Pulmonology Practice Questions

Q: A 70-year-old male smoker presents with cough and sputum production, but is afebrile. Lung examination reveals left-sided crackles, rhonchi, and egophony in the left upper lobe. The patient is being treated for an acute exacerbation of chronic bronchitis, and sputum is negative for AFB. What is the most likely cause of the observed chest X-ray findings in the left upper lobe?

Old granulomatous disease. ***Old granulomatous disease*** - **Healed tuberculosis** commonly causes **fibrotic scarring** and **calcifications** in the left upper lobe, which appear as persistent radiographic changes on chest X-ray. - The **AFB-negative sputum** and **afebrile** presentation rule out active TB, while the **upper lobe predilection** and **chronic radiographic changes** are characteristic of old granulomatous disease. *Chronic bronchitis* - Typically causes **hyperinflation** and **increased bronchovascular markings** throughout both lungs, not localized upper lobe changes. - Does not produce the **consolidation** or **fibrotic changes** that would cause **egophony** and localized crackles in one specific lobe. *Left upper lobe pneumonia* - Would present with **fever**, **acute onset** of symptoms, and **leukocytosis**, which are absent in this afebrile patient. - **Pneumonia** typically shows **acute consolidation** rather than the **chronic fibrotic changes** suggested by the clinical context and imaging findings. *Asbestos exposure* - Primarily causes **bilateral lower lobe fibrosis** and **pleural plaques**, not upper lobe predominant changes. - Associated with **restrictive lung disease** and **pleural effusions**, rather than the upper lobe consolidation pattern described.

Q: A 62-year-old man with a 40-pack/year history of smoking presents with increased sputum production and marked shortness of breath. On examination, he is using accessory muscles of respiration, and breath sounds are diminished with expiratory wheezes. Your clinical diagnosis is chronic obstructive pulmonary disease (COPD) exacerbation. For the above patient, select the characteristic arterial pulse finding.

Pulsus paradoxus. ### Explanation **Correct Answer: B. Pulsus paradoxus** **Why it is correct:** Pulsus paradoxus is defined as an exaggerated fall in systolic blood pressure (>10 mmHg) during inspiration. In severe **COPD or Asthma exacerbations**, the patient generates extreme negative intrathoracic pressure to overcome airway obstruction. This negative pressure increases venous return to the right ventricle (RV), causing the interventricular septum to bulge into the left ventricle (LV). This reduces LV filling and stroke volume. Additionally, the hyperinflated lungs and high negative pressure increase the "afterload" on the LV by making it harder to pump blood out of the thorax, further dropping the systolic pressure during inspiration [1]. **Why the other options are incorrect:** * **A. Pulsus tardus:** A slow-rising, low-amplitude pulse characteristic of **Aortic Stenosis**. * **C. Hyperkinetic pulse:** A bounding pulse seen in high-output states like **Anemia, Thyrotoxicosis, or Aortic Regurgitation**. * **D. Bisferiens pulse:** A pulse with two systolic peaks, typically seen in **HOCM** or combined **Aortic Stenosis and Regurgitation**. **Clinical Pearls for NEET-PG:** * **Classic Causes of Pulsus Paradoxus:** Cardiac Tamponade (most common association), Severe COPD/Asthma, Constrictive Pericarditis, and Restrictive Cardiomyopathy [1]. * **Reverse Pulsus Paradoxus:** Seen in patients on **positive pressure ventilation** and in **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. * **Mechanism Tip:** In Tamponade, the mechanism is "ventricular interdependence" within a fixed pericardial space; in COPD, it is primarily due to extreme fluctuations in intrathoracic pressure.

Q: Which of the following is NOT a recognized cause of adult respiratory distress syndrome?

Malignant hypertension. **Explanation:** Acute Respiratory Distress Syndrome (ARDS) is characterized by diffuse alveolar-capillary damage leading to non-cardiogenic pulmonary edema [1]. The pathophysiology involves an inflammatory trigger that increases permeability, causing protein-rich fluid to leak into the alveoli. **Why Malignant Hypertension is the correct answer:** Malignant hypertension (hypertensive emergency) typically causes **cardiogenic pulmonary edema**. The mechanism is hemodynamic: extreme systemic vascular resistance leads to left ventricular strain and increased pulmonary capillary hydrostatic pressure. Unlike ARDS, the alveolar-capillary membrane remains intact initially, and the edema fluid is transudative (low protein) rather than exudative [2]. **Analysis of Incorrect Options:** * **Smoke Inhalation:** This is a direct lung injury. Toxic chemicals and heat cause chemical pneumonitis and direct damage to the alveolar epithelium, a classic trigger for ARDS. * **Gastric Aspiration:** One of the most common causes of ARDS. The low pH of gastric acid causes immediate chemical burns to the lung parenchyma, triggering a massive inflammatory response. * **Viral Pneumonia:** A common infectious cause of ARDS (e.g., Influenza, COVID-19). The virus infects type II pneumocytes, leading to diffuse alveolar damage (DAD). **NEET-PG High-Yield Pearls:** * **Berlin Criteria for ARDS:** 1) Acute onset (within 1 week); 2) Bilateral opacities on imaging; 3) Respiratory failure not fully explained by heart failure (PCWP < 18 mmHg); 4) PaO2/FiO2 ratio < 300 [1]. * **Pathological Hallmark:** Diffuse Alveolar Damage (DAD) with the formation of **Hyaline Membranes**. * **Most common cause:** Sepsis (indirect injury) is the overall most common cause of ARDS.

Q: True about pleural effusion?

Amylase content is usually high in pancreatic effusion. Explanation: 1. Why Option A is Correct: Pleural fluid amylase levels are considered elevated when they exceed the upper limit of normal for serum amylase or the fluid-to-serum amylase ratio is >1.0. High amylase is a hallmark of pancreatic pleural effusion (caused by acute/chronic pancreatitis or pancreatic pseudocyst), where levels can reach thousands. Other causes include esophageal rupture (salivary amylase) and certain malignancies (adenocarcinoma). 2. Why Other Options are Incorrect: * Option B: While Congestive Cardiac Failure (CCF) is the most common cause of bilateral effusion, it is not the only cause. Bilateral effusions can also occur in cirrhosis, nephrotic syndrome, and systemic lupus erythematosus (SLE). Therefore, saying it is "due to CCF" is an overgeneralization. * Option C: In Tuberculous pleurisy, the yield of TB bacilli in pleural fluid via direct microscopy (AFB stain) is extremely low ( 40 U/L), or PCR. * Option D: Hemorrhagic effusion is commonly associated with malignancy, but it is not pathognomonic [1]. It can also be seen in pulmonary embolism with infarction, trauma, and asbestos-related diseases [1]. Clinical Pearls for NEET-PG: * Light’s Criteria: Used to differentiate Exudate from Transudate (Protein ratio >0.5, LDH ratio >0.6, or Fluid LDH >2/3rd upper limit of serum) [1]. * Low Glucose ( 40-70 U/L, suspect Tuberculosis in endemic areas.

Q: SIADH is associated with which type of lung malignancy?

Small cell carcinoma of the lung. **Small cell carcinoma of the lung (SCLC)** is the correct answer because it is a neuroendocrine tumor derived from Kulchitsky cells. These cells have the metabolic machinery to produce ectopic hormones [1]. In approximately 7–10% of cases, SCLC cells secrete **Arginine Vasopressin (AVP/ADH)**, leading to the Syndrome of Inappropriate Antidiuretic Hormone (SIADH) [2]. This results in dilutional hyponatremia, concentrated urine, and euvolemic status. **Analysis of Incorrect Options:** * **Squamous cell carcinoma (SCC):** This is classically associated with the ectopic production of **Parathyroid Hormone-related Protein (PTHrP)**, leading to hypercalcemia [1]. A common mnemonic is "Squamous starts with S, and so does Stones (hypercalcemia)." * **Adenocarcinoma:** This is the most common lung cancer in non-smokers and is typically associated with **Hypertrophic Osteoarthropathy (HOA)** and digital clubbing rather than SIADH [2]. * **Mixed cell tumor:** While these can exhibit features of multiple cell types, they are not the primary or classic association for SIADH in medical examinations. **High-Yield Clinical Pearls for NEET-PG:** * **SCLC Associations:** SIADH, ACTH production (Cushing Syndrome), and Lambert-Eaton Myasthenic Syndrome (LEMS) [1], [3]. * **Diagnosis of SIADH:** Characterized by hyponatremia (Na 100 mOsm/kg). * **Management:** The mainstay of treatment for SIADH in SCLC is fluid restriction and treating the underlying malignancy. For refractory cases, Vasopressin receptor antagonists (Vaptans) may be used.

Q: Which of the following is NOT associated with pulmonary arterial hypertension?

Left ventricular hypertrophy. **Explanation:** The classification of Pulmonary Hypertension (PH) is divided into five groups based on etiology. Understanding these groups is key to identifying the correct answer. **Why Left Ventricular Hypertrophy (LVH) is the correct answer:** Pulmonary Arterial Hypertension (PAH) specifically refers to **WHO Group 1 PH**, which is characterized by primary disease of the small pulmonary arteries (pre-capillary PH). **Left Ventricular Hypertrophy (LVH)** is a consequence of systemic hypertension or aortic stenosis and leads to left-sided heart failure. This falls under **WHO Group 2 PH** (PH due to left heart disease). In Group 2, the pathology is "post-capillary" due to back-pressure from the left atrium, which is distinct from the "arterial" pathology of Group 1. **Analysis of Incorrect Options:** * **Interstitial Lung Disease (ILD):** Falls under **WHO Group 3**. Chronic hypoxia in ILD leads to pulmonary vasoconstriction and remodeling, causing PH [1]. * **Mitral Stenosis:** A classic cause of **WHO Group 2** PH. While it is "venous" or "post-capillary" PH, it is a well-known cause of elevated pulmonary pressures. * **Cor Pulmonale:** This is defined as right ventricular hypertrophy and failure resulting from diseases of the lungs or pulmonary vasculature (PH) [1]. Therefore, it is a direct **consequence** and clinical manifestation associated with chronic PH [1]. **NEET-PG High-Yield Pearls:** * **WHO Group 1 (PAH):** Includes Idiopathic, Heritable (BMPR2 mutation), and drug-induced (Aminorex, Fenfluramine). * **Hemodynamic Definition:** PH is now defined as Mean Pulmonary Artery Pressure **(mPAP) > 20 mmHg** (revised from 25 mmHg). * **Drug of Choice:** For PAH with a positive vasaoreactivity test, **Calcium Channel Blockers** are used. For others, Bosentan (Endothelin antagonist) or Sildenafil (PDE-5 inhibitor) are common. * **Gold Standard Diagnosis:** Right Heart Catheterization [1].

Q: A woman presents with a 6-week history of low-grade fever. A chest radiograph shows bihilar adenopathy with clear lung fields. Which of the following investigations would NOT be useful in the differential diagnosis?

CD4/CD8 counts in the blood. The clinical presentation of **bihilar lymphadenopathy** with a low-grade fever in a patient with clear lung fields is a classic "textbook" description of **Stage I Sarcoidosis** [1]. The goal of investigations is to confirm the diagnosis and rule out differentials like tuberculosis or lymphoma. **Why Option A is the correct answer:** While the **CD4/CD8 ratio in Bronchoalveolar Lavage (BAL) fluid** is a highly useful diagnostic marker for sarcoidosis (typically showing a ratio >3.5:1), the **CD4/CD8 ratio in peripheral blood** is non-specific and does not reflect the localized pulmonary inflammatory process. Therefore, blood counts do not aid in the differential diagnosis of hilar adenopathy. **Analysis of other options:** * **Serum ACE levels (B):** Elevated in about 60-80% of patients with active sarcoidosis. While not specific, it helps support the diagnosis and monitor disease activity. * **CECT Chest (C):** This is the gold standard for evaluating mediastinal and hilar lymphadenopathy [2]. It helps differentiate sarcoidosis (typically symmetrical) from malignancy or TB (often asymmetrical or necrotic) and detects subtle parenchymal involvement. * **Gallium-67 Scan (D):** Though less commonly used now, it shows characteristic uptake patterns like the **"Panda sign"** (lacrimal/parotid glands) and **"Lambda sign"** (bihilar/paratracheal nodes) in sarcoidosis. **NEET-PG High-Yield Pearls:** * **Lofgren’s Syndrome:** A specific acute presentation of sarcoidosis consisting of the triad: Erythema nodosum, Bilateral hilar lymphadenopathy, and Polyarthritis/Arthralgia [1]. * **Kveim Test:** An older skin test for sarcoidosis (now largely obsolete). * **Biopsy:** The definitive diagnosis of sarcoidosis requires the demonstration of **non-caseating granulomas** on histopathology.

Q: Alpha-1 antitrypsin deficiency presents as which of the following conditions?

Emphysema. ### Explanation **Correct Answer: A. Emphysema** **Pathophysiology:** Alpha-1 Antitrypsin (AAT) is a protease inhibitor synthesized in the liver [1]. Its primary role is to inhibit **Neutrophil Elastase**, an enzyme that breaks down elastin in the alveolar walls [1]. In AAT deficiency, the lack of this protective "anti-elastase" leads to unchecked destruction of the lung parenchyma, resulting in **Panacinar (Panlobular) Emphysema** [1]. Unlike smoking-related emphysema (which is typically centriacinar and affects the upper lobes), AAT deficiency characteristically involves the **lower lobes**. **Analysis of Incorrect Options:** * **B. Bronchiectasis:** While chronic lung destruction in AAT deficiency can occasionally lead to secondary bronchiectasis, it is not the primary or classic presentation. Bronchiectasis is more typically associated with Cystic Fibrosis or Kartagener syndrome. * **C. Empyema:** This refers to pus in the pleural space, usually secondary to bacterial pneumonia or thoracic surgery. It is an infectious process, not a genetic protease-antiprotease imbalance. * **D. Bronchogenic carcinoma:** While chronic lung inflammation is a risk factor for malignancy, AAT deficiency is specifically linked to emphysema and liver cirrhosis, not primarily as a cause of lung cancer. **Clinical Pearls for NEET-PG:** 1. **Genetics:** Autosomal codominant inheritance; the **PiZZ** genotype is associated with the most severe clinical disease [1]. 2. **Liver Involvement:** Misfolded AAT proteins accumulate in the endoplasmic reticulum of hepatocytes, leading to **Liver Cirrhosis**. Histology shows **PAS-positive, diastase-resistant globules**. 3. **Diagnosis:** Suspect in a young, non-smoker (age <45) presenting with lower-lobe emphysema. 4. **Radiology:** Chest X-ray shows hyperinflation and flattening of the diaphragm, predominantly at the bases.

Question 1

A 70-year-old male smoker presents with cough and sputum production, but is afebrile. Lung examination reveals left-sided crackles, rhonchi, and egophony in the left upper lobe. The patient is being treated for an acute exacerbation of chronic bronchitis, and sputum is negative for AFB. What is the most likely cause of the observed chest X-ray findings in the left upper lobe?

Accepted Answer

Old granulomatous disease

Answer

Chronic bronchitis

Answer

Left upper lobe pneumonia

Answer

Asbestos exposure

Question 2

A 62-year-old man with a 40-pack/year history of smoking presents with increased sputum production and marked shortness of breath. On examination, he is using accessory muscles of respiration, and breath sounds are diminished with expiratory wheezes. Your clinical diagnosis is chronic obstructive pulmonary disease (COPD) exacerbation. For the above patient, select the characteristic arterial pulse finding.

Accepted Answer

Pulsus paradoxus

Answer

Pulsus tardus

Answer

Hyperkinetic pulse

Answer

Bisferiens pulse

Question 3

Which of the following is NOT a recognized cause of adult respiratory distress syndrome?

Accepted Answer

Malignant hypertension

Answer

Smoke inhalation

Answer

Gastric aspiration

Answer

Viral pneumonia

Question 4

True about pleural effusion?

Accepted Answer

Amylase content is usually high in pancreatic effusion

Answer

Bilateral effusion is due to congestive cardiac failure

Answer

TB bacilli can be isolated if it is due to TB

Answer

Hemorrhagic effusion is due to malignancy

Question 5

SIADH is associated with which type of lung malignancy?

Accepted Answer

Small cell carcinoma of the lung

Answer

Adenocarcinoma of the lung

Answer

Squamous cell carcinoma of the lung

Answer

Mixed cell tumor of the lung

Question 6

Which of the following is NOT associated with pulmonary arterial hypertension?

Accepted Answer

Left ventricular hypertrophy

Answer

Interstitial lung disease

Answer

Mitral Stenosis

Answer

Cor pulmonale

Question 7

Type I respiratory failure best relates to which of the following?

Accepted Answer

Alveolar flooding

Answer

Alveolar hypoventilation

Answer

Hypoperfusion of respiratory muscles

Answer

Lung atelectasis

Question 8

A woman presents with a 6-week history of low-grade fever. A chest radiograph shows bihilar adenopathy with clear lung fields. Which of the following investigations would NOT be useful in the differential diagnosis?

Accepted Answer

CD4/CD8 counts in the blood

Answer

Serum ACE levels

Answer

Contrast-enhanced computed tomography (CECT) of the chest

Answer

Gallium scan

Question 9

A 25-year-old man presents with infertility, a lifelong history of productive cough, recurrent pulmonary infections, chronic abdominal pain, diarrhea, difficulty gaining weight, and diabetes mellitus. His chest x-ray suggests bronchiectasis. What is the most likely diagnosis?

Accepted Answer

Cystic fibrosis

Answer

Immunoglobulin deficiency

Answer

Whipple disease

Answer

Chronic obstructive pulmonary disease (COPD)

Question 10

Alpha-1 antitrypsin deficiency presents as which of the following conditions?

Accepted Answer

Emphysema

Answer

Bronchiectasis

Answer

Empyema

Answer

Bronchogenic carcinoma

Pulmonology — MCQs

Pulmonology — MCQs

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