Pulmonology Practice Questions

Q: A 48-year-old man, residing near a textile mill, presents with respiratory symptoms. A chest X-ray reveals a fine reticular and nodular pattern in the lower lung zones with loss of clarity of the diaphragmatic and cardiac outlines, and possible small pleural effusion. What is the probable diagnosis?

Asbestosis. **Explanation:** The clinical presentation and radiological findings point directly to **Asbestosis**. **Why Asbestosis is correct:** Asbestosis is a chronic fibrotic lung disease caused by inhaling asbestos fibers (common in textile mills, insulation, and shipbuilding). Key diagnostic features mentioned in the question include: * **Lower Zone Involvement:** Unlike most pneumoconioses, asbestosis predominantly affects the lower lobes. * **Ground-glass/Reticular Pattern:** Fine reticulation indicates interstitial fibrosis. * **Shaggy Heart Sign:** The "loss of clarity of diaphragmatic and cardiac outlines" is a classic radiological sign (Shaggy Heart Sign) caused by pleural thickening and parenchymal fibrosis blurring the borders. * **Pleural Involvement:** Asbestos is unique among these options for causing pleural plaques and effusions. **Why other options are incorrect:** * **Stannosis:** Caused by tin oxide; it presents with very dense, discrete micronodules but is generally asymptomatic and does not cause significant fibrosis or pleural changes. * **Silicosis:** Characteristically affects the **upper lobes**. Radiologically, it shows "eggshell calcification" of hilar lymph nodes and discrete nodules, not a shaggy heart border. * **Coal Worker’s Pneumoconiosis (CWP):** Also primarily affects the **upper lobes** with small rounded opacities. It does not typically involve the pleura or cause the blurring of cardiac outlines seen here. **NEET-PG High-Yield Pearls:** * **Asbestosis:** Lower lobes + Pleural plaques + Increased risk of Bronchogenic Carcinoma (most common) and Mesothelioma (most specific). * **Silicosis:** Upper lobes + Eggshell calcification + Increased risk of Tuberculosis. * **Siderosis:** Iron dust; **Stannosis:** Tin dust (both are "Benign Pneumoconioses"). * **Byssinosis:** Cotton dust; "Monday Morning Fever."

Q: A 17-year-old male complains of recurrent episodes of cough, wheezing, and shortness of breath, particularly at night, for the last 3 days. His sibling has a history of similar symptoms. A skin test with pollen produces an immediate wheal and flare. What is the most appropriate initial treatment?

Bronchodilators. ### Explanation **Diagnosis: Acute Exacerbation of Bronchial Asthma** The clinical presentation of recurrent cough, wheezing, and nocturnal dyspnea, combined with a positive family history and evidence of atopy (positive skin test for pollen), strongly points toward **Bronchial Asthma**. The immediate wheal and flare reaction indicates a Type I Hypersensitivity reaction. **Why Bronchodilators are the Correct Choice:** In an acute symptomatic episode (exacerbation), the primary goal is to reverse **bronchoconstriction**. Short-acting beta-2 agonists (SABA), such as Salbutamol, are the first-line "reliever" medications. They act rapidly on the smooth muscles of the airways to provide immediate symptomatic relief. **Analysis of Incorrect Options:** * **B. Steroids:** While inhaled corticosteroids (ICS) are the mainstay for long-term *maintenance* and control of airway inflammation, they do not provide immediate relief during an acute episode. Systemic steroids are used in severe cases but are secondary to bronchodilators in the initial management. * **C. Antibiotics:** Asthma is an inflammatory condition, not an infectious one. Antibiotics are only indicated if there is clear evidence of a secondary bacterial infection (e.g., fever, purulent sputum). * **D. Cough suppressants:** These are generally contraindicated in asthma as they can lead to the retention of secretions and worsening of airway obstruction. **NEET-PG High-Yield Pearls:** * **Gold Standard for Diagnosis:** Spirometry showing reversible airway obstruction (increase in FEV1 >12% and >200ml after bronchodilator inhalation). * **Pathology:** Characterized by Curschmann spirals (mucus plugs) and Charcot-Leyden crystals (eosinophil breakdown products) in sputum. * **Drug of Choice (Acute):** Inhaled SABA (Salbutamol). * **Drug of Choice (Chronic/Maintenance):** Inhaled Corticosteroids (ICS).

Q: Pulmonary hypertension may occur in all of the following conditions, EXCEPT?

Argemone mexicana poisoning. Explanation: The correct answer is **Argemone mexicana poisoning**. This condition is clinically known as **Epidemic Dropsy**, caused by the ingestion of mustard oil contaminated with Sanguinarine and Dihydrosanguinarine alkaloids. The hallmark of Epidemic Dropsy is **congestive heart failure** (high-output failure) due to extensive capillary leakage and peripheral vasodilatation, rather than pulmonary hypertension. **Why the other options are incorrect:** * **Toxic Oil Syndrome:** This occurred due to the ingestion of denatured rapeseed oil. It is a multisystemic disease where the chronic phase is characterized by severe **pre-capillary pulmonary hypertension** due to vascular endothelial damage. * **Progressive Systemic Sclerosis (Scleroderma):** This is a classic cause of Group 1 Pulmonary Arterial Hypertension (PAH). It occurs due to intimal proliferation and fibrosis of the pulmonary arterioles, independent of interstitial lung disease. * **Sickle Cell Anaemia:** Pulmonary hypertension is a major complication of chronic hemolytic anemias. It occurs due to chronic hemolysis leading to decreased Nitric Oxide (NO) bioavailability and recurrent pulmonary thromboembolism (Group 1 and Group 4 mechanisms). **NEET-PG High-Yield Pearls:** * **Epidemic Dropsy:** Look for the triad of **bilateral pitting edema, erythema (flushing), and cardiac failure**. A specific ocular complication is **Glaucoma**. * **WHO Classification of PH:** * **Group 1:** PAH (includes Scleroderma, HIV, Schistosomiasis). * **Group 2:** Due to Left Heart Disease. * **Group 3:** Due to Lung Disease/Hypoxia. * **Group 4:** Chronic Thromboembolic PH (CTEPH). * **Group 5:** Multifactorial (includes Sickle Cell Disease).

Q: In hemoptysis, from where does the blood usually originate?

Bronchial arteries. **Explanation:** The lungs have a dual blood supply: the **pulmonary circulation** (low pressure, involved in gas exchange) and the **bronchial circulation** (high pressure, provides systemic oxygenated blood to the airway tissues). **Why Bronchial Arteries are the correct answer:** In approximately **90% of cases of massive hemoptysis**, the bleeding originates from the **bronchial arteries**. Because these arteries arise directly from the aorta or intercostal arteries, they carry blood at **systemic arterial pressure**. In chronic inflammatory conditions (like Tuberculosis, Bronchiectasis, or Aspergilloma), these vessels undergo hypertrophy, neovascularization, and become fragile. Under high systemic pressure, these remodeled vessels are prone to rupture, leading to significant bleeding. **Analysis of Incorrect Options:** * **Pulmonary Arteries (D):** Although they carry the bulk of blood to the lungs, they are a **low-pressure system** (mean pressure ~15 mmHg). They account for only about 5-10% of hemoptysis cases, usually involving specialized pathologies like Rasmussen aneurysms or pulmonary infarcts. * **Bronchial Veins (A) & Pulmonary Veins (B):** These are low-pressure venous systems. While they can bleed in conditions like Mitral Stenosis (due to pulmonary venous hypertension), they are rarely the primary source of significant hemoptysis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of hemoptysis in India:** Tuberculosis. * **Most common cause of hemoptysis worldwide:** Acute Bronchitis. * **Rasmussen’s Aneurysm:** A rare cause of massive hemoptysis where a pulmonary artery aneurysm forms in the wall of a tuberculous cavity. * **Management:** The gold standard for identifying and stopping the source of massive hemoptysis is **Bronchial Artery Embolization (BAE)**.

Q: What is the treatment of choice in a patient of acute pulmonary embolism with right ventricular hypokinesis and compromised cardiac output but normal blood pressure?

Thrombolytic agent. This question addresses the management of **Submassive (Intermediate-risk) Pulmonary Embolism (PE)**. ### **Explanation** The patient presents with **Right Ventricular (RV) hypokinesis** and **compromised cardiac output** (signs of RV strain) but remains **normotensive**. This clinical picture defines **Submassive PE**. While anticoagulation is the standard for stable PE, the presence of RV dysfunction and clinical signs of low output (even without frank hypotension) indicates a high risk of clinical deterioration and obstructive shock. In such cases, **Thrombolytic therapy** is indicated to rapidly dissolve the clot, reduce RV afterload, and improve cardiac output [1]. ### **Why the other options are incorrect:** * **Low Molecular Weight Heparin (LMWH):** This is the treatment of choice for *stable* (Low-risk) PE. It prevents further clot formation but does not actively dissolve the existing life-threatening thrombus. * **Warfarin:** This is an oral anticoagulant used for long-term maintenance therapy [1]. It has a slow onset of action (days) and is never used for the acute management of PE. * **IVC Filters:** These are indicated only when anticoagulation is strictly contraindicated or has failed despite therapeutic levels. They do not treat the current pulmonary obstruction. ### **Clinical Pearls for NEET-PG:** 1. **Massive PE:** Hypotension (SBP <90 mmHg) or shock. **Tx: Immediate Thrombolysis.** 2. **Submassive PE:** Normal BP + RV strain (Echo/CT) or elevated Biomarkers (Troponin/BNP). **Tx: Thrombolysis** (especially if clinical output is compromised) [1]. 3. **Drug of Choice:** Recombinant tissue plasminogen activator (**rtPA/Alteplase**) is preferred over Streptokinase due to its shorter infusion time [2]. 4. **Gold Standard Diagnosis:** CT Pulmonary Angiography (CTPA) [3]. 5. **Most Common ECG Finding:** Sinus tachycardia (S1Q3T3 is specific but less common).

Q: All of the following are features of Superior Vena Cava (SVC) Syndrome except?

Hoarseness of voice. **Explanation:** Superior Vena Cava (SVC) Syndrome results from the obstruction of blood flow through the SVC, most commonly due to extrinsic compression by intrathoracic malignancies (e.g., Bronchogenic carcinoma, Lymphoma) [1]. **Why Hoarseness of Voice is the Correct Answer:** Hoarseness of voice is **not** a feature of SVC syndrome itself. It typically occurs due to the involvement of the **Recurrent Laryngeal Nerve**. While a mediastinal tumor (like lung cancer) can cause both SVC syndrome and hoarseness simultaneously, the hoarseness is a sign of nerve infiltration/compression, not a result of venous congestion [1]. **Analysis of Incorrect Options:** * **Facial Swelling:** This is the hallmark clinical feature. Obstruction leads to increased venous pressure in the upper body, causing edema of the face, neck, and upper extremities (often worse in the morning). * **Dilatation and Congestion of Neck Veins:** Due to the blockage of the SVC, blood is shunted through collateral pathways. This leads to prominent, non-pulsatile distention of neck and chest wall veins. * **Headache:** Increased intracranial venous pressure leads to cerebral congestion, which commonly manifests as a dull headache, dizziness, or a feeling of "fullness" in the head, especially when bending forward. **Clinical Pearls for NEET-PG:** * **Most Common Cause:** Bronchogenic carcinoma (Small cell lung cancer is the most frequent histological type associated) [1]. * **Pemberton’s Sign:** Facial flushing and inspiratory stridor upon elevating both arms above the head; a classic sign of SVC obstruction (often seen in retrosternal goiters). * **Management:** Emergency treatment includes stenting, radiation, or chemotherapy depending on the tumor type [1]. Diuretics and head elevation provide symptomatic relief.

Q: Which of the following syndromes is associated with bronchiectasis?

Kartagener syndrome. Explanation: **Kartagener Syndrome (Option B)** is a subset of **Primary Ciliary Dyskinesia (PCD)**, an autosomal recessive disorder characterized by defective dynein arms in cilia. This leads to impaired mucociliary clearance, resulting in chronic respiratory infections and permanent dilation of the bronchi, known as **bronchiectasis** [1]. It is classically defined by a clinical triad: 1. **Situs Inversus** (transposition of viscera) 2. **Chronic Sinusitis** 3. **Bronchiectasis** **Why other options are incorrect:** * **Kallmann Syndrome (A):** A genetic condition characterized by hypogonadotropic hypogonadism and **anosmia** (loss of smell) due to failure of GnRH-producing neurons to migrate. It has no association with bronchiectasis. * **Kostmann Syndrome (C):** Also known as Severe Congenital Neutropenia. It presents with life-threatening bacterial infections in infancy due to a maturation arrest of neutrophils in the bone marrow, but it is not a primary cause of bronchiectasis. * **Klinefelter Syndrome (D):** A chromosomal anomaly (47, XXY) characterized by testicular atrophy, gynecomastia, and infertility. It does not involve the respiratory system. **High-Yield Clinical Pearls for NEET-PG:** * **Infertility connection:** Males with Kartagener syndrome are usually infertile due to immotile spermatozoa (flagella share the same structural dynein defect as cilia) [1]. * **Diagnosis:** Screening is done via **nasal Nitric Oxide (nNO)** levels (which are low in PCD); definitive diagnosis is via electron microscopy of ciliary ultrastructure or genetic testing. * **Dextrocardia:** Always look for "heart sounds loudest on the right side" in clinical vignettes describing chronic cough and sinusitis.

Q: A 37-year-old truck driver presents with recent onset of shortness of breath, aggravated by bending over, lying down, and exertion. Physical examination reveals normal vital signs, decreased air movement at the left base with an area of dullness posteriorly on lung auscultation, and a soft abdomen without palpable organomegaly. A chest X-ray is shown. Which diagnostic test would best confirm the diagnosis?

Sniff test. ***Sniff test*** - The **sniff test (fluoroscopy)** is the gold standard for diagnosing **diaphragmatic paralysis**, showing **paradoxical upward movement** of the affected diaphragm during inspiration. - The patient's **positional dyspnea** (worse when bending/lying down) and **unilateral basal dullness** strongly suggest **left hemidiaphragm paralysis**, common in truck drivers due to **phrenic nerve injury**. *Ultrasound of abdomen* - While ultrasound can show **diaphragm position**, it cannot assess **diaphragmatic movement** or confirm paralysis during respiratory cycles. - The **soft abdomen** without organomegaly makes intra-abdominal pathology unlikely as the primary cause of respiratory symptoms. *Bronchoscopy* - Bronchoscopy evaluates **airway pathology** and **endobronchial lesions**, not diaphragmatic function or paralysis. - The **decreased air movement** is due to **mechanical restriction** from diaphragm elevation, not airway obstruction requiring bronchoscopic evaluation. *Pulmonary function test* - PFTs would show **restrictive pattern** but are **non-specific** and cannot differentiate between various causes of restriction. - While useful for assessing **functional impairment**, PFTs cannot **confirm the diagnosis** of diaphragmatic paralysis or identify the specific anatomical defect.

Question 1

A 48-year-old man, residing near a textile mill, presents with respiratory symptoms. A chest X-ray reveals a fine reticular and nodular pattern in the lower lung zones with loss of clarity of the diaphragmatic and cardiac outlines, and possible small pleural effusion. What is the probable diagnosis?

Accepted Answer

Asbestosis

Answer

Stannosis

Answer

Silicosis

Answer

Coal worker's pneumoconiosis

Question 2

A 17-year-old male complains of recurrent episodes of cough, wheezing, and shortness of breath, particularly at night, for the last 3 days. His sibling has a history of similar symptoms. A skin test with pollen produces an immediate wheal and flare. What is the most appropriate initial treatment?

Accepted Answer

Bronchodilators

Answer

Steroids

Answer

Antibiotics

Answer

Cough suppressants

Question 3

Pulmonary hypertension may occur in all of the following conditions, EXCEPT?

Accepted Answer

Argemone mexicana poisoning

Answer

Toxic oil syndrome

Answer

Progressive systemic sclerosis

Answer

Sickle cell anaemia

Question 4

In hemoptysis, from where does the blood usually originate?

Accepted Answer

Bronchial arteries

Answer

Bronchial veins

Answer

Pulmonary veins

Answer

Pulmonary arteries

Question 5

What is the treatment of choice in a patient of acute pulmonary embolism with right ventricular hypokinesis and compromised cardiac output but normal blood pressure?

Accepted Answer

Thrombolytic agent

Answer

Low molecular weight heparin

Answer

Warfarin

Answer

IV filters

Question 6

A middle-aged man presented with blood in the sputum. Which artery is primarily responsible for bleeding in hemoptysis?

Accepted Answer

Bronchial artery

Answer

Pulmonary artery

Answer

Intersegmental artery

Answer

Intercostal collaterals

Question 7

All of the following are features of Superior Vena Cava (SVC) Syndrome except?

Accepted Answer

Hoarseness of voice

Answer

Facial swelling

Answer

Dilatation and congestion of neck veins

Answer

Headache

Question 8

Which of the following syndromes is associated with bronchiectasis?

Accepted Answer

Kartagener syndrome

Answer

Kallmann syndrome

Answer

Kostmann syndrome

Answer

Klinefelter syndrome

Question 9

Which of the following statements regarding hypersensitivity pneumonitis is FALSE?

Accepted Answer

Bronchoalveolar lavage in hypersensitivity pneumonitis characteristically shows increased eosinophils.

Answer

It is typically caused by exposure to organic dusts or proteins.

Answer

It can lead to fibrosis of the lung parenchyma, resulting in interstitial lung disease.

Answer

Farmer's lung is a classic example of hypersensitivity pneumonitis.

Question 10

A 37-year-old truck driver presents with recent onset of shortness of breath, aggravated by bending over, lying down, and exertion. Physical examination reveals normal vital signs, decreased air movement at the left base with an area of dullness posteriorly on lung auscultation, and a soft abdomen without palpable organomegaly. A chest X-ray is shown. Which diagnostic test would best confirm the diagnosis?

Accepted Answer

Sniff test

Answer

Ultrasound of abdomen

Answer

Bronchoscopy

Answer

Pulmonary function test

Pulmonology — MCQs

Pulmonology — MCQs

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