Pulmonology Practice Questions

Q: Which of the following is an obstructive lung disease?

All of the above. **Explanation:** Obstructive lung diseases are characterized by **increased resistance to airflow** due to partial or complete obstruction at any level of the respiratory tract. The hallmark physiological finding is a **decreased FEV1/FVC ratio (<0.7)** [1]. * **Bronchial Asthma:** Characterized by reversible airway hyperresponsiveness and chronic inflammation, leading to bronchoconstriction and mucus plugging [1]. * **Chronic Bronchitis:** Defined clinically as a productive cough for at least 3 months in 2 consecutive years. It involves hypertrophy of mucus-secreting glands in the large airways, causing luminal narrowing. * **Bronchiectasis:** A condition of permanent, abnormal dilation of the bronchi and bronchioles caused by destruction of muscle and elastic tissue, resulting in impaired clearance of secretions and airway collapse. Since all three conditions involve pathology that impedes the outflow of air, they are all classified as obstructive lung diseases. **High-Yield Clinical Pearls for NEET-PG:** * **The "Big Four" Obstructive Diseases:** Asthma, Chronic Bronchitis, Emphysema, and Bronchiectasis [2]. (Note: Chronic Bronchitis + Emphysema = COPD). * **PFT Pattern:** In obstructive disease, FEV1 is decreased significantly more than FVC, leading to a **decreased FEV1/FVC ratio** [1]. In contrast, restrictive diseases (like ILD) show a normal or increased ratio. * **Flow-Volume Loop:** Look for a **"scooped-out"** appearance on the expiratory limb [1]. * **Reversibility:** A post-bronchodilator increase in FEV1 of **>12% and >200 mL** suggests Asthma over COPD [1].

Q: Kallmann syndrome is characterized by which of the following?

All of the above. The question refers to **Kartagener Syndrome**, which is a specific subset of **Primary Ciliary Dyskinesia (PCD)**. It is an autosomal recessive disorder characterized by a classic clinical triad: **Situs inversus, Chronic sinusitis, and Bronchiectasis.** 1. **Situs Inversus (Option A):** During embryonic development, normal ciliary beating is required for the proper left-right positioning of internal organs. Defective cilia lead to a 50% chance of random organ orientation, resulting in situs inversus (reversal of organs). 2. **Bronchiectasis and Sinusitis (Option B):** Cilia are essential for the "mucociliary escalator." In PCD, impaired ciliary motility leads to poor clearance of mucus from the respiratory tract, causing recurrent infections, chronic sinusitis, and permanent dilation of the bronchi (bronchiectasis). 3. **Male Infertility (Option C):** The structural defect (most commonly a lack of **dynein arms**) that affects respiratory cilia also affects the flagella of spermatozoa. This results in immotile sperm, leading to infertility. **Note on Nomenclature:** While the prompt mentions "Kallmann syndrome" (which is actually Hypogonadotropic Hypogonadism with Anosmia) [1], the options and the marked correct answer clearly describe **Kartagener Syndrome**. In the context of NEET-PG, this is a common "trap" or typo; always prioritize the clinical triad presented in the options. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Defect:** Most commonly mutations in *DNAI1* and *DNAH5* genes. * **Diagnostic Test:** Screening with **Nasal Nitric Oxide (nNO)** levels (low in PCD); gold standard is **Electronic Microscopy** of ciliary ultrastructure or genetic testing. * **Dextrocardia:** Often the first clue on a chest X-ray (heart apex on the right). * **Female Fertility:** Can also be reduced due to impaired ciliary action in the fallopian tubes.

Q: Precapillary Pulmonary hypertension is caused by all EXCEPT:

Mitral stenosis. **Explanation:** Pulmonary Hypertension (PH) is hemodynamically classified into two main types based on the site of resistance: **Pre-capillary** and **Post-capillary**. 1. **Why Mitral Stenosis is the correct answer:** Mitral stenosis is a classic cause of **Post-capillary PH** (WHO Group 2). In this condition, the narrowing of the mitral valve leads to increased pressure in the left atrium, which is transmitted backward into the pulmonary veins and then the pulmonary capillaries. Hemodynamically, this is characterized by an elevated **Pulmonary Capillary Wedge Pressure (PCWP >15 mmHg)**. 2. **Why the other options are incorrect (Pre-capillary causes):** Pre-capillary PH occurs when the pathology is located *before* the pulmonary capillaries (PCWP remains normal, ≤15 mmHg). * **Primary Pulmonary Hypertension (Idiopathic PAH):** Involves intrinsic remodeling of the pulmonary arteries (WHO Group 1). * **Pulmonary Vasculitis:** Causes inflammation and narrowing of the arterial bed (WHO Group 1). * **Thromboembolism:** Leads to Chronic Thromboembolic Pulmonary Hypertension (CTEPH) by physically obstructing the arterial flow (WHO Group 4). **High-Yield Clinical Pearls for NEET-PG:** * **Hemodynamic Definition:** Pre-capillary PH is defined by a Mean Pulmonary Artery Pressure (mPAP) >20 mmHg AND a PCWP ≤15 mmHg. * **WHO Groups:** * **Group 1:** PAH (Idiopathic, Drugs, Connective Tissue Disease). * **Group 2:** Left Heart Disease (Mitral/Aortic valve disease, Heart Failure) — **Most common cause of PH overall.** * **Group 3:** Lung Disease/Hypoxia (COPD, ILD). * **Group 4:** CTEPH. * **Group 5:** Multifactorial. * **Groups 1, 3, and 4 are all Pre-capillary.** Only Group 2 is Post-capillary.

Q: Which of the following is not found as a presentation of sarcoidosis?

Myocardial infarction. Explanation: Sarcoidosis is a multisystem, chronic granulomatous disease of unknown etiology characterized by the formation of **non-caseating granulomas**. While it can affect almost any organ, its cardiovascular manifestations are specific. **Why Myocardial Infarction (Option B) is the Correct Answer:** Myocardial Infarction (MI) is typically caused by atherosclerotic plaque rupture or coronary artery occlusion. Sarcoidosis does not directly cause typical MI. While cardiac sarcoidosis involves the infiltration of granulomas into the myocardium, it leads to restrictive cardiomyopathy, heart failure, or conduction defects rather than acute coronary syndrome. **Analysis of Incorrect Options:** * **A. Erythema Nodosum:** This is a classic cutaneous manifestation of sarcoidosis [1]. When seen alongside bilateral hilar lymphadenopathy and arthralgia, it is known as **Löfgren syndrome**, which carries a favorable prognosis [1]. * **C. Arrhythmias:** Cardiac sarcoidosis most commonly involves the basal septum. Granulomatous infiltration and subsequent scarring disrupt the electrical conduction system, leading to heart blocks, ventricular arrhythmias, and sudden cardiac death [1]. * **D. CNS Involvement (Neurosarcoidosis):** Occurs in about 5–10% of patients. The most common presentation is **Cranial Nerve VII (Facial nerve) palsy** [1]. It can also cause meningitis, diabetes insipidus, and hypothalamic dysfunction [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Lungs:** 90% of cases show bilateral hilar lymphadenopathy [1]. * **Eyes:** Anterior uveitis is the most common ocular finding [1]. * **Heerfordt’s Syndrome:** Uveitis, Parotid swelling, and Facial nerve palsy. * **Diagnosis:** Elevated Serum ACE levels (non-specific) and biopsy showing non-caseating granulomas. * **Asteroid bodies** and **Schaumann bodies** are characteristic microscopic findings within the granulomas.

Q: What is the diagnostic test for acute pulmonary embolism?

D-dimer assay. **Explanation:** The diagnosis of acute pulmonary embolism (PE) relies on a high index of clinical suspicion followed by a structured diagnostic algorithm [1]. **Why D-dimer is the correct answer:** D-dimer is a fibrin degradation product that rises during active clot formation and lysis. In the context of acute PE, a **D-dimer assay (specifically ELISA)** has a very high **negative predictive value (>95%)**. This makes it the ideal initial "rule-out" test in patients with a low-to-moderate clinical probability (based on Wells’ Criteria). If the D-dimer is negative, PE can be safely excluded without further imaging. **Analysis of Incorrect Options:** * **A. Chest Radiograph:** Usually normal or shows non-specific findings (e.g., atelectasis) [1]. While classic signs like **Hampton’s Hump** (wedge-shaped opacity) or **Westermark sign** (oligemia) exist, they are rare and not diagnostic. * **B. ESR:** This is a non-specific marker of inflammation and has no diagnostic utility for PE. * **C. ECG changes:** The most common ECG finding in PE is **Sinus Tachycardia** [1]. The "classic" **S1Q3T3 pattern** (deep S in lead I, Q wave and inverted T in lead III) is specific for right heart strain but is only seen in about 20% of cases [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard (Investigation of Choice):** CT Pulmonary Angiography (CTPA). * **Definitive Gold Standard (Historical):** Conventional Pulmonary Angiography (rarely used now). * **Best Initial Test:** D-dimer (for low/intermediate risk) or CTPA (for high risk). * **Pregnancy/Renal Failure:** Ventilation-Perfusion (V/Q) scan is the preferred alternative to CTPA [1]. * **Treatment of Choice (Hemodynamically Stable):** Low Molecular Weight Heparin (LMWH) or Fondaparinux. * **Treatment of Choice (Hemodynamically Unstable/Massive PE):** Systemic Thrombolysis (e.g., Alteplase).

Q: All drugs cause interstitial lung disease, except:

Alpha methyl dopa. Drug-induced Interstitial Lung Disease (DILD) is a common cause of diffuse parenchymal lung disease [1]. The correct answer is **Alpha-methyl dopa**, as it is primarily associated with drug-induced autoimmune hemolytic anemia and hepatitis, but not typically with interstitial lung disease (ILD). **Why the other options are incorrect:** * **Phenytoin sodium:** This anticonvulsant is a known cause of hypersensitivity pneumonitis and can lead to pulmonary fibrosis or a pseudolymphoma-like syndrome. * **Sulphonamides:** These are associated with Eosinophilic Pneumonia (Loeffler’s syndrome) [1] and hypersensitivity reactions that manifest as interstitial infiltrates. * **Busulphan:** This alkylating agent is a classic cause of "Busulphan Lung." It causes chronic interstitial fibrosis, often occurring months to years after the initiation of therapy. **High-Yield Clinical Pearls for NEET-PG:** To master DILD questions, remember these high-yield categories: 1. **Cytotoxic/Chemo agents:** **Bleomycin** (most common, dose-dependent), Busulphan, Methotrexate (causes hypersensitivity pneumonitis) [1], and Cyclophosphamide. 2. **Anti-arrhythmics:** **Amiodarone** (highly high-yield; causes foamy macrophages in alveoli and "gold-standard" drug-induced fibrosis). 3. **Antibiotics:** **Nitrofurantoin** (causes both acute hypersensitivity and chronic fibrosis) and Sulphonamides. 4. **Others:** Gold salts [1], Penicillamine, and Phenytoin. **Mnemonic for common causes:** "**B**-**A**-**N**-**M**-**E**" (**B**leomycin, **A**miodarone, **N**itrofurantoin, **M**ethotrexate, **E**thyl alcohol/others). Alpha-methyl dopa is a "distractor" often used because it causes many other side effects, but the lung is not its primary target.

Question 1

What is the most reliable investigation in the diagnosis of pulmonary embolism?

Accepted Answer

Angiography

Answer

Lung scan

Answer

Differential gas tension

Answer

ECG

Question 2

Which of the following is an obstructive lung disease?

Accepted Answer

All of the above

Answer

Bronchial asthma

Answer

Chronic bronchitis

Answer

Bronchiectasis

Question 3

Kallmann syndrome is characterized by which of the following?

Accepted Answer

All of the above

Answer

Situs inversus

Answer

Bronchiectasis and sinusitis

Answer

Male infertility

Question 4

Precapillary Pulmonary hypertension is caused by all EXCEPT:

Accepted Answer

Mitral stenosis

Answer

Pulmonary vasculitis

Answer

Primary pulmonary hypertension

Answer

Thromboembolism

Question 5

A 29-year-old anxious lady presents with a history of progressive breathlessness and exercise intolerance for four months. Her FVC is 90% and FEV1/FVC is 86%. Oxygen saturation after exercise dropped from 92% to 86%. What is the likely diagnosis?

Accepted Answer

Primary pulmonary hypertension

Answer

Primary alveolar hypoventilation

Answer

Anxiety disorder

Answer

Interstitial lung disease

Question 6

Which of the following is not found as a presentation of sarcoidosis?

Accepted Answer

Myocardial infarction

Answer

Erythema nodosum

Answer

Arrhythmias

Answer

CNS involvement

Question 7

What is the diagnostic test for acute pulmonary embolism?

Accepted Answer

D-dimer assay

Answer

Chest radiograph

Answer

ESR

Answer

ECG changes

Question 8

Regarding Sarcoidosis, which of the following statements are true?
1. The most commonly involved organ is the lung.
2. Lupus pernio is a type of sarcoid skin lesion.
3. 90% of patients will have an abnormal chest X-ray sometime during the course of the disease.
4. Blindness is not a complication of sarcoidosis.
5. Tissue biopsy is not mandatory to establish the diagnosis.

Accepted Answer

Statements 1, 2, and 3 are true; statements 4 and 5 are false.

Answer

Statements 1 and 5 are true; statements 2, 3, and 4 are false.

Answer

Statements 1, 2, 4, and 5 are true; statement 3 is false.

Answer

Statements 1 and 2 are true; statements 3, 4, and 5 are false.

Question 9

A 60-year-old man, a heavy smoker, presents for advice to stop smoking. He is thin, has a ruddy complexion, a productive cough, and a barrel-shaped chest. He sits leaning forward with pursed lips to facilitate his breathing. A diagnosis of emphysema is made. Which of the following is the most likely histologic finding in the lungs?

Accepted Answer

Dilation of air spaces with destruction of alveolar walls

Answer

Bronchial smooth muscle hypertrophy with proliferation of eosinophils

Answer

Diffuse alveolar damage with leakage of protein-rich fluid into alveolar spaces

Answer

Hyperplasia of bronchial mucus-secreting submucosal glands

Question 10

All drugs cause interstitial lung disease, except:

Accepted Answer

Alpha methyl dopa

Answer

Phenytoin sodium

Answer

Sulphonamides

Answer

Busulphan

Pulmonology — MCQs

Pulmonology — MCQs

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