Pulmonology Practice Questions

Q: In the management of pulmonary emboli, what is the recommended infusion time for alteplase?

1-3 hours. **Explanation:** In the management of hemodynamically unstable (massive) pulmonary embolism (PE), thrombolytic therapy is indicated to rapidly dissolve the clot and reduce right ventricular strain [1]. **Alteplase (rt-PA)** is the preferred thrombolytic agent [2]. **1. Why Option A is Correct:** The standard FDA-approved regimen for alteplase in acute PE is **100 mg administered as a continuous intravenous infusion over 2 hours**. This rapid infusion (1-3 hour window) is preferred over older, prolonged regimens because it achieves faster clot lysis and hemodynamic improvement without a significant increase in major bleeding complications. In extreme cases of cardiac arrest, a "bolus" dose may be considered, but the 2-hour infusion remains the gold standard for massive PE. **2. Why Other Options are Incorrect:** * **Options B, C, and D:** These timeframes (4-12 hours) represent outdated protocols. Historically, first-generation thrombolytics like Streptokinase were administered over 12–24 hours [2]. However, for Alteplase, prolonged infusions do not offer additional efficacy and significantly increase the risk of bleeding, particularly intracranial hemorrhage [1]. **3. Clinical Pearls for NEET-PG:** * **Indication:** Thrombolysis is reserved for **Massive PE** (defined by hypotension: SBP <90 mmHg) or select cases of Submassive PE with evidence of severe RV dysfunction [1]. * **Drug of Choice:** Alteplase (100 mg over 2 hours). * **Alternative:** Tenecteplase (TNK-tPA) is often used in MI but is currently being studied for PE (not yet the primary standard over Alteplase in all guidelines). * **Contraindication:** Always screen for absolute contraindications like recent intracranial hemorrhage, active internal bleeding, or recent ischemic stroke (within 3 months) [1]. * **Post-Thrombolysis:** Heparin therapy should be initiated/resumed once the aPTT falls below twice the upper limit of normal.

Q: Which of the following is NOT a feature of tuberculous pleural effusion?

Increased mesothelial cells. ### Explanation **Correct Answer: D. Increased mesothelial cells** In **Tuberculous Pleural Effusion (TPE)**, the hallmark finding is a **paucity or near-absence of mesothelial cells** (typically 60% of serum LDH:** TPE is a classic **exudate**. According to Light’s Criteria, an exudate must meet at least one of three criteria: Pleural fluid/Serum Protein ratio >0.5, Pleural fluid/Serum LDH ratio >0.6, or Pleural fluid LDH >2/3rd the upper limit of normal serum LDH [1]. * **B. Adenosine Deaminase (ADA):** ADA is a high-yield marker for TPE. Levels **>40 U/L** have high sensitivity and specificity. It reflects the activation of T-lymphocytes in response to mycobacterial antigens. * **C. WBC count 5000 - 10000:** TPE typically presents with a total leukocyte count in the range of 1,000 to 10,000 cells/µL, with a marked **lymphocyte predominance** (>80-90%) [1]. **Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Pleural biopsy (showing granulomas) is more sensitive than fluid culture or AFB staining [1]. * **IFN-gamma:** High levels of Interferon-gamma in pleural fluid are also highly suggestive of TPE. * **Glucose:** Usually low to normal; if extremely low (<30 mg/dL), consider empyema or malignancy [1]. * **Rule of Thumb:** If you see "many mesothelial cells" on a cytology report, think of other causes like pulmonary infarction or congestive heart failure, not TB [1].

Q: All of the following constitute primary diagnostic criteria for ABPA, except:

Identification of A. fumigatus from sputum. Allergic Bronchopulmonary Aspergillosis (ABPA) is a complex hypersensitivity reaction to Aspergillus fumigatus colonization in the airways, typically seen in patients with Asthma or Cystic Fibrosis. Why Option D is the correct answer: The identification of A. fumigatus from sputum is not a primary diagnostic criterion. Aspergillus is ubiquitous in the environment; its presence in sputum may represent simple colonization or environmental contamination and does not confirm an active immunological disease process. Diagnosis relies on immunological evidence and radiological findings rather than a positive culture. Analysis of other options (Primary Criteria): Elevated Serum IgE (>417 IU/ml or >1000 ng/ml): This is a mandatory "obligatory" criterion. A level 500 cells/µL): This is a classic secondary/supportive criterion (often part of the ISHAM criteria) reflecting the Type I and Type III hypersensitivity nature of the disease. Central/Proximal Bronchiectasis: This is a hallmark radiological finding. Unlike post-tubercular bronchiectasis, ABPA typically affects the inner two-thirds of the lung fields (central), sparing the periphery. High-Yield Clinical Pearls for NEET-PG: Obligatory Criteria (ISHAM 2013): 1. Positive Type I skin test for Aspergillus OR elevated IgE specific to A. fumigatus. 2. Elevated Total Serum IgE (>1000 IU/mL). [1] Radiology: Look for "Finger-in-glove" appearance and "High-attenuation mucus" (HAM) on CT—the latter is pathognomonic for ABPA. Treatment: The mainstay is Oral Corticosteroids to suppress the immune response, often combined with Itraconazole to reduce the fungal burden.

Q: Thermoplasty is used in which condition?

Asthma. **Explanation:** **Bronchial Thermoplasty (BT)** is an innovative, FDA-approved bronchoscopic procedure specifically designed for the management of **severe, persistent asthma** that remains uncontrolled despite optimal medical therapy (high-dose inhaled corticosteroids and long-acting beta-agonists) [1]. **Why Asthma is the Correct Answer:** The pathophysiology of asthma involves hypertrophy and hyperplasia of the **bronchial smooth muscle (BSM)**, leading to airway hyperresponsiveness and narrowing. Bronchial thermoplasty uses controlled **radiofrequency energy** (thermal energy) delivered via a catheter to the airways. This heat selectively reduces the mass of the smooth muscle, thereby decreasing the lung's ability to constrict during an asthma attack. It typically involves three separate sessions targeting different lobes of the lungs. **Why Other Options are Incorrect:** * **COPD:** While COPD involves airway obstruction, the primary pathology is alveolar destruction (emphysema) and chronic inflammation/mucus production (bronchitis), rather than reversible smooth muscle constriction. * **Bronchiectasis:** This is characterized by permanent, abnormal dilation of the bronchi due to chronic infection and inflammation. Treatment focuses on airway clearance and antibiotics, not smooth muscle reduction. * **Carcinoma Lung:** Treatment modalities for lung cancer include surgery, chemotherapy, radiotherapy, or endobronchial interventions like stenting or laser ablation, but not thermoplasty. **High-Yield Clinical Pearls for NEET-PG:** * **Indication:** Severe persistent asthma in patients ≥18 years old [1]. * **Mechanism:** Reduction of airway smooth muscle (ASM) mass. * **Contraindication:** Patients with pacemakers, internal defibrillators, or those experiencing an active asthma exacerbation. * **Common Side Effect:** Transient worsening of respiratory symptoms (cough, wheeze) immediately following the procedure.

Q: A 34-year-old man presents with increasing shortness of breath. He has a history of asthma that was previously well controlled, but two weeks ago he developed cold symptoms and has noticed increased coughing and shortness of breath since then. He reports no fevers or chills and denies sputum production. He is currently using his salbutamol inhaler six times a day for rescue therapy and feels unwell. His physical examination reveals wheezing on expiration, but is otherwise normal. A chest X-ray is normal. He is prescribed prednisone 30 mg once daily for one week. What is the primary mechanism of glucocorticoids in the management of asthma?

Anti-inflammatory effect. **Explanation:** **Why Option A is correct:** Asthma is fundamentally a **chronic inflammatory disorder** of the airways. Glucocorticoids (like Prednisone) are the most effective anti-inflammatory agents used in its management. Their primary mechanism involves: 1. **Inhibition of inflammatory mediators:** They inhibit the synthesis of cytokines (IL-4, IL-5), leukotrienes, and prostaglandins. 2. **Reduction of inflammatory cells:** They induce apoptosis of eosinophils and T-lymphocytes and decrease mast cell density. 3. **Up-regulation of Beta-2 receptors:** They increase the expression of $\beta_2$-adrenergic receptors on airway smooth muscle, which enhances the responsiveness to bronchodilators (synergistic effect). **Why the other options are incorrect:** * **B. Bronchodilatory effect:** Glucocorticoids do **not** have a direct relaxant effect on airway smooth muscle. Bronchodilation is achieved by $\beta_2$-agonists (e.g., Salbutamol) or anticholinergics (e.g., Ipratropium) [1]. * **C. Sedative effect:** Glucocorticoids do not cause sedation; in fact, they can cause CNS side effects like insomnia, euphoria, or psychosis. * **D. Mucolytic effect:** While steroids reduce mucus hypersecretion by decreasing inflammation, they do not chemically break down mucus (the role of mucolytics like N-acetylcysteine). **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Inhaled Corticosteroids (ICS) are the first-line maintenance therapy for persistent asthma [1]. * **Systemic Steroids:** Reserved for acute exacerbations (as seen in this patient) to prevent relapse and speed up recovery [1]. * **Side Effects:** Long-term ICS use carries a risk of **oropharyngeal candidiasis** (prevented by using a spacer and rinsing the mouth) and dysphonia. * **Mechanism Tip:** Steroids act via **intracellular receptors** to alter gene transcription (genomic effect), which is why their clinical onset takes several hours. [1]

Q: All of the following are features of sarcoidosis except?

Malabsorption syndrome. Explanation: Sarcoidosis is a multisystem, chronic granulomatous disease characterized by the formation of **non-caseating granulomas**. **Why Malabsorption Syndrome is the correct answer:** While sarcoidosis can affect almost any organ, the gastrointestinal tract is involved in less than 1% of cases [1]. When it does occur, it most commonly affects the stomach (gastritis). **Malabsorption syndrome** is not a feature of sarcoidosis; it is more characteristic of conditions like Celiac disease, Tropical sprue, or Whipple’s disease. [1] **Analysis of incorrect options:** * **Right paratracheal lymphadenopathy:** This is a classic radiological finding. Sarcoidosis typically presents with **bilateral hilar lymphadenopathy** often accompanied by right paratracheal lymphadenopathy (forming the "1-2-3 sign" or Garland’s triad) [1]. * **Cardiomyopathy:** Cardiac sarcoidosis occurs in about 5% of patients [1]. Granulomatous infiltration of the myocardium can lead to restrictive cardiomyopathy, heart block, arrhythmias, and sudden cardiac death [1]. * **Hypercalcemia:** This is a high-yield metabolic feature. Epithelioid cells within the granulomas contain the enzyme **1-alpha-hydroxylase**, which converts Vitamin D to its active form (1,25-dihydroxyvitamin D), leading to increased intestinal calcium absorption and hypercalciuria/hypercalcemia [1]. **NEET-PG Clinical Pearls:** * **Lofgren’s Syndrome:** A triad of Erythema nodosum, bilateral hilar lymphadenopathy, and polyarthritis (Good prognosis) [1]. * **Heerfordt’s Syndrome (Uveoparotid fever):** Parotid enlargement, facial nerve palsy, and anterior uveitis. * **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.

Question 1

In the management of pulmonary emboli, what is the recommended infusion time for alteplase?

Accepted Answer

1-3 hours

Answer

4-6 hours

Answer

7-9 hours

Answer

10-12 hours

Question 2

A 30-year-old man presents with coughing up blood and sputum. There is no associated dyspnea, fever, or pleuritic chest pain. His past medical history is significant for recurrent pneumonias and a chronic cough productive of foul-smelling purulent sputum. The sputum production is usually worse when lying down and in the morning. He quit smoking 5 years ago and started when he was 18 years old. On physical examination, he appears chronically ill with clubbing of the fingers. Wet inspiratory crackles are heard at the lung bases posteriorly. Chest imaging reveals scarring in the right lower lobe, identified as airway dilatation, bronchial wall thickening, and grapelike cysts. Which of the following is the most likely diagnosis?

Accepted Answer

Bronchiectasis

Answer

Chronic bronchitis

Answer

Disseminated pulmonary tuberculosis

Answer

Pulmonary neoplasm

Question 3

Which of the following is NOT a feature of tuberculous pleural effusion?

Accepted Answer

Increased mesothelial cells

Answer

LDH > 60% of serum LDH

Answer

Adenosine deaminase

Answer

WBC count 5000 - 10000

Question 4

All of the following constitute primary diagnostic criteria for ABPA, except:

Accepted Answer

Identification of A. fumigatus from sputum

Answer

Elevated serum IgE levels > 417 IU/ml

Answer

Peripheral eosinophilia >500 cells/ml

Answer

Central/Proximal bronchiectasis

Question 5

Thermoplasty is used in which condition?

Accepted Answer

Asthma

Answer

COPD

Answer

Bronchiectasis

Answer

Carcinoma lung

Question 6

A 34-year-old man presents with increasing shortness of breath. He has a history of asthma that was previously well controlled, but two weeks ago he developed cold symptoms and has noticed increased coughing and shortness of breath since then. He reports no fevers or chills and denies sputum production. He is currently using his salbutamol inhaler six times a day for rescue therapy and feels unwell. His physical examination reveals wheezing on expiration, but is otherwise normal. A chest X-ray is normal. He is prescribed prednisone 30 mg once daily for one week. What is the primary mechanism of glucocorticoids in the management of asthma?

Accepted Answer

Anti-inflammatory effect

Answer

Bronchodilatory effect

Answer

Sedative effect

Answer

Mucolytic effect

Question 7

A 80-year-old male presented with a lung abscess in the left upper zone. What is the best initial treatment modality?

Accepted Answer

Antibiotics guided by identified organisms

Answer

Surgical drainage

Answer

Tube thoracostomy

Answer

Observation (wait and watch)

Question 8

Clinical manifestations of bronchogenic carcinoma include the following except?

Accepted Answer

Gastroparesis due to vagal involvement

Answer

Hoarseness of voice due to involvement of left recurrent laryngeal nerve

Answer

Horner's syndrome

Answer

Diaphragmatic palsy due to infiltration of phrenic nerve

Question 9

All of the following are features of sarcoidosis except?

Accepted Answer

Malabsorption syndrome

Answer

Right paratracheal lymphadenopathy

Answer

Cardiomyopathy

Answer

Hypercalcemia

Question 10

A patient presents with non-productive cough, hemoptysis, and grade III clubbing. Chest X-ray reveals an upper left zone lesion. What is the likely cause?

Accepted Answer

Non-small cell carcinoma of the lung

Answer

Small cell carcinoma of the lung

Answer

Tuberculosis

Answer

Fungal infection of the lung

Pulmonology — MCQs

Pulmonology — MCQs

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