Pulmonology Practice Questions

Q: Central bronchiectasis is seen with

Cystic fibrosis. ***Cystic fibrosis*** - **Cystic Fibrosis (CF)** is a genetic disorder commonly associated with **central bronchiectasis**, particularly affecting the upper lobes and central airways. - The abnormal mucus production in CF leads to chronic infection, inflammation, and eventual **dilation of the bronchi**, prominent in the central regions. *Bronchogenic carcinoma* - **Bronchogenic carcinoma** can cause **post-obstructive bronchiectasis** distal to the tumor due to airway obstruction and reduced clearance. - However, the bronchiectasis tends to be **localized** to the segment supplied by the obstructed bronchus, rather than being diffusely central. *Tuberculosis* - **Tuberculosis (TB)** can lead to bronchiectasis, often affecting the **upper lobes** and causing localized airway damage. - While TB can cause changes in the bronchi, it is typically linked with **focal or segmental bronchiectasis** resulting from inflammatory destruction, not diffuse central bronchiectasis like CF. *Cystic Adenomatoid Malformation (CAM)* - **Cystic Adenomatoid Malformation (CAM)** is a **congenital lung lesion** with abnormal airway development, but it does not primarily involve bronchiectasis. - CAM is characterized by **cystic structures** or abnormal lung tissue, not the permanent dilation of the bronchi seen in typical bronchiectasis.

Q: Post-tubercular bronchiectasis is most commonly seen with

Tuberculosis. ***Tuberculosis*** - **Tuberculosis (TB)**, particularly childhood TB, is a leading cause of post-infectious bronchiectasis, especially in regions with high TB prevalence [1]. - The inflammatory and destructive processes associated with TB infection in the lungs can lead to irreversible dilation and damage of the bronchi [1]. *Pertussis* - While **pertussis** can cause severe respiratory inflammation and chronic cough, it is a less common cause of widespread, irreversible bronchiectasis compared to tuberculosis [1]. - The damage caused by pertussis is typically more acute and less likely to lead to long-term structural changes like those seen in post-tubercular bronchiectasis. *Cystic fibrosis* - **Cystic fibrosis** is a genetic disorder that causes thick, sticky mucus to build up in the lungs, leading to chronic infections and bronchiectasis [1]. - However, post-tubercular bronchiectasis refers specifically to bronchiectasis developing *after* a tuberculosis infection, not as a primary genetic condition. *Kartagener syndrome* - **Kartagener syndrome** is a genetic disorder characterized by defects in ciliary function, leading to impaired mucociliary clearance and recurrent respiratory infections, which can result in bronchiectasis [1]. - Similar to cystic fibrosis, this is a primary genetic cause of bronchiectasis, distinct from bronchiectasis occurring as a sequela of tuberculosis.

Q: Which of the following is the common cause of respiratory failure type 2 ?

Chronic bronchitis exacerbation. ***Chronic bronchitis exacerbation*** - **Chronic bronchitis** is a common cause of **Type 2 respiratory failure**, characterized by **hypercapnia** (elevated CO2) due to impaired alveolar ventilation [1]. - An exacerbation worsens **airflow obstruction** and leads to increased work of breathing and CO2 retention [1]. *Acute attack asthma* - While severe asthma can cause respiratory failure, it typically presents initially as **Type 1 (hypoxemic)**, with severe bronchospasm and V/Q mismatch [2]. - **Hypercapnia** in asthma is a sign of **severe, impending respiratory collapse** rather than the primary cause of respiratory failure. *ARDS* - **Acute Respiratory Distress Syndrome (ARDS)** is a classic cause of **Type 1 (hypoxemic) respiratory failure**, characterized by widespread inflammation and fluid accumulation in the lungs [2]. - ARDS primarily involves impaired oxygenation rather than CO2 elimination issues, unless it progresses to severe stages with significant muscle fatigue. *Pneumonia* - **Pneumonia** predominantly causes **Type 1 (hypoxemic) respiratory failure** due to consolidation and V/Q mismatch in affected lung areas, leading to impaired oxygen diffusion [2]. - While severe, widespread pneumonia can eventually lead to ventilatory failure, its initial and primary impact is on oxygenation.

Q: Which of the following is seen in sarcoidosis

Increased calcium levels in the blood (Hypercalcemia). ***Increased calcium levels in the blood (Hypercalcemia)*** - In sarcoidosis, activated macrophages in granulomas produce **1-alpha hydroxylase**, which converts **25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol)** [1]. - This increased calcitriol leads to enhanced intestinal **calcium absorption** and occasional bone resorption, resulting in **hypercalcemia** [1]. *Decreased calcium levels in the blood (Hypocalcemia)* - **Hypocalcemia** is not characteristic of sarcoidosis; the disease typically involves dysregulated vitamin D metabolism causing elevated, not decreased, calcium [1]. - Conditions like **hypoparathyroidism** or **vitamin D deficiency** (unrelated to the sarcoidosis pathogenesis) would cause hypocalcemia. *Increased phosphate levels in the blood (Hyperphosphatemia)* - **Hyperphosphatemia** is not a feature of sarcoidosis. Calcium and phosphate levels often have an inverse relationship, so with hypercalcemia, phosphate levels tend to be normal or slightly decreased due to suppression of parathyroid hormone. - Hyperphosphatemia is more commonly associated with **renal failure** or certain **endocrine disorders**. *Decreased phosphate levels in the blood (Hypophosphatemia)* - While **hypophosphatemia** can occur in conditions with high vitamin D activity (as increased active vitamin D can promote renal phosphate excretion), it is not the primary or most notable electrolyte disturbance specifically linked to sarcoidosis. - **Hypercalcemia** is the more consistently observed electrolyte abnormality in sarcoidosis related to ectopic vitamin D production [1].

Q: In a patient with COPD, what is the best management option?

Quit smoking. ***Quit smoking*** - **Smoking cessation** is the single most effective intervention for slowing the progression of **COPD** and improving lung function [1]. - It reduces exacerbation rates and improves overall mortality, making it the cornerstone of management [1]. *Bronchodilators* - **Bronchodilators** (e.g., beta-agonists, anticholinergics) are crucial for symptomatic relief by opening airways, but they do not alter the disease progression [1]. - While essential for managing symptoms, they are not the "best" in terms of modifying the disease course. *Low flow oxygen* - **Oxygen therapy** is indicated for patients with **severe hypoxemia** (PaO2 < 55 mmHg or SaO2 < 88%) to improve survival and quality of life [2]. - It is a supportive treatment for advanced disease and does not prevent or slow the progression of COPD itself. *Mucolytics* - **Mucolytics** may be used in some patients with COPD and chronic productive cough to reduce sputum viscosity and improve clearance. - Their benefit is primarily symptomatic, and they do not have a significant impact on disease progression or mortality.

Q: Clicking noise in Pneumomediastinum is known as

Hamman's sign. Hamman's sign - Hamman's sign is a crunching, bubbling, or clicking sound synchronous with the heartbeat, audible on auscultation over the precordium. - It is pathognomonic for pneumomediastinum, caused by the heart beating against air-filled tissues. Traube's sign - Traube's sign refers to a pistol-shot sound heard over the femoral artery in severe aortic regurgitation [1]. - It is a vascular sign and not related to pneumomediastinum. Kussmaul's sign - Kussmaul's sign is a paradoxical rise in jugular venous pressure (JVP) during inspiration. - It is typically seen in conditions like constrictive pericarditis or right ventricular infarction, not pneumomediastinum. None of the options - This option is incorrect because Hamman's sign accurately describes the clicking noise associated with pneumomediastinum. - The other options refer to different clinical phenomena unrelated to pneumomediastinum.

Q: In a patient with high clinical suspicion of pulmonary thromboembolism, best investigation would be?

CT angiography. ***CT angiography*** - In a patient with **high clinical suspicion** of pulmonary embolism (PE), CT angiography of the pulmonary arteries is the preferred and often definitive diagnostic test. - It allows for direct visualization of thrombi within the pulmonary arterial tree with high sensitivity and specificity. *D-dimer* - While useful for **ruling out PE** in patients with low or intermediate pre-test probability, a positive D-dimer is non-specific and requires further investigation in high-suspicion cases. - It has a high **negative predictive value** but a low positive predictive value, meaning a normal D-dimer makes PE unlikely, but an elevated one does not confirm it. *Catheter angiography* - This is an **invasive procedure** that is typically reserved for cases where CT angiography is inconclusive or contraindicated, or when interventional treatment is contemplated. - It carries risks such as **bleeding** and **contrast-induced nephropathy**, making it less appropriate as a first-line diagnostic in most situations. *Color Doppler* - Color Doppler ultrasound is primarily used to diagnose **deep vein thrombosis (DVT)** in the lower extremities, which is a common source of PE. - It is **not used to directly diagnose PE** in the pulmonary arteries; however, finding a DVT can support the diagnosis of PE indirectly.

Q: What is the best immediate management strategy for a patient experiencing respiratory alkalosis due to anxiety-induced hyperventilation?

Rebreathing in paper bag. ***Rebreathing in paper bag*** - This helps to **increase the inspired CO2 concentration**, thereby correcting the hypocapnia (low CO2) caused by hyperventilation. - It's a simple, non-invasive method to raise arterial PCO2 and normalize blood pH in acute respiratory alkalosis. *IPPV* - **Intermittent positive pressure ventilation (IPPV)** would further reduce CO2 by assisting ventilation and is typically used for respiratory *acidosis* or failure [1]. - This intervention would worsen the patient's respiratory alkalosis rather than alleviating it. *Normal saline* - **Normal saline** administration is primarily used for volume expansion or to correct electrolyte imbalances; it does not directly address respiratory alkalosis. - It would not correct the underlying issue of excessive CO2 exhalation. *Acetazolamide* - **Acetazolamide** is a carbonic anhydrase inhibitor that reduces bicarbonate reabsorption and is used to treat metabolic alkalosis or as a diuretic. - It would not be an immediate or appropriate solution for acute respiratory alkalosis and might even worsen the acid-base balance if used improperly.

Q: Which of the following is not a clinical feature of Bronchiectasis?

Night sweats. ***Night sweats*** - While **night sweats** can be present in chronic infections, they are not considered a primary or defining clinical feature directly associated with the pathology of bronchiectasis itself. - They are more commonly linked with systemic conditions like **tuberculosis** or malignancy, which would require alternative diagnostic pathways. *Hemoptysis* - **Hemoptysis** (coughing up blood) is a common and often alarming symptom of bronchiectasis due to the inflammation and damage to the bronchial walls and underlying vasculature [1]. - Blood vessels in damaged airways are prone to rupture, leading to bleeding, which can range from blood-streaked sputum to massive hemorrhage [1]. *Chest pain* - **Chest pain** can occur in bronchiectasis, often related to the chronic cough, pleural inflammation, or musculoskeletal strain from persistent coughing. - It can also be a symptom if there's an associated infection or inflammation extending to the pleura. *Productive cough* - A **chronic productive cough** with significant amounts of purulent sputum is the hallmark symptom of bronchiectasis [1]. - This is due to the impaired mucociliary clearance and chronic infection within the dilated, damaged airways .

Question 1

Central bronchiectasis is seen with

Accepted Answer

Cystic fibrosis

Answer

Tuberculosis

Answer

Bronchogenic carcinoma

Answer

Cystic Adenomatoid Malformation (CAM)

Question 2

Post-tubercular bronchiectasis is most commonly seen with

Accepted Answer

Tuberculosis

Answer

Pertussis

Answer

Cystic fibrosis

Answer

Kartagener syndrome

Question 3

Which of the following is the common cause of respiratory failure type 2 ?

Accepted Answer

Chronic bronchitis exacerbation

Answer

Acute attack asthma

Answer

ARDS

Answer

Pneumonia

Question 4

Which of the following is seen in sarcoidosis

Accepted Answer

Increased calcium levels in the blood (Hypercalcemia)

Answer

Decreased calcium levels in the blood (Hypocalcemia)

Answer

Increased phosphate levels in the blood (Hyperphosphatemia)

Answer

Decreased phosphate levels in the blood (Hypophosphatemia)

Question 5

In a patient with COPD, what is the best management option?

Accepted Answer

Quit smoking

Answer

Bronchodilators

Answer

Low flow oxygen

Answer

Mucolytics

Question 6

Clicking noise in Pneumomediastinum is known as

Accepted Answer

Hamman's sign

Answer

Traube's sign

Answer

Kussmaul's sign

Answer

None of the options

Question 7

In a patient with high clinical suspicion of pulmonary thromboembolism, best investigation would be?

Accepted Answer

CT angiography

Answer

D-dimer

Answer

Catheter angiography

Answer

Color Doppler

Question 8

What is the best immediate management strategy for a patient experiencing respiratory alkalosis due to anxiety-induced hyperventilation?

Accepted Answer

Rebreathing in paper bag

Answer

IPPV

Answer

Normal saline

Answer

Acetazolamide

Question 9

Which of the following is not a clinical feature of Bronchiectasis?

Accepted Answer

Night sweats

Answer

Hemoptysis

Answer

Chest pain

Answer

Productive cough

Question 10

Which of the following statements is true regarding the diagnostic criteria for Chronic Obstructive Pulmonary Disease (COPD)?

Accepted Answer

A post-bronchodilator FEV1/FVC ratio below the threshold indicates airflow limitation.

Answer

A post-bronchodilator FEV1/FVC ratio above the threshold indicates normal lung function.

Answer

Residual Volume (RV) is normal.

Answer

Total Lung Capacity (TLC) is decreased.

Pulmonology — MCQs

Pulmonology — MCQs

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