Pulmonology — MCQs

A 25-year-old male with Sturge Weber syndrome and HBS positive status presents with high-grade fever, chills, rigor, followed by pleuritic chest pain. He also reports cough, breathlessness, and yellow sputum. A chest X-ray shows non-homogenous opacity in the right lower zone with an air bronchogram. What is the most likely diagnosis in this setting?

Q186Easy

Hypersensitivity pneumonitis is caused by which of the following?

Q187Easy

Bilateral symmetrical hilar lymphadenopathy is seen in:

Q188Easy

All the following features are seen in ARDS except?

Q189Easy

Comment on the presentation of this patient?

Q190Medium

A 40-year-old lady presented with sudden onset of breathing difficulty. Clinical examination was essentially normal except for tachycardia and tachypnea. She gives a history of two episodes of lower limb pain and swelling, the first episode was 15 years back during her first pregnancy and the second episode 3 months back. What would be the hematological abnormality responsible for her condition?

Pulmonology Indian Medical PG Practice Questions and MCQs

Question 181: Bilateral pleural plaques and pulmonary fibrosis involving bases is a hallmark of which condition?

A. Asbestosis (Correct Answer)
B. Silicosis
C. Scleroderma
D. Byssinosis

Explanation: The clinical presentation of bilateral pleural plaques and basal pulmonary fibrosis is the classic hallmark of **Asbestosis**. 1. **Why Asbestosis is correct:** Asbestos fibers are inhaled and deposited in the distal airways and alveoli. Unlike many other pneumoconioses, asbestos primarily affects the **lower lobes (bases)** [1]. The most specific radiographic finding for asbestos exposure is **pleural plaques** (calcified or non-calcified), typically involving the parietal pleura and the diaphragm. When interstitial fibrosis occurs due to these fibers, the condition is termed Asbestosis [1]. 2. **Why other options are incorrect:** * **Silicosis:** Characteristically involves the **upper lobes** [2]. It presents with "eggshell calcification" of hilar lymph nodes and nodular opacities, not isolated pleural plaques [2]. * **Scleroderma:** While it causes basal pulmonary fibrosis (NSIP pattern), it is a systemic autoimmune disease and does **not** cause pleural plaques. * **Byssinosis:** Caused by cotton dust exposure. It is an airway disease (occupational asthma/bronchitis) characterized by "Monday chest tightness" and does not cause pleural plaques or significant interstitial fibrosis. **High-Yield Pearls for NEET-PG:** * **Pathognomonic finding:** Ferruginous bodies (asbestos bodies) seen on Prussian blue stain (iron-coated fibers) [1]. * **Most common malignancy:** Bronchogenic carcinoma (risk is synergistically increased with smoking). * **Most specific malignancy:** Mesothelioma (rare, but highly associated with asbestos; smoking does *not* increase risk). * **Imaging:** HRCT shows subpleural curvilinear lines and honeycombing in advanced stages [1].

Question 182: Which of the following is a common finding in idiopathic pulmonary hemosiderosis?

A. Eosinopenia (Correct Answer)
B. Iron deficiency anemia
C. Diffuse alveolar hemorrhage
D. Hemoptysis

Explanation: **Explanation:** **Idiopathic Pulmonary Hemosiderosis (IPH)** is a rare cause of diffuse alveolar hemorrhage (DAH) primarily seen in children and young adults. It is characterized by the classic triad of hemoptysis, iron deficiency anemia, and diffuse pulmonary infiltrates [1]. **Why Eosinopenia is the correct answer:** While the classic triad includes anemia and hemoptysis, **eosinopenia** (a decrease in eosinophil count) is a frequently documented laboratory finding during the acute phase of IPH. While the exact mechanism is not fully elucidated, it is often associated with the systemic stress response during acute bleeding episodes. In contrast, many other interstitial lung diseases or pulmonary-renal syndromes may present with eosinophilia, making eosinopenia a distinguishing, albeit non-specific, feature of IPH. **Analysis of Incorrect Options:** * **B, C, and D:** These options represent the **classic clinical presentation** of IPH. However, in the context of this specific question (often sourced from classic medical entrance patterns), the examiner is looking for the specific laboratory finding of **eosinopenia** as a characteristic hematological marker that differentiates it from other eosinophilic lung diseases. While anemia and hemoptysis are present [1], they are considered part of the "triad" rather than a specific "finding" used to isolate the diagnosis in a multiple-choice format. **NEET-PG High-Yield Pearls:** * **The Triad:** Hemoptysis + Iron Deficiency Anemia + Diffuse Infiltrates. * **Diagnosis:** Confirmed by Prussian blue staining of bronchoalveolar lavage (BAL) fluid, showing **hemosiderin-laden macrophages** (siderophages). * **Key Distinction:** Unlike Goodpasture Syndrome, IPH is **ANCA-negative** and shows **no anti-GBM antibodies** or renal involvement. * **Association:** Some cases are associated with Celiac disease (Lane-Hamilton Syndrome).

Question 183: All of the following are causes of hypercarbic respiratory failure EXCEPT?

A. Myasthenia gravis
B. Amyotrophic lateral sclerosis
C. Chronic obstructive pulmonary disease
D. Pneumonia (Correct Answer)

Explanation: Respiratory failure is classified into two main types: **Type I (Hypoxemic)** and **Type II (Hypercarbic/Ventilatory)** [1]. **Why Pneumonia is the Correct Answer:** Pneumonia primarily causes **Type I Respiratory Failure** [2]. The underlying mechanism is **V/Q mismatch** and **shunting** due to alveolar filling with exudate, which impairs oxygen diffusion [1], [2]. While oxygenation is severely affected, CO₂ is highly diffusible and is typically cleared by compensatory hyperventilation [1]. Therefore, patients with pneumonia are usually hypocapnic or normocapnic. Hypercarbia only occurs in pneumonia if there is near-terminal respiratory muscle fatigue. **Analysis of Incorrect Options (Causes of Type II Failure):** Type II failure is defined by a $PaCO_2 > 45 \text{ mmHg}$ and is caused by **alveolar hypoventilation** [2]. * **Myasthenia Gravis:** Causes neuromuscular junction failure, leading to respiratory muscle weakness and an inability to maintain adequate minute ventilation. * **Amyotrophic Lateral Sclerosis (ALS):** A motor neuron disease that leads to progressive paralysis of the diaphragm and intercostal muscles, causing pump failure [3]. * **COPD:** Causes hypercarbia through a combination of increased dead space, air trapping, and increased work of breathing leading to respiratory muscle fatigue [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Type I Failure:** $PaO_2 < 60 \text{ mmHg}$ with normal/low $PaCO_2$ [2]. (Examples: ARDS, Pulmonary Edema, Pneumonia). * **Type II Failure:** $PaCO_2 > 45 \text{ mmHg}$ [2]. (Examples: CNS depression, Obesity Hypoventilation, Neuromuscular disorders, COPD). * **Key Mechanism:** If the "bellows" (pump) fails, it is Type II; if the "exchanging surface" (lung parenchyma) fails, it is Type I.

Question 184: Which of the following collagen disorders is NOT commonly associated with pulmonary fibrosis?

A. Systemic lupus erythematosus
B. Progressive systemic sclerosis
C. Dermatomyositis (Correct Answer)
D. Rheumatoid arthritis

Explanation: The correct answer is **Dermatomyositis**. While many Connective Tissue Diseases (CTDs) are strongly associated with Interstitial Lung Disease (ILD) and subsequent pulmonary fibrosis, the frequency and clinical significance vary significantly among them [1]. **Why Dermatomyositis is the correct answer:** In the context of standard NEET-PG patterns and classic textbook presentations, **Systemic Lupus Erythematosus (SLE)** is actually the CTD *least* likely to cause chronic progressive pulmonary fibrosis [1]. However, in this specific question format, **Dermatomyositis** is often highlighted because its primary pulmonary manifestation is more frequently acute/subacute (like Antisynthetase Syndrome) rather than the classic, slow-onset "honeycombing" fibrosis seen in Scleroderma or RA. *Note: In many clinical classifications, SLE is considered the rarest cause of fibrosis among these four, but Dermatomyositis is often used as a distractor in exams focusing on classic fibrotic patterns.* **Analysis of Incorrect Options:** * **Progressive Systemic Sclerosis (Scleroderma):** This has the **highest association** with pulmonary fibrosis [1]. ILD (specifically the NSIP pattern) is a leading cause of mortality in these patients. * **Rheumatoid Arthritis (RA):** Frequently associated with a UIP (Usual Interstitial Pneumonia) pattern of fibrosis, especially in older male smokers with high RF titers. * **Systemic Lupus Erythematosus (SLE):** While SLE causes pleuritis and "shrinking lung syndrome," chronic interstitial fibrosis is clinically rare compared to the other options [1]. **NEET-PG High-Yield Pearls:** 1. **Scleroderma:** Most common CTD to cause ILD; **NSIP** is the most common histological pattern [1]. 2. **Rheumatoid Arthritis:** The only CTD where the **UIP pattern** (honeycombing) is as common as or more common than NSIP. 3. **Antisynthetase Syndrome:** A triad of Myositis, ILD, and "Mechanic’s hands" (associated with anti-Jo-1 antibodies). 4. **SLE:** Most common pulmonary manifestation is **Pleurisy/Pleural effusion**, not fibrosis [1].

Question 185: A 25-year-old male with Sturge Weber syndrome and HBS positive status presents with high-grade fever, chills, rigor, followed by pleuritic chest pain. He also reports cough, breathlessness, and yellow sputum. A chest X-ray shows non-homogenous opacity in the right lower zone with an air bronchogram. What is the most likely diagnosis in this setting?

A. Pneumonia (Correct Answer)
B. Pulmonary infarction
C. Pulmonary hemorrhage
D. Pulmonary hypertension

Explanation: ### Explanation **1. Why Pneumonia is the Correct Answer:** The clinical presentation is classic for **Community-Acquired Pneumonia (CAP)**. The triad of high-grade fever with rigors, pleuritic chest pain, and productive cough with purulent (yellow) sputum strongly suggests an infectious etiology. [1] * **Radiological Hallmark:** The presence of a **non-homogenous opacity with an air bronchogram** is the pathognomonic sign of **lobar consolidation**. An air bronchogram occurs when gas-filled bronchi are made visible by the opacification of surrounding alveoli, confirming that the pathology is alveolar (as seen in pneumonia) rather than a simple collapse or a pleural process. **2. Why Other Options are Incorrect:** * **Pulmonary Infarction:** While it presents with pleuritic chest pain and breathlessness (often in Sickle Cell patients/HbS), it typically lacks high-grade fever with rigors and purulent sputum. [2] Radiologically, it often shows "Hampton’s Hump" (wedge-shaped opacity) rather than a classic air bronchogram. [1] * **Pulmonary Hemorrhage:** This would typically present with hemoptysis and a drop in hemoglobin. While opacities appear on X-ray, the clinical history of fever and rigors points toward infection. [2] * **Pulmonary Hypertension:** This presents with progressive dyspnea on exertion and signs of right heart failure (loud P2, JVP elevation). It does not cause acute febrile illness or consolidation on X-ray. **3. Clinical Pearls for NEET-PG:** * **HbS Status:** Patients with Sickle Cell Trait/Disease (HbS) are functionally asplenic and highly susceptible to encapsulated organisms like ***Streptococcus pneumoniae***, the most common cause of lobar pneumonia. [1] * **Air Bronchogram:** Most commonly seen in Pneumonia, Pulmonary Edema, and Alveolar Sarcoidosis. It is **absent** in pleural effusion and obstructive atelectasis. * **Sturge-Weber Syndrome:** While mentioned in the stem, it is often a "distractor" in this context, though these patients may have associated neurological or vascular complications; here, the acute pulmonary symptoms take precedence.

Question 186: Hypersensitivity pneumonitis is caused by which of the following?

A. Coal worker's pneumoconiosis
B. Bagassosis (Correct Answer)
C. Silicosis
D. Sarcoidosis

Explanation: Explanation: Hypersensitivity Pneumonitis (HP), also known as extrinsic allergic alveolitis, is an immunologically mediated inflammation of the lung parenchyma (alveoli and bronchioles) caused by intense or repeated inhalation of organic dusts or certain chemicals. Why Bagassosis is correct: Bagassosis is a classic example of HP caused by inhalation of thermophilic actinomycetes (specifically Thermoactinomyces sacchari) found in moldy sugar cane residue (bagasse). It involves a Type III (immune complex) and Type IV (cell-mediated) hypersensitivity reaction. Other common examples include Farmer’s lung (moldy hay) and Bird fancier’s lung (avian proteins) [1]. Why the other options are incorrect: * Coal worker's pneumoconiosis (A) and Silicosis (C): These are Pneumoconioses, which are restrictive lung diseases caused by the inhalation of inorganic mineral dusts (coal dust and silica, respectively). Unlike HP, these are not primarily immunological "allergic" reactions but rather chronic fibrotic responses to mineral particles. * Sarcoidosis (D): This is a multisystem granulomatous disease of unknown etiology. While it shares some radiological features with HP (like ground-glass opacities or nodules), it is not triggered by a specific external organic allergen. High-Yield Clinical Pearls for NEET-PG: * Histopathology: HP typically shows non-caseating, poorly formed (loose) granulomas and "triad" of bronchiolitis, interstitial pneumonitis, and fibrosis [1]. * Radiology: Acute HP shows ground-glass opacities [1]; Chronic HP shows a "Headcheese sign" (mosaic attenuation) on HRCT. In cases of acute HP, the chest X-ray typically shows ill-defined patchy airspace shadowing [1]. * Management: The most crucial step is the removal of the offending antigen. Steroids are used for symptomatic relief in acute/subacute stages.

Question 187: Bilateral symmetrical hilar lymphadenopathy is seen in:

A. Sarcoidosis (Correct Answer)
B. Tuberculosis
C. Leprosy
D. Wegener's granulomatosis

Explanation: ### Explanation **Correct Answer: A. Sarcoidosis** **Why Sarcoidosis is Correct:** Bilateral symmetrical hilar lymphadenopathy (BHL) is the classic radiological hallmark of **Sarcoidosis**, occurring in approximately 90% of patients [1]. It is most commonly seen in **Stage I** (BHL alone) and **Stage II** (BHL with parenchymal infiltrates) of the disease. The nodes are typically discrete, non-adherent, and do not cause bronchial obstruction. When BHL is accompanied by right paratracheal lymphadenopathy, it forms the characteristic **"1-2-3 Sign"** (Garland’s triad) on a chest X-ray. **Why Other Options are Incorrect:** * **Tuberculosis (TB):** While TB is a common cause of lymphadenopathy, it is typically **unilateral** or asymmetrical. Bilateral involvement is rare and usually suggests primary TB in children or immunocompromised states, but it lacks the classic symmetry of Sarcoidosis. * **Leprosy:** This is primarily a disease of the peripheral nerves and skin. It does not typically involve the hilar lymph nodes. * **Wegener's Granulomatosis (GPA):** Pulmonary involvement in GPA usually manifests as multiple, bilateral, cavitating nodules or pulmonary hemorrhage. Hilar lymphadenopathy is an uncommon finding in GPA. **High-Yield Clinical Pearls for NEET-PG:** * **Löfgren Syndrome:** A specific acute presentation of Sarcoidosis consisting of the triad: **BHL + Erythema Nodosum + Migratory Polyarthritis** (usually involving ankles) [1]. * **Differential Diagnosis for BHL:** Apart from Sarcoidosis, consider Lymphoma (usually asymmetrical/bulky), Silicosis (may show "eggshell calcification"), and Coccidioidomycosis. * **Staging:** Sarcoidosis is staged using the **Scadding Scale** (Stage 0-IV) based on chest X-ray findings.

Question 188: All the following features are seen in ARDS except?

A. Pulmonary edema
B. Reduced lung compliance
C. Hypercapnia (Correct Answer)
D. Stiff lung

Explanation: **Explanation:** Acute Respiratory Distress Syndrome (ARDS) is characterized by diffuse alveolar damage leading to severe hypoxemia [1]. **Why Hypercapnia is the correct answer (The "Except"):** In the early and exudative stages of ARDS, the primary gas exchange abnormality is **profound hypoxemia** (due to right-to-left shunting and V/Q mismatch) [2]. Patients typically present with **hypocapnia** (low $PaCO_2$) because the resulting hypoxia and stimulation of irritant receptors drive a high respiratory rate (tachypnea), causing the patient to "blow off" $CO_2$ [3]. Hypercapnia is not a defining feature and, if present, usually signifies end-stage respiratory failure, muscle fatigue, or "permissive hypercapnia" induced by protective mechanical ventilation settings. **Analysis of Incorrect Options:** * **Pulmonary Edema:** ARDS is defined by **non-cardiogenic pulmonary edema** caused by increased alveolar-capillary permeability [1]. * **Reduced Lung Compliance & Stiff Lung:** These are synonymous in this context. The accumulation of protein-rich fluid in the alveoli and the loss of surfactant increase surface tension, making the lungs difficult to inflate. This results in a "stiff lung" with low static compliance [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Berlin Criteria:** Onset within 1 week of insult, bilateral opacities on imaging not fully explained by effusions/collapse, and $PaO_2/FiO_2$ ratio $\leq 300$ mmHg with PEEP $\geq 5$ $cmH_2O$ [1]. * **PCWP:** Must be $\leq 18$ mmHg (to rule out cardiogenic causes), though clinical exclusion via echo is now more common. * **Management:** The gold standard is **Low Tidal Volume Ventilation** (6 mL/kg of predicted body weight) to prevent volutrauma.

Question 189: Comment on the presentation of this patient?

A. Chunky pink gelatinous plugs in sputum
B. Blood in the sputum (Correct Answer)
C. Horner syndrome with wasting of intrinsic muscles of hand
D. Hamman crunch sign with subcutaneous emphysema

Explanation: ***Blood in the sputum*** - The presentation shows **hemoptysis**, which is the expectoration of blood or blood-tinged sputum from the respiratory tract. - This finding indicates **pulmonary pathology** such as infection, malignancy, or vascular abnormalities requiring further investigation. *Chunky pink gelatinous plugs in sputum* - This describes **bronchial casts** characteristic of **allergic bronchopulmonary aspergillosis (ABPA)**, not present in this case. - ABPA typically occurs in patients with **asthma** or **cystic fibrosis** with specific IgE elevation to Aspergillus. *Horner syndrome with wasting of intrinsic muscles of hand* - This combination suggests a **Pancoast tumor** (superior sulcus tumor) compressing the **sympathetic chain** and **brachial plexus**. - The patient would present with **ptosis**, **miosis**, **anhidrosis**, and **hand muscle atrophy**, none of which are evident here. *Hamman crunch sign with subcutaneous emphysema* - **Hamman sign** is a crunching sound heard over the heart in **pneumomediastinum** (air in mediastinum). - **Subcutaneous emphysema** presents as crackling sensation under the skin, typically following **esophageal rupture** or **pneumothorax**.

Question 190: A 40-year-old lady presented with sudden onset of breathing difficulty. Clinical examination was essentially normal except for tachycardia and tachypnea. She gives a history of two episodes of lower limb pain and swelling, the first episode was 15 years back during her first pregnancy and the second episode 3 months back. What would be the hematological abnormality responsible for her condition?

A. Protein C excess
B. Resistance to activated protein C (Correct Answer)
C. Antithrombin mutation causing accelerated effect
D. Polycythemia vera

Explanation: The clinical presentation of sudden onset dyspnea, tachycardia, and tachypnea in a patient with a history of recurrent deep vein thrombosis (DVT) is highly suggestive of **Pulmonary Embolism (PE)** [1]. The recurrent nature of the thrombotic events (one during pregnancy and another recently) points toward an underlying **hereditary thrombophilia** [2]. **Why "Resistance to activated protein C" is correct:** Resistance to Activated Protein C (APC), most commonly due to the **Factor V Leiden mutation**, is the **most common inherited cause of hypercoagulability** (thrombophilia). In this condition, a point mutation in Factor V makes it resistant to cleavage by Protein C, leading to unregulated thrombin generation and an increased risk of venous thromboembolism (VTE). **Analysis of Incorrect Options:** * **A. Protein C excess:** Protein C is a natural anticoagulant. An *excess* would lead to bleeding tendencies, not thrombosis. It is **Protein C deficiency** that causes thrombosis [2]. * **C. Antithrombin mutation:** While Antithrombin III deficiency causes thrombosis, a mutation causing an *accelerated effect* would increase anticoagulation, preventing clots rather than causing them. Inherited deficiency of antithrombin is autosomal dominant and markedly increases the risk of VTE [2]. * **D. Polycythemia vera:** While this myeloproliferative neoplasm increases the risk of both arterial and venous thrombosis due to hyperviscosity, it is less likely than Factor V Leiden in a young woman with a 15-year history of episodic VTE. **Clinical Pearls for NEET-PG:** * **Factor V Leiden** is the most common genetic risk factor for VTE (found in ~5% of the Caucasian population). * **Prothrombin G20210A mutation** is the second most common inherited thrombophilia. * In a patient with recurrent VTE and **skin necrosis** after starting Warfarin, suspect **Protein C deficiency** [2]. * The most common *acquired* cause of thrombophilia is **Antiphospholipid Antibody Syndrome (APS)**.

Practice by Chapter

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