaging findings. - There is no clinical information provided that would suggest renal involvement. *Hepatocellular carcinoma* - This is a **primary liver cancer** typically associated with chronic liver diseases like **hepatitis B** or **C infections**, **cirrhosis**, or **alcohol abuse**, none of which are suggested in the patient's history. - The patient's symptoms and diagnostic findings are entirely focused on the respiratory system, with no indication of liver disease.

Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 3: A 70-year-old man comes to the physician because of intermittent shortness of breath while going up stairs and walking his dog. It began about 1 month ago and seems to be getting worse. He has also developed a dry cough. He has not had any wheezing, fevers, chills, recent weight loss, or shortness of breath at rest. He has a history of Hodgkin lymphoma, for which he was treated with chemotherapy and radiation to the chest 7 years ago. He also has hypertension, for which he takes lisinopril. Ten years ago, he retired from work in the shipbuilding industry. He has smoked half a pack of cigarettes daily since the age of 21. Vital signs are within normal limits. On lung auscultation, there are mild bibasilar crackles. A plain x-ray of the chest shows bilateral ground-glass opacities at the lung bases and bilateral calcified pleural plaques. Which of the following is the greatest risk factor for this patient's current condition?

• A. Family history
• B. Smoking
• C. Radiation therapy
• D. Occupational exposure (Correct Answer)
• E. Advanced age

Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Occupational exposure*** - The patient's history of working in the **shipbuilding industry** and the presence of **calcified pleural plaques** strongly suggest **asbestosis**, a chronic lung disease caused by inhaling asbestos fibers. - **Asbestosis** typically presents with **progressive shortness of breath** and a **dry cough**, along with bibasilar crackles and ground-glass opacities, consistent with the patient's symptoms and chest X-ray findings. *Family history* - While genetics can play a role in some interstitial lung diseases (e.g., familial pulmonary fibrosis), there is no specific family history mentioned that would strongly link it to the patient's present illness. - The patient's presentation with **pleural plaques** points away from a primary genetic cause and towards environmental exposure. *Smoking* - Smoking is a risk factor for various lung conditions, including **emphysema** and **lung cancer**, and can exacerbate other lung diseases. However, the presence of **pleural plaques** is not caused by smoking. - While smoking can worsen the prognosis of asbestos-related diseases, it is not the primary cause of the pleural plaques or the most likely underlying condition in this specific clinical picture. *Radiation therapy* - **Radiation pneumonitis** and **fibrosis** can occur following chest radiation, and the patient received radiation for Hodgkin lymphoma 7 years ago. However, the **calcified pleural plaques** are highly characteristic of asbestos exposure, not radiation. - Radiation-induced lung changes are typically more localized to the irradiated field and would not specifically cause pleural plaques. *Advanced age* - While the incidence of many chronic diseases increases with age, age itself is not a specific risk factor for the characteristic findings of **calcified pleural plaques** and the described clinical picture. - The presence of specific radiological findings (pleural plaques) strongly points to an environmental exposure rather than simply advanced age.

Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 4: A 68-year-old, overweight gentleman with a 20-pack-year history of smoking presents to the primary care physician after noticing multiple blood-stained tissues after coughing attacks in the last month. His vital signs are within normal limits except for an O2 saturation of 93% on room air. He states that over the last 5 years his cough has continued to worsen and has never truly improved. He states that his shortness of breath has also worsened over this time period, as now he can barely make it up the flight of stairs in his home. In this patient, what is the most likely cause of his hemoptysis?

• A. Chronic bronchitis
• B. Bronchogenic carcinoma (Correct Answer)
• C. Lung abscess
• D. Acute pulmonary edema
• E. Goodpasture's disease

Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Bronchogenic carcinoma (Lung cancer)*** - **Hemoptysis in a smoker is lung cancer until proven otherwise** - this is a critical clinical principle in respiratory medicine. - This patient has major risk factors: **20-pack-year smoking history**, age 68, and chronic progressive symptoms. - **Hemoptysis** is a common presenting symptom of lung cancer, occurring in 20-50% of patients, caused by tumor invasion of bronchial vessels. - The **chronic progressive dyspnea** and **worsening cough over 5 years** suggest an evolving mass lesion or bronchial obstruction. - **Hypoxemia** (O2 sat 93%) indicates significant pulmonary compromise. - While this patient likely has underlying COPD/chronic bronchitis as a comorbidity, the presence of hemoptysis mandates urgent evaluation for malignancy. *Chronic bronchitis* - While this patient likely has chronic bronchitis (a type of COPD) given the smoking history and chronic productive cough, **hemoptysis is NOT a typical feature** of uncomplicated chronic bronchitis. - Hemoptysis in chronic bronchitis is rare and usually minimal; its presence should prompt investigation for other causes, particularly malignancy. - Chronic bronchitis explains the dyspnea and chronic cough but does not explain the hemoptysis. *Lung abscess* - A lung abscess typically presents with **acute onset of fever**, chills, night sweats, and **foul-smelling purulent sputum**, none of which are mentioned in this case. - The **chronic, progressive nature over five years** is inconsistent with an acute infectious process. *Acute pulmonary edema* - Acute pulmonary edema presents with **sudden onset of severe dyspnea**, orthopnea, and often pink frothy sputum due to acute cardiac decompensation. - The **gradual progression over five years** rules out an acute cardiac event. - Vital signs are stable, with no mention of cardiac findings. *Goodpasture's disease* - This rare autoimmune disorder causes **pulmonary-renal syndrome** with glomerulonephritis and pulmonary hemorrhage. - Typically affects younger patients (20s-30s) with acute presentation. - There are **no renal symptoms** (hematuria, oliguria, elevated creatinine) to suggest this diagnosis.

Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 5: A 70-year-old man presents to a physician with a cough and difficulty breathing during the last 7 years. He has smoked since his teenage years and regularly inhales tiotropium, formoterol, and budesonide and takes oral theophylline. The number of exacerbations has been increasing over the last 6 months. His temperature is 37.2°C (99°F), the heart rate is 92/min, the blood pressure is 134/88 mm Hg and the respiratory rate is 26/min. On chest auscultation breath sounds are diffusely decreased and bilateral rhonchi are present. Pulse oximetry shows his resting oxygen saturation to be 88%. Chest radiogram shows a flattened diaphragm, hyperlucency of the lungs, and a long, narrow heart shadow. The physician explains this condition to the patient and emphasizes the importance of smoking cessation. In addition to this, which of the following is most likely to reduce the risk of mortality from the condition?

• A. Roflumilast
• B. Low-dose oral prednisone
• C. Pulmonary rehabilitation
• D. Supplemental oxygen (Correct Answer)
• E. Prophylactic azithromycin

Pulmonology (COPD, asthma, interstitial lung disease) Explanation: ***Supplemental oxygen*** - The patient's **resting oxygen saturation of 88%** indicates significant hypoxemia, which, if chronic, places a high burden on the cardiovascular system and is a strong predictor of premature mortality in **COPD**. - **Long-term oxygen therapy (LTOT)** for at least 15 hours a day has been shown to improve survival in patients with severe chronic hypoxemia due to COPD. *Roflumilast* - **Roflumilast** is a phosphodiesterase-4 inhibitor that reduces inflammation and is used to decrease exacerbations in severe COPD associated with chronic bronchitis and a history of frequent exacerbations. - While it can improve lung function and reduce exacerbations, it has not been shown to reduce mortality directly. *Low-dose oral prednisone* - **Oral corticosteroids** are primarily used for acute exacerbations of COPD, not for long-term maintenance due to significant systemic side effects like osteoporosis, muscle weakness, and increased infection risk. - While they can temporarily reduce inflammation, chronic low-dose use is not recommended for mortality benefit and may cause harm in the long run. *Pulmonary rehabilitation* - **Pulmonary rehabilitation** is a comprehensive program that improves exercise tolerance, dyspnea, and quality of life in patients with COPD. - It does not directly reduce mortality but significantly improves functional status and potentially reduces hospitalizations. *Prophylactic azithromycin* - **Prophylactic azithromycin** can reduce the frequency of exacerbations in select patients with severe COPD, likely due to its anti-inflammatory and immunomodulatory properties, as well as its bactericidal effect. - Similar to roflumilast, it reduces exacerbations but has not been shown to reduce mortality directly in COPD patients.

Pulmonology (COPD, asthma, interstitial lung disease) US Medical PG Question 6: 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 7: 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 8: 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 9: 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 10: 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.

Pulmonology (COPD, asthma, interstitial lung disease) Flashcard 1 of 2

Question: What signs/symptoms define Kartagener syndrome?

Answer: Subset of PCD with triad of bronchiectasis, chronic sinusitis, and situs inversus

Pulmonology (COPD, asthma, interstitial lung disease) Flashcard 2 of 2

Question: When primary ciliary dyskinesia (PCD) presents with the triad of bronchiectasis, chronic sinusitis, and situs inversus, what is it called?

Answer: Kartagener syndrome