Pulmonology Practice Questions

Q: All of the following statements are true regarding asbestosis except?

It begins in an upper zone.. **Explanation:** Asbestosis is a chronic fibrotic interstitial lung disease caused by the inhalation of asbestos fibers. The correct answer is **B** because asbestosis characteristically involves the **lower zones** of the lungs, unlike many other pneumoconioses (like Silicosis or Coal Worker’s Pneumoconiosis) which typically affect the upper zones. **Analysis of Options:** * **Option B (Correct):** Asbestosis begins in the lower lobes. The fibers settle deep into the respiratory bronchioles and alveolar ducts in the lower zones due to gravity and the linear flow of air. * **Option A:** Asbestos fibers are divided into Serpentine (Chrysotile) and **Amphiboles** (Crocidolite, Amosite). Amphiboles are straight, needle-like, and more resistant to clearance, making them significantly more pathogenic and carcinogenic. * **Option C:** Asbestos exposure is the primary risk factor for **Mesothelioma** (malignancy of the pleura). While bronchogenic carcinoma is the most common cancer in asbestos workers, mesothelioma is the most specific. * **Option D:** Chronic interstitial fibrosis leads to destruction of the pulmonary capillary bed and hypoxia, resulting in **Pulmonary Hypertension** and potentially Cor Pulmonale in advanced stages. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic Finding:** **Asbestos bodies** (Ferruginous bodies) – golden-brown, dumbbell-shaped fibers coated with iron and protein. * **Radiology:** Presence of **Pleural Plaques** (calcified diaphragmatic pleura) is the most common radiological sign of exposure. * **Ground Glass Appearance:** Early radiological sign of asbestosis. * **Synergy:** Smoking and asbestos exposure have a synergistic (multiplicative) effect on the risk of lung cancer.

Q: Kallmann syndrome includes all of the following except?

Cystic fibrosis. 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).

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

Diffusion Lung Capacity for carbon monoxide is decreased. **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.

Q: What is the most diagnostic test for pulmonary embolism in a high-risk case?

Multidetector CT angiography. The diagnosis of Pulmonary Embolism (PE) depends on the patient's clinical probability. In high-risk cases, the goal is rapid, definitive visualization of the pulmonary vasculature. **1. Why Multidetector CT Angiography (MDCTA) is correct:** MDCTA is currently the **first-line diagnostic investigation** and the "gold standard" in clinical practice for PE [1]. It offers high sensitivity and specificity (PIOPED II study) and has the advantage of being non-invasive, widely available, and capable of identifying alternative diagnoses (e.g., pneumonia, aortic dissection) [2]. Modern multidetector scanners can visualize even subsegmental emboli with high precision. **2. Why the other options are incorrect:** * **Catheter Angiography:** Historically the "reference standard," it is now rarely performed because it is invasive, carries a higher risk of complications, and MDCTA provides comparable diagnostic accuracy. * **D-dimer:** This test has a high negative predictive value but very low specificity. It is used to **rule out** PE in low-to-moderate risk patients. In a high-risk case, a D-dimer is unnecessary as a negative result would not override clinical suspicion. * **Ventilation-Perfusion (V/Q) Scan:** This is a second-line test, primarily reserved for patients with contraindications to CT contrast (e.g., renal failure or severe allergy) [1]. It often yields "indeterminate" results, requiring further testing. **Clinical Pearls for NEET-PG:** * **Initial Investigation of choice:** MDCTA. * **Best Initial Test (Screening):** Chest X-ray (to rule out other causes), though often normal or showing non-specific signs like *Westermark sign* [2] or *Hampton’s hump*. * **Investigation of choice in Pregnancy:** V/Q scan is often preferred to limit maternal breast radiation, though CTPA is also used. * **Gold Standard (Historical):** Invasive Pulmonary Angiography.

Q: Amylase increased in pleural fluid is seen in all of the following conditions except:

Rheumatoid arthritis. Pleural fluid amylase is considered elevated when it exceeds the upper limit of normal for serum amylase or when the pleural fluid-to-serum amylase ratio is >1.0. **Why Rheumatoid Arthritis (RA) is the correct answer:** In RA-associated pleural effusion, the characteristic biochemical markers are **very low glucose levels** (often <30 mg/dL), high LDH, and low pH [1]. Amylase levels are typically **normal**. Therefore, it is the "except" in this list. **Analysis of Incorrect Options:** * **Esophageal Perforation:** This causes the highest levels of pleural fluid amylase [1]. The amylase is **salivary** in origin, leaking through the mediastinum into the pleural space. * **Gallstone Pancreatitis:** Acute or chronic pancreatitis leads to elevated **pancreatic** amylase in the pleural fluid (usually left-sided) due to transdiaphragmatic lymphatic spread or fistula formation [2]. * **Malignancy:** Approximately 10% of malignant effusions (most commonly Adenocarcinoma of the lung or ovary) show elevated amylase [1]. In these cases, the amylase is usually the salivary isoenzyme produced by the tumor cells themselves. **High-Yield NEET-PG Pearls:** 1. **Differential for High Pleural Amylase:** Remember the mnemonic **"PEAM"** — **P**ancreatitis, **E**sophageal rupture, **A**denocarcinoma (Malignancy), and **M**esothelioma. 2. **RA Effusion Triad:** Low Glucose + High LDH + Low pH (and presence of RA cells/Ragocytes) [1]. 3. **Esophageal Rupture:** Look for low pH (often <6.0) and presence of squamous epithelial cells or food particles in the fluid [1]. 4. **Pancreatic Effusion:** The pleural fluid amylase level is often significantly higher than the concomitant serum amylase level [2].

Q: About respiratory failure, which of the following statements is false?

Type II failure does not have a fall in PaO2 (hypoxia).. ### Explanation **Why Option B is the Correct (False) Statement:** Respiratory failure is defined by the inability of the respiratory system to maintain adequate gas exchange [1]. **Type II respiratory failure (Hypercapnic)** is characterized by a primary failure of ventilation leading to elevated $PaCO_2$ (>45 mmHg) [2]. However, according to the alveolar gas equation, as $PaCO_2$ rises, the partial pressure of alveolar oxygen ($PAO_2$) must fall. Therefore, **Type II failure always involves hypoxia ($PaO_2$ < 60 mmHg)** unless the patient is breathing supplemental oxygen [2]. The statement that it does not have a fall in $PaO_2$ is physiologically incorrect. **Analysis of Other Options:** * **Option A (True):** Type III respiratory failure is specifically associated with **perioperative** conditions. It occurs due to decreased functional residual capacity (FRC) in the setting of abnormal abdominal wall mechanics, leading to basal atelectasis. * **Option C (True):** Type I respiratory failure is **Hypoxemic** failure [2]. It is defined by a $PaO_2$ < 60 mmHg with a normal or low $PaCO_2$. It is the most common form of respiratory failure [1]. * **Option D (True):** Pneumonia causes a V/Q mismatch and inflammatory exudate in the alveoli, which impairs oxygen diffusion [1]. This typically results in Type I failure [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Type IV Respiratory Failure:** Refers to respiratory failure due to **shock** (hypoperfusion), where respiratory muscles consume a disproportionate amount of cardiac output. * **A-a Gradient:** Useful for differentiating causes of Type I failure. It is **increased** in pneumonia/PE but **normal** in hypoventilation (e.g., opioid overdose) or high altitude. * **Gold Standard Diagnosis:** Arterial Blood Gas (ABG) analysis is essential to classify respiratory failure [2].

Question 1

All of the following statements are true regarding asbestosis except?

Accepted Answer

It begins in an upper zone.

Answer

Amphiboles are more pathogenic.

Answer

It can cause mesothelioma.

Answer

Pulmonary hypertension may be seen.

Question 2

Kallmann syndrome includes all of the following except?

Accepted Answer

Cystic fibrosis

Answer

Situs inversus

Answer

Bronchiectasis

Answer

Sinusitis

Question 3

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

Accepted Answer

Diffusion Lung Capacity for carbon monoxide is decreased

Answer

FEV1 increases by more than 200 mL within 15 minutes after administering a bronchodilator

Answer

PEFR shows diurnal variation of more than 20%

Answer

More than 12% reversibility in FEV1 on administering a bronchodilator

Question 4

Mark the false statement about Pulmonary artery hypertension.

Accepted Answer

Mutations in the gene encoding bone morphogenetic protein receptor type 1.

Answer

Large a waves leading to elevated JVP.

Answer

In severe PAH, early pulmonic regurgitation can occur.

Answer

On histopathology, plexiform arteriopathy is seen.

Question 5

A 53-year-old patient presents with dyspnea and physical examination reveals facial swelling with engorged veins over the chest, raising suspicion for Superior Vena Cava (SVC) obstruction. Chest X-ray shows mediastinal enlargement. What is the next step in management?

Accepted Answer

CT thorax

Answer

Complete blood count with peripheral smear

Answer

Start cyclophosphamide

Answer

Urgent referral to a cardiologist

Question 6

What is the most diagnostic test for pulmonary embolism in a high-risk case?

Accepted Answer

Multidetector CT angiography

Answer

Catheter angiography

Answer

D-dimer

Answer

Ventilation perfusion scan

Question 7

Amylase increased in pleural fluid is seen in all of the following conditions except:

Accepted Answer

Rheumatoid arthritis

Answer

Esophageal perforation

Answer

Malignancy

Answer

Gallstone pancreatitis

Question 8

What is the most common cause of acute cor pulmonale?

Accepted Answer

Pulmonary thromboembolism

Answer

Pneumonia

Answer

Chronic obstructive pulmonary disease

Answer

Primary spontaneous pneumothorax

Question 9

About respiratory failure, which of the following statements is false?

Accepted Answer

Type II failure does not have a fall in PaO2 (hypoxia).

Answer

Type III failure involves post-operative atelectasis.

Answer

Type I failure involves hypoxia (PaO2).

Answer

Pneumonia usually presents with type I respiratory failure.

Question 10

Which of the following are features of pulmonary embolism?

Accepted Answer

Respiratory alkalosis, Right axis deviation, Ventricular strain

Answer

Right axis deviation, Normal A-a Gradient, Ventricular strain

Answer

Respiratory alkalosis, Right axis deviation

Pulmonology — MCQs

Pulmonology — MCQs

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