Pulmonology Practice Questions

Q: Pulmonary embolism is best diagnosed by:

Angiography. **Explanation:** The diagnosis of Pulmonary Embolism (PE) involves a tiered approach ranging from screening to definitive confirmation. **Why Angiography is correct:** **Pulmonary Angiography** is considered the **Gold Standard** (definitive) investigation for diagnosing pulmonary embolism. It allows for the direct visualization of an intraluminal filling defect or the abrupt "cutoff" of a pulmonary vessel. While CT Pulmonary Angiography (CTPA) is the modern clinical investigation of choice due to its non-invasive nature [2], conventional catheter-based angiography remains the most accurate reference standard against which other tests are measured. **Why other options are incorrect:** * **ECG:** Non-specific. The most common finding is sinus tachycardia [1]. The "classic" S1Q3T3 pattern is specific but seen in fewer than 20% of patients [1]. It is used to rule out myocardial infarction rather than diagnose PE [1]. * **Perfusion Scan (V/Q Scan):** This is a screening tool. While a "high probability" scan in a patient with high clinical suspicion is suggestive, it is often indeterminate in patients with underlying lung disease [2]. * **Plain X-ray:** Usually normal in PE [1]. Its primary role is to rule out other causes of chest pain (like pneumonia or pneumothorax) [1]. Classic signs like Hampton’s Hump or Westermark sign are rare. **Clinical Pearls for NEET-PG:** * **Investigation of Choice (IOC):** CT Pulmonary Angiography (CTPA) [2]. * **Gold Standard:** Conventional Pulmonary Angiography. * **Best Initial Test:** Chest X-ray (to rule out mimics) or D-dimer (to rule out PE in low-risk patients). * **Most common ECG finding:** Sinus Tachycardia [1]. * **Most common symptom:** Tachypnea/Dyspnea.

Q: What is the drug of choice for diffuse panbronchiolitis?

Erythromycin. **Explanation:** **Diffuse Panbronchiolitis (DPB)** is an idiopathic inflammatory airway disease characterized by chronic inflammation of the respiratory bronchioles, commonly associated with chronic sinusitis and a high prevalence in East Asian populations. **1. Why Erythromycin is the Correct Answer:** The cornerstone of DPB management is **long-term, low-dose Macrolide therapy** (specifically Erythromycin). The therapeutic benefit is derived not from its antimicrobial properties, but from its **immunomodulatory and anti-inflammatory effects**. Macrolides inhibit mucus hypersecretion, reduce neutrophil infiltration, and decrease the production of pro-inflammatory cytokines (IL-8, TNF-α). This treatment has revolutionized the prognosis of DPB, increasing the 10-year survival rate from <25% to over 90%. **2. Why Other Options are Incorrect:** * **Tetracyclines:** While they possess some anti-inflammatory properties, they have not shown the specific clinical efficacy required to alter the course of DPB compared to macrolides. * **Prednisolone:** Although DPB is an inflammatory condition, corticosteroids alone are generally ineffective in halting the progression of the disease and are not considered first-line therapy. * **Cyclophosphamide:** This is a potent immunosuppressant used in vasculitis or interstitial lung diseases (like GPA); it has no role in the standard management of DPB. **Clinical Pearls for NEET-PG:** * **Classic Triad:** Chronic sinusitis, bilateral small nodular shadows on CXR/HRCT, and obstructive lung defect. * **HRCT Finding:**

Q: Rasmussen's aneurysm involves which of the following arteries?

Pulmonary artery. **Explanation:** **Rasmussen’s aneurysm** is a pseudoaneurysm of the **pulmonary artery** branch that occurs as a late complication of pulmonary tuberculosis. **1. Why the Pulmonary Artery is Correct:** In patients with chronic cavitary tuberculosis, the inflammatory process leads to the erosion of the vessel wall of a pulmonary artery branch located in the wall of a tuberculous cavity. The weakened wall undergoes aneurysmal dilatation (pseudoaneurysm). If this aneurysm ruptures into the cavity, it leads to life-threatening, massive hemoptysis. **2. Why the Other Options are Incorrect:** * **Bronchial Artery:** While the bronchial arteries are the most common source of massive hemoptysis in general (due to high systemic pressure), they are not the vessels involved in the specific pathological entity known as Rasmussen’s aneurysm. * **Intercostal Artery:** These are systemic arteries supplying the chest wall. They may be involved in hemoptysis related to pleural diseases or chronic infections via transpleural collaterals, but not in Rasmussen’s. * **Aorta:** Aorto-bronchial fistulas can cause catastrophic hemoptysis, but this is usually related to aortic aneurysms or prior surgery, not tuberculous cavitation. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of massive hemoptysis:** Bronchial artery (85-90% of cases). * **Rasmussen’s Aneurysm:** A rare but classic cause of massive hemoptysis in TB. * **Gold Standard Investigation:** Bronchial Artery Angiography (to identify the bleeding site). * **Management:** Bronchial Artery Embolization (BAE) is the first-line treatment for stabilizing massive hemoptysis. For Rasmussen’s specifically, pulmonary artery embolization may be required.

Q: Which of the following conditions may lead to exudative pleural effusion?

Bronchogenic carcinoma. ### Explanation Pleural effusions are classified into **transudates** and **exudates** based on Light’s Criteria. This distinction is crucial for narrowing down the differential diagnosis [1]. **Correct Answer: D. Bronchogenic carcinoma** Bronchogenic carcinoma causes an **exudative** effusion [1]. The underlying mechanism involves direct pleural involvement by the tumor or lymphatic obstruction, which increases capillary permeability and prevents the drainage of proteins and cells from the pleural space [2]. Malignancy is one of the most common causes of exudative effusions, often presenting with hemorrhagic fluid and low glucose levels [1]. **Incorrect Options:** * **A, B, and C (Cirrhosis, Nephrotic Syndrome, Congestive Heart Failure):** These conditions lead to **transudative** effusions. * **CHF** increases pulmonary capillary hydrostatic pressure. * **Cirrhosis and Nephrotic Syndrome** result in hypoalbuminemia, which decreases plasma oncotic pressure. * In these cases, the pleural membranes are intact, but systemic factors alter the balance of fluid filtration and reabsorption. **High-Yield Clinical Pearls for NEET-PG:** * **Light’s Criteria:** An effusion is exudative if it meets at least one of the following: 1. Pleural fluid protein/Serum protein ratio **> 0.5** 2. Pleural fluid LDH/Serum LDH ratio **> 0.6** 3. Pleural fluid LDH **> 2/3rd** the upper limit of normal serum LDH. * **Most common cause of Transudate:** Congestive Heart Failure (usually bilateral). * **Most common cause of Exudate:** Parapneumonic effusion, followed by Malignancy and Tuberculosis [1]. * **Pseudochylothorax:** Seen in chronic Rheumatoid Arthritis or TB effusions (high cholesterol, but no chylomicrons).

Q: Bronchial asthma is characterized by which of the following?

Hyperresponsiveness of the airway. **Explanation:** **Bronchial Asthma** is defined as a chronic inflammatory disorder of the airways characterized by reversible airflow obstruction and **Airway Hyperresponsiveness (AHR)** [1]. **Why Option D is Correct:** Airway Hyperresponsiveness is the physiological hallmark of asthma. It refers to an exaggerated bronchoconstrictor response to stimuli that are otherwise harmless to healthy individuals (e.g., cold air, exercise, or histamine) [2]. This hyper-reactivity leads to the classic symptoms of wheezing, breathlessness, and coughing [3]. While inflammation triggers AHR, the hyperresponsiveness itself is the defining functional characteristic that distinguishes asthma from other chronic lung diseases [2]. **Why Other Options are Incorrect:** * **Option A & B:** While asthma involves inflammation and often has an allergic (atopic) component, these are **pathological mechanisms** rather than the defining physiological characteristic [1]. Not all asthma is allergic (e.g., intrinsic or non-atopic asthma), and many inflammatory lung diseases (like COPD) are not asthma. * **Option C:** This is the opposite of the clinical reality. **Hyporesponsiveness** would imply a lack of reaction to triggers, whereas asthmatic airways are hypersensitive. **NEET-PG High-Yield Pearls:** * **Diagnosis:** The gold standard for demonstrating AHR in clinical practice is the **Methacholine Challenge Test** (a provocative test where a $\text{PC}_{20} < 8 \text{ mg/mL}$ indicates asthma) [2]. * **Pathology:** Look for **Curschmann spirals** (mucus plugs) and **Charcot-Leyden crystals** (eosinophil breakdown products) in sputum. * **Airway Remodeling:** Chronic untreated inflammation leads to subepithelial fibrosis and smooth muscle hypertrophy, making the obstruction irreversible over time.

Q: What is the basic genetic abnormality in primary pulmonary hypertension?

Bone morphogenetic protein receptor type II. **Explanation:** **Primary Pulmonary Hypertension (now classified as Idiopathic Pulmonary Arterial Hypertension - IPAH)** is characterized by the remodeling of pulmonary arterioles, leading to increased vascular resistance. **1. Why Option A is Correct:** The most significant genetic discovery in IPAH is a mutation in the **Bone Morphogenetic Protein Receptor Type II (BMPR2)** gene, located on chromosome 2q33 [1]. BMPR2 is a member of the TGF-̢ receptor superfamily. Under normal conditions, BMPR2 signaling inhibits the proliferation of vascular smooth muscle cells. A "loss-of-function" mutation [1] leads to uncontrolled proliferation of endothelial and smooth muscle cells, resulting in the characteristic **plexiform lesions** and vascular narrowing. **2. Why Other Options are Incorrect:** * **Option B (Endothelin):** While Endothelin-1 levels are elevated in pulmonary hypertension and contribute to vasoconstriction, it is a **mediator** [2] of the disease process, not the primary genetic abnormality. * **Option C (Homeobox gene):** These genes are involved in anatomical development and pattern formation during embryogenesis, not the pathogenesis of IPAH. * **Option D (PAX-II):** PAX genes are transcription factors involved in organogenesis (specifically renal and eye development); they have no established link to pulmonary hypertension. **Clinical Pearls for NEET-PG:** * **Inheritance:** BMPR2 mutations follow an **Autosomal Dominant** pattern with **incomplete penetrance** (only ~20% of carriers develop the disease). * **Histology:** The pathognomonic finding is the **Plexiform lesion**. * **Demographics:** Most common in young females (Female:Male ratio ≈ 3:1). * **Diagnosis:** Gold standard is **Right Heart Catheterization** (Mean Pulmonary Artery Pressure >20 mmHg at rest).

Question 1

Pulmonary embolism is best diagnosed by:

Accepted Answer

Angiography

Answer

ECG

Answer

Perfusion scan

Answer

Plain X-ray

Question 2

What is the drug of choice for diffuse panbronchiolitis?

Accepted Answer

Erythromycin

Answer

Tetracyclines

Answer

Prednisolone

Answer

Cyclophosphamide

Question 3

Rasmussen's aneurysm involves which of the following arteries?

Accepted Answer

Pulmonary artery

Answer

Bronchial artery

Answer

Intercostal artery

Answer

Aorta

Question 4

Which of the following conditions may lead to exudative pleural effusion?

Accepted Answer

Bronchogenic carcinoma

Answer

Cirrhosis

Answer

Nephrotic syndrome

Answer

Congestive heart failure

Question 5

Pleural glucose less than 60 mg/dl is seen in which of the following conditions?

Accepted Answer

Tuberculosis

Answer

Malignancy

Answer

Fungal infection

Answer

Pancreatitis

Question 6

What is the recommended treatment for cough variant asthma?

Accepted Answer

Inhaled corticosteroids (ICS) low dose once a day

Answer

Long-acting beta-agonists (LABA) once at night

Answer

Short-acting beta-agonists (SABA) twice daily

Answer

Anti-tussive lozenges as needed

Question 7

Bronchial asthma is characterized by which of the following?

Accepted Answer

Hyperresponsiveness of the airway

Answer

Inflammatory disease of the airway

Answer

Allergic disease of the airway

Answer

Hyporesponsiveness of the airway

Question 8

What is the basic genetic abnormality in primary pulmonary hypertension?

Accepted Answer

Bone morphogenetic protein receptor type II

Answer

Endothelin

Answer

Homeobox gene

Answer

PAX-II

Question 9

Clubbing is commonly seen in all of the following except?

Accepted Answer

Tropical eosinophilia

Answer

Mesothelioma

Answer

Bronchiectasis

Answer

Fibrosing alveolitis

Question 10

What is the treatment most likely to benefit a patient with massive pulmonary embolism presenting in shock?

Accepted Answer

Thrombolytic therapy

Answer

Inotropic agent

Answer

Vasodilator therapy

Answer

Diuretic therapy

Pulmonology — MCQs

Pulmonology — MCQs

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