Pulmonology — MCQs

Pulmonology Indian Medical PG Practice Questions and MCQs

Question 471: Hemoptysis is commonly seen in:

A. Pulmonary thromboembolism (Correct Answer)
B. Miliary tuberculosis
C. Pneumoconiosis
D. None of the above

Explanation: **Explanation:** **Pulmonary Thromboembolism (PTE)** is a classic cause of hemoptysis, occurring in approximately 10–30% of cases. The underlying mechanism is **pulmonary infarction** [1]. When a peripheral pulmonary artery is occluded, the lung tissue distal to the block undergoes necrosis and hemorrhage into the alveolar spaces. This typically presents as small amounts of bright red blood or blood-streaked sputum, often accompanied by pleuritic chest pain and dyspnea [1]. **Analysis of Options:** * **Miliary Tuberculosis (Option B):** While pulmonary TB is the most common cause of hemoptysis in India, *miliary* TB typically presents with hematogenous spread, resulting in millet-sized tubercles throughout the lung parenchyma. It usually presents with fever, weight loss, and dyspnea; hemoptysis is rare in the miliary form compared to cavitary TB. * **Pneumoconiosis (Option C):** Occupational lung diseases like silicosis or asbestosis primarily cause progressive pulmonary fibrosis [2]. Hemoptysis is not a standard feature unless there is a complication like Progressive Massive Fibrosis (PMF) or a superimposed infection (e.g., Silicotuberculosis). **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of hemoptysis (Global):** Acute Bronchitis [3]. * **Most common cause of hemoptysis (India):** Tuberculosis. * **Massive Hemoptysis:** Defined as >200–600 ml of blood in 24 hours. The most common source is the **Bronchial Arteries** (high pressure) rather than the Pulmonary Arteries. * **PTE Triad:** Hemoptysis, pleuritic chest pain, and dyspnea (seen in <20% of patients). * **Chest X-ray in PTE:** Usually normal, but may show **Hampton’s Hump** (wedge-shaped opacity indicating infarction) or **Westermark sign** (focal oligemia).

Question 472: What is true about sarcoidosis?

A. Causes large cavitary lesions
B. Spontaneous remission may occur (Correct Answer)
C. Tuberculin test is negative
D. Caseation and necrosis may occur

Explanation: **Explanation:** Sarcoidosis is a multisystem, idiopathic disease characterized by the formation of **non-caseating granulomas**. **1. Why Option B is Correct:** Spontaneous remission is a hallmark of sarcoidosis, occurring in approximately **60-70% of patients**. This is particularly common in patients with Stage I disease (bilateral hilar lymphadenopathy) and those presenting with **Löfgren syndrome** (erythema nodosum, hilar adenopathy, and arthralgia) [1]. Most remissions occur within the first two years of diagnosis. **2. Why the Other Options are Incorrect:** * **Option A:** Sarcoidosis typically presents with interstitial lung disease or hilar lymphadenopathy. While rare "cystic" changes can occur in end-stage fibrosis, **large cavitary lesions** are characteristic of Tuberculosis or fungal infections, not sarcoidosis [2]. * **Option C:** While it is true that many sarcoidosis patients exhibit **cutaneous anergy** (a negative Tuberculin Skin Test/Mantoux), this is a *clinical finding*, not a defining rule. More importantly, Option B is the "most true" classic teaching regarding the natural history of the disease. (Note: In exams, spontaneous remission is the preferred high-yield fact). * **Option D:** By definition, sarcoidosis granulomas are **non-caseating**. The presence of caseation or central necrosis strongly suggests an infectious etiology like Tuberculosis [2]. **Clinical Pearls for NEET-PG:** * **Biochemical Marker:** Elevated **Serum ACE levels** (reflects total granuloma burden). * **Bronchoalveolar Lavage (BAL):** Shows an increased **CD4+:CD8+ ratio** (usually >3.5:1). * **Kveim-Siltzbach Test:** Historically used but now obsolete due to infection risks. * **Scadding Stages:** Stage I (Hilar nodes), Stage II (Nodes + Infiltrates), Stage III (Infiltrates only), Stage IV (Fibrosis). * **Asteroid bodies** and **Schaumann bodies** are characteristic microscopic findings within the giant cells.

Question 473: Extensive pleural thickening, especially involving the diaphragmatic pleura, is a classical feature of which condition?

A. Coal worker's pneumoconiosis
B. Asbestosis (Correct Answer)
C. Silicosis
D. Siderosis

Explanation: **Explanation:** The correct answer is **Asbestosis** (specifically, asbestos-related pleural disease) [1]. **1. Why Asbestosis is correct:** Asbestos fibers are unique among mineral dusts for their ability to migrate to the periphery of the lung and reach the visceral and parietal pleura [1]. The hallmark of asbestos exposure is the development of **pleural plaques**, which are areas of dense, collagenous thickening [1]. These plaques characteristically involve the **parietal pleura**, particularly the **posterolateral chest wall** and the **diaphragmatic pleura** (often sparing the costophrenic angles). Diaphragmatic calcification is considered nearly pathognomonic for prior asbestos exposure. **2. Why other options are incorrect:** * **Coal Worker’s Pneumoconiosis (CWP):** Primarily involves the lung parenchyma (macules and nodules) with a predilection for the upper lobes [1]. Pleural involvement is rare. * **Silicosis:** Characterized by "eggshell calcification" of hilar lymph nodes and silicotic nodules in the upper lobes [1]. While it can cause some pleural thickening, it does not classically target the diaphragmatic pleura. * **Siderosis:** Caused by iron oxide inhalation (common in welders) [1]. It is a "benign" pneumoconiosis that causes reticulonodular opacities on X-ray but typically does not cause fibrosis or pleural disease. **3. NEET-PG High-Yield Pearls:** * **Most common manifestation of asbestos exposure:** Pleural plaques (asymptomatic). * **Most common malignancy in asbestosis:** Bronchogenic carcinoma (Risk is synergistically increased with smoking). * **Most specific malignancy:** Mesothelioma (Not related to smoking). * **Radiology:** Look for "Holly leaf" appearance of pleural plaques on chest X-ray. * **Histology:** Ferruginous bodies (asbestos bodies) – golden-brown, fusiform rods with beaded appearance (Prussian blue positive) [1].

Question 474: Kartagener's syndrome is characterized by which of the following?

A. Infertility
B. Differential pulse
C. Ciliary dyskinesia
D. All of the above (Correct Answer)

Explanation: **Explanation:** Kartagener’s syndrome is a clinical subtype of **Primary Ciliary Dyskinesia (PCD)**, an autosomal recessive disorder characterized by a structural defect in the **dynein arms** of cilia. This leads to impaired ciliary motility throughout the body. **Why "All of the above" is correct:** 1. **Ciliary Dyskinesia:** This is the fundamental pathophysiology. Defective cilia in the respiratory tract lead to impaired mucociliary clearance, causing chronic sinusitis and bronchiectasis [1]. 2. **Infertility:** In males, the flagella of spermatozoa (which are structurally identical to cilia) are immobile, leading to infertility. In females, defective cilia in the fallopian tubes can lead to reduced fertility or ectopic pregnancies. 3. **Differential Pulse:** Kartagener’s syndrome is defined by the triad of **Situs Inversus**, bronchiectasis, and sinusitis [1]. In Situs Inversus, the heart is located on the right side (**Dextrocardia**). If a clinician palpates the pulses or measures blood pressure normally without accounting for the reversed anatomy, or if there are associated rare vascular anomalies, pulse discrepancies may be noted. (Note: In the context of NEET-PG, "Differential Pulse" is often included in this question to reflect the cardiovascular displacement/dextrocardia associated with the syndrome). **Clinical Pearls for NEET-PG:** * **The Triad:** Bronchiectasis, Sinusitis, and Situs Inversus [1]. * **Pathology:** Absence of inner or outer **dynein arms** (most common defect). * **Screening Test:** Saccharin test (prolonged time) or Nasal Nitric Oxide (low levels). * **Gold Standard Diagnosis:** Electron microscopy of ciliary biopsy. * **Sperm Motility:** Sperm are alive (viable) but non-motile (unlike necrozoospermia). * **Prognosis:** The disease is progressive when associated with ciliary dysfunction [2].

Question 475: Breath sounds are decreased in all the following conditions except?

A. Lobar pneumonia (Correct Answer)
B. Pneumothorax
C. Pleural effusion
D. Atelectasis

Explanation: ### Explanation The intensity of breath sounds depends on the transmission of sound from the airways to the chest wall. **Why Lobar Pneumonia is the Correct Answer:** In **Lobar Pneumonia**, the alveoli are filled with inflammatory exudate (consolidation), but the conducting airways (bronchi) usually remain **patent** (open) [1]. Because solid medium conducts sound better than air, the breath sounds are not decreased; instead, they are **increased** in intensity and change in quality to **Bronchial Breath Sounds**. Additionally, vocal resonance and fremitus are increased over the area of consolidation. **Why the other options are incorrect:** * **Pneumothorax:** Air in the pleural space acts as an insulator, separating the lung from the chest wall and preventing the transmission of sound, leading to **decreased or absent** breath sounds [2]. * **Pleural Effusion:** Fluid in the pleural space similarly acts as a physical barrier that reflects and dampens sound waves, resulting in **decreased** breath sounds over the effusion [1]. * **Atelectasis (Collapse):** In most cases of atelectasis (especially obstructive), the bronchus is blocked. Since no air can enter the segment, no sound is generated or transmitted, leading to **decreased** breath sounds. **High-Yield Clinical Pearls for NEET-PG:** 1. **Consolidation (Pneumonia):** The only common condition where breath sounds are **increased** (Bronchial) and Vocal Fremitus is **increased**. 2. **Pleural Effusion vs. Consolidation:** Both show dullness on percussion, but Effusion has **decreased** fremitus, while Consolidation has **increased** fremitus. 3. **Silent Chest:** A clinical emergency in severe asthma where breath sounds are absent due to minimal air movement. 4. **Bronchial Breath Sounds:** Characterized by a high pitch, a gap between inspiration and expiration, and a louder/longer expiratory phase.

Question 476: Loeffler's syndrome is characterized by?

A. Transient, migratory pulmonary infiltrations (Correct Answer)
B. Fibrosis in the pulmonary apices
C. Fibrosis in the base of one or both lungs
D. Miliary mottling

Explanation: **Explanation:** **Loeffler’s Syndrome** (Simple Pulmonary Eosinophilia) is a specific type of eosinophilic lung disease characterized by the clinical triad of **transient pulmonary infiltrates**, **peripheral blood eosinophilia**, and a benign, self-limiting course. 1. **Why Option A is Correct:** The hallmark of Loeffler’s syndrome is the presence of **"fleeting" or migratory infiltrates** on chest X-ray [1]. These are non-segmental opacities that shift in location over days or weeks. The underlying mechanism is usually a Type I hypersensitivity reaction to the transpulmonary passage of helminth larvae (most commonly *Ascaris lumbricoides*, but also *Ancylostoma* and *Necator americanus*) [1]. 2. **Why the Other Options are Incorrect:** * **Options B & C (Fibrosis):** Loeffler’s syndrome is an acute, reversible condition. It does not lead to permanent structural damage or fibrosis. Apical fibrosis is characteristic of conditions like Tuberculosis or Ankylosing Spondylitis, while basal fibrosis is seen in Idiopathic Pulmonary Fibrosis (IPF) or Asbestosis [2]. * **Option D (Miliary mottling):** This refers to 1–2 mm "millet seed" spots typical of Miliary Tuberculosis, Sarcoidosis, or Silicosis, not the fluffy, migratory opacities seen in eosinophilic pneumonia. **High-Yield Clinical Pearls for NEET-PG:** * **Etiology:** Most common cause is *Ascaris lumbricoides* [1]. * **Clinical Presentation:** Usually asymptomatic or presents with a dry cough and wheezing [1]. * **Diagnosis:** Elevated absolute eosinophil count (AEC) and migratory shadows on CXR. * **Management:** Usually self-limiting; symptoms resolve within 2–4 weeks. * **Differential:** Tropical Pulmonary Eosinophilia (TPE) is more severe, caused by *Wuchereria bancrofti*, and requires Diethylcarbamazine (DEC) [3].

Question 477: What is the most common cause of Superior Vena Cava (SVC) syndrome?

A. Lung cancer (Correct Answer)
B. Trauma
C. Thymoma
D. Fibrosis of the SVC

Explanation: **Explanation:** Superior Vena Cava (SVC) syndrome occurs due to the obstruction of blood flow through the SVC, typically caused by external compression or direct invasion by a mediastinal mass [1]. **1. Why Lung Cancer is the Correct Answer:** Malignancy is responsible for approximately 60–90% of all SVC syndrome cases. Among these, **Lung Cancer** (specifically Small Cell Lung Cancer and Squamous Cell Carcinoma) is the most common cause [1]. This is due to the proximity of the right mainstem bronchus and right hilar lymph nodes to the thin-walled, low-pressure SVC, making it highly susceptible to compression by enlarging tumors. **2. Analysis of Incorrect Options:** * **Trauma:** While trauma can cause vascular injury, it rarely leads to the chronic obstructive clinical picture of SVC syndrome. * **Thymoma:** This is a known cause of mediastinal masses, but it is significantly less frequent than lung cancer or lymphoma [1]. * **Fibrosis of the SVC:** Historically, infectious causes like Syphilitic aortitis or Tuberculosis (causing fibrosing mediastinitis) were common. Today, benign causes are more often related to iatrogenic factors like indwelling catheters or pacemaker leads rather than idiopathic fibrosis. **3. NEET-PG High-Yield Pearls:** * **Most common malignancy:** Lung Cancer (Small cell > Squamous). * **Second most common malignancy:** Non-Hodgkin Lymphoma. * **Most common benign cause:** Iatrogenic (thrombosis due to central venous catheters/pacemakers). * **Clinical Presentation:** Facial puffiness (Pemberton’s sign), "plethora," and dilated collateral veins on the upper chest [1]. * **Management:** The priority is treating the underlying cause (Chemotherapy for Small Cell; Radiotherapy for Non-Small Cell). Endovascular stenting is the gold standard for rapid symptomatic relief.

Question 478: Exudative pleural effusion is seen in:

A. Pneumonia (Correct Answer)
B. Nephrotic syndrome
C. Congestive cardiac failure
D. Cirrhosis

Explanation: **Explanation:** Pleural effusions are classified into **Transudates** and **Exudates** based on the underlying pathophysiology. **1. Why Pneumonia is Correct:** Pneumonia causes an **Exudative effusion** (specifically a parapneumonic effusion). The mechanism involves local inflammation of the pleura, which increases capillary permeability. This allows protein-rich fluid and cells to leak into the pleural space. According to **Light’s Criteria**, an exudate meets at least one of the following: * Pleural fluid protein/Serum protein ratio > 0.5 * Pleural fluid LDH/Serum LDH ratio > 0.6 * Pleural fluid LDH > 2/3rd the upper limit of normal serum LDH. **2. Why Other Options are Incorrect:** * **Congestive Cardiac Failure (CCF):** The most common cause of transudative effusion. It occurs due to increased hydrostatic pressure in the systemic or pulmonary circulation. * **Nephrotic Syndrome:** Causes a transudative effusion due to decreased oncotic pressure (hypoalbuminemia). * **Cirrhosis:** Leads to "Hepatic Hydrothorax" (usually right-sided), a transudative effusion caused by decreased oncotic pressure and the movement of peritoneal fluid through diaphragmatic defects. **Clinical Pearls for NEET-PG:** * **Most common cause of Transudate:** Congestive Heart Failure. * **Most common cause of Exudate:** Pneumonia (Parapneumonic) followed by Malignancy and TB. * **Meigs’ Syndrome:** Triad of Benign Ovarian Tumor (Fibroma), Ascites, and Pleural Effusion (Transudative). * **Chylothorax:** Exudative fluid with Triglycerides > 110 mg/dL. * **Low Glucose in Effusion:** Suggests Rheumatoid Arthritis, Empyema, Malignancy, or TB.

Question 479: Which investigation is most diagnostic of pulmonary emboli?

A. CTPA (Correct Answer)
B. V/P scan
C. HRCT
D. D-Dimer Assay

Explanation: **CT Pulmonary Angiography (CTPA)** is currently the **gold standard and investigation of choice** for diagnosing Pulmonary Embolism (PE) [1]. Its high sensitivity (>83%) and specificity (>96%) allow for direct visualization of thrombi within the pulmonary arteries as intraluminal filling defects [1]. It is preferred because it is rapid, widely available, and can provide alternative diagnoses (like pneumonia or aortic dissection) if PE is ruled out. **Analysis of Incorrect Options:** * **V/Q Scan (Ventilation/Perfusion):** Previously the mainstay, it is now a second-line investigation. It is primarily used when CTPA is contraindicated (e.g., severe renal failure or contrast allergy) [1]. It provides a probability (High, Intermediate, Low) rather than a definitive "yes/no" diagnosis. * **HRCT (High-Resolution CT):** This is used to visualize lung parenchyma and interstitial diseases (e.g., ILD, bronchiectasis). It does not involve the contrast bolus timing required to opacify pulmonary arteries and is therefore not used for PE. * **D-Dimer Assay:** This is a **screening tool** with high negative predictive value. It is used to *rule out* PE in low-probability patients. It is not diagnostic because it can be elevated in many conditions (surgery, trauma, pregnancy, malignancy). **Clinical Pearls for NEET-PG:** * **Initial Investigation:** Chest X-ray (usually normal, but may show **Westermark sign** or **Hampton’s Hump**). * **Best Initial Test:** CTPA. * **Gold Standard (Historical):** Invasive Catheter Pulmonary Angiography (rarely used now). * **Investigation of choice in Pregnancy:** Compression Ultrasonography of leg veins is often first; if negative, V/Q scan is generally preferred over CTPA to minimize maternal breast radiation [1].

Question 480: What is the most common cause of pulmonary embolism?

A. Amniotic fluid embolism
B. Calf vein thrombi
C. Pelvic vein thrombosis (Correct Answer)
D. Cardio thoracic surgery

Explanation: **Explanation:** The most common source of a pulmonary embolism (PE) is **Deep Vein Thrombosis (DVT)** of the lower extremities and pelvis [1]. While many thrombi originate in the calf, they are less likely to embolize unless they propagate proximally [1]. **Why Pelvic Vein Thrombosis is Correct:** Clinically significant and fatal pulmonary emboli most frequently arise from the **proximal deep veins** of the lower limbs (popliteal, femoral, and iliac veins) and the **pelvic venous plexus**. Thrombi in these larger, proximal vessels have a higher volume and are more likely to detach and travel through the inferior vena cava to the pulmonary arteries compared to distal thrombi. **Analysis of Incorrect Options:** * **Amniotic fluid embolism:** This is a rare, catastrophic obstetric complication. While it is a type of embolism, it is not the "most common" cause of PE in the general population. * **Calf vein thrombi:** Although DVT frequently begins in the calf (soleal sinuses), distal thrombi are generally small and often resolve spontaneously [1]. They account for only about 10-20% of PE cases unless they extend proximally. * **Cardio thoracic surgery:** While surgery is a major risk factor for DVT/PE due to stasis and hypercoagulability (Virchow’s Triad), it is a *predisposing factor*, not the anatomical source of the embolus itself. **High-Yield Clinical Pearls for NEET-PG:** * **Virchow’s Triad:** Stasis, endothelial injury, and hypercoagulability are the three pillars of thrombus formation. * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA) is the investigation of choice for PE. * **Most Common EKG Finding:** Sinus tachycardia (Most common). The classic **S1Q3T3** pattern is specific but seen in less than 20% of cases. * **Homan’s Sign:** Calf pain on dorsiflexion of the foot (low sensitivity and specificity for DVT).

Practice by Chapter

Obstructive Airway Diseases (Asthma, COPD)

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Interstitial Lung Diseases

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Pulmonary Infections

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Pulmonary Vascular Diseases

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Pleural Diseases

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Sleep-Disordered Breathing

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Respiratory Failure

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Mediastinal Disorders

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Occupational Lung Diseases

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Pulmonary Function Testing

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Bronchiectasis and Cystic Fibrosis

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Lung Cancer Approach

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