Pulmonology — MCQs

Pulmonology Indian Medical PG Practice Questions and MCQs

Question 41: A 67-year-old woman presents with symptoms of dyspnea. Pulmonary function tests reveal a prominent reduction in the FEV1/FVC ratio. What is the most likely diagnosis?

A. COPD (Correct Answer)
B. Ankylosing spondylitis
C. Pickwickian syndrome
D. Scleroderma of the chest wall

Explanation: ### Explanation The core of this question lies in distinguishing between **Obstructive** and **Restrictive** lung diseases based on Pulmonary Function Tests (PFTs). **1. Why COPD is Correct:** A reduction in the **FEV1/FVC ratio (typically <0.70)** is the hallmark of **Obstructive Lung Disease** [1]. In conditions like COPD (Chronic Obstructive Pulmonary Disease) and Asthma, airway resistance is increased [2]. While both FEV1 and FVC may decrease, the FEV1 (forced expiratory volume in 1 second) drops disproportionately more because the narrowed airways collapse during forced expiration, leading to a low ratio [1]. **2. Why the Other Options are Incorrect:** * **Ankylosing Spondylitis (B):** This causes "bamboo spine" and fixation of the thoracic cage, leading to **extrapulmonary restrictive lung disease**. In restrictive patterns, the FEV1/FVC ratio is **normal or even increased**, though the absolute values of both FEV1 and FVC are reduced [3]. * **Pickwickian Syndrome (C):** Also known as Obesity Hypoventilation Syndrome. The excess adipose tissue restricts chest wall expansion, resulting in a **restrictive pattern** (normal ratio). * **Scleroderma of the Chest Wall (D):** Similar to the above, skin tightening and fibrosis of the chest wall limit thoracic excursion, leading to **extrinsic restriction** (normal ratio). **Clinical Pearls for NEET-PG:** * **Obstructive Pattern:** ↓ FEV1, ↓ FVC, **↓ FEV1/FVC ratio**, ↑ TLC (due to air trapping). Examples: COPD, Asthma, Bronchiectasis, Cystic Fibrosis [1]. * **Restrictive Pattern:** ↓ FEV1, ↓ FVC, **Normal/↑ FEV1/FVC ratio**, ↓ TLC. Examples: ILD, Scoliosis, Obesity, Myasthenia Gravis [3]. * **High-Yield Tip:** If the ratio is low, it's obstructive. If the ratio is normal but the FVC is low, it's restrictive.

Question 42: A patient presents with cough and expectoration. Diagnosis of farmer's lung is suspected. Which statement regarding this condition is true?

A. Seasonal occurrence from May to June
B. Persistent cough with expectoration
C. X-ray features show upper lobe predominance in chronic hypersensitivity pneumonitis (Correct Answer)
D. Pleural effusions are common

Explanation: Farmer's lung is a classic example of **Hypersensitivity Pneumonitis (HP)**, an immune-mediated inflammatory lung disease caused by the inhalation of organic dusts (specifically thermophilic actinomycetes like *Saccharopolyspora rectivirgula*) found in moldy hay. ### **Explanation of Options** * **Correct Answer (C):** In the **chronic stage** of hypersensitivity pneumonitis, repetitive exposure leads to progressive interstitial fibrosis. Radiologically, this is characterized by reticular opacities, volume loss, and honeycombing. Crucially, HP typically involves the **upper and middle lobes**, distinguishing it from Idiopathic Pulmonary Fibrosis (IPF), which is predominantly basal. * **Option A:** Farmer’s lung is not strictly seasonal from May to June. It occurs most frequently in **late winter and early spring** when stored, moldy hay is moved or used for fodder in confined spaces. * **Option B:** While cough occurs, the hallmark of the acute phase is **dyspnea, fever, and chills** occurring 4–8 hours after exposure. Persistent productive cough is more characteristic of chronic bronchitis or bronchiectasis rather than the interstitial inflammation seen in HP. * **Option D:** Pleural effusions, hilar lymphadenopathy, and cavitation are **rare or absent** in HP. Their presence should prompt a search for alternative diagnoses like tuberculosis or malignancy. ### **NEET-PG High-Yield Pearls** * **Pathology:** Characterized by the "Triad" of interstitial pneumonitis, non-caseating granulomas (poorly formed), and bronchiolitis obliterans. * **BAL Findings:** Bronchoalveolar lavage typically shows significant **Lymphocytosis** (often >50%) with a **decreased CD4:CD8 ratio** (unlike Sarcoidosis, where the ratio is increased). * **Management:** The most critical step is the **complete avoidance of the offending antigen**. Systemic corticosteroids are used for acute/severe symptoms but do not alter the long-term prognosis of chronic disease.

Question 43: Which of the following statements about sarcoidosis is false?

A. Elevated level of angiotensin converting enzyme (ACE)
B. Bilateral parotid enlargement is the rule
C. Pleural effusion is common (Correct Answer)
D. Facial nerve palsy may be seen

Explanation: Explanation: Sarcoidosis is a multisystem granulomatous disease characterized by non-caseating granulomas. Understanding its classic presentations versus its rare manifestations is crucial for NEET-PG. **Why Option C is the correct (False) statement:** While sarcoidosis primarily affects the lungs (90% of cases), **pleural effusion is rare**, occurring in less than 5% of patients. The hallmark pulmonary finding is bilateral hilar lymphadenopathy and interstitial lung disease, not pleural involvement. **Analysis of other options:** * **Option A (ACE levels):** Elevated serum Angiotensin-Converting Enzyme (ACE) is a classic marker produced by the epithelioid cells of the granulomas. While not specific enough for diagnosis, it is elevated in roughly 60-80% of active cases. * **Option B (Parotid enlargement):** Bilateral parotid gland enlargement is a recognized feature, especially in **Heerfordt’s syndrome** (Uveoparotid fever), which consists of parotitis, uveitis, fever, and cranial nerve palsy. * **Option D (Facial nerve palsy):** Neurosarcoidosis can affect any cranial nerve, but the **facial nerve (CN VII)** is the most commonly involved, often presenting as a lower motor neuron palsy [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Löfgren’s Syndrome:** A classic triad of Erythema nodosum, bilateral hilar lymphadenopathy, and polyarthritis (excellent prognosis) [1]. * **Diagnosis:** Requires a biopsy showing **non-caseating granulomas** and exclusion of other causes (like TB). * **Asteroid bodies** and **Schaumann bodies** are characteristic microscopic findings within the granulomas. * **Hypercalcemia/Hypercalciuria:** Occurs because macrophages in the granulomas convert Vitamin D to its active form (1,25-dihydroxyvitamin D) [1].

Question 44: Type I Respiratory failure is seen in which of the following conditions?

A. Anaemia
B. Emphysema (Correct Answer)
C. Pulmonary oedema
D. Adult respiratory distress syndrome

Explanation: **Explanation:** Respiratory failure is classified based on arterial blood gas (ABG) patterns [1]. **Type I Respiratory Failure (Hypoxemic)** is characterized by a low partial pressure of arterial oxygen ($PaO_2 < 60$ mmHg) with a normal or low partial pressure of carbon dioxide ($PaCO_2$) [2]. The primary mechanism is **Ventilation-Perfusion (V/Q) mismatch** [4] or diffusion impairment. **Why Emphysema is the correct answer:** In **Emphysema**, there is permanent destruction of the alveolar walls and capillary beds. This leads to a significant V/Q mismatch and a reduced surface area for gas exchange [3]. While it is a component of COPD, early to moderate emphysema typically presents as Type I failure. Type II failure (hypercapnia) usually occurs only in the terminal stages or during acute exacerbations when the work of breathing becomes unsustainable. **Analysis of Incorrect Options:** * **Anaemia:** This causes "Hemic Hypoxia." While the total oxygen content of the blood is low due to decreased hemoglobin, the $PaO_2$ (dissolved oxygen) remains normal. Therefore, it does not fulfill the criteria for respiratory failure. * **Pulmonary Oedema & ARDS:** These are classic causes of **Acute Type I Respiratory Failure**. However, in the context of standard medical examinations, if a single best answer must be chosen among chronic conditions versus acute syndromes, the examiner often focuses on the underlying pathophysiology of obstructive diseases like Emphysema. *(Note: In clinical practice, B, C, and D all cause Type I failure; however, Emphysema is a high-yield textbook example of V/Q mismatch leading to hypoxemia).* **High-Yield Clinical Pearls for NEET-PG:** * **Type I (Hypoxemic):** $PaO_2 \downarrow$, $PaCO_2$ Normal/$\downarrow$. Causes: Pneumonia, Pulmonary Embolism, ARDS, Emphysema [2]. * **Type II (Hypercapnic):** $PaO_2 \downarrow$, $PaCO_2 \uparrow$ ($>50$ mmHg). Causes: Hypoventilation, Neuromuscular disorders (GBS, Myasthenia), OSA, and late-stage COPD [2]. * **Key differentiator:** The **A-a gradient** is increased in Type I failure but remains normal in Type II failure caused by pure hypoventilation (e.g., opioid overdose).

Question 45: All of the following statements are false regarding sarcoidosis, except?

A. Schaumann bodies and asteroid bodies are not seen
B. Broncho-alveolar lavage fluid shows a CD4/CD8 T cell ratio of 4:1
C. Hilar and mediastinal lymph nodes are spared
D. Can be associated with unilateral or bilateral iritis or iridocyclitis (Correct Answer)

Explanation: **Explanation:** Sarcoidosis is a multisystem, idiopathic disease characterized by the formation of **non-caseating granulomas**. **Why Option D is Correct:** Ocular involvement occurs in approximately 25% of patients with sarcoidosis [1]. The most common manifestation is **anterior uveitis** (iritis or iridocyclitis), which can be unilateral or bilateral. It often presents with blurred vision, photophobia, and floaters. Chronic involvement can lead to glaucoma or blindness, making it a critical clinical feature to monitor. **Analysis of Incorrect Options:** * **Option A:** Schaumann bodies (laminated calcium-protein concretions) and Asteroid bodies (stellate inclusions within giant cells) are **characteristic histopathological findings** in sarcoidosis, though they are not pathognomonic. * **Option B:** Sarcoidosis is a T-helper cell-mediated disease. Broncho-alveolar lavage (BAL) typically shows a **lymphocytic alveolitis** with a **CD4/CD8 ratio > 3.5:1** (often cited as 4:1). While the ratio in the option is correct, the statement is phrased as "false except," and since the ratio is a hallmark finding, it is a true statement. *Note: In many MCQ formats, the most definitive clinical association is preferred.* * **Option C:** Bilateral **hilar lymphadenopathy** (BHL) with or without mediastinal involvement is the most common radiographic finding, seen in over 90% of patients (Stage I) [1]. **NEET-PG High-Yield Pearls:** * **Lofgren’s Syndrome:** Triad of Erythema nodosum, Bilateral hilar lymphadenopathy, and Polyarthritis (Good prognosis) [1]. * **Heerfordt’s Syndrome (Uveoparotid fever):** Parotid enlargement, Anterior uveitis, Facial nerve palsy, and Fever. * **Diagnosis:** Elevated Serum ACE levels and hypercalciuria/hypercalcemia (due to 1-alpha hydroxylase activity in macrophages). * **Gold Standard:** Transbronchial lung biopsy showing non-caseating granulomas.

Question 46: Which of the following is the least common cause of ARDS?

A. Aspiration
B. Severe pneumonia with sepsis
C. Shock
D. All of the above (Correct Answer)

Explanation: The correct answer is **All of the above** because, according to current clinical data and major textbooks (like Harrison’s Principles of Internal Medicine), the conditions listed—Aspiration, Severe Pneumonia, and Sepsis—are actually the **most common** causes of Acute Respiratory Distress Syndrome (ARDS). Therefore, none of them can be classified as the "least common." **Understanding the Concept:** ARDS is a clinical syndrome of diffuse alveolar-capillary damage. Causes are categorized into **Direct Lung Injury** (e.g., pneumonia, aspiration) and **Indirect Lung Injury** (e.g., non-pulmonary sepsis, trauma). [1] * **Sepsis (Option B):** This is the single most common cause of ARDS overall (indirect injury). * **Severe Pneumonia (Option B):** The most common cause of direct lung injury leading to ARDS. [1] * **Aspiration (Option A):** A very frequent cause, especially in patients with altered consciousness or gastric reflux. [1] * **Shock (Option C):** While shock itself leads to systemic inflammatory response syndrome (SIRS), it is a well-recognized and frequent precursor to ARDS. Since options A, B, and C represent the "top tier" of etiologies, the question implies that none of these are rare; thus, "All of the above" is the logical choice to indicate that none of these are the "least common." **High-Yield Clinical Pearls for NEET-PG:** * **Berlin Definition:** ARDS is defined by acute onset (<1 week), bilateral opacities on imaging, and a **PaO2/FiO2 ratio <300 mmHg** with PEEP ≥5 cm H2O. [2] * **PCWP:** In ARDS, the Pulmonary Capillary Wedge Pressure is typically **<18 mmHg** (to rule out cardiogenic edema). [2] * **Pathology:** The hallmark pathological finding is **Diffuse Alveolar Damage (Dad)** with hyaline membrane formation. [2] * **Ventilation Strategy:** Use **Low Tidal Volume (6 mL/kg)** to prevent volutrauma.

Question 47: Kallmann syndrome includes all of the following except?

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

Explanation: The question asks to identify the condition **not** associated with **Kartagener Syndrome** (Note: The question likely refers to Kartagener syndrome, a subset of Primary Ciliary Dyskinesia, as Kallmann syndrome is a separate neuroendocrine disorder characterized by hypogonadotropic hypogonadism and anosmia [4]. In the context of the options provided—Situs inversus, Bronchiectasis, and Sinusitis—the clinical triad described is classic for Kartagener Syndrome [1]). **1. Why Cystic Fibrosis is the Correct Answer:** Cystic Fibrosis (CF) is a distinct genetic disorder caused by mutations in the **CFTR gene**, leading to thick, viscous secretions [2]. While both CF and Kartagener syndrome cause bronchiectasis and sinusitis, CF is **not a component** of Kartagener syndrome [1],[3]. They are two different etiologies of obstructive lung disease. **2. Analysis of Incorrect Options (Components of Kartagener’s Triad):** Kartagener syndrome is a subtype of **Primary Ciliary Dyskinesia (PCD)** characterized by the classic triad: * **Situs Inversus (Option A):** Due to the failure of ciliary motion during embryogenesis. * **Bronchiectasis (Option B):** Chronic impaired mucociliary clearance leads to recurrent infections and permanent dilation of the bronchi [1]. * **Sinusitis (Option C):** Defective cilia in the paranasal sinuses lead to chronic inflammation and infection [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** PCD is mostly autosomal recessive; the most common defect is the absence of **dynein arms** in the cilia. * **Infertility:** Males are infertile due to immotile spermatozoa. * **Screening:** The initial screening test is the **Saccharin test** or measuring **nasal Nitric Oxide (nNO)** levels. * **Confining the confusion:** Do not confuse *Kartagener* (cilia) with *Kallmann* (GnRH deficiency [4]) or *Young’s syndrome* (bronchiectasis + obstructive azoospermia but normal cilia).

Question 48: All of the following are used to diagnose asthma, except?

A. FEV1 increases by more than 200 mL within 15 minutes after administering a bronchodilator
B. PEFR shows diurnal variation of more than 20%
C. More than 12% reversibility in FEV1 on administering a bronchodilator
D. Diffusion Lung Capacity for carbon monoxide is decreased (Correct Answer)

Explanation: **Explanation:** The diagnosis of Asthma is primarily based on demonstrating **reversible airflow obstruction** [1]. **Why Option D is the Correct Answer:** In Asthma, the **Diffusion Lung Capacity for carbon monoxide (DLCO)** is typically **normal or even increased**. This occurs because of increased pulmonary capillary blood volume and higher subatmospheric pressure during inspiration. A **decreased DLCO** is a hallmark of **Emphysema** (due to alveolar destruction) or Interstitial Lung Disease, not Asthma. Therefore, a decreased DLCO is the "except" in this list. **Analysis of Other Options:** * **Options A & C:** These represent the criteria for **Bronchodilator Reversibility**. A positive test is defined as an increase in FEV1 of **>12% AND >200 mL** from the baseline, 15–20 minutes after inhaling a short-acting beta-agonist (SABA) [1]. * **Option B:** Asthma is characterized by airway hyper-responsiveness. **Diurnal variation** in Peak Expiratory Flow Rate (PEFR) of **>20%** (calculated over 1–2 weeks) is a diagnostic indicator of the bronchial lability seen in asthmatic patients [1]. **Clinical Pearls for NEET-PG:** * **Gold Standard:** Spirometry is the investigation of choice to demonstrate reversible obstruction. * **Methacholine Challenge:** Used when spirometry is normal but asthma is suspected; a **20% fall in FEV1** (PC20) indicates airway hyper-responsiveness [2]. * **FeNO (Fractional Exhaled Nitric Oxide):** A high FeNO (>50 ppb) suggests eosinophilic airway inflammation and helps predict response to inhaled corticosteroids. * **Key Distinction:** Asthma = Normal/High DLCO; COPD (Emphysema) = Low DLCO.

Question 49: Mark the false statement about Pulmonary artery hypertension.

A. Mutations in the gene encoding bone morphogenetic protein receptor type 1. (Correct Answer)
B. Large a waves leading to elevated JVP.
C. In severe PAH, early pulmonic regurgitation can occur.
D. On histopathology, plexiform arteriopathy is seen.

Explanation: **Explanation:** **1. Why Option A is the Correct Answer (False Statement):** The genetic basis of heritable Pulmonary Arterial Hypertension (PAH) is primarily associated with mutations in the **BMPR2** gene (Bone Morphogenetic Protein Receptor type **2**), not type 1. BMPR2 is a member of the TGF-β receptor superfamily; its deficiency leads to the proliferation of vascular smooth muscle cells and endothelial cells, causing vessel narrowing. **2. Analysis of Other Options:** * **Option B (Large 'a' waves):** In PAH, the right ventricle faces high afterload, leading to right ventricular hypertrophy (RVH). This results in a "stiff" ventricle, requiring a forceful right atrial contraction to complete filling, which manifests as prominent or **giant 'a' waves** in the Jugular Venous Pulse (JVP) [1]. * **Option C (Early Pulmonic Regurgitation):** Severe PAH causes dilation of the pulmonary artery root, leading to functional valvular incompetence. This produces a high-pitched, decrescendo diastolic murmur known as the **Graham Steell murmur**, heard best at the left sternal edge. * **Option D (Plexiform Arteriopathy):** This is the histopathological hallmark of advanced PAH (WHO Group 1). It consists of glomeruloid-like tufts of proliferating endothelial cells and smooth muscle cells within the lumen of small pulmonary arteries. **Clinical Pearls for NEET-PG:** * **Definition:** PAH is defined as a Mean Pulmonary Artery Pressure (mPAP) **>20 mmHg** at rest (updated from 25 mmHg). * **Drug of Choice:** For vasoreactive patients (positive vasoreactivity test), **Calcium Channel Blockers** are used. For non-reactive patients, Endothelin receptor antagonists (Bosentan), PDE-5 inhibitors (Sildenafil), or Prostacyclin analogues (Epoprostenol) are preferred. * **Physical Sign:** A loud, palpable **P2** (pulmonary component of the second heart sound) is the most common physical finding [1].

Question 50: Bilateral ronchi are seen in which of the following conditions?

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

Explanation: The presence of **bilateral rhonchi** (or wheezing) in the setting of **Pulmonary Embolism (PE)** is a classic clinical finding often referred to as "cardiac asthma" or reflex bronchoconstriction. **1. Why Pulmonary Embolism is Correct:** When a thrombus occludes the pulmonary vasculature, it triggers the release of humoral mediators such as **serotonin, histamine, and prostaglandins** from activated platelets. These mediators cause widespread **reflex bronchoconstriction** of the small airways. Additionally, the resulting regional alveolar hypoxia can further induce bronchospasm. This manifests clinically as diffuse, bilateral wheezing or rhonchi, which can sometimes lead to a misdiagnosis of bronchial asthma or COPD exacerbation. **2. Analysis of Incorrect Options:** * **A. Pulmonary Edema:** Typically presents with **fine, crepitant rales (crackles)**, usually starting at the lung bases. While "cardiac asthma" can occur in left heart failure, the hallmark is crackles due to fluid in the alveoli [2]. * **C. Bronchiectasis:** Characterized by permanent dilation of bronchi, leading to **coarse crackles** and localized rhonchi due to mucus plugging. It is usually not a sudden-onset bilateral rhonchi presentation unless there is a severe secondary infection. * **D. Pulmonary AV Fistula:** This is a vascular malformation. It typically presents with a **continuous bruit** heard over the site of the fistula, not generalized airway sounds like rhonchi. **Clinical Pearls for NEET-PG:** * **Triad of PE:** Dyspnea, chest pain, and hemoptysis (present in <20% of cases). * **ECG Finding:** Most common is sinus tachycardia; most specific is **S1Q3T3** [1]. * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA). * **Auscultation Hint:** If a patient has sudden onset dyspnea, clear lungs on X-ray, but bilateral wheezing, always consider Pulmonary Embolism.

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

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