Pulmonology Practice Questions

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.

Q: Which of the following classes of drugs is a precipitant of acute asthma?

NSAIDs. **Explanation:** **NSAIDs (Non-Steroidal Anti-inflammatory Drugs)** are well-known precipitants of acute asthma exacerbations [1], particularly in a subset of patients with **Aspirin-Exacerbated Respiratory Disease (AERD)**, also known as Samter’s Triad (Asthma, Nasal Polyposis, and Aspirin Sensitivity) [1]. **Pathophysiology:** The underlying mechanism involves the inhibition of the **Cyclooxygenase-1 (COX-1)** enzyme [3]. When COX-1 is blocked, the metabolism of arachidonic acid is shifted away from the prostaglandin pathway and shunted toward the **5-Lipoxygenase pathway**. This leads to an overproduction of **cysteinyl leukotrienes** (LTC4, LTD4, and LTE4), which are potent bronchoconstrictors that induce airway edema and mucus secretion, triggering an acute asthma attack [3]. **Analysis of Incorrect Options:** * **A. Beta-adrenergic receptor agonists:** These are the mainstay of treatment for acute asthma (e.g., Salbutamol) as they cause bronchodilation. However, **Beta-blockers** (especially non-selective ones like Propranolol) are known precipitants [1]. * **C. Calcium channel blockers:** These drugs generally have a neutral effect on the airways or may cause mild bronchodilation; they do not precipitate asthma. * **D. H1 blockers:** These are antihistamines used to treat allergic rhinitis and urticaria [2]. They do not cause bronchoconstriction and are often used as adjunctive therapy in allergic asthma [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Samter’s Triad:** Asthma + Nasal polyps + Aspirin sensitivity [1]. * **Safe Alternative:** Acetaminophen (Paracetamol) is generally safe in aspirin-sensitive asthmatics at low doses (<1000mg). * **Other common precipitants:** Beta-blockers (even topical eye drops like Timolol), Sulfites (food preservatives), and Tartrazine (yellow food dye) [1]. * **Treatment of AERD:** Leukotriene receptor antagonists (e.g., Montelukast) are particularly effective in these patients.

Q: Which of the following findings is true in Acute Respiratory Distress Syndrome (ARDS)?

Decreased lung compliance. ### Explanation **Correct Option: B. Decreased lung compliance** **Mechanism:** Acute Respiratory Distress Syndrome (ARDS) is characterized by diffuse alveolar damage leading to increased permeability of the alveolar-capillary membrane. This results in the leakage of protein-rich fluid into the alveoli (non-cardiogenic pulmonary edema) and the inactivation of surfactant. The combination of fluid-filled alveoli and alveolar collapse (atelectasis) makes the lungs stiff [1]. In medical terms, this is a **decrease in static lung compliance**, requiring higher pressures to achieve the same tidal volume—often referred to as the **"Baby Lung"** concept [3]. **Analysis of Incorrect Options:** * **A. Type 2 respiratory failure:** ARDS typically presents with **Type 1 respiratory failure** (Hypoxemic) [2]. It is defined by severe hypoxemia ($PaO_2/FiO_2$ ratio $\leq 300$ mmHg) with a normal or low $PaCO_2$ due to compensatory tachypnea. Type 2 failure involves hypercapnia, which is not a primary feature of early ARDS. * **C. Increased diffusion capacity:** In ARDS, the diffusion capacity ($DLCO$) is **decreased**. The accumulation of edema fluid and the formation of hyaline membranes increase the thickness of the blood-gas barrier, severely impairing gas exchange. **High-Yield Clinical Pearls for NEET-PG:** * **Berlin Criteria:** Acute onset (within 1 week), bilateral opacities on imaging, and respiratory failure not fully explained by heart failure (PCWP $\leq 18$ mmHg) [1]. * **Pathological Hallmark:** Hyaline membranes in the alveolar walls. * **Management Strategy:** **Low Tidal Volume Ventilation** (6 mL/kg of predicted body weight) is the gold standard to prevent Ventilator-Induced Lung Injury (VILI). * **Prone Positioning:** Recommended for severe ARDS ($PaO_2/FiO_2 < 150$) to improve V/Q matching.

Q: Which of the following is the most common abnormality in ECG manifestation of pulmonary embolism?

T wave inversion V1 to V4. The most common ECG abnormality in Pulmonary Embolism (PE) is **Sinus Tachycardia**. However, among the specific morphological changes, **T-wave inversion in the precordial leads (V1 to V4)** is the most frequent and specific finding. **1. Why T-wave inversion (V1-V4) is correct:** Acute PE causes a sudden increase in pulmonary artery pressure, leading to **Right Ventricular (RV) strain**. This pressure overload causes RV ischemia and repolarization abnormalities, manifesting as T-wave inversions in the right precordial leads (V1-V4) and sometimes lead III. This finding is more common and has higher diagnostic sensitivity than the classic S1Q3T3 pattern. **2. Why other options are incorrect:** * **Sinus bradycardia:** PE typically causes tachycardia due to sympathetic activation and hypoxia. Bradycardia is rare and usually signifies a pre-terminal event or severe vagal response. * **U wave:** This is associated with hypokalemia or certain drugs, not PE. * **S1Q3T3 pattern (McGinn-White Sign):** While highly "classic" and frequently tested, it is **not** the most common finding. It is seen in only about 10-20% of cases and indicates acute cor pulmonale. **Clinical Pearls for NEET-PG:** * **Most common ECG finding:** Sinus Tachycardia. * **Most common "abnormality" (if tachycardia is absent):** Non-specific ST-T wave changes. * **Most specific morphological pattern:** T-wave inversion in V1-V4 (Right ventricular strain pattern). * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA). * **Initial Investigation of choice:** Chest X-ray (usually normal, but helps rule out other causes).

Q: All of the following are associated with pulmonary eosinophilic pneumonia, except?

Wegner's granulomatosis. **Explanation:** The core concept tested here is the classification of **Pulmonary Eosinophilia (PE)**, a group of disorders characterized by pulmonary infiltrates on chest X-ray and an excess of eosinophils in the blood, lung tissue, or bronchoalveolar lavage (BAL) fluid. **Why Wegener’s Granulomatosis (Granulomatosis with Polyangiitis - GPA) is the correct answer:** GPA is a small-vessel vasculitis characterized by a triad of necrotizing granulomas of the respiratory tract, vasculitis, and glomerulonephritis. It is classically associated with **neutrophilic** inflammation and **c-ANCA (PR3-ANCA)** positivity [1]. Unlike other vasculitides, eosinophilia is **not** a feature of GPA. **Analysis of Incorrect Options:** * **ABPA (Allergic Bronchopulmonary Aspergillosis):** A hypersensitivity reaction to *Aspergillus fumigatus*. It is a classic cause of pulmonary eosinophilia, presenting with high IgE levels, peripheral eosinophilia, and central bronchiectasis. * **Loeffler’s Syndrome:** Also known as Simple Pulmonary Eosinophilia, it is often caused by trans-pulmonary migration of helminth larvae (e.g., *Ascaris*). It presents with transient, migratory "fleeting" opacities and peripheral eosinophilia. * **Churg-Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis - EGPA):** This is the prototypical eosinophilic vasculitis [1]. It presents with asthma, prominent peripheral eosinophilia (>1500/µL), and **p-ANCA (MPO-ANCA)** positivity. **NEET-PG High-Yield Pearls:** 1. **Fleeting Infiltrates:** Think Loeffler’s Syndrome or ABPA. 2. **ANCA Association:** GPA = c-ANCA; EGPA = p-ANCA. 3. **Tropical Pulmonary Eosinophilia (TPE):** Caused by *Wuchereria bancrofti*; characterized by nocturnal cough and massive eosinophilia. 4. **Drug-Induced PE:** Common culprits include Nitrofurantoin, Sulfonamides, and NSAIDs.

Q: A 31-year-old man with severe kyphoscoliosis due to cerebral palsy presents with worsening shortness of breath on exertion. He denies chest discomfort, fever, chills, cough, or sputum production. Examination reveals severe scoliosis to the left with decreased air entry on that side. His right lung is clear, JVP is at 3 cm, and heart sounds are normal. Which of the following is the most likely abnormality to be seen on the pulmonary function tests?

Decreased TLC. The patient presents with severe **kyphoscoliosis**, a classic cause of **Extrapulmonary Restrictive Lung Disease**. In this condition, the structural deformity of the chest wall and spine physically limits the expansion of the lungs, leading to a reduction in all lung volumes [1]. **1. Why Decreased TLC is correct:** In restrictive lung diseases, the hallmark is a **reduction in Total Lung Capacity (TLC)**. Kyphoscoliosis increases the stiffness of the chest wall (decreased chest wall compliance), which prevents the lungs from inflating fully [1]. This results in a "small lung" physiology where TLC, Vital Capacity (VC), and Functional Residual Capacity (FRC) are all characteristically decreased [3]. **2. Why other options are incorrect:** * **A & B (Increased TLC/FRC):** These are features of **Obstructive Lung Diseases** (e.g., COPD, Emphysema, Asthma) due to air trapping and hyperinflation [2]. In kyphoscoliosis, the chest wall restriction makes it impossible to achieve high volumes. * **D (Increased Compliance):** Kyphoscoliosis causes **decreased** chest wall compliance. Increased compliance is seen in emphysema, where the loss of elastic recoil makes the lungs "floppy" and easy to distend. **Clinical Pearls for NEET-PG:** * **PFT Pattern in Kyphoscoliosis:** Decreased TLC, Decreased FRC, Decreased VC, but a **Normal or Increased FEV1/FVC ratio** (typical of restriction) [3]. * **Work of Breathing:** These patients have a high work of breathing and typically adopt a breathing pattern of **low tidal volume and high respiratory rate** (rapid shallow breathing) to minimize energy expenditure. * **Complications:** Long-standing severe kyphoscoliosis leads to chronic alveolar hypoventilation, pulmonary hypertension, and eventually **Cor Pulmonale** (Right heart failure).

Question 1

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 2

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

Question 3

A patient presents with sudden respiratory distress. On examination, bilateral basal crepitations are noted, suggestive of pulmonary edema with normal alveolar-wedge pressure. What is the likely cause?

Accepted Answer

Narcotic overdose

Answer

Congestive heart failure

Answer

Myocardial infarction

Answer

Cardiogenic shock

Question 4

Which of the following classes of drugs is a precipitant of acute asthma?

Accepted Answer

NSAIDs

Answer

Beta–adrenergic receptor agonists

Answer

Calcium channel blockers

Answer

H1 blockers

Question 5

A 35-year-old man presents with shortness of breath and no history of lung or heart disease. He smokes half a pack a day and has for 10 years. Examination reveals a JVP of 2 cm, normal heart sounds, and clear lungs. Chest X-ray shows hyperinflation and increased lucency of the lung fields. A chest CT reveals bullae and emphysematous changes. Pulmonary function tests show an FEV1/FVC ratio of less than 70%. His family history is significant for other affected individuals. What is the most likely diagnosis?

Accepted Answer

alpha-1-antitrypsin deficiency

Answer

beta-glycosidase deficiency

Answer

glucose-6-phosphatase deficiency

Answer

glucocerebroside deficiency

Question 6

Which of the following findings is true in Acute Respiratory Distress Syndrome (ARDS)?

Accepted Answer

Decreased lung compliance

Answer

Type 2 respiratory failure

Answer

Increased diffusion capacity

Answer

None of the above

Question 7

Which of the following is the most common abnormality in ECG manifestation of pulmonary embolism?

Accepted Answer

T wave inversion V1 to V4

Answer

Sinus bradycardia

Answer

U wave

Answer

S1Q3T3 pattern

Question 8

All of the following are associated with pulmonary eosinophilic pneumonia, except?

Accepted Answer

Wegner's granulomatosis

Answer

ABPA

Answer

Loeffler's pneumonia

Answer

Churg Strauss syndrome

Question 9

A 48-year-old alcoholic man presents with a 6-day history of productive cough and fever. The temperature is 38.7°C (103°F), respirations are 32 per minute, and blood pressure is 126/86 mm Hg. The patient's cough worsens, and he begins expectorating large amounts of foul-smelling sputum. A chest X-ray shows a right upper and middle lobe infiltrate. A CBC demonstrates leukocytosis (WBC = 38,000/mL), with 80% slightly immature neutrophils and toxic granulation. Laboratory studies reveal elevated leukocyte alkaline phosphatase. Which of the following best describes this patient's hematologic condition?

Accepted Answer

Leukemoid reaction

Answer

Acute myelogenous leukemia

Answer

Chronic lymphocytic leukemia

Answer

Chronic myelogenous leukemia

Question 10

A 31-year-old man with severe kyphoscoliosis due to cerebral palsy presents with worsening shortness of breath on exertion. He denies chest discomfort, fever, chills, cough, or sputum production. Examination reveals severe scoliosis to the left with decreased air entry on that side. His right lung is clear, JVP is at 3 cm, and heart sounds are normal. Which of the following is the most likely abnormality to be seen on the pulmonary function tests?

Accepted Answer

Decreased TLC

Answer

Increased total lung capacity (TLC)

Answer

Increased functional residual capacity (FRC)

Answer

Increased compliance

Pulmonology — MCQs

Pulmonology — MCQs

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