Pulmonology — MCQs

Pulmonology Indian Medical PG Practice Questions and MCQs

Question 281: Which of the following is NOT seen in a Pancoast tumor?

A. Pain in shoulder and arm
B. Horner's syndrome
C. Rib erosion
D. Hemoptysis (Correct Answer)

Explanation: **Explanation:** A **Pancoast tumor** (Superior Sulcus Tumor) is typically a non-small cell lung carcinoma (most commonly squamous cell or adenocarcinoma) located at the extreme apex of the lung [2]. Because of its peripheral and apical location, it presents more as a neurological and musculoskeletal syndrome rather than a typical pulmonary one. **Why Hemoptysis is NOT seen:** Hemoptysis occurs when a tumor invades the central airways or causes endobronchial friability [1]. Since Pancoast tumors are located at the **peripheral apex**, they are far from the hilum and major bronchi [2]. Therefore, pulmonary symptoms like cough and hemoptysis are characteristically **absent** or occur very late in the disease course. **Analysis of Incorrect Options:** * **Pain in shoulder and arm:** This is the most common presenting symptom. It results from the tumor invading the **brachial plexus** (specifically C8, T1, and T2 nerve roots), leading to pain radiating down the ulnar distribution of the arm. * **Horner’s Syndrome:** This occurs due to the involvement of the **paravertebral sympathetic chain** and the stellate ganglion. It is characterized by the triad of miosis, partial ptosis, and anhidrosis. * **Rib Erosion:** Due to its local invasiveness, the tumor frequently erodes the **first and second ribs** and sometimes the upper thoracic vertebrae, which is visible on a chest X-ray or CT scan. **High-Yield Clinical Pearls for NEET-PG:** * **Pancoast Syndrome:** Includes Pancoast tumor + Horner’s syndrome + Brachial plexopathy + Rib destruction. * **Most common cell type:** Squamous cell carcinoma (traditionally), though Adenocarcinoma is now frequently cited [2]. * **Initial Investigation:** Chest X-ray (look for apical thickening or a mass). * **Gold Standard Investigation:** MRI (superior for evaluating brachial plexus and spinal cord involvement).

Question 282: What is the treatment most likely to benefit a patient with massive pulmonary embolism presenting in shock?

A. Thrombolytic therapy (Correct Answer)
B. Inotropic agent
C. Vasodilator therapy
D. Diuretic therapy

Explanation: ### Explanation **Correct Answer: A. Thrombolytic therapy** **Why it is correct:** A **massive pulmonary embolism (PE)** is defined by the presence of hemodynamic instability (systolic BP <90 mmHg or a drop of ≥40 mmHg for >15 minutes). The underlying pathophysiology involves a sudden increase in pulmonary vascular resistance, leading to acute right ventricular (RV) failure and obstructive shock. **Thrombolytic therapy** (e.g., Alteplase, Tenecteplase, or Streptokinase) is the treatment of choice because it rapidly dissolves the obstructing clot, reduces pulmonary artery pressure, and improves RV function, thereby restoring cardiac output and systemic perfusion [1]. **Why the other options are incorrect:** * **B. Inotropic agents:** While inotropes (like Dobutamine) may be used as temporary supportive measures to improve cardiac contractility, they do not address the primary mechanical obstruction. * **C. Vasodilator therapy:** Systemic vasodilators can worsen hypotension and shock. While inhaled nitric oxide may selectively dilate pulmonary vessels, it is not the standard of care for reversing the obstruction in massive PE. * **D. Diuretic therapy:** Diuretics reduce preload. In acute RV failure due to PE, the RV is "preload dependent" to maintain stroke volume across the high-resistance pulmonary circuit. Diuretics can further decrease cardiac output and worsen shock. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** CT Pulmonary Angiography (CTPA) [1]. * **ECG Findings:** Most common is sinus tachycardia; most specific is the **S1Q3T3 pattern** (sign of acute cor pulmonale). * **McConnell’s Sign:** A specific echocardiographic finding (RV free wall akinesia with sparing of the apex). * **Absolute Contraindications to Thrombolysis:** Prior intracranial hemorrhage, known structural cerebrovascular lesion, ischemic stroke within 3 months, or active internal bleeding [1]. * **Alternative:** If thrombolysis is contraindicated or fails, the next step is **Surgical Embolectomy** or catheter-directed fragmentation [1].

Question 283: Hypoxemia occurring after pulmonary thromboembolism is a result of which of the following?

A. Perfusion of areas poorly ventilated because of airway constriction (Correct Answer)
B. Increased dead-space ventilation in the area of vascular occlusion
C. Increased right heart filling pressures
D. Tachycardia

Explanation: ### Explanation **1. Why Option A is Correct: Ventilation-Perfusion (V/Q) Mismatch** The primary cause of hypoxemia in Pulmonary Thromboembolism (PTE) is **V/Q mismatch**, specifically **shunting** [1]. When a pulmonary artery is occluded, blood is diverted to non-obstructed areas of the lung [2]. Simultaneously, the release of inflammatory mediators (like histamine and serotonin) and a local decrease in CO₂ lead to **reflex bronchoconstriction** in the affected and surrounding areas. This results in the perfusion of poorly ventilated alveoli (low V/Q ratio), leading to a physiological shunt and subsequent hypoxemia [1]. **2. Why the Other Options are Incorrect:** * **Option B:** While increased **dead-space ventilation** (ventilation without perfusion) is the hallmark pathophysiological change in PTE, it explains the increase in work of breathing and hypercapnia risk, but it does **not** directly cause hypoxemia. Hypoxemia is caused by where the blood *goes* (the non-occluded zones), not where it *cannot go* [1]. * **Option C & D:** Increased right heart filling pressures and tachycardia are hemodynamic consequences of pulmonary hypertension and compensatory sympathetic activation, respectively. While they reflect the severity of the PE, they are not the primary mechanisms responsible for the gas exchange defect (hypoxemia). **3. NEET-PG High-Yield Pearls:** * **Most common finding on ABG in PTE:** Hypoxemia with Respiratory Alkalosis (due to hyperventilation) and an **increased A-a gradient** [2]. * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA). * **Classic ECG finding:** S1Q3T3 (Sign of acute right heart strain; however, Sinus Tachycardia is the *most common* ECG finding). * **Westermark Sign:** Focal oligemia on CXR (represents dead space). * **Hampton’s Hump:** Wedge-shaped opacity (represents pulmonary infarction).

Question 284: Which of the following findings is characteristic of pulmonary thromboembolism?

A. S1 Q3 T3 (Correct Answer)
B. S2 Q3 T3
C. S3 Q3 T1
D. S3 Q3 T2

Explanation: ### Explanation **Correct Answer: A. S1 Q3 T3** #### 1. Why S1 Q3 T3 is Correct The **S1 Q3 T3 pattern** (also known as the McGinn-White sign) is the classic, though non-specific, ECG finding associated with acute pulmonary thromboembolism (PTE) [1]. It reflects **acute right ventricular (RV) strain** caused by a sudden increase in pulmonary vascular resistance. * **S1:** A deep S-wave in Lead I (indicating a rightward shift in the QRS axis). * **Q3:** A pathological Q-wave in Lead III. * **T3:** T-wave inversion in Lead III. This pattern occurs because the massive embolus obstructs pulmonary flow, leading to RV dilation and clockwise rotation of the heart. #### 2. Why Other Options are Incorrect Options **B, C, and D** are simply incorrect permutations of the letters and numbers. There are no recognized clinical entities or ECG patterns known as S2Q3T3 or S3Q3T2. These are common distractors used in medical examinations to test the precision of a candidate's rote memorization of the McGinn-White sign. #### 3. High-Yield Clinical Pearls for NEET-PG * **Most Common ECG Finding:** While S1Q3T3 is the most "famous" sign, the **most common** ECG finding in PTE is actually **Sinus Tachycardia** [1]. * **Most Specific Finding:** T-wave inversions in the right precordial leads (V1–V4) are highly suggestive of RV strain [1]. * **Sensitivity:** The S1Q3T3 pattern is present in only about **10–15%** of patients with PTE; its absence does *not* rule out the diagnosis. * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA). * **Initial Screening:** D-dimer (high negative predictive value). * **Chest X-ray Signs:** Look for **Westermark sign** (focal oligemia) and **Hampton’s Hump** (wedge-shaped opacity) [1].

Question 285: What is the most common causative organism of community-acquired pneumonia?

A. Klebsiella pneumoniae
B. Streptococcus pneumoniae (Correct Answer)
C. Mycoplasma pneumoniae
D. Legionella pneumoniae

Explanation: **Explanation:** **Streptococcus pneumoniae** (Pneumococcus) remains the **most common cause** of community-acquired pneumonia (CAP) worldwide across all age groups [1]. It is a Gram-positive, lancet-shaped diplococcus [1]. The underlying medical concept involves its high prevalence in the nasopharyngeal flora and its potent virulence factor—the polysaccharide capsule—which allows it to evade phagocytosis and cause typical lobar pneumonia. **Analysis of Incorrect Options:** * **Klebsiella pneumoniae:** While a significant cause of CAP, it is typically associated with specific risk factors such as **chronic alcoholism**, diabetes mellitus, or nursing home residents [1]. It is classic for causing "currant jelly sputum" and upper lobe cavitation [1]. * **Mycoplasma pneumoniae:** This is the most common cause of **atypical pneumonia**, particularly in young adults and school-aged children. It lacks a cell wall and often presents with a "walking pneumonia" clinical picture (milder symptoms, interstitial infiltrates). * **Legionella pneumoniae:** This is an important cause of severe CAP, often linked to contaminated water systems or air conditioning [1]. It is characterized by multisystem involvement, such as hyponatremia and gastrointestinal symptoms (diarrhea). **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Sputum culture and Gram stain, though urinary antigen tests are highly specific for *S. pneumoniae* [1]. * **Radiology:** *S. pneumoniae* typically presents as **lobar consolidation**. * **Vaccination:** Two types are available (PPSV23 and PCV13), recommended for the elderly and immunocompromised to prevent invasive pneumococcal disease. * **Drug of Choice:** Beta-lactams (like Amoxicillin or Ceftriaxone) are first-line, though resistance patterns must be monitored.

Question 286: What is the effect of rheumatoid arthritis on the lung?

A. DLco normal
B. CXR is normal
C. Exudative pleural effusion (Correct Answer)
D. Flow volume pattern showing an obstructive pattern

Explanation: **Explanation:** Rheumatoid Arthritis (RA) is a systemic autoimmune disease that frequently involves the lungs [1]. Pleuropulmonary manifestations occur in approximately 30-40% of patients. **Why Option C is Correct:** Pleural involvement is the most common thoracic manifestation of RA. The resulting **pleural effusion is typically exudative** (based on Light’s criteria). A classic, high-yield diagnostic feature of rheumatoid pleural effusion is a **very low glucose level** (often <30 mg/dL), which is attributed to impaired glucose transport across the inflamed pleura. Other findings include high LDH and low pH. **Why Other Options are Incorrect:** * **A. DLco normal:** RA most commonly causes **Interstitial Lung Disease (ILD)**, specifically the UIP (Usual Interstitial Pneumonia) pattern. ILD leads to a thickened alveolar-capillary membrane, which **decreases** the Diffusing Capacity of the Lungs for Carbon Monoxide (DLco) [1]. * **B. CXR is normal:** While early stages may be clear, RA frequently shows abnormalities on Chest X-ray, such as reticular opacities (ILD), pleural thickening, or **Caplan syndrome** (rheumatoid nodules associated with coal worker's pneumoconiosis). * **D. Obstructive pattern:** RA primarily causes a **restrictive pattern** on pulmonary function tests (PFTs) due to ILD [1]. While bronchiolitis obliterans (an obstructive condition) can occur, it is much less common than the restrictive pathology of ILD. **High-Yield Clinical Pearls for NEET-PG:** 1. **Glucose Paradox:** RA and Empyema are the two most common causes of pleural effusion with glucose levels <30 mg/dL. 2. **Gender Predisposition:** While RA is more common in females, **RA-associated ILD and pleural effusions** are more frequently seen in **males**. 3. **Caplan Syndrome:** Combination of RA + Pneumoconiosis + Multiple pulmonary nodules. 4. **Drug-Induced ILD:** Always remember that **Methotrexate**, a first-line treatment for RA, can itself cause hypersensitivity pneumonitis [1].

Question 287: All of the following are seen in massive pulmonary embolism except:

A. Inter-ventricular septum deviation
B. Fall of SBP
C. Pulmonary plethora (Correct Answer)
D. Elevated JVP

Explanation: Massive pulmonary embolism (PE) is defined by hemodynamic instability, specifically a sustained drop in systolic blood pressure (SBP <90 mmHg) or the need for inotropic support [1]. **Why Pulmonary Plethora is the Correct Answer:** Pulmonary plethora refers to increased pulmonary vascular markings seen on a chest X-ray, typically associated with left-to-right shunts (e.g., ASD, VSD). In massive PE, the opposite occurs: there is a mechanical obstruction of the pulmonary arteries. This leads to **oligemia** (decreased blood flow) distal to the site of the occlusion, a classic radiological sign known as **Westermark’s sign** [1]. Therefore, plethora is not a feature of PE. **Analysis of Other Options:** * **Fall of SBP:** By definition, massive PE involves obstructive shock. The large clot increases pulmonary vascular resistance, leading to right ventricular (RV) failure and a subsequent drop in left ventricular preload, causing systemic hypotension [2]. * **Elevated JVP:** Acute RV pressure overload leads to RV dysfunction and backup of pressure into the venous system, manifesting clinically as an elevated Jugular Venous Pressure (JVP) [1]. * **Inter-ventricular Septum (IVS) Deviation:** Due to acute RV dilation and high intra-cavitary pressure, the IVS shifts or "bows" toward the left ventricle (seen on echocardiography). This reduces LV filling and further compromises cardiac output. **NEET-PG High-Yield Pearls:** * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA). * **ECG Findings:** Most common is sinus tachycardia; most specific is the **S1Q3T3** pattern [1]. * **CXR Signs:** Westermark sign (focal oligemia) and Hampton’s hump (wedge-shaped opacity indicating infarction) [1]. * **Treatment of Massive PE:** Systemic thrombolysis (e.g., Alteplase) is the first-line treatment if there are no contraindications [2].

Question 288: Proximal bronchiectasis is a feature of which condition?

A. Allergic bronchopulmonary aspergillosis (Correct Answer)
B. Tuberculosis
C. Measles pneumonia
D. All of the above

Explanation: ### Explanation **Correct Answer: A. Allergic bronchopulmonary aspergillosis (ABPA)** **1. Why ABPA is the correct answer:** ABPA is a hypersensitivity reaction to *Aspergillus fumigatus* colonization in the airways, typically occurring in patients with asthma or cystic fibrosis. The underlying pathophysiology involves the formation of thick, tenacious mucus plugs containing fungal hyphae in the segmental and subsegmental bronchi. These plugs cause chronic inflammation and destruction of the bronchial wall, leading to **central (proximal) bronchiectasis** [1]. On imaging, this classically presents as the "finger-in-glove" sign. **2. Why the other options are incorrect:** * **Tuberculosis (TB):** Post-tubercular bronchiectasis is typically **traction-based** and localized to the **upper lobes** (apical and posterior segments) [1]. While it can be proximal, it is not the classic "proximal bronchiectasis" pattern described in medical literature, which specifically points toward ABPA. * **Measles pneumonia:** Viral and bacterial infections (like Measles, Pertussis, or Adenovirus) usually cause **distal (peripheral) bronchiectasis** due to necroizing inflammation in the smaller, more peripheral airways. **3. High-Yield Clinical Pearls for NEET-PG:** * **Classic Imaging Sign:** "Finger-in-glove" appearance (mucus-filled dilated bronchi). * **Diagnostic Criteria (Rosenberg-Patterson):** Look for asthma, immediate skin reactivity to *Aspergillus*, elevated serum IgE (>1000 IU/mL), and central bronchiectasis. * **CT Finding:** High Attenuation Mucus (HAM) is a highly specific sign for ABPA. * **Treatment:** The mainstay of treatment is **Oral Corticosteroids** (to reduce inflammation) and **Itraconazole** (to reduce fungal burden). **Summary:** While many conditions cause bronchiectasis, **proximal/central** distribution is a hallmark diagnostic feature of ABPA, whereas post-infectious causes (like Measles) typically affect the distal airways.

Question 289: Kartagener’s syndrome is characterized by which of the following?

A. Situs Solitus (Correct Answer)
B. Dextrocardia
C. Chronic sinusitis
D. Situs inversus

Explanation: **Explanation:** Kartagener’s syndrome is a subset of **Primary Ciliary Dyskinesia (PCD)**, an autosomal recessive disorder caused by structural defects in the cilia (most commonly a deficiency of outer/inner dynein arms). This leads to impaired mucociliary clearance and organ lateralization defects [1]. **Why Situs Solitus is the Correct Answer (Context of the Question):** In the context of NEET-PG "except" or "characteristic" questions, it is vital to distinguish between normal and abnormal anatomy. **Situs Solitus** refers to the normal arrangement of thoracic and abdominal organs. Kartagener’s syndrome is classically defined by a **clinical triad**: 1. **Situs Inversus** (Transposition of organs) 2. **Bronchiectasis** [1] 3. **Chronic Sinusitis** [1] Therefore, **Situs Solitus is NOT a feature** of Kartagener’s syndrome; its presence (Situs Inversus) is what defines the syndrome within the spectrum of PCD. **Analysis of Options:** * **B. Dextrocardia:** This is a component of Situs Inversus where the heart is located on the right side. It is a hallmark finding in Kartagener’s. * **C. Chronic Sinusitis:** Due to dysfunctional cilia in the paranasal sinuses, patients suffer from recurrent infections and nasal polyps [1]. * **D. Situs Inversus:** This is the defining feature that differentiates Kartagener’s from other forms of Primary Ciliary Dyskinesia. **High-Yield Clinical Pearls for NEET-PG:** * **Infertility:** Males are infertile due to immotile spermatozoa (flagella defect); females have reduced fertility due to ciliary dysfunction in the fallopian tubes. * **Diagnosis:** Initial screening via **Nasal Nitric Oxide (nNO)** levels (low in PCD). Definitive diagnosis via **High-speed video microscopy** or **Electron microscopy** (showing dynein arm defects). * **Genetics:** Most common mutations involve **DNAI1 and DNAH5** genes.

Question 290: Hamman's sign is seen with which of the following conditions?

A. Acute pericarditis
B. Aortic dissection
C. Tracheal compression
D. Esophageal perforation (Correct Answer)

Explanation: ### Explanation **Hamman’s sign** (also known as Hamman’s crunch) is a clinical finding characterized by a **crunching, clicking, or rasping sound** heard over the precordium during auscultation. It is synchronous with the heartbeat and is caused by the heart beating against air-filled tissues. #### Why Esophageal Perforation is Correct: Esophageal perforation (e.g., **Boerhaave syndrome**) allows air to escape from the esophagus into the mediastinum, leading to **pneumomediastinum**. As the heart beats, it compresses this trapped air against the pleura and mediastinal structures, producing the characteristic "crunching" sound. This sign is most audible when the patient is in the left lateral decubitus position. #### Analysis of Incorrect Options: * **A. Acute pericarditis:** Characterized by a **pericardial friction rub**, which is a high-pitched, scratchy sound (triphasic or biphasic) caused by the inflamed layers of the pericardium rubbing together, not by air. * **B. Aortic dissection:** Typically presents with tearing chest pain radiating to the back and unequal pulses. While it can cause a murmur of aortic regurgitation, it does not produce Hamman’s sign. * **C. Tracheal compression:** Usually presents with **stridor** or wheezing due to narrowed airways, but it does not involve air in the mediastinal space. #### High-Yield Clinical Pearls for NEET-PG: * **Triad of Boerhaave Syndrome (Mackler’s Triad):** Vomiting, chest pain, and subcutaneous emphysema. * **Hamman’s Sign vs. Hamman-Rich Syndrome:** Do not confuse them. Hamman-Rich syndrome is an older term for **Acute Interstitial Pneumonia (AIP)**. * **Common Causes of Hamman’s Sign:** Pneumomediastinum (most common), esophageal rupture, and occasionally tension pneumothorax. * **Diagnosis:** If Hamman’s sign is heard, the next best step is often a **Chest X-ray** (looking for "continuous diaphragm sign" or "V sign of Naclerio") or a **CT Thorax**.

Practice by Chapter

Obstructive Airway Diseases (Asthma, COPD)

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Interstitial Lung Diseases

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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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