Respiratory Pathology — MCQs

A 46-year-old man presents with a year of increasing dyspnea and nonproductive cough. Physical examination reveals clubbing of digits and no fever. Pulmonary function tests show a mild restrictive abnormality and reduced DLCO. A transbronchial biopsy reveals numerous alveolar macrophages containing lamellar bodies and iron pigment, along with plump epithelial cells, mild interstitial fibrosis, and loss of respiratory bronchioles. What is the most likely etiology for his pulmonary disease?

Q147Easy

Which of the following histopathological findings is most commonly associated with COVID-19?

Q148Easy

Hyaline membrane disease is associated with which of the following conditions?

Q149Medium

Which of the following morphological changes in the lungs would be found in a patient of asthma?

Q150Easy

Miliary tuberculosis is classified as:

Respiratory Pathology Indian Medical PG Practice Questions and MCQs

Question 141: Which tumor is not seen in the anterior mediastinum?

A. Teratoma
B. Thymic tumors
C. Thyroid tumors
D. Neurofibroma (Correct Answer)

Explanation: ### Explanation The mediastinum is anatomically divided into compartments, each associated with specific characteristic pathologies. This is a high-yield topic for NEET-PG, often remembered by the **"4 Ts" rule for anterior mediastinal masses.** **1. Why Neurofibroma is the Correct Answer:** Neurofibroma is a nerve sheath tumor. In the mediastinum, neurogenic tumors (including neurofibromas, schwannomas, and ganglioneuromas) are almost exclusively located in the **posterior mediastinum**, arising from the paravertebral sympathetic chain or spinal nerves. Therefore, it is not typically seen in the anterior compartment. **2. Analysis of Incorrect Options (Anterior Mediastinal Masses):** The anterior mediastinum is the space between the sternum and the pericardium. The most common masses follow the **"4 Ts" mnemonic**: * **Thymic tumors (Option B):** Including thymomas, thymic hyperplasia, and thymic carcinoma [1]. Thymoma is the most common anterior mediastinal mass in adults. * **Teratoma (Option A):** And other Germ Cell Tumors (GCTs). These are common in young adults; mature cystic teratomas are the most frequent subtype [1]. * **Thyroid tumors (Option C):** Specifically retrosternal or ectopic thyroid goiters. * **"Terrible" Lymphoma:** Often presenting with bulky lymphadenopathy [1]. **3. Clinical Pearls for NEET-PG:** * **Most common posterior mediastinal mass:** Neurogenic tumors (e.g., Schwannoma). * **Most common anterior mediastinal mass:** Thymoma. * **Thymoma Association:** Strongly associated with **Myasthenia Gravis** (approx. 30–45% of thymoma patients have MG) [2]. * **Imaging Gold Standard:** CT chest is the preferred initial investigation to localize and characterize mediastinal masses. * **Biomarkers:** In anterior masses, elevated **AFP or beta-hCG** suggests a non-seminomatous germ cell tumor. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 571-574. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 634.

Question 142: Adenocarcinoma of the lung is NOT associated with which of the following features?

A. Is not associated with cigarette smoking
B. Is usually found in the periphery of the lung
C. Is more common in women than men
D. Often produces ectopic hormones (Correct Answer)

Explanation: **Explanation:** The correct answer is **D (Often produces ectopic hormones)** because paraneoplastic syndromes involving ectopic hormone production are classically associated with **Small Cell Lung Carcinoma (SCLC)** and **Squamous Cell Carcinoma (SCC)**, rather than Adenocarcinoma [3], [4]. Specifically, SCLC is known for producing ACTH (Cushing syndrome) and ADH (SIADH), while SCC is associated with PTHrP (Hypercalcemia) [3]. Adenocarcinoma is more frequently associated with **Hypertrophic Osteoarthropathy (clubbing)** and Trousseau syndrome (migratory thrombophlebitis). **Analysis of Incorrect Options:** * **Option A:** While smoking increases the risk of all lung cancers, Adenocarcinoma is the most common subtype found in **non-smokers**. It has the weakest association with smoking compared to SCLC and SCC [2]. * **Option B:** Adenocarcinoma typically arises from the bronchial mucosal glands or alveolar epithelium in the **periphery** of the lung, often involving the pleura [1], [2]. * **Option C:** It is the most common histological subtype of lung cancer in **women** and young adults. **High-Yield NEET-PG Pearls:** * **Most Common:** Adenocarcinoma is now the most common type of lung cancer overall in both men and women. * **Driver Mutations:** Frequently associated with **EGFR** (especially in non-smoking Asian women), **ALK** rearrangements, and **KRAS** mutations [1], [4]. * **Precursor Lesion:** Atypical Adenomatous Hyperplasia (AAH) → Adenocarcinoma in situ (formerly Bronchioloalveolar carcinoma) → Invasive Adenocarcinoma [1]. * **Microscopy:** Characterized by gland formation and/or mucin production (detected by Mucin or PAS stains). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 335-336. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 336-337. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 338-339. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 725-727.

Question 143: Ciliocytophthoria is seen in which of the following conditions?

A. Kartagener syndrome
B. Situs inversus
C. Acute respiratory infection (Correct Answer)
D. Cystic fibrosis

Explanation: **Explanation:** **Ciliocytophthoria (CCP)** refers to a specific cytopathological change characterized by the **degeneration and fragmentation of ciliated columnar epithelial cells**. In this process, the apical portion of the cell (containing the cilia and a pyknotic nucleus or nuclear fragment) separates from the basal portion. 1. **Why "Acute Respiratory Infection" is correct:** CCP is most commonly associated with **viral respiratory infections**, particularly those caused by **Adenovirus**, Influenza, and Parainfluenza. The virus induces a cytopathic effect that leads to the tufting and detachment of the ciliated border. Recognizing CCP is clinically significant in sputum or bronchoalveolar lavage (BAL) cytology because it can be mistaken for protozoa (like *Balantidium coli*) or malignant cells, potentially leading to a misdiagnosis. 2. **Why other options are incorrect:** * **Kartagener Syndrome & Situs Inversus:** These are related to **Primary Ciliary Dyskinesia (PCD)**, which involves a structural/functional defect in the dynein arms of cilia. While the cilia are dysfunctional, they do not typically undergo the specific fragmentation (CCP) seen in acute viral insults. * **Cystic Fibrosis:** This is a genetic disorder affecting chloride channels (CFTR), leading to thick mucus and secondary chronic infections. While chronic inflammation occurs, CCP is not a hallmark diagnostic feature of this condition. **High-Yield Pearls for NEET-PG:** * **Key Association:** Adenovirus infection is the classic trigger for CCP. * **Morphology:** Look for "tufts" of cilia attached to a small rim of cytoplasm with a pyknotic nucleus. * **Differential Diagnosis:** Must be distinguished from *Lophomonas blattarum* (a multiflagellated protozoan) in respiratory samples. * **Clinical Context:** It is a non-specific marker of epithelial injury but strongly points toward a viral etiology in the respiratory tract.

Question 144: Which of the following types of asbestos is LEAST associated with mesothelioma?

A. Chrysolite
B. Crocidolite
C. Amosite (Correct Answer)
D. Tremolite

Explanation: **Explanation:** The association between asbestos and mesothelioma depends primarily on the physical structure and chemical composition of the fibers [1]. Asbestos fibers are classified into two main groups: **Serpentine** and **Amphibole**. 1. **Chrysolite (Serpentine):** These are curly, flexible fibers. Due to their shape, they are often trapped in the upper airways and cleared by the mucociliary escalator. They are more soluble and more easily removed from lung tissue, making them **least likely** to cause mesothelioma compared to the amphibole group. 2. **Amphiboles (Crocidolite, Amosite, Tremolite):** These are straight, stiff, needle-like fibers. Their aerodynamic properties allow them to penetrate deep into the distal airways and pleura. They are highly biopersistent and induce chronic inflammation and DNA damage. **Why the options are structured this way:** * **Crocidolite (Blue Asbestos):** This is the **most carcinogenic** form and has the strongest association with mesothelioma [1]. * **Amosite (Brown Asbestos):** A highly fibrogenic amphibole with a significant risk for both asbestosis and mesothelioma. * **Tremolite:** Often found as a contaminant in talc; it is an amphibole and highly associated with pleural plaques and malignancy. * **Chrysolite (White Asbestos):** This is the correct answer (Note: The provided key in the prompt marked Amosite, but standard pathology textbooks like **Robbins** state that **Chrysolite** is the least associated with mesothelioma due to its rapid clearance). **High-Yield NEET-PG Pearls:** * **Most common** asbestos-related lesion: **Pleural Plaques** (usually involving the parietal pleura) [1]. * **Most common** malignancy in asbestos workers: **Bronchogenic Carcinoma** (not mesothelioma). * **Synergistic effect:** Smoking increases the risk of lung cancer in asbestos workers by ~55-fold but does **not** increase the risk of mesothelioma. * **Ferruginous bodies:** Asbestos fibers coated with iron-containing protein (Prussian blue positive). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 697-698.

Question 145: Pleural calcification is found in all of the following conditions except?

A. Asbestosis
B. Hemothorax (Correct Answer)
C. Tuberculous pleural effusion
D. Coal workers' pneumoconiosis

Explanation: **Explanation:** Pleural calcification is a chronic sequela of persistent inflammation or mineral fiber deposition in the pleural space. **Why Hemothorax is the correct answer:** While a chronic, organized hemothorax (fibrothorax) can occasionally lead to calcification, it is **not** a classic or characteristic feature of an acute or standard hemothorax. In the context of NEET-PG questions, hemothorax is typically associated with acute trauma or hemorrhage, where the primary complication is organization into fibrous tissue rather than dystrophic calcification. **Analysis of Incorrect Options:** * **Asbestosis:** This is the most classic cause. Asbestos exposure leads to **pleural plaques**, which are well-circumscribed areas of dense collagen that frequently undergo calcification [1]. These are typically found on the parietal pleura and the domes of the diaphragm [3]. * **Tuberculous Pleural Effusion:** Chronic inflammation from TB (especially empyema necessitans) often results in extensive, "eggshell" or "plaster-like" calcification of the visceral pleura, often leading to restrictive lung patterns [2]. * **Coal Workers' Pneumoconiosis (CWP):** While CWP primarily affects the lung parenchyma, advanced stages (Progressive Massive Fibrosis) and associated silica exposure can lead to pleural thickening and secondary calcification. **High-Yield Clinical Pearls for NEET-PG:** * **Asbestos:** The most common manifestation of asbestos exposure is **pleural plaques**, but the most common malignancy is **Bronchogenic Carcinoma** (not Mesothelioma) [1]. * **Holly Leaf Sign:** This is the characteristic radiological appearance of calcified pleural plaques on a chest X-ray. * **Diaphragmatic Calcification:** If you see calcification on the diaphragmatic pleura, it is almost pathognomonic for **asbestos exposure** [1]. * **Dystrophic Calcification:** All pleural calcifications are examples of dystrophic calcification (occurs in damaged/necrotic tissue with normal serum calcium levels). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 699. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 698-699.

Question 146: A 46-year-old man presents with a year of increasing dyspnea and nonproductive cough. Physical examination reveals clubbing of digits and no fever. Pulmonary function tests show a mild restrictive abnormality and reduced DLCO. A transbronchial biopsy reveals numerous alveolar macrophages containing lamellar bodies and iron pigment, along with plump epithelial cells, mild interstitial fibrosis, and loss of respiratory bronchioles. What is the most likely etiology for his pulmonary disease?

A. Type I hypersensitivity
B. Cigarette smoking (Correct Answer)
C. Ciliary dyskinesia
D. Inhalation of mold spores

Explanation: This question describes a classic case of **Desquamative Interstitial Pneumonia (DIP)**, a smoking-related interstitial lung disease [1]. ### **Explanation of the Correct Answer** The key diagnostic feature is the accumulation of **"smoker’s macrophages"**—alveolar macrophages containing dusty brown iron pigment (hemosiderin) and **lamellar bodies** (surfactant-derived) within the alveolar spaces [1]. Clinical findings of progressive dyspnea, clubbing, and a restrictive pattern on PFTs with reduced DLCO are characteristic. DIP is almost exclusively seen in **cigarette smokers** (90% of cases) [1]. The "desquamative" name is a historical misnomer; the cells filling the alveoli are macrophages, not desquamated epithelial cells [1]. ### **Why Other Options are Incorrect** * **A. Type I Hypersensitivity:** This is associated with Asthma, characterized by eosinophils, Charcot-Leyden crystals, and Curschmann spirals, rather than pigmented macrophages and fibrosis. * **C. Ciliary Dyskinesia:** This leads to Kartagener syndrome, presenting with bronchiectasis, sinusitis, and situs inversus. It does not typically present with interstitial macrophage accumulation. * **D. Inhalation of mold spores:** This causes Hypersensitivity Pneumonitis (Type III/IV reaction). Histology would show poorly formed non-caseating granulomas and patchy mononuclear interstitial infiltrates, not diffuse pigmented macrophages. ### **NEET-PG High-Yield Pearls** * **Smoking-Related ILDs:** Include DIP and **Respiratory Bronchiolitis-Associated Interstitial Lung Disease (RB-ILD)**. The main difference is that RB-ILD is patchy/bronchiolocentric, while DIP is diffuse. * **Histology Keyword:** "Smoker's macrophages" (brown-pigmented) are the hallmark [1]. * **Prognosis:** DIP has an excellent prognosis with smoking cessation and steroid therapy, unlike Idiopathic Pulmonary Fibrosis (UIP). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 702-703.

Question 147: Which of the following histopathological findings is most commonly associated with COVID-19?

A. Pulmonary fibrosis
B. Massive pulmonary hemorrhage
C. Diffuse alveolar damage (Correct Answer)
D. Changes of pulmonary arterial hypertension

Explanation: **Explanation:** **Diffuse Alveolar Damage (DAD)** is the hallmark histopathological finding of **Acute Respiratory Distress Syndrome (ARDS)**, which is the primary cause of respiratory failure in severe COVID-19 [1]. 1. **Why DAD is correct:** COVID-19-associated DAD typically progresses through two phases: * **Exudative Phase:** Characterized by capillary congestion, intra-alveolar edema, and the formation of **hyaline membranes** (composed of fibrin and cell debris) lining the alveolar walls [1]. * **Proliferative/Organizing Phase:** Involves the proliferation of Type II pneumocytes and fibroblasts as the lung attempts to repair the damage [1]. 2. **Analysis of Incorrect Options:** * **Pulmonary Fibrosis (A):** While fibrosis can occur as a late-stage sequela (post-COVID lung disease) due to persistent organizing pneumonia, it is a complication rather than the primary acute histopathological feature. * **Massive Pulmonary Hemorrhage (B):** Though micro-hemorrhages and focal intra-alveolar hemorrhage are seen due to coagulopathy, "massive" hemorrhage is not a characteristic or defining feature of COVID-19 pathology. * **Pulmonary Arterial Hypertension (D):** While COVID-19 causes significant endothelial dysfunction and microthrombi (immunothrombosis), chronic changes of PAH (like plexiform lesions) are not acute findings of the infection. **High-Yield Clinical Pearls for NEET-PG:** * **Key Microscopic Feature:** Hyaline membranes [1]. * **Vascular Findings:** COVID-19 is unique for its high incidence of **microvascular thrombi** and **intussusceptive angiogenesis** compared to Influenza. * **Cytopathic Effect:** Multinucleated giant cells (syncytial cells) and prominent nucleoli in pneumocytes are often noted. * **Receptor:** SARS-CoV-2 enters via the **ACE2 receptor**, which is highly expressed on Type II pneumocytes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 679-681.

Question 148: Hyaline membrane disease is associated with which of the following conditions?

A. Respiratory distress syndrome (Correct Answer)
B. Bronchopulmonary dysplasia
C. Sudden infant death syndrome
D. Bronchiolitis obliterans

Explanation: **Explanation:** **Hyaline Membrane Disease (HMD)**, also known as **Infant Respiratory Distress Syndrome (IRDS)**, is the primary cause of respiratory distress in preterm infants [1]. **1. Why Option A is Correct:** The core pathology of HMD is a **deficiency of pulmonary surfactant** (produced by Type II pneumocytes) [1]. Surfactant normally reduces surface tension; its absence leads to widespread alveolar collapse (atelectasis) [2]. This results in hypoxia and endothelial damage, causing a protein-rich fluid to leak into the alveolar spaces. This exudate clots into a fibrin-rich, eosinophilic membrane—the **"Hyaline Membrane"**—which further impairs gas exchange [3]. **2. Why Other Options are Incorrect:** * **B. Bronchopulmonary Dysplasia (BPD):** This is a *complication* of HMD and its treatment (prolonged oxygen therapy/ventilation). It is characterized by alveolar hypoplasia rather than the acute formation of hyaline membranes. * **C. Sudden Infant Death Syndrome (SIDS):** This is the unexplained death of an infant under one year of age. While its etiology is multifactorial (e.g., sleeping position), it is not pathologically defined by hyaline membranes. * **D. Bronchiolitis Obliterans:** This involves the fibrotic occlusion of the bronchioles, often seen in post-transplant rejection or toxic inhalations, not neonatal surfactant deficiency. **Clinical Pearls for NEET-PG:** * **Risk Factors:** Prematurity (most common), Maternal Diabetes (insulin inhibits surfactant synthesis), and Cesarean section (lack of "vaginal squeeze" stress which triggers cortisol/surfactant release). * **L/S Ratio:** A Lecithin-to-Sphingomyelin ratio of **<2:1** in amniotic fluid indicates fetal lung immaturity. * **X-ray Finding:** Characterized by a diffuse **"Ground Glass Appearance"** and air bronchograms. * **Treatment:** Antenatal corticosteroids (e.g., Betamethasone) to the mother and postnatal exogenous surfactant to the neonate [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 464-466. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, p. 466. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 313-314.

Question 149: Which of the following morphological changes in the lungs would be found in a patient of asthma?

A. Destruction and dilation of the bronchi and bronchioles
B. Free air in the interstitium
C. Viscid mucus plugs in the small airways (Correct Answer)
D. Peribronchiolar fibrosis

Explanation: **Explanation:** **Correct Answer: C. Viscid mucus plugs in the small airways** Bronchial asthma is a chronic inflammatory disorder of the airways characterized by reversible bronchoconstriction [1]. The hallmark gross morphological finding in a patient who dies of status asthmaticus is the presence of **thick, tenacious, viscid mucus plugs** that occlude the lumens of the bronchi and bronchioles [1]. These plugs contain shed epithelium, eosinophils, and spiral-shaped mucus strands known as **Curschmann spirals**. **Analysis of Incorrect Options:** * **A. Destruction and dilation of the bronchi and bronchioles:** This describes **Bronchiectasis**, a permanent dilation caused by chronic necrotizing infections. In asthma, the airway wall is thickened, not destroyed. * **B. Free air in the interstitium:** This refers to **Interstitial Emphysema**, which occurs when air enters the connective tissue stroma of the lung, often due to alveolar rupture. * **D. Peribronchiolar fibrosis:** While "airway remodeling" in asthma involves subepithelial fibrosis (thickening of the basement membrane), extensive peribronchiolar fibrosis is more characteristic of **Bronchiolitis Obliterans** or chronic interstitial lung diseases. **High-Yield NEET-PG Pearls:** * **Microscopic Findings (The "Asthma Triad"):** 1. **Curschmann Spirals:** Whorled mucus plugs. 2. **Charcot-Leyden Crystals:** Eosinophil-derived galectin-10 (diamond-shaped). 3. **Creola Bodies:** Clusters of exfoliated bronchial epithelial cells. * **Airway Remodeling:** Includes hypertrophy of bronchial smooth muscle, hyperplasia of goblet cells, and **thickening of the subepithelial basement membrane** (Type I and III collagen). * **Key Cytokines:** Th2-mediated response involving **IL-4** (IgE isotype switching), **IL-5** (eosinophil activation), and **IL-13** (mucus production) [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 328-329. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689.

Question 150: Miliary tuberculosis is classified as:

A. Primary tuberculosis
B. Post-primary tuberculosis (Correct Answer)
C. Extra-pulmonary tuberculosis
D. None of the above

Explanation: **Explanation:** Miliary tuberculosis (TB) refers to the hematogenous dissemination of *Mycobacterium tuberculosis*, resulting in tiny, millet-sized (1-2 mm) granulomatous lesions throughout various organs [1]. **Why Post-primary TB is correct:** While hematogenous spread can occur during primary infection in immunocompromised individuals, miliary TB is classically categorized under **Post-primary (Secondary) tuberculosis**. It occurs due to the reactivation of a latent focus or a fresh re-infection in a previously sensitized host. The erosion of a necrotic granuloma into a blood vessel or lymphatic duct allows the bacilli to enter the systemic circulation, leading to widespread "miliary" seeding [1]. In adults, this is most commonly a feature of secondary TB when host immunity fails to contain the infection. **Analysis of Incorrect Options:** * **A. Primary Tuberculosis:** This is the initial infection in a non-sensitized host, typically characterized by the Ghon Complex. While "progressive primary TB" can lead to dissemination, the term miliary TB is more synonymous with the complications of the secondary stage in standard pathology curricula [1]. * **C. Extra-pulmonary Tuberculosis:** While miliary TB involves extra-pulmonary organs (liver, spleen, bone marrow), it is a **systemic** manifestation that frequently involves the lungs simultaneously. It is a pattern of spread rather than a localized extra-pulmonary site (like TB lymphadenitis or Pott’s disease). **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** The "millet seed" appearance is due to small, firm, grey-white sub-millimetric tubercles [2]. * **Most common site:** The **Lungs** are the most common site for miliary TB (miliary pulmonary TB), followed by the liver, spleen, and bone marrow [1]. * **Microscopy:** Look for epithelioid granulomas with central caseous necrosis and Langhans giant cells [2]. * **Clinical sign:** Choroid tubercles on fundoscopy are pathognomonic for miliary TB. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384.

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Lung Tumors

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Pleural Diseases

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Interstitial Lung Diseases

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Occupational Lung Diseases

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