Respiratory Pathology — MCQs

Respiratory Pathology Indian Medical PG Practice Questions and MCQs

Question 71: Pleural fibroma is differentiated from mesothelioma by the presence of which of the following markers in the former?

A. CD14
B. CD24
C. Cytokeratin (Correct Answer)
D. ERBB2 positive

Explanation: **Explanation:** The differentiation between **Pleural Fibroma** (also known as Solitary Fibrous Tumor - SFT) and **Malignant Mesothelioma** is a classic high-yield pathology topic. [1] **1. Why Cytokeratin is the correct answer:** The primary distinction lies in the cell of origin. **Mesothelioma** arises from mesothelial cells, which are epithelial-like and strongly express **Cytokeratin** (CK) [2]. In contrast, **Pleural Fibroma** (SFT) is a mesenchymal tumor arising from submesothelial fibroblasts [1]. Therefore, Pleural Fibroma is typically **Cytokeratin negative**, while Mesothelioma is **Cytokeratin positive**. *(Note: The question asks for the marker used to differentiate them; the absence of CK in SFT vs. its presence in Mesothelioma is the diagnostic gold standard.)* **2. Analysis of Incorrect Options:** * **CD14:** This is a marker primarily for monocytes and macrophages; it has no diagnostic utility in pleural tumors. * **CD24:** This is a cell adhesion molecule used in some breast and ovarian cancer studies but is not a standard marker for pleural pathology. * **ERBB2 (HER2/neu):** This is a growth factor receptor commonly associated with breast and gastric adenocarcinomas, not used to differentiate SFT from mesothelioma. **3. Clinical Pearls for NEET-PG:** * **SFT Marker:** The most specific and sensitive modern marker for Solitary Fibrous Tumor (Pleural Fibroma) is **STAT6** (due to the NAB2-STAT6 gene fusion). It is also **CD34 positive**. [1] * **Mesothelioma Markers:** Positive for **Calretinin**, **WT-1**, and **Cytokeratin 5/6**. [2] * **Clinical Association:** Pleural Fibroma is famously associated with **Doege-Potter Syndrome** (paraneoplastic hypoglycemia due to secretion of IGF-2). Unlike mesothelioma, it is **not** related to asbestos exposure. [1] **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 339-340. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 731.

Question 72: What is the most common termination of lobar pneumonia?

A. Consolidation
B. Resolution (Correct Answer)
C. Abscess formation
D. Empyema

Explanation: **Explanation:** **Lobar pneumonia** is characterized by an acute bacterial infection (most commonly *Streptococcus pneumoniae*) that involves a large portion of a lobe or an entire lobe of the lung [1]. **1. Why Resolution is the correct answer:** In the majority of cases (approximately 90%), especially with appropriate antibiotic therapy, the inflammatory exudate within the alveolar spaces undergoes enzymatic digestion by neutrophil-derived enzymes and macrophage activity [5]. This process, known as **Resolution**, restores the lung parenchyma to its normal structural and functional state without permanent scarring [4]. It is the most common and favorable outcome [1]. **2. Analysis of Incorrect Options:** * **Consolidation (A):** This is not a termination but rather a **stage** of the disease process (specifically the stages of Red and Gray Hepatization) where the air spaces are filled with exudate, making the lung tissue firm and liver-like [3]. * **Abscess formation (C):** This is a **complication** occurring due to localized tissue destruction and necrosis, often associated with more virulent organisms like *Staphylococcus aureus* or *Klebsiella* [2]. * **Empyema (D):** This refers to the spread of infection to the pleural cavity, resulting in a purulent pleural effusion [4]. It is a serious complication, not the standard termination. **High-Yield Clinical Pearls for NEET-PG:** * **Stages of Lobar Pneumonia:** Congestion (Day 1-2) → Red Hepatization (Day 3-4) → Gray Hepatization (Day 5-7) → **Resolution (Day 8+).** [1] * **Organization:** If the exudate is not resolved, it may undergo "organization," where fibroblasts grow into the exudate, converting it into permanent fibrous tissue (carnification) [4]. * **Most common cause:** *Streptococcus pneumoniae* (Pneumococcus) is responsible for 90-95% of lobar pneumonia cases. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 711-712. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 715. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 194-195. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 193-194.

Question 73: What is true about alpha-1 antitrypsin deficiency?

A. It is an autosomal dominant condition.
B. It can lead to pulmonary emphysema. (Correct Answer)
C. It makes hepatic cells resistant to disease.
D. Hepatic cells are orcein stain positive in this condition.

Explanation: ### Explanation **1. Why Option B is Correct:** Alpha-1 Antitrypsin (AAT) is a serum glycoprotein synthesized in the liver [1] that acts as a major **protease inhibitor**. Its primary role is to inhibit **Neutrophil Elastase** [2], an enzyme capable of digesting alveolar elastic fibers. In AAT deficiency, the lack of this "protective shield" allows elastase to cause unchecked destruction of the alveolar walls, leading to **Panacinar Emphysema** [3]. This typically presents in young patients and is more severe in the lower lobes. **2. Why Other Options are Incorrect:** * **Option A:** AAT deficiency is an **Autosomal Codominant** condition (often described as recessive in context of phenotypic expression) [1]. The most common normal allele is *PiM*, while the most common deficiency allele is *PiZ* [2]. Homozygotes (*PiZZ*) have the highest risk of disease. * **Option C:** It does not make hepatic cells resistant; rather, it causes **Liver Cirrhosis** and Hepatocellular Carcinoma [1]. The misfolded mutant protein (Z-variant) cannot be secreted and accumulates within the endoplasmic reticulum of hepatocytes, causing toxic injury. * **Option D:** While hepatic cells show characteristic inclusions, they are **PAS-positive and Diastase-resistant**. Orcein stain is typically used to identify HBsAg in Hepatitis B or copper-binding proteins, not AAT globules. **3. High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Gene located on **Chromosome 14** [1]. * **Morphology:** Characteristic **round-to-oval acidophilic cytoplasmic globules** in hepatocytes. * **Emphysema Pattern:** **Panacinar** (affects the entire acinus), unlike smoking-related emphysema which is Centriacinar [3]. * **Diagnosis:** Low serum AAT levels and phenotype testing (Isoelectric focusing). * **Clinical Triad:** Young age + Non-smoker + Lower lobe emphysema = Think AAT deficiency. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 856-858. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 683-684. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 684-685.

Question 74: Alpha-1 antitrypsin deficiency is associated with which type of emphysema?

A. Panacinar emphysema (Correct Answer)
B. Centriacinar emphysema
C. Paraseptal emphysema
D. Irregular emphysema

Explanation: **Explanation:** **Alpha-1 Antitrypsin (AAT) Deficiency** is a genetic disorder characterized by a lack of the protease inhibitor AAT, which normally neutralizes **neutrophil elastase** [2], [3]. Without AAT, elastase unchecked destroys the alveolar walls [1]. 1. **Why Panacinar Emphysema is Correct:** In AAT deficiency, the lack of protective enzymes is systemic, affecting the entire secondary pulmonary lobule uniformly. This leads to **Panacinar (or Panlobular) emphysema** [1], [3], where there is permanent enlargement of airspaces from the respiratory bronchiole to the terminal blind alveoli [4]. It characteristically involves the **lower lobes** of the lungs because of higher perfusion in these areas. 2. **Why Other Options are Incorrect:** * **Centriacinar Emphysema:** This is the most common type and is strongly associated with **cigarette smoking** [1]. It primarily affects the central/proximal parts of the acini (respiratory bronchioles) while sparing distal alveoli [4]. It typically involves the **upper lobes**. * **Paraseptal Emphysema:** This involves the distal part of the acinus near the pleura and connective tissue septa [4]. It is a common cause of **spontaneous pneumothorax** in young adults [4]. * **Irregular Emphysema:** This is associated with **scarring** (healed inflammatory diseases) and is usually asymptomatic [4]. **NEET-PG High-Yield Pearls:** * **Genetics:** AAT deficiency is caused by mutations in the **SERPINA1 gene** (Chromosome 14). The most severe phenotype is **PiZZ** [3]. * **Liver Involvement:** AAT deficiency also causes **liver cirrhosis** due to the accumulation of misfolded AAT proteins in hepatocytes, which appear as **PAS-positive, diastase-resistant globules** [2]. * **Radiology:** Look for "hyperlucency at the lung bases" on a chest X-ray to differentiate AAT deficiency from smoking-related emphysema. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 684-685. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 856-858. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 683-684. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 683.

Question 75: A lung section from an autopsy of an AIDS patient with a CD4 count less than 100/mm³ shows desquamation of type 1 pneumocytes with prominent intranuclear basophilic inclusion bodies surrounded by a clear halo. What is the most likely diagnosis causing these features?

A. Acute respiratory distress syndrome
B. Pneumocystis jirovecii pneumonia
C. CMV pneumonia (Correct Answer)
D. Mycobacterium avium-intracellulare pneumonia

Explanation: The clinical presentation and histopathology point directly to **Cytomegalovirus (CMV) pneumonia**, a common opportunistic infection in immunocompromised patients (especially those with AIDS and CD4 counts <50–100/mm³). **1. Why CMV Pneumonia is correct:** The hallmark of CMV infection is the presence of **"Owl’s eye" inclusion bodies**. These are large, dark, basophilic intranuclear inclusions surrounded by a clear halo (perinuclear clearing). CMV causes massive enlargement of both the nucleus and the entire cell (cytomegaly). It typically infects alveolar macrophages, endothelial cells, and type 1 pneumocytes, leading to desquamation and interstitial inflammation. **2. Why other options are incorrect:** * **Acute Respiratory Distress Syndrome (ARDS):** Characterized by the formation of waxy **hyaline membranes** lining the alveolar walls, not specific viral inclusions. * **Pneumocystis jirovecii pneumonia (PCP):** Shows a characteristic **"crushed strawberry" or "cotton candy"** intra-alveolar foamy exudate [1]. On Silver stain (GMS), it reveals cup-shaped or boat-shaped cysts [1]. * **Mycobacterium avium-intracellulare (MAC):** Typically presents with granulomatous inflammation (often poorly formed in AIDS) and contains numerous **acid-fast bacilli (AFB)** within macrophages. It does not produce large nuclear inclusions. **High-Yield Clinical Pearls for NEET-PG:** * **CMV Inclusions:** Can be intranuclear (Owl's eye) AND intracytoplasmic (basophilic). * **Target Organs in AIDS:** CMV most commonly causes **retinitis** (pizza-pie appearance), followed by colitis and pneumonitis. * **Diagnosis:** While histopathology is classic, PCR and viral culture are used for definitive diagnosis [2]. * **Treatment:** Ganciclovir is the drug of choice. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 318-319. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 260-261.

Question 76: All of the following statements are true regarding the histological features of emphysema, except?

A. There is loss of attachments of the alveoli to the outer wall of small airways.
B. The pores of Kohn become narrower and obstructed. (Correct Answer)
C. It causes a decrease in the capillary bed area.
D. There are large abnormal airspaces, blebs, and bullae.

Explanation: **Explanation:** Emphysema is characterized by the **permanent, abnormal enlargement** of airspaces distal to the terminal bronchioles [1], accompanied by the destruction of their walls without significant fibrosis [2]. **Why Option B is the correct answer (The False Statement):** In emphysema, the destruction of alveolar septa actually causes the **Pores of Kohn to enlarge and coalesce**, rather than becoming narrow or obstructed. These pores are openings in the alveolar walls that allow collateral ventilation; as the septal tissue is destroyed by proteases (like elastase) [1], these openings expand, eventually leading to the formation of large, confluent airspaces. **Analysis of other options:** * **Option A:** Emphysema involves the destruction of elastic tissue. This leads to the **loss of radial traction** (loss of alveolar attachments to the outer walls of small airways), causing these airways to collapse during expiration, leading to air trapping. * **Option C:** As the alveolar walls are destroyed, the **capillary bed area decreases** significantly [2]. This reduction in the surface area for gas exchange contributes to ventilation-perfusion mismatch and can eventually lead to pulmonary hypertension. * **Option D:** The coalescence of destroyed alveoli results in **large abnormal airspaces** [3]. When these occur subpleurally and are >1 cm in diameter, they are termed **bullae** or **blebs** [2], which can rupture and cause spontaneous pneumothorax [3]. **High-Yield NEET-PG Pearls:** * **Panacinar Emphysema:** Associated with **$\alpha$1-antitrypsin deficiency** [1]; involves the lower lobes. * **Centriacinar Emphysema:** Most common type in **smokers** [1]; involves the upper lobes (specifically the respiratory bronchioles). * **Pathogenesis:** Driven by the **Protease-Antiprotease imbalance** [1] and Oxidant-Antioxidant imbalance. * **Morphology:** Characterized by "voluminous lungs" that overlap the heart. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 683-685. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 326-328. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 683.

Question 77: In a patient of mesothelioma, what is often found?

A. Hypoglycaemia
B. An association with asbestosis
C. Haemorrhagic pleural effusion
D. All of the above (Correct Answer)

Explanation: **Explanation:** Malignant Mesothelioma is a rare neoplasm of the mesothelial cells, most commonly involving the pleura [2]. The correct answer is **"All of the above"** due to the following clinico-pathological features: 1. **Association with Asbestosis (Option B):** Asbestos exposure is the primary risk factor, present in up to 90% of cases [2]. While it is linked to asbestos exposure, it is important to note that unlike bronchogenic carcinoma, smoking does *not* increase the risk of mesothelioma. 2. **Haemorrhagic Pleural Effusion (Option C):** This is the most common clinical presentation. The tumor spreads widely over the pleural surface, often encasing the lung in a thick "rind" of tumor tissue. This leads to the accumulation of bloody (haemorrhagic) fluid in the pleural space [1]. 3. **Hypoglycaemia (Option A):** This is a recognized **paraneoplastic syndrome** associated with large mesenchymal tumors and mesotheliomas. It is caused by the secretion of **IGF-2 (Insulin-like Growth Factor 2)**, also known as "Non-Islet Cell Tumor Hypoglycemia" (NICTH). **High-Yield Facts for NEET-PG:** * **Latent Period:** Long interval (25–40 years) between asbestos exposure and tumor development [2]. * **Gross Appearance:** Diffuse pleural thickening forming a firm, grayish-white "rind." * **Microscopy:** Can be Epithelioid (most common), Sarcomatoid, or Biphasic. * **Immunohistochemistry (IHC):** Positive for **Calretinin** (most specific), WT-1, and Cytokeratin 5/6. It is negative for CEA (which helps differentiate it from Adenocarcinoma). * **Electron Microscopy:** Characterized by **long, slender microvilli**. **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. 339-340.

Question 78: The Reid index is increased in which of the following conditions?

A. Chronic bronchitis (Correct Answer)
B. Emphysema
C. Bronchiectasis
D. ARDS

Explanation: **Explanation:** **Reid Index** is a pathological measurement used to assess the severity of **Chronic Bronchitis**. It is defined as the ratio of the thickness of the submucosal mucus-secreting glands to the total thickness of the bronchial wall (measured from the epithelium to the inner surface of the cartilage). 1. **Why Chronic Bronchitis is correct:** In chronic bronchitis, chronic irritation (usually from smoking) leads to **hypertrophy and hyperplasia of the submucosal mucous glands** in the trachea and bronchi [1]. This increases the numerator of the ratio. A Reid Index **> 0.4** (normal is < 0.4) is diagnostic of chronic bronchitis. 2. **Why other options are incorrect:** * **Emphysema:** This involves the permanent enlargement of airspaces distal to the terminal bronchioles due to alveolar wall destruction, not glandular hypertrophy [2]. * **Bronchiectasis:** This is characterized by permanent dilation of bronchi and bronchioles due to destruction of muscle and elastic tissue, typically following chronic necrotizing infections. * **ARDS:** This is an acute condition characterized by diffuse alveolar damage (DAD) and hyaline membrane formation, involving the alveolar-capillary unit rather than bronchial glandular changes. **High-Yield Clinical Pearls for NEET-PG:** * **Normal Reid Index:** < 0.4 (or 1:3). * **Chronic Bronchitis Definition:** Clinical diagnosis based on a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years [1]. * **Location:** The Reid Index is measured in the **bronchi**, as bronchioles lack submucosal glands and cartilage. * **Key Histology:** Increased Goblet cell density in small airways is also a feature of chronic bronchitis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 681-686. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 326-327.

Question 79: Emphysema is associated with a deficiency of which of the following?

A. Trypsin
B. Trypsinogen
C. Bradykinin
D. Alpha-1 Anti-trypsin (Correct Answer)

Explanation: **Explanation:** **Emphysema** is a chronic obstructive pulmonary disease (COPD) characterized by the permanent enlargement of airspaces distal to the terminal bronchioles due to the destruction of alveolar walls [3], [4]. **Why Option D is Correct:** The pathogenesis of emphysema is primarily explained by the **Protease-Antiprotease Hypothesis** [1]. Normally, neutrophils and macrophages in the lungs release **elastase** (a protease) that can digest lung tissue. **Alpha-1 Anti-trypsin (AAT)** is a serum glycoprotein (produced in the liver) that acts as a major inhibitor of these proteases, particularly neutrophil elastase [1], [2]. A deficiency in AAT—whether genetic or acquired (e.g., via smoking, which inactivates AAT)—leads to unchecked elastic tissue destruction, resulting in the loss of alveolar recoil and emphysema [1]. **Why Incorrect Options are Wrong:** * **A & B (Trypsin/Trypsinogen):** Trypsin is a pancreatic digestive enzyme. While AAT inhibits trypsin in vitro (hence the name), its primary physiological role in the lung is inhibiting **elastase** [1], [2]. A deficiency of trypsin itself does not cause lung disease. * **C (Bradykinin):** This is a vasodilator peptide involved in inflammation and blood pressure regulation. It is inactivated by ACE (Angiotensin-Converting Enzyme), and its accumulation is associated with the dry cough seen with ACE inhibitors, not emphysema. **NEET-PG High-Yield Pearls:** * **Genetic Association:** AAT deficiency is linked to the **PiZZ genotype** (most severe) [1]. * **Morphology:** Genetic AAT deficiency typically causes **Panacinar emphysema** (lower lobes), whereas smoking typically causes **Centriacinar emphysema** (upper lobes) [3]. * **Liver Involvement:** In genetic deficiency, misfolded AAT proteins accumulate in the liver, appearing as **PAS-positive, diastase-resistant globules**, which can lead to cirrhosis [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 683-684. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 856-858. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 684-685. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 326-327.

Question 80: A 45-year-old coal mine worker presents with cutaneous nodules, joint pain, and occasional cough with dyspnea. His chest radiograph shows multiple small (1-4 cm) nodules in bilateral lung fields. Some of the nodules show cavitation and specks of calcification. What is the most likely diagnosis?

A. Sjogren's syndrome
B. Caplan's syndrome (Correct Answer)
C. Silicosis
D. Wegener's granulomatosis

Explanation: ### Explanation **Correct Answer: B. Caplan’s Syndrome** **Why it is correct:** Caplan’s syndrome (also known as rheumatoid pneumoconiosis) is the combination of **Rheumatoid Arthritis (RA)** and **Pneumoconiosis** (most commonly Coal Worker’s Pneumoconiosis) [2]. * **Clinical Presentation:** The patient exhibits systemic features of RA (joint pain, cutaneous rheumatoid nodules) alongside occupational exposure (coal mining) [1]. * **Radiological Features:** It is characterized by the sudden appearance of multiple, well-defined, bilateral "Caplan nodules" (1–5 cm in diameter) in the lung periphery. These nodules may undergo **cavitation** or **calcification**, distinguishing them from simple coal macules. **Why the other options are incorrect:** * **A. Sjogren’s Syndrome:** While associated with RA, it primarily presents with sicca symptoms (dry eyes/mouth) [1]. It does not typically cause large cavitating lung nodules in coal workers. * **C. Silicosis:** Though silicosis presents with nodules and eggshell calcification, it does not explain the **joint pain and cutaneous nodules** (extrapulmonary RA manifestations) described in the stem. * **D. Wegener’s Granulomatosis (GPA):** While GPA causes cavitating lung nodules, it is a systemic vasculitis usually involving the upper respiratory tract (sinusitis) and kidneys (glomerulonephritis), unrelated to coal dust exposure. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of Caplan Syndrome:** Rheumatoid Arthritis + Pneumoconiosis + Multiple peripheral lung nodules [2]. * **Pathology:** Histologically, Caplan nodules resemble rheumatoid nodules but have a peripheral zone of inflammation containing dust-laden macrophages. * **Association:** Most common in coal miners, but can also occur in silicosis and asbestosis. * **Progression:** The lung nodules often appear rapidly and can precede the onset of clinical arthritis [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 678-679. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 333-334.

Practice by Chapter

Congenital Anomalies

Practice Questions

Atelectasis and Acute Lung Injury

Practice Questions

Obstructive Pulmonary Diseases

Practice Questions

Restrictive Pulmonary Diseases

Practice Questions

Lung Infections

Practice Questions

Pulmonary Vascular Diseases

Practice Questions

Lung Tumors

Practice Questions

Pleural Diseases

Practice Questions

Interstitial Lung Diseases

Practice Questions

Occupational Lung Diseases

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free