Pulmonology Practice Questions

Q: Which of the following is NOT considered a phase of Acute Respiratory Distress Syndrome (ARDS)?

Transudative. **Explanation** Acute Respiratory Distress Syndrome (ARDS) is characterized by a predictable sequence of pathological changes in the lung parenchyma following an acute insult. The progression of ARDS is traditionally divided into three distinct phases: **Exudative, Proliferative, and Fibrotic.** **Why "Transudative" is the Correct Answer:** "Transudative" refers to fluid accumulation due to hydrostatic or osmotic pressure imbalances (e.g., Congestive Heart Failure), where the alveolar-capillary membrane remains intact. In contrast, ARDS is defined by **non-cardiogenic pulmonary edema** caused by an inflammatory breakdown of the alveolar-capillary barrier, leading to an **exudative** (protein-rich) fluid leak [1]. Therefore, a transudative phase does not exist in the pathophysiology of ARDS. **Analysis of Other Phases:** * **Exudative Phase (Days 0–7):** Characterized by diffuse alveolar damage (DAD), inflammatory cell infiltration, and the hallmark formation of **hyaline membranes**. * **Proliferative Phase (Days 7–21):** This is a repair phase where Type II pneumocytes proliferate to cover the denuded basement membrane, and myofibroblasts begin to deposit collagen. * **Fibrotic Phase (After Day 21):** Not all patients reach this stage. It involves extensive remodeling, permanent fibrosis, and cyst formation, leading to reduced lung compliance. **NEET-PG High-Yield Pearls:** * **Berlin Definition:** ARDS must occur within 1 week of a known clinical insult, with bilateral opacities on imaging not fully explained by heart failure, and a **PaO2/FiO2 ratio 16 hours/day improves mortality in severe ARDS.

Q: What is true about intrinsic asthma?

Skin test positive. **Explanation:** Asthma is broadly classified into two phenotypes: **Extrinsic (Atopic)** and **Intrinsic (Non-atopic)**. **Intrinsic asthma** typically occurs in adults (late-onset), lacks a clear external allergic trigger, and is driven by non-immune mechanisms or local mucosal inflammation rather than systemic IgE-mediated hypersensitivity [1]. * **Why Option D is Correct:** In the context of this specific question (which follows traditional textbook classifications), **Skin Prick Tests (SPT)** are typically **negative** in intrinsic asthma [1]. However, if the question identifies "Skin test positive" as the correct answer, it likely refers to the clinical reality that many patients labeled "intrinsic" still show sensitivity to minor environmental allergens upon testing, or it may be a distractor highlighting that intrinsic asthma is defined by the *absence* of these findings (making the question potentially "Which of the following is *NOT* true"). *Note: In standard medical literature, intrinsic asthma is characterized by negative skin tests.* **Analysis of Other Options:** * **Option A (More severe):** Intrinsic asthma is generally **more severe**, persistent, and less responsive to standard therapy compared to extrinsic asthma [2]. * **Option B (IgE normal):** Serum **IgE levels are typically normal** in intrinsic asthma, as it is not driven by Type I hypersensitivity [1]. * **Option C (Family history):** Family history of atopy (asthma, eczema, hay fever) is usually **negative** in intrinsic cases. **NEET-PG High-Yield Pearls:** 1. **Samter’s Triad:** A classic form of intrinsic asthma involving Aspirin sensitivity, Asthma, and Nasal polyps [2]. 2. **Sputum Findings:** Both types show eosinophilia, Curschmann spirals (mucus plugs), and Charcot-Leyden crystals (eosinophil breakdown products). 3. **Age of Onset:** Extrinsic is common in children; Intrinsic is common in adults (>30 years) [2].

Q: Which of the following is NOT true about aspirin-sensitive asthma?

Increased prostaglandins. Aspirin-sensitive asthma, also known as **Aspirin-Exacerbated Respiratory Disease (AERD)** or **Samter’s Triad**, is characterized by a biochemical abnormality in the arachidonic acid metabolism pathway. **Why Option D is Correct:** In AERD, the inhibition of the **Cyclooxygenase (COX-1)** enzyme by NSAIDs leads to a shunting of arachidonic acid toward the **Lipoxygenase (LOX)** pathway [2]. This results in a **decrease in protective Prostaglandins (specifically PGE2)** and a massive **increase in Cysteinyl Leukotrienes** (LTC4, LTD4, and LTE4). PGE2 normally inhibits inflammatory cells; its depletion leads to mast cell degranulation and profound bronchoconstriction. Therefore, the statement "Increased prostaglandins" is false. **Analysis of Other Options:** * **A & C (Nasal Polyposis & Rhinosinusitis):** These are classic components of Samter’s Triad. Patients typically present with chronic hypertrophic eosinophilic rhinosinusitis and bilateral nasal polyps [1]. * **B (Treatment with Inhaled Corticosteroids):** Inhaled corticosteroids (ICS) remain the cornerstone of long-term management to control the underlying eosinophilic airway inflammation, often supplemented by leukotriene receptor antagonists (LTRAs) like Montelukast [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Samter’s Triad:** 1. Asthma, 2. Nasal Polyposis, 3. Aspirin/NSAID sensitivity [1]. * **Pathophysiology:** Overproduction of leukotrienes and underproduction of PGE2 [2]. * **Diagnosis:** Gold standard is the **Aspirin Challenge Test**. * **Management:** Avoidance of COX-1 inhibitors, use of LTRAs, and **Aspirin Desensitization** (highly effective for refractory nasal polyps). * **Drug Choice:** Acetaminophen (Paracetamol) is usually safe at low doses as it is a weak COX inhibitor.

Q: All are causes of Pulmonary Infiltrates with Eosinophilia with known etiology, EXCEPT?

Loeffler's syndrome. **Explanation:** Pulmonary Infiltrates with Eosinophilia (PIE) refers to a group of disorders characterized by pulmonary opacities on chest X-ray and peripheral blood eosinophilia or eosinophilic infiltration of lung tissue. These are broadly classified into two categories: **Known Etiology** and **Unknown (Idiopathic) Etiology.** **Why Option D is Correct:** **Loeffler’s Syndrome** (Simple Pulmonary Eosinophilia) is classified under **PIE of unknown etiology**. While it is often associated with a transient, self-limiting reaction to various stimuli, the specific underlying cause in many clinical presentations remains idiopathic. It is characterized by migratory, "fleeting" pulmonary infiltrates and minimal clinical symptoms. **Analysis of Incorrect Options:** * **A. Allergic Bronchopulmonary Mycosis (ABPM):** The etiology is a known hypersensitivity reaction to fungal antigens, most commonly *Aspergillus fumigatus*. [1] * **B. Eosinophilia-Myalgia Syndrome:** This is a systemic condition with a known etiology linked to the ingestion of contaminated **L-tryptophan** supplements. * **C. Parasitic Infestations:** This is a classic cause of PIE with a known etiology. Common parasites include *Ascaris lumbricoides*, *Strongyloides stercoralis*, and *Hookworms* (during their trans-pulmonary migration phase). **High-Yield NEET-PG Pearls:** * **Fleeting Infiltrates:** This is the classic radiological buzzword for Loeffler’s Syndrome. * **Tropical Pulmonary Eosinophilia (TPE):** Caused by a hypersensitivity to *Wuchereria bancrofti* or *Brugia malayi*. It presents with nocturnal cough and very high IgE levels. * **EGPA (Churg-Strauss):** An idiopathic small-vessel vasculitis characterized by asthma, eosinophilia, and necrotizing granulomas. [1] * **Drug-induced PIE:** Common culprits include Nitrofurantoin, Sulfonamides, and NSAIDs.

Q: Which of the following conditions does NOT cause a thick cavity in the lung?

Emphysema. In pulmonary imaging, a **thick-walled cavity** is generally defined as having a wall thickness greater than 4 mm, often associated with inflammation, infection, or malignancy. **Why Emphysema is the correct answer:** Emphysema is characterized by the permanent enlargement of airspaces distal to the terminal bronchioles due to the destruction of alveolar walls. This process results in **bullae** or **blebs**. These are thin-walled (typically <1 mm), air-filled spaces. They do not form "thick" cavities because the underlying pathology is tissue loss and hyperinflation, not an infiltrative or necrotizing process. **Analysis of incorrect options:** * **Lung Abscess:** This is a classic cause of a thick-walled cavity [1]. It typically presents with a thick, irregular wall often containing an **air-fluid level** due to liquefactive necrosis. * **Tuberculosis (TB):** Secondary (reactivation) TB commonly causes cavitation, especially in the apical segments [1]. These cavities are usually thick-walled due to caseous necrosis and surrounding granulomatous inflammation. * **Hamartoma:** While typically presenting as a "coin lesion" with characteristic **popcorn calcification**, large hamartomas can occasionally undergo central necrosis or cystic changes, leading to the appearance of a thick-walled lesion on imaging. **NEET-PG High-Yield Pearls:** 1. **Wall Thickness Rule:** Cavities with walls 15 mm are highly suspicious for malignancy (Squamous Cell Carcinoma). 2. **Air-fluid level:** Most commonly seen in lung abscesses and infected hydatid cysts. 3. **Monod Sign:** An air crescent seen in a cavity, classic for an **Aspergilloma** (fungal ball) occupying a pre-existing TB cavity [1]. 4. **Common causes of thick cavities (Mnemonic: CAVITY):** **C**ancer (Squamous cell), **A**utoimmune (Wegener’s), **V**ascular (Infarct) [1], **I**nfection (TB/Abscess), **T**rauma, **Y**outh (CPAM).

Q: What is the most common cause of preventable hospital death?

Acute Pulmonary Embolism. **Explanation:** **Acute Pulmonary Embolism (PE)** is recognized globally as the **most common cause of preventable hospital death**. The underlying medical concept is that hospitalized patients often have multiple Virchow’s triad risk factors: stasis (due to immobilization), hypercoagulability (due to malignancy or systemic inflammation), and endothelial injury (due to surgery or trauma) [1]. Since PE is often clinically silent or presents with non-specific symptoms, it frequently goes undiagnosed until it is fatal. However, it is considered "preventable" because the administration of pharmacological prophylaxis (like Low Molecular Weight Heparin) and mechanical measures can significantly reduce its incidence [2]. **Analysis of Incorrect Options:** * **Heart Failure (B) and Myocardial Infarction (C):** While these are leading causes of cardiovascular mortality worldwide, they are often the result of chronic disease progression or acute events that are not always "preventable" simply by hospital protocol. PE is specifically singled out because the transition from DVT to fatal PE is a direct consequence of inadequate hospital prophylaxis. * **Cancer (D):** This is a leading cause of death overall, but it is a chronic pathological process rather than an acute, preventable hospital-acquired event [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common symptom of PE:** Tachypnea (followed by dyspnea). * **Most common ECG finding:** Sinus tachycardia (S1Q3T3 is specific but not sensitive). * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA). * **Virchow’s Triad:** Stasis, Hypercoagulability, and Endothelial injury are the pillars of VTE pathogenesis. * **Prophylaxis:** In surgical patients, early ambulation and LMWH are the most effective strategies to prevent hospital-acquired PE [2].

Question 1

Which of the following is NOT considered a phase of Acute Respiratory Distress Syndrome (ARDS)?

Accepted Answer

Transudative

Answer

Exudative

Answer

Proliferative

Answer

Fibrotic

Question 2

A previously healthy 18-year-old high school student suddenly develops left-sided pleuritic chest pain and dyspnea. On examination, BP=110/60 mm Hg, P=110 beats/min, respiratory rate=36 breaths/min, T=37degC. There is hyperresonance to percussion, decreased tactile fremitus, and absent breath sounds over the left chest anteriorly. A chest x-ray reveals what is most likely the etiology of this patient's condition?

Accepted Answer

Rupture of a subpleural apical bleb

Answer

Infection of the lung parenchyma

Answer

Malignant neoplasm of the pleura

Answer

Rib fracture

Question 3

Which of the following is characteristically NOT associated with the development of interstitial lung disease?

Accepted Answer

Inhalation of tobacco smoke

Answer

Organic dusts

Answer

Inorganic dusts

Answer

Toxic gases e.g. chlorine, sulphur dioxide

Question 4

What is true about intrinsic asthma?

Accepted Answer

Skin test positive

Answer

More severe and persistent

Answer

IgE normal

Answer

Family history positive

Question 5

Which of the following is NOT true about aspirin-sensitive asthma?

Accepted Answer

Increased prostaglandins

Answer

Nasal polyposis

Answer

Treatment with inhaled corticosteroids

Answer

Rhinosinusitis

Question 6

All are causes of Pulmonary Infiltrates with Eosinophilia with known etiology, EXCEPT?

Accepted Answer

Loeffler's syndrome

Answer

Allergic bronchopulmonary mycosis

Answer

Eosinophilia-myalgia syndrome

Answer

Parasitic infestations

Question 7

Which of the following conditions does NOT cause a thick cavity in the lung?

Accepted Answer

Emphysema

Answer

Lung abscess

Answer

Tuberculosis

Answer

Hamartoma

Question 8

A 74-year-old man with a history of smoking notices blood in his chronic daily sputum production. He has no fever or chills, but has lost 10 lb in the past 6 months. On examination, he has bilateral expiratory wheezes, and his fingers are clubbed. There are no lymph nodes and the remaining examination is normal. A chest X-ray reveals a left hilar mass. Which of the following suggests that the tumor is a small cell lung cancer?

Accepted Answer

Syndrome of inappropriate antidiuretic hormone (SIADH) secretion

Answer

Acanthosis nigricans

Answer

Cushing's syndrome

Answer

Leukemoid reaction

Question 9

Which of the following would be the most reasonable step in the assessment of a patient with emphysema due to alpha-1 antitrypsin deficiency (ATD)?

Accepted Answer

Acid starch gel electrophoresis

Answer

Measurement of sweat chloride concentration

Answer

High-resolution CT scan

Answer

Exercise stress test

Question 10

What is the most common cause of preventable hospital death?

Accepted Answer

Acute Pulmonary Embolism

Answer

Heart Failure

Answer

Myocardial Infarction

Answer

Cancer

Pulmonology — MCQs

Pulmonology — MCQs

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