Pulmonology — MCQs

A 65-year-old patient with chronic obstructive airway disease presented with headache, rhinorrhoea, myalgia, and retro-orbital and throat pain. He was managed conservatively. After 3-4 days, he presented again with cough, fever, and severe dyspnoea, requiring oxygen therapy. His condition deteriorated further, and ABG analysis showed pH 7.42, pCO2 41 mm Hg, pO2 34 mm Hg, and HCO3- 26 mmol/L. Blood cultures and sputum samples were negative for bacterial infections. Which of the following statements about the causative organism of this condition is FALSE?

Q316Easy

Hamman's sign is most characteristic of which condition?

Q317Easy

Which of the following is the LEAST likely cause of hemoptysis?

Q318Medium

Bilateral rhonchi may be seen in all of the following conditions except?

Q319Medium

What is true about sarcoidosis?

Q320Easy

ARDS is characterized by all except:

Pulmonology Indian Medical PG Practice Questions and MCQs

Question 311: Kartagener's syndrome includes which of the following EXCEPT?

A. Situs inversus
B. Bronchitis (Correct Answer)
C. Sinusitis
D. Bronchiectasis

Explanation: **Explanation:** Kartagener’s syndrome is a specific subset of **Primary Ciliary Dyskinesia (PCD)**, an autosomal recessive disorder characterized by structural defects in the dynein arms of cilia [2]. This leads to impaired mucociliary clearance throughout the body [2]. **Why Bronchitis is the correct answer (The Exception):** While patients with Kartagener’s syndrome suffer from recurrent respiratory infections, **Bronchitis** is not considered a defining component of the classic clinical triad. Bronchitis refers to acute or chronic inflammation of the bronchial tubes, whereas Kartagener’s involves permanent, irreversible structural damage known as **Bronchiectasis** [1, 3]. In the context of NEET-PG, "Bronchiectasis" is the specific pathological hallmark, making "Bronchitis" the incorrect descriptor for the syndrome. **Analysis of other options:** * **Situs Inversus (A):** Present in 50% of PCD patients (defining Kartagener’s). It occurs due to the failure of nodal cilia to determine left-right asymmetry during embryonic development. * **Sinusitis (C):** Chronic rhinosinusitis occurs because impaired cilia cannot clear mucus from the paranasal sinuses, leading to secondary bacterial infections [2]. * **Bronchiectasis (D):** Persistent stasis of secretions and recurrent infections lead to permanent dilation of the bronchi, a core feature of the syndrome [3, 4]. **High-Yield Clinical Pearls for NEET-PG:** 1. **The Classic Triad:** Situs inversus, Chronic sinusitis, and Bronchiectasis. 2. **Infertility:** Common in males (immotile spermatozoa) and females (impaired ciliary action in fallopian tubes). 3. **Diagnostic Gold Standard:** Electron microscopy showing **absence of dynein arms** (inner or outer). 4. **Screening Test:** Nasal Nitric Oxide (nNO) levels are characteristically very low in these patients.

Question 312: Which of the following is a feature of acute severe asthma?

A. Heart rate of 110 beats/min
B. PaO2 of 70 mmHg
C. Peak expiratory flow rate of < 40% (Correct Answer)
D. All of the above

Explanation: In clinical practice and for NEET-PG, distinguishing between the grades of asthma severity is crucial for management. The classification of **Acute Severe Asthma** (formerly known as

Question 313: Which of the following conditions can produce hemothorax?

A. Myxoma
B. Congestive heart failure
C. Rheumatoid arthritis
D. Uremia (Correct Answer)

Explanation: Explanation: Hemothorax is defined as the presence of pleural fluid with a hematocrit level ≥50% of the peripheral blood hematocrit. While trauma is the most common cause, non-traumatic (spontaneous) hemothorax can occur due to underlying systemic conditions. Why Uremia is the correct answer: Uremia (chronic kidney disease) is a recognized cause of hemorrhagic pleural effusions and, in severe cases, frank hemothorax. The underlying mechanism involves uremic toxins causing increased capillary permeability and, more significantly, platelet dysfunction (impaired adhesion and aggregation). This uremic coagulopathy predisposes patients to spontaneous bleeding into serous cavities, including the pleura. Analysis of Incorrect Options: * Myxoma (Atrial Myxoma): Typically presents with constitutional symptoms (fever, weight loss) and embolic phenomena. While it can cause pulmonary edema or congestive heart failure, it does not directly cause hemothorax. * Congestive Heart Failure (CHF): This is the most common cause of transudative pleural effusion [1, 5]. The fluid is typically clear/straw-colored with low protein and LDH levels, not hemorrhagic. * Rheumatoid Arthritis (RA): RA typically causes an exudative effusion characterized by very low glucose levels (<30 mg/dL), high LDH, and low pH [1]. While the fluid can occasionally be turbid, it is not a classic cause of hemothorax. High-Yield Pearls for NEET-PG: * Definition: Pleural fluid hematocrit >50% of blood hematocrit = Hemothorax. * Spontaneous Hemothorax Causes: Malignancy (most common non-traumatic), anticoagulant therapy, vascular ruptures (Aortic dissection), and coagulopathies (Uremia). * Uremic Effusion: Usually serosanguinous; if it becomes a hemothorax, it often indicates severe platelet dysfunction or concurrent anticoagulant use during dialysis. * Management: Immediate tube thoracostomy (chest tube) is the treatment of choice for hemothorax to drain the blood and monitor for ongoing bleeding.

Question 314: A patient tested positive for MTB on sputum CBNAAT and did not return for follow-up despite reminders. The patient now presents with massive hemoptysis. What is the next best step for this patient?

A. Urgent coagulation studies
B. Perform multi-slice CT scan of the chest (Correct Answer)
C. Schedule a flexible fiber-optic bronchoscopy
D. Urgent rigid bronchoscopy with prophylactic balloon tamponade

Explanation: The patient has a history of pulmonary tuberculosis (MTB) and presents with **massive hemoptysis** (typically defined as >200–600 mL of blood in 24 hours). In the context of TB, massive hemoptysis is most commonly caused by the rupture of a **Rasmussen’s aneurysm** (a pulmonary artery aneurysm within a tuberculous cavity) or hypertrophied bronchial arteries. [1] **Why Option B is correct:** Multi-slice CT (MSCT) angiography has replaced conventional angiography as the initial diagnostic tool of choice. It is non-invasive, rapid, and highly sensitive in identifying the **site and cause of bleeding** (e.g., cavity, aneurysm, or bronchiectasis). It serves as a "roadmap" for the interventional radiologist if Bronchial Artery Embolization (BAE)—the definitive non-surgical treatment—is required. [2] **Why other options are incorrect:** * **Option A:** While coagulation profiles are part of the workup, they are supportive and do not identify the source of life-threatening bleeding. * **Option C:** Flexible bronchoscopy has a limited role in massive hemoptysis because the large volume of blood obscures the field of vision, making it difficult to localize the bleed. * **Option D:** Rigid bronchoscopy is an excellent tool for airway stabilization and suctioning, but it is technically demanding and usually reserved for cases where MSCT is unavailable or the patient is too unstable to leave the ICU. **Clinical Pearls for NEET-PG:** 1. **Most common source of massive hemoptysis:** Bronchial arteries (90%), despite the lungs having a dual blood supply. 2. **Rasmussen’s Aneurysm:** A classic TB-associated cause involving the pulmonary artery. 3. **Immediate Management:** Position the patient with the **bleeding lung in the dependent (downward) position** to prevent aspiration into the healthy lung. 4. **Gold Standard Treatment:** Bronchial Artery Embolization (BAE). [2]

Question 315: A 65-year-old patient with chronic obstructive airway disease presented with headache, rhinorrhoea, myalgia, and retro-orbital and throat pain. He was managed conservatively. After 3-4 days, he presented again with cough, fever, and severe dyspnoea, requiring oxygen therapy. His condition deteriorated further, and ABG analysis showed pH 7.42, pCO2 41 mm Hg, pO2 34 mm Hg, and HCO3- 26 mmol/L. Blood cultures and sputum samples were negative for bacterial infections. Which of the following statements about the causative organism of this condition is FALSE?

A. The organism is mostly spherical but filamentous in fresh isolates.
B. The organism is segmented with 8 pieces of RNA.
C. Haemolysins are present. (Correct Answer)
D. The diameter of the nucleocapsid is 9nm.

Explanation: ### Explanation The clinical presentation describes a classic case of **Influenza** infection leading to **Secondary Viral Pneumonia** or **ARDS**. The patient initially had "flu-like" symptoms (rhinorrhoea, myalgia, retro-orbital pain), followed by a "biphasic" worsening characterized by severe respiratory distress and profound hypoxemia (pO2 34 mmHg) [1]. The negative bacterial cultures and the rapid deterioration in a COPD patient point toward the **Influenza virus** (Orthomyxoviridae family). #### Why Option C is False: Influenza viruses possess two major surface glycoproteins: **Hemagglutinin (HA)** and **Neuraminidase (NA)** [1]. While Hemagglutinin allows the virus to bind to sialic acid receptors and agglutinate red blood cells, the virus **does not possess Haemolysins** (enzymes that rupture RBCs). Haemolysins are typically associated with bacteria like *Streptococcus* or *Staphylococcus*. #### Analysis of Other Options: * **Option A (True):** Influenza viruses are pleomorphic. While generally spherical (80–120 nm), fresh clinical isolates often demonstrate **filamentous forms**. * **Option B (True):** Influenza A and B viruses have a **segmented genome** consisting of **8 single-stranded, negative-sense RNA segments**. This segmentation allows for "genetic reassortment," leading to antigenic shift [1]. * **Option D (True):** The nucleocapsid of the Influenza virus (Type A/B) has a helical symmetry with a diameter of approximately **9 nm**. #### Clinical Pearls for NEET-PG: * **Antigenic Shift:** Major changes due to gene reassortment (causes Pandemics) [1]. * **Antigenic Drift:** Minor point mutations (causes Epidemics) [1]. * **Complications:** The most common secondary bacterial pneumonia after Influenza is caused by *Streptococcus pneumoniae*, but the most "classic" or severe post-viral pneumonia is caused by *Staphylococcus aureus* [1]. * **Diagnosis:** Gold standard is RT-PCR. * **Treatment:** Oseltamivir (Neuraminidase inhibitor) is most effective when started within 48 hours of symptom onset.

Question 316: Hamman's sign is most characteristic of which condition?

A. Subcutaneous emphysema
B. Pneumothorax
C. Pneumopericardium
D. Pneumomediastinum (Correct Answer)

Explanation: **Explanation:** **Hamman’s Sign** (also known as Hamman’s crunch) is a pathognomonic physical finding for **Pneumomediastinum**. It is characterized by a series of precordial crackles, clicks, or gurgling sounds synchronous with the heartbeat rather than respiration. **Why Pneumomediastinum is correct:** When air is trapped within the mediastinum, the mechanical contraction and relaxation of the heart against these air pockets create a "crunching" sound. This is best heard over the left sternal border with the patient in the left lateral decubitus position. It is often associated with Mackler’s triad (seen in Boerhaave syndrome). **Why other options are incorrect:** * **Subcutaneous emphysema:** While often co-existing with pneumomediastinum, it presents with "crepitus" (a rice-krispy popping sensation) upon palpation of the skin, not a rhythmic crunching sound synchronous with the heart. * **Pneumothorax:** This typically presents with decreased breath sounds and hyper-resonance on percussion. While a "clicking" sound can rarely occur in a left-sided spontaneous pneumothorax, it is not the classic Hamman’s sign. * **Pneumopericardium:** This involves air within the pericardial sac. It classically produces a "mill-wheel murmur" (bruit de moulin), which is a loud, splashing sound, distinct from the crunching of Hamman’s sign. **Clinical Pearls for NEET-PG:** * **Hamman’s Syndrome:** Refers to spontaneous pneumomediastinum, often triggered by activities involving the Valsalva maneuver (e.g., childbirth, weightlifting, or forceful coughing). * **Chest X-ray:** Look for the "continuous diaphragm sign" or "spinnaker sail sign" (in pediatrics) to diagnose pneumomediastinum. * **Differential:** Always rule out esophageal rupture (Boerhaave syndrome) when Hamman’s sign is present in a patient with chest pain and vomiting.

Question 317: Which of the following is the LEAST likely cause of hemoptysis?

A. Pneumonia
B. Empyema (Correct Answer)
C. Bronchiectasis
D. Mitral stenosis

Explanation: Hemoptysis is the expectoration of blood originating from the lower respiratory tract, typically due to the erosion of bronchial or pulmonary vessels. **Why Empyema is the Correct Answer:** Empyema is a collection of **pus** within the pleural space (the cavity between the lung and the chest wall) [1]. Because the infection is localized outside the lung parenchyma and the bronchial tree, there is no direct communication with the airways. Therefore, while empyema causes chest pain and fever, it does not typically cause hemoptysis unless it is complicated by a bronchopleural fistula [1]. **Analysis of Incorrect Options:** * **Pneumonia:** Inflammation and necrosis of the lung parenchyma can cause localized vascular damage [2]. "Rusty sputum" is a classic finding in *Streptococcus pneumoniae* [2]. * **Bronchiectasis:** This is one of the most common causes of massive hemoptysis [2]. Chronic inflammation leads to the hypertrophy and tortuosity of high-pressure **bronchial arteries**, which can easily rupture [2]. * **Mitral Stenosis:** This is a classic cardiovascular cause of hemoptysis. Elevated left atrial pressure leads to pulmonary venous hypertension, causing the rupture of small bronchial submucosal veins (often termed "cardiac asthma" or "pink frothy sputum" in acute failure). **Clinical Pearls for NEET-PG:** * **Most common cause of hemoptysis (Global/India):** Tuberculosis. * **Most common cause of hemoptysis (Western world):** Bronchitis / Bronchogenic carcinoma. * **Massive Hemoptysis:** Defined as >200–600 mL of blood in 24 hours. The **bronchial arteries** (systemic circulation) are responsible for 90% of massive hemoptysis cases, not the pulmonary arteries [2]. * **Initial Investigation of choice:** Chest X-ray. * **Gold standard for localizing the site of bleeding:** Bronchoscopy.

Question 318: Bilateral rhonchi may be seen in all of the following conditions except?

A. Pulmonary edema
B. Bronchiectasis
C. Pulmonary embolism (Correct Answer)
D. Emphysema

Explanation: **Explanation:** The presence of **bilateral rhonchi** (polyphonic wheezing) indicates widespread narrowing of the small airways, typically due to bronchospasm, mucosal edema, or excessive secretions. **Why Pulmonary Embolism (PE) is the correct answer:** Pulmonary embolism is primarily a **vascular pathology**, not an airway disease. It involves the occlusion of pulmonary arteries by a thrombus. While massive PE can occasionally cause localized wheezing due to the release of bronchoconstrictive mediators (like serotonin), it typically presents with sudden onset dyspnea, pleuritic chest pain, and clear lung fields on auscultation [1]. It does **not** characteristically cause bilateral rhonchi. **Analysis of Incorrect Options:** * **Pulmonary Edema:** Known as "Cardiac Asthma," left-sided heart failure leads to peribronchial edema and fluid in the airways, resulting in bilateral rhonchi and crepitations [2]. * **Bronchiectasis:** This involves permanent dilatation of bronchi with chronic inflammation and copious secretions. The presence of thick mucus in the dilated airways frequently produces bilateral rhonchi and coarse crackles. * **Emphysema:** As a component of COPD, emphysema involves airway inflammation and loss of elastic recoil, leading to expiratory airflow obstruction and characteristic bilateral polyphonic rhonchi [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Monophonic Rhonchi:** Suggests a fixed local obstruction (e.g., Foreign body or Bronchogenic Carcinoma). * **Polyphonic Rhonchi:** Suggests generalized airway disease (e.g., Asthma, COPD) [2]. * **Silent Chest:** A dangerous sign in acute severe asthma where airflow is too low to even produce a rhonchus. * **Classic PE Triad:** Dyspnea, Chest Pain, and Hemoptysis (seen in <20% of cases). The most common ECG finding is Sinus Tachycardia; the most specific is S1Q3T3 [1].

Question 319: What is true about sarcoidosis?

A. Kveim test is helpful in diagnosis (Correct Answer)
B. May be associated with positive RA factor
C. Associated with pleural effusion
D. Common in 50-year-old males

Explanation: **Explanation:** **Sarcoidosis** is a multisystem, chronic granulomatous disease of unknown etiology characterized by the formation of non-caseating granulomas. **1. Why Option A is Correct:** The **Kveim-Siltzbach test** is a historical diagnostic tool where a suspension of sarcoid tissue (usually from the spleen or lymph node) is injected intradermally. A positive result is the formation of a nodule 4–6 weeks later, which shows non-caseating granulomas on biopsy. While largely replaced by modern imaging and transbronchial biopsy (TBB), it remains a classic "textbook" diagnostic association for Sarcoidosis in exams. **2. Why the other options are Incorrect:** * **Option B:** While sarcoidosis is an inflammatory condition, it is classically associated with **Hypergammaglobulinemia** and an **elevated ACE (Angiotensin-Converting Enzyme) level**, rather than a positive Rheumatoid Factor (which is specific to RA and other connective tissue diseases). * **Option C:** Pleural involvement is **rare** in sarcoidosis (occurring in <5% of cases). The hallmark pulmonary finding is bilateral hilar lymphadenopathy and interstitial lung disease. * **Option D:** Sarcoidosis typically affects **younger adults (20–40 years)** and shows a slight **female predominance** [1]. It is not a disease primarily of 50-year-old males. **High-Yield Clinical Pearls for NEET-PG:** * **Lofgren’s Syndrome:** A triad of Erythema nodosum, Bilateral hilar lymphadenopathy, and Arthralgia (Good prognosis) [1]. * **Heerfordt’s Syndrome (Uveoparotid fever):** Parotid enlargement, Uveitis, and Facial nerve palsy [1]. * **Histology:** Non-caseating granulomas containing **Schaumann bodies** (laminated calcium-protein concretions) and **Asteroid bodies** (star-shaped inclusions). * **Imaging:** Stage I is characterized by bilateral hilar lymphadenopathy alone [1]. * **Biochemical marker:** Elevated serum ACE levels (reflects total body granuloma burden).

Question 320: ARDS is characterized by all except:

A. Decreased surfactant
B. Alveolar transudate (Correct Answer)
C. Decreased lung compliance
D. PaO2/FiO2 < 200

Explanation: **Explanation:** Acute Respiratory Distress Syndrome (ARDS) is characterized by **non-cardiogenic pulmonary edema** resulting from diffuse alveolar-capillary damage. **Why "Alveolar Transudate" is the correct answer:** In ARDS, the primary pathology is increased permeability of the alveolar-capillary membrane due to inflammatory injury. This leads to the leakage of protein-rich fluid into the alveolar space, known as an **exudate**. In contrast, a *transudate* occurs due to hydrostatic pressure changes (e.g., Congestive Heart Failure), which ARDS specifically excludes by definition. **Analysis of Incorrect Options:** * **Decreased Surfactant:** Damage to Type II pneumocytes and the presence of proteinaceous fluid lead to the inactivation and decreased production of surfactant. This increases surface tension, causing alveolar collapse. * **Decreased Lung Compliance:** The combination of alveolar edema, loss of surfactant, and subsequent fibrosis makes the lungs "stiff." This reduction in compliance increases the work of breathing. * **PaO2/FiO2 < 200:** According to the **Berlin Criteria**, ARDS is categorized by the severity of hypoxemia (Mild: 200–300; Moderate: 100–200; Severe: <100). Thus, a ratio <200 is a classic feature of moderate-to-severe ARDS. **High-Yield Clinical Pearls for NEET-PG:** * **Berlin Criteria:** Acute onset (<1 week), bilateral opacities on imaging not fully explained by effusions/collapse, and respiratory failure not fully explained by heart failure (PCWP <18 mmHg). * **Pathological Hallmark:** Diffuse Alveolar Damage (DAD) and **Hyaline membrane** formation. * **Management:** Low tidal volume ventilation (6 mL/kg) is the gold standard to prevent Volutrauma.

Practice by Chapter

Obstructive Airway Diseases (Asthma, COPD)

Practice Questions

Interstitial Lung Diseases

Practice Questions

Pulmonary Infections

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Pulmonary Vascular Diseases

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Pleural Diseases

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Sleep-Disordered Breathing

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Respiratory Failure

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Mediastinal Disorders

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Occupational Lung Diseases

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Pulmonary Function Testing

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Bronchiectasis and Cystic Fibrosis

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Lung Cancer Approach

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