Pulmonology Practice Questions

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

Asbestosis. 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].

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

Eosinopenia. **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).

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

Pneumonia. 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:** $PaO_2 45 \text{ mmHg}$ [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.

Q: Hypersensitivity pneumonitis is caused by which of the following?

Bagassosis. 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.

Q: Bilateral symmetrical hilar lymphadenopathy is seen in:

Sarcoidosis. ### 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.

Q: All the following features are seen in ARDS except?

Hypercapnia. **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.

Q: Comment on the presentation of this patient?

Blood in the sputum. ***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 1

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

Accepted Answer

Asbestosis

Answer

Silicosis

Answer

Scleroderma

Answer

Byssinosis

Question 2

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

Accepted Answer

Eosinopenia

Answer

Iron deficiency anemia

Answer

Diffuse alveolar hemorrhage

Answer

Hemoptysis

Question 3

All of the following are causes of hypercarbic respiratory failure EXCEPT?

Accepted Answer

Pneumonia

Answer

Myasthenia gravis

Answer

Amyotrophic lateral sclerosis

Answer

Chronic obstructive pulmonary disease

Question 4

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

Accepted Answer

Dermatomyositis

Answer

Systemic lupus erythematosus

Answer

Progressive systemic sclerosis

Answer

Rheumatoid arthritis

Question 5

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?

Accepted Answer

Pneumonia

Answer

Pulmonary infarction

Answer

Pulmonary hemorrhage

Answer

Pulmonary hypertension

Question 6

Hypersensitivity pneumonitis is caused by which of the following?

Accepted Answer

Bagassosis

Answer

Coal worker's pneumoconiosis

Answer

Silicosis

Answer

Sarcoidosis

Question 7

Bilateral symmetrical hilar lymphadenopathy is seen in:

Accepted Answer

Sarcoidosis

Answer

Tuberculosis

Answer

Leprosy

Answer

Wegener's granulomatosis

Question 8

All the following features are seen in ARDS except?

Accepted Answer

Hypercapnia

Answer

Pulmonary edema

Answer

Reduced lung compliance

Answer

Stiff lung

Question 9

Comment on the presentation of this patient?

Accepted Answer

Blood in the sputum

Answer

Chunky pink gelatinous plugs in sputum

Answer

Horner syndrome with wasting of intrinsic muscles of hand

Answer

Hamman crunch sign with subcutaneous emphysema

Question 10

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?

Accepted Answer

Resistance to activated protein C

Answer

Protein C excess

Answer

Antithrombin mutation causing accelerated effect

Answer

Polycythemia vera

Pulmonology — MCQs

Pulmonology — MCQs

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