Pulmonology — MCQs

A 40-year-old male patient presents with a complaint of dry cough and dyspnea. Lung function tests reveal a restrictive pattern with decreased lung function. A chest X-ray shows few reticular opacities in the bilateral lungs. HRCT of the lungs demonstrates ground-glass opacities (GGO) in bilateral lung fields, sparing the subpleural region. What is the most probable diagnosis?

Q664Easy

What is the most common cause of pleural effusion?

Q665Medium

A 53-year-old man develops weakness, malaise, cough with bloody sputum, and night sweats. A chest X-ray reveals numerous apical densities bilaterally, some of which are cavitary. Exposure to Mycobacterium tuberculosis was documented 20 years ago, and M. tuberculosis is identified in his sputum. Which of the following describes the expected lung pathology in this patient?

Q666Easy

What is the most common symptom seen in pulmonary tuberculosis?

Q667Medium

A 45-year-old man presents with a history of recurrent hemoptysis and purulent sputum. His chest X-ray is normal. What is the next best investigation for him?

Q668Easy

Allergic bronchopulmonary Aspergillosis is commonly a complication of:

Q669Medium

Pulmonary edema with normal pulmonary capillary wedge pressure (PCWP) is typically seen in which of the following conditions?

Q670Medium

A 24-year-old male law student presents with a 3-week history of increasing dyspnea. He has a history of chronic sputum production of about 100 cc of purulent material each day for many years. In the past, he was hospitalized for a left pneumothorax. He is on inhaled bronchodilator as an outpatient. What is the most helpful treatment option?

Pulmonology Indian Medical PG Practice Questions and MCQs

Question 661: Allergic bronchopulmonary aspergillosis is characterized by which of the following EXCEPT?

A. Bronchial asthma
B. Pleural effusion
C. Central bronchiectasis
D. Lack of response to steroids (Correct Answer)

Explanation: **Explanation:** Allergic Bronchopulmonary Aspergillosis (ABPA) is a complex hypersensitivity reaction to *Aspergillus fumigatus* that occurs primarily in patients with long-standing bronchial asthma or cystic fibrosis. **Why "Lack of response to steroids" is the correct answer:** This statement is incorrect because **systemic corticosteroids are the mainstay of treatment** for ABPA. They are highly effective in suppressing the immune response, reducing eosinophilia, and clearing pulmonary infiltrates. In fact, a dramatic clinical and radiological improvement following steroid therapy is a hallmark of the disease management. **Analysis of other options:** * **Bronchial Asthma:** This is a prerequisite for the diagnosis of ABPA. It typically presents as poorly controlled or steroid-dependent asthma [1]. * **Central Bronchiectasis:** This is a pathognomonic radiological finding in ABPA. Unlike post-infectious bronchiectasis which is usually peripheral, ABPA causes "inner two-thirds" or central bronchiectasis (often seen as "ring shadows" or "tram-track" appearances). * **Pleural Effusion:** While not a classic diagnostic criterion, pleural involvement is **rare** in ABPA. In the context of this specific MCQ, "Lack of response to steroids" is the definitive "false" statement because steroids are the primary treatment, whereas pleural effusion is simply an uncommon clinical finding. **NEET-PG High-Yield Pearls:** * **Diagnostic Criteria (Rosenberg-Patterson):** Look for Asthma, immediate skin reactivity to *Aspergillus*, elevated total IgE (>1000 IU/mL), and peripheral eosinophilia [1]. * **Radiology:** "Finger-in-glove" appearance (due to mucoid impaction) and "Toothpaste shadows." * **Treatment:** Oral Prednisolone is the first line; Itraconazole is added as a steroid-sparing agent to reduce fungal burden.

Question 662: What is the drug of choice for the treatment of type 2 Brittle Asthma?

A. b-adrenergic agonist
B. Inhaled corticosteroids
C. Antileukotrienes
D. Subcutaneous epinephrine (Correct Answer)

Explanation: **Explanation:** **Brittle Asthma** is a rare but severe form of asthma characterized by wide variations in Peak Expiratory Flow (PEF) despite high doses of inhaled therapy. It is categorized into two types: * **Type 1:** Persistent wide diurnal variability in PEF (often >40%). * **Type 2:** Sudden, unpredictable, and life-threatening drops in PEF occurring on a background of otherwise well-controlled asthma. **Why Subcutaneous Epinephrine is the Correct Answer:** Type 2 Brittle Asthma is characterized by "sudden asphyxiation" or "thunderclap" attacks. These episodes are so rapid and severe that inhaled medications (like Salbutamol) often cannot reach the distal airways due to profound bronchoconstriction and mucus plugging. **Subcutaneous Epinephrine** is the drug of choice because it provides rapid systemic bronchodilation, bypassing the obstructed airway route to stabilize the patient during these acute, life-threatening episodes. **Why Other Options are Incorrect:** * **A. β-adrenergic agonists (Inhaled):** While used in standard asthma, they are often ineffective in Type 2 Brittle Asthma during an acute crash because the delivery to the site of action is compromised. * **B. Inhaled Corticosteroids (ICS):** These are the cornerstone for long-term control of airway inflammation but have no role in the emergency management of an acute brittle attack [1]. * **C. Antileukotrienes:** These are used as add-on maintenance therapy (e.g., Montelukast) and are not indicated for acute rescue in brittle asthma. **High-Yield Clinical Pearls for NEET-PG:** * **Type 1 Brittle Asthma** is best managed with a **Continuous Subcutaneous Terbutaline Infusion (CSLI)**. * Patients with Type 2 Brittle Asthma should always carry a **pre-filled Epinephrine syringe (EpiPen)** for self-administration. * A key trigger for Type 2 Brittle Asthma is often **food allergy** (e.g., nuts, shellfish).

Question 663: A 40-year-old male patient presents with a complaint of dry cough and dyspnea. Lung function tests reveal a restrictive pattern with decreased lung function. A chest X-ray shows few reticular opacities in the bilateral lungs. HRCT of the lungs demonstrates ground-glass opacities (GGO) in bilateral lung fields, sparing the subpleural region. What is the most probable diagnosis?

A. Usual Interstitial Pneumonia (UIP)
B. Non-Specific Interstitial Pneumonia (NSIP) (Correct Answer)
C. Hypersensitivity Pneumonitis
D. Respiratory Bronchiolitis

Explanation: The clinical presentation of a middle-aged patient with dry cough, dyspnea, and a restrictive pattern on PFT points towards **Interstitial Lung Disease (ILD)** [1]. **Why NSIP is the correct answer:** The hallmark radiological feature of **Non-Specific Interstitial Pneumonia (NSIP)** on HRCT is the presence of bilateral, symmetrical **ground-glass opacities (GGO)** with a characteristic **subpleural sparing**. Unlike UIP, NSIP typically involves the lower lobes but preserves the immediate area adjacent to the pleura. It is the most common pattern of ILD associated with connective tissue diseases (e.g., Scleroderma). **Why other options are incorrect:** * **Usual Interstitial Pneumonia (UIP):** Characterized by honeycombing, traction bronchiectasis, and a predilection for the **subpleural** and basal regions [1]. It lacks significant GGO and does not show subpleural sparing. * **Hypersensitivity Pneumonitis:** Typically presents with centrilobular nodules, air trapping (mosaic attenuation), and a history of organic dust exposure. It usually involves the upper and middle lung zones. * **Respiratory Bronchiolitis (RB-ILD):** Strongly associated with heavy smoking. HRCT typically shows centrilobular ground-glass nodules and patchy GGO, but not the classic subpleural sparing seen in NSIP. **Clinical Pearls for NEET-PG:** * **NSIP Key Word:** "Subpleural Sparing" is the pathognomonic HRCT sign. * **Prognosis:** NSIP has a significantly better prognosis and better response to steroids compared to UIP/IPF. * **Histology:** NSIP shows a "temporally uniform" appearance (all lesions are at the same stage of development), whereas UIP shows "temporal heterogeneity" (fibroblastic foci alongside old scars).

Question 664: What is the most common cause of pleural effusion?

A. Cirrhosis
B. Left ventricular failure (Correct Answer)
C. Pulmonary embolism
D. Pneumonia

Explanation: **Explanation:** **Left Ventricular Failure (LVF)** is the most common cause of pleural effusion overall. The underlying mechanism is an increase in pulmonary capillary hydrostatic pressure. This pressure gradient forces fluid from the pulmonary capillaries into the interstitial space and across the visceral pleura into the pleural cavity, resulting in a **transudative** effusion. Typically, these effusions are bilateral; however, if unilateral, they occur more frequently on the right side. **Analysis of Incorrect Options:** * **Cirrhosis (A):** Causes "Hepatic Hydrothorax" due to the movement of ascitic fluid through small diaphragmatic defects. While a significant cause of transudative effusion, it is less frequent than heart failure. * **Pulmonary Embolism (C):** A common cause of pleural effusion, but it can be either transudative or exudative (though usually exudative). It is statistically less common than LVF. * **Pneumonia (D):** This is the most common cause of an **exudative** pleural effusion (specifically termed a parapneumonic effusion), but it ranks behind LVF when considering all types of effusions [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Light’s Criteria:** Used to differentiate between transudate and exudate. An effusion is **exudative** if it meets any one of the following: 1. Pleural fluid protein/Serum protein ratio > 0.5 2. Pleural fluid LDH/Serum LDH ratio > 0.6 3. Pleural fluid LDH > 2/3rd the upper limit of normal serum LDH. * **Most common cause of Exudative effusion:** Parapneumonic effusion (Pneumonia) [1]. * **Most common cause of Hemorrhagic effusion:** Malignancy or Trauma [1]. * **Most common cause of Massive effusion:** Malignancy (e.g., Lung CA, Breast CA) or Tuberculosis.

Question 665: A 53-year-old man develops weakness, malaise, cough with bloody sputum, and night sweats. A chest X-ray reveals numerous apical densities bilaterally, some of which are cavitary. Exposure to Mycobacterium tuberculosis was documented 20 years ago, and M. tuberculosis is identified in his sputum. Which of the following describes the expected lung pathology in this patient?

A. Dense fibrosis
B. Eosinophilic infiltration
C. Granulomas (Correct Answer)
D. Plasma cell infiltration

Explanation: ### Explanation The clinical presentation of chronic cough, hemoptysis, night sweats, and apical cavitary lesions in a patient with a history of exposure is classic for **Secondary (Reactivation) Tuberculosis**. **Why Granulomas are the Correct Answer:** The hallmark of *Mycobacterium tuberculosis* (MTB) infection is the formation of **caseating granulomas** [1]. This is a Type IV (delayed-type) hypersensitivity reaction. When MTB enters the lungs, alveolar macrophages ingest the bacilli but cannot initially kill them. Th1 cells then release **Interferon-gamma (IFN-γ)**, which activates macrophages, transforming them into **epithelioid histiocytes** and **Langhans giant cells** [1]. These cells surround the bacteria to form a granuloma with central "cheesy" caseous necrosis, effectively sequestering the infection [1]. **Analysis of Incorrect Options:** * **A. Dense fibrosis:** While healing of TB lesions involves fibrosis (fibrocalcific nodules), the active, cavitary stage described in the question is characterized by granulomatous inflammation and necrosis. * **B. Eosinophilic infiltration:** This is characteristic of parasitic infections or allergic conditions (e.g., ABPA, Churg-Strauss), not mycobacterial infections. * **D. Plasma cell infiltration:** Plasma cells are seen in chronic non-specific inflammation and certain conditions like Syphilis or Plasma Cell Myeloma, but they are not the diagnostic hallmark of TB. **NEET-PG High-Yield Pearls:** * **Ghon Focus:** Subpleural lesion in the mid/lower lobes (Primary TB) [1]. * **Ghon Complex:** Ghon focus + involved hilar lymph node [1]. * **Ranke Complex:** Calcified Ghon complex (seen on X-ray) [1]. * **Assmann Focus:** Infraclavicular lesion seen in Secondary TB. * **Cytokine Key:** **TNF-alpha** is essential for maintaining granuloma integrity. (Anti-TNF drugs like Infliximab can cause TB reactivation).

Question 666: What is the most common symptom seen in pulmonary tuberculosis?

A. Chest pain
B. Breathlessness
C. High temperature
D. Chronic cough (Correct Answer)

Explanation: **Explanation:** **Pulmonary Tuberculosis (PTB)** is a chronic granulomatous infection caused by *Mycobacterium tuberculosis*. The hallmark of the disease is its insidious onset and predilection for the lung parenchyma. **Why Chronic Cough is the Correct Answer:** Cough is the **most common and earliest symptom** of pulmonary TB, occurring in over 95% of symptomatic cases. It is initially dry but typically becomes productive as the disease progresses and lung tissue undergoes necrosis (cavitation). According to RNTCP (now NTEP) guidelines, any cough lasting **2 weeks or more** is the primary screening criterion for TB in endemic regions like India [1]. **Analysis of Incorrect Options:** * **A. Chest Pain:** Usually occurs only if the infection involves the pleura (pleuritic chest pain) or due to muscle strain from persistent coughing. It is a late or secondary feature. * **B. Breathlessness (Dyspnea):** This is generally seen in advanced stages with extensive lung parenchymal destruction, large pleural effusions, or miliary TB [1]. It is not the presenting symptom in most cases. * **C. High Temperature:** While fever is common in TB, it is characteristically **low-grade** and follows a **diurnal variation** (evening rise of temperature with nocturnal sweating) [1]. High-grade fever is more typical of acute bacterial pneumonias. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Upper lobes (Apical and posterior segments) due to higher oxygen tension. * **Gold Standard Diagnosis:** Sputum culture (MGIT/LJ Medium); however, **CBNAAT (GeneXpert)** is the initial diagnostic test of choice under NTEP. * **Constitutional Symptoms:** Weight loss (most common systemic symptom), anorexia, and evening rise of temperature [1]. * **Hemoptysis:** Occurs due to erosion of a blood vessel or the formation of a **Rasmussen aneurysm** in a tuberculous cavity.

Question 667: A 45-year-old man presents with a history of recurrent hemoptysis and purulent sputum. His chest X-ray is normal. What is the next best investigation for him?

A. High-resolution computed tomography (HRCT) (Correct Answer)
B. CT-guided angiography
C. Angiography
D. Spiral CT

Explanation: ### Explanation **Correct Answer: A. High-resolution computed tomography (HRCT)** The clinical presentation of recurrent hemoptysis and purulent sputum in a patient with a normal chest X-ray is highly suggestive of **Bronchiectasis**. While a chest X-ray may show "tram-track" opacities or ring shadows in advanced cases, it is normal in up to 10–20% of patients [1]. **HRCT is the gold standard** and the investigation of choice for diagnosing bronchiectasis, as it can detect bronchial wall thickening and dilation (e.g., the "signet ring sign") that are invisible on standard radiography [1]. **Why other options are incorrect:** * **B & C (CT-guided angiography / Angiography):** These are used to identify the site of bleeding in cases of *massive* or life-threatening hemoptysis when bronchial artery embolization (BAE) is planned [2]. They are not diagnostic tools for the underlying parenchymal or airway disease. * **D (Spiral CT):** While useful for detecting pulmonary embolisms or masses, it lacks the thin-slice resolution (1–2 mm) required to visualize the subtle airway changes characteristic of bronchiectasis, which HRCT provides. **Clinical Pearls for NEET-PG:** * **Gold Standard for Bronchiectasis:** HRCT (Look for a broncho-arterial ratio >1). * **Most common cause of Bronchiectasis in India:** Post-tubercular sequelae. * **Kartagener Syndrome Triad:** Bronchiectasis, Situs inversus, and Sinusitis [3]. * **Dry Bronchiectasis:** Hemoptysis without purulent sputum, typically involving the upper lobes (often post-TB). * **Initial Investigation for Hemoptysis:** Always start with a Chest X-ray, but if symptoms persist despite a normal X-ray, proceed to HRCT.

Question 668: Allergic bronchopulmonary Aspergillosis is commonly a complication of:

A. Tuberculosis
B. Bronchogenic carcinoma
C. Cystic fibrosis (Correct Answer)
D. Wegener's granulomatosis

Explanation: **Explanation:** **Allergic Bronchopulmonary Aspergillosis (ABPA)** is a complex hypersensitivity reaction to the fungus *Aspergillus fumigatus* that occurs almost exclusively in patients with pre-existing chronic airway diseases. 1. **Why Cystic Fibrosis (CF) is correct:** The underlying pathophysiology of ABPA involves an exaggerated Th2-mediated immune response to *Aspergillus* colonizing the thick, tenacious mucus in the airways. This is most commonly seen in patients with **Bronchial Asthma** and **Cystic Fibrosis**. In CF patients, the impaired mucociliary clearance provides an ideal environment for fungal colonization, leading to the development of ABPA in approximately 2–15% of cases [1]. 2. **Why other options are incorrect:** * **Tuberculosis:** While TB can lead to "Aspergilloma" (a fungal ball in a pre-existing cavity), it does not typically trigger the systemic hypersensitivity reaction characteristic of ABPA [1]. * **Bronchogenic Carcinoma:** This is a neoplastic condition. While fungal infections can occur in immunocompromised cancer patients, ABPA is not a recognized complication of malignancy. * **Wegener’s Granulomatosis (GPA):** This is a systemic vasculitis. While it affects the lungs (nodules/cavities), its pathogenesis is autoimmune (ANCA-associated) and unrelated to *Aspergillus* hypersensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Asthma/CF + Central Bronchiectasis + Eosinophilia. * **Radiological Sign:** "Finger-in-glove" appearance (due to mucoid impaction) and "Tram-line" shadows. * **Diagnosis:** Elevated total Serum IgE (>1000 IU/mL) and specific IgE/IgG against *Aspergillus*. * **Treatment:** Oral Corticosteroids (to suppress inflammation) and Itraconazole (to reduce fungal burden).

Question 669: Pulmonary edema with normal pulmonary capillary wedge pressure (PCWP) is typically seen in which of the following conditions?

A. Left atrial myxoma
B. High altitude (Correct Answer)
C. Mitral stenosis
D. Left ventricular systolic dysfunction

Explanation: **Explanation:** The core concept in this question is the differentiation between **Cardiogenic (Hydrostatic)** and **Non-Cardiogenic** pulmonary edema. Pulmonary Capillary Wedge Pressure (PCWP) is a surrogate measure of Left Atrial Pressure (LAP). **Why High Altitude is Correct:** High Altitude Pulmonary Edema (HAPE) is a form of **non-cardiogenic pulmonary edema** [1]. At high altitudes, the low partial pressure of oxygen (hypoxia) triggers **Hypoxic Pulmonary Vasoconstriction (HPV)**. This constriction is often uneven, leading to high pressure in the pulmonary arteries that is transmitted to the capillaries (overperfusion injury), causing fluid leakage into the alveoli [1]. Crucially, the left heart remains unaffected; therefore, the **LAP and PCWP remain normal (<18 mmHg).** **Why Other Options are Incorrect:** * **A, C, and D (Left Atrial Myxoma, Mitral Stenosis, and LV Dysfunction):** These are all causes of **Cardiogenic Pulmonary Edema**. In these conditions, there is a "back-pressure" effect from the left heart into the pulmonary veins. This increases the hydrostatic pressure in the pulmonary capillaries, leading to an **elevated PCWP (>18 mmHg).** **High-Yield Clinical Pearls for NEET-PG:** * **PCWP vs. PAP:** In HAPE, Pulmonary Artery Pressure (PAP) is elevated, but PCWP is normal. * **Other causes of Normal PCWP Edema:** ARDS (increased permeability), Neurogenic pulmonary edema, and Re-expansion pulmonary edema. * **Treatment of HAPE:** The definitive treatment is immediate descent and oxygen [1]. Pharmacologically, **Nifedipine** (a pulmonary vasodilator) is used for prevention and treatment, unlike cardiogenic edema where diuretics are mainstay. * **Radiology:** HAPE typically shows patchy, peripheral opacities rather than the perihilar "bat-wing" appearance seen in heart failure.

Question 670: A 24-year-old male law student presents with a 3-week history of increasing dyspnea. He has a history of chronic sputum production of about 100 cc of purulent material each day for many years. In the past, he was hospitalized for a left pneumothorax. He is on inhaled bronchodilator as an outpatient. What is the most helpful treatment option?

A. Increase bronchodilator therapy
B. Start broad-spectrum antibiotic therapy
C. Initiate anti-pseudomonas antibiotic regimen (Correct Answer)
D. Start oral steroids

Explanation: ### Explanation **Diagnosis: Bronchiectasis with Acute Exacerbation** The clinical presentation of chronic, voluminous (100 cc/day), purulent sputum production in a young patient is classic for **Bronchiectasis**. The history of a prior pneumothorax further suggests structural lung damage. In patients with bronchiectasis presenting with worsening dyspnea (an acute exacerbation), the primary goal is to treat the underlying bacterial infection [1]. **Why Option C is Correct:** * **Microbiology:** The most common and clinically significant pathogen isolated from the sputum of patients with bronchiectasis is ***Pseudomonas aeruginosa*** [1]. * **Impact:** Colonization with *Pseudomonas* is associated with more frequent exacerbations, accelerated decline in lung function, and higher mortality. Therefore, empiric therapy for an exacerbation must prioritize an **anti-pseudomonal antibiotic regimen** (e.g., Piperacillin-Tazobactam, Ceftazidime, or Ciprofloxacin) until cultures return [1]. **Why Other Options are Incorrect:** * **Option A:** While bronchodilators help with airflow obstruction, they do not treat the underlying infectious trigger causing the increased dyspnea and sputum. * **Option B:** "Broad-spectrum" is too vague. In bronchiectasis, therapy must specifically cover Gram-negative organisms, particularly *Pseudomonas*, which many standard broad-spectrum antibiotics do not cover adequately. * **Option D:** Oral steroids are indicated for Asthma or COPD exacerbations. In bronchiectasis, they are not the primary treatment unless there is a comorbid allergic component (like ABPA). **NEET-PG High-Yield Pearls:** * **Gold Standard Investigation:** High-Resolution CT (HRCT) Chest. Look for the **"Signet Ring Sign"** (bronchial lumen wider than the accompanying pulmonary artery). * **Most Common Organism:** *Haemophilus influenzae* is common, but *Pseudomonas aeruginosa* indicates more severe disease and worse prognosis [1]. * **Kartagener Syndrome:** A classic triad associated with bronchiectasis: Situs inversus, chronic sinusitis, and bronchiectasis (due to Primary Ciliary Dyskinesia). * **Management Priority:** Airway clearance (chest physiotherapy) and targeted antibiotic therapy [2].

Practice by Chapter

Obstructive Airway Diseases (Asthma, COPD)

Practice Questions

Interstitial Lung Diseases

Practice Questions

Pulmonary Infections

Practice Questions

Pulmonary Vascular Diseases

Practice Questions

Pleural Diseases

Practice Questions

Sleep-Disordered Breathing

Practice Questions

Respiratory Failure

Practice Questions

Mediastinal Disorders

Practice Questions

Occupational Lung Diseases

Practice Questions

Pulmonary Function Testing

Practice Questions

Bronchiectasis and Cystic Fibrosis

Practice Questions

Lung Cancer Approach

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free