Respiratory Pathology — MCQs

A 53-year-old man presents with weakness, malaise, cough with bloody sputum, and night sweats. A chest X-ray shows bilateral apical densities, some cavitary. The patient has a history of documented exposure to Mycobacterium tuberculosis 20 years ago, and M. tuberculosis has been identified in his sputum. Which of the following best describes the expected lung pathology in this patient?

Q309Medium

What pathological findings are revealed in status asthmaticus?

Q310Easy

Carcinoma of the lung is associated with exposure to which of the following?

Respiratory Pathology Indian Medical PG Practice Questions and MCQs

Question 301: Emphysema is due to deficiency of?

A. Tumor necrosis factor
B. Prostaglandins
C. Leukotrienes
D. Alpha-1 antitrypsin (Correct Answer)

Explanation: The correct answer is **Alpha-1 antitrypsin (AAT)**. Emphysema is characterized by the permanent enlargement of airspaces distal to the terminal bronchioles due to the destruction of alveolar walls [3]. **1. Why Alpha-1 Antitrypsin is correct:** The pathogenesis of emphysema is best explained by the **Protease-Antiprotease Hypothesis**. Normally, neutrophils in the lung release **Neutrophil Elastase**, a potent protease that digests elastin in alveolar walls. Alpha-1 antitrypsin is a major serum protein (an antielastase) produced by the liver that inhibits this enzyme [1]. A deficiency in AAT—either genetic or acquired (smoking inactivates AAT)—leads to an imbalance where unchecked elastase destroys the lung parenchyma, resulting in emphysema [1][2]. **2. Why other options are incorrect:** * **A. Tumor Necrosis Factor (TNF):** This is a pro-inflammatory cytokine. While it plays a role in chronic inflammation, its deficiency does not cause emphysema; rather, its excess is often associated with systemic symptoms of COPD. * **B & C. Prostaglandins and Leukotrienes:** These are arachidonic acid metabolites. While leukotrienes (especially LTB4) are chemotactic for neutrophils, their deficiency is not the primary cause of the structural destruction seen in emphysema. **Clinical Pearls for NEET-PG:** * **Genetic Locus:** The AAT gene (SERPINA1) is located on **Chromosome 14** [1][2]. * **Phenotypes:** **PiMM** is normal; **PiZZ** is the most severe deficiency state associated with panacinar emphysema and liver cirrhosis [1]. * **Morphology:** AAT deficiency typically causes **Panacinar emphysema** (lower lobes), whereas smoking typically causes **Centriacinar emphysema** (upper lobes) [3]. * **Histology:** In the liver, AAT deficiency shows **PAS-positive, diastase-resistant globules** within hepatocytes. **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.

Question 302: Inhalation of asbestos particles of 15 micrometers will cause which of the following?

A. Mesothelioma (Correct Answer)
B. Carcinoma of the liver
C. Carcinoma of the larynx
D. Carcinoma of the colon

Explanation: **Explanation:** The correct answer is **Mesothelioma (Option A)**. **Pathophysiology and Mechanism:** Asbestos fibers are categorized into two types: **Serpentine** (curly) and **Amphibole** (straight/needle-like). While serpentine fibers are more common, amphibole fibers are more pathogenic because they are aerodynamic and can penetrate deep into the distal airways. [1] Fibers measuring **>10–15 μm** in length are particularly significant. While smaller particles are often cleared by alveolar macrophages, longer fibers cannot be fully ingested (frustrated phagocytosis). This leads to the chronic release of pro-inflammatory cytokines and reactive oxygen species, causing DNA damage. These long fibers reach the **pleural space** via lymphatic drainage, where they induce chronic inflammation and malignant transformation of mesothelial cells, leading to **Mesothelioma**. [1] **Analysis of Incorrect Options:** * **Option B (Liver):** There is no established causal link between asbestos inhalation and hepatic malignancy. * **Option C & D (Larynx and Colon):** While some epidemiological studies suggest a slight increase in the risk of laryngeal and gastrointestinal cancers in asbestos-exposed workers, **Mesothelioma** (and Bronchogenic Carcinoma) remains the classic, high-yield association tested in exams. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Malignancy:** Although Mesothelioma is the most *specific* cancer associated with asbestos, **Bronchogenic Carcinoma** is actually the *most common* cancer in asbestos-exposed individuals. [1] * **Synergy:** Smoking does **not** increase the risk of Mesothelioma, but it has a **multiplicative effect** on the risk of Bronchogenic Carcinoma in asbestos workers. * **Marker:** The presence of **Ferruginous bodies** (asbestos bodies coated with iron-containing protein) in the lungs is a hallmark of exposure. [1] * **Latency:** Mesothelioma has a long latency period, often appearing **20–40 years** after initial exposure. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 695-699.

Question 303: Charcot-Leyden crystals are derived from which cell type?

A. Eosinophils (Correct Answer)
B. Basophils
C. Bronchial goblet cells
D. Mast cells

Explanation: **Explanation:** **Charcot-Leyden crystals** are hallmark microscopic findings in conditions characterized by eosinophilic inflammation, most notably **Bronchial Asthma**, allergic rhinitis, and certain parasitic infections. [1] 1. **Why Eosinophils are correct:** These crystals are composed of **Galectin-10**, a protein that makes up nearly 7–10% of the total cellular protein in eosinophils. When eosinophils degranulate and undergo lysis (eosinoptosis) at the site of inflammation, the released Galectin-10 molecules aggregate and crystallize into the characteristic hexagonal, bipyramidal, needle-like shapes known as Charcot-Leyden crystals. 2. **Why other options are incorrect:** * **Basophils:** While basophils contain some Galectin-10, they are present in much smaller numbers in respiratory secretions compared to eosinophils and are not the primary source of these crystals. * **Bronchial goblet cells:** These cells are responsible for mucus production (hyperplasia leads to Curschmann spirals), not crystal formation. * **Mast cells:** These cells release histamine and leukotrienes during Type I hypersensitivity but do not contain the Galectin-10 protein required to form these specific crystals. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Hexagonal, bipyramidal, "needle-shaped" crystals. * **Associated Finding:** Often seen alongside **Curschmann spirals** (coiled mucus plugs) and **Creola bodies** (ciliated columnar epithelial clusters) in the sputum of asthmatic patients. * **Biochemical Marker:** Remember the protein **Galectin-10** (formerly known as lysophospholipase). * **Staining:** They stain purplish-red with Romanowsky stains. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689.

Question 304: Which of the following is a marker for small cell carcinoma of the lung?

A. Chromogranin (Correct Answer)
B. Cytokeratin
C. Dermin
D. Vimentin

Explanation: **Explanation:** **Small Cell Carcinoma (SCLC)** is a highly aggressive, high-grade neuroendocrine tumor of the lung [2]. Because it originates from neuroendocrine cells (Kulchitsky cells), it expresses specific markers associated with neurosecretory granules [2]. * **Why Chromogranin is correct:** **Chromogranin A** is a protein found within the secretory granules of neuroendocrine cells. Along with **Synaptophysin** and **CD56 (NCAM)**, it is a classic immunohistochemical (IHC) marker used to confirm SCLC [2]. Its presence confirms the neuroendocrine nature of the tumor. **Analysis of Incorrect Options:** * **Cytokeratin:** This is a marker for epithelial cells. While SCLC is a carcinoma and may show focal positivity for cytokeratin (often in a "perinuclear dot-like" pattern), it is not specific to SCLC and is found in almost all epithelial malignancies (like Squamous Cell Carcinoma or Adenocarcinoma) [3]. * **Desmin:** This is a marker for **muscle differentiation** (skeletal, smooth, or cardiac). It is used to diagnose tumors like Rhabdomyosarcoma or Leiomyosarcoma, not lung carcinomas. * **Vimentin:** This is a marker for **mesenchymal cells**. It is typically expressed in sarcomas, melanomas, and lymphomas. While some carcinomas undergo epithelial-mesenchymal transition, it is not a diagnostic marker for SCLC. **High-Yield Clinical Pearls for NEET-PG:** * **Origin:** Derived from neuroendocrine (Kulchitsky) cells; strongly associated with **smoking** [4]. * **Genetics:** Nearly 100% show **TP53** and **RB1** mutations [4]. * **Paraneoplastic Syndromes:** SCLC is most commonly associated with **SIADH** (ectopic ADH) and **Cushing Syndrome** (ectopic ACTH) [1]. It is also linked to **Lambert-Eaton Myasthenic Syndrome**. * **Histology:** Shows "Azzopardi effect" (DNA encrustation of vessel walls) and nuclear molding [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 725-727. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 337-338. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 723-724. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 721.

Question 305: In Respiratory Distress Syndrome (RDS), which cells are damaged?

A. Type 2 pneumocytes
B. Type 1 pneumocytes (Correct Answer)
C. Clara cells
D. Type 1 pneumocytes

Explanation: **Explanation:** In **Respiratory Distress Syndrome (RDS)**, specifically Neonatal RDS (Hyaline Membrane Disease), the primary insult is a deficiency of pulmonary surfactant [1]. However, the question asks which cells are **damaged** as a result of this process. The fundamental pathophysiology involves surfactant deficiency leading to widespread alveolar atelectasis [1]. This causes localized hypoxia and acidosis, which triggers a cascade of endothelial and epithelial injury. **Type 1 pneumocytes** are thin, squamous cells that cover 95% of the alveolar surface area. Due to their large surface area and metabolic vulnerability, they are the primary targets of injury [2]. Damage to these cells leads to increased alveolar permeability, allowing a protein-rich fluid to leak into the alveoli, which subsequently organizes into the characteristic **hyaline membranes** [2]. **Analysis of Options:** * **Type 1 Pneumocytes (Correct):** These are the structural cells that undergo necrosis and sloughing during the exudative phase of RDS [2]. * **Type 2 Pneumocytes:** These cells are the *source* of the problem (due to prematurity and decreased surfactant production), but they are relatively more resistant to injury than Type 1 cells [1]. In the recovery phase, Type 2 pneumocytes actually proliferate to repair the damaged alveolar epithelium [2]. * **Clara Cells (Club Cells):** These are found in the bronchioles, not the alveoli. While they protect the bronchiolar epithelium, they are not the primary site of damage in RDS. **NEET-PG High-Yield Pearls:** * **Lecithin/Sphingomyelin (L/S) ratio:** A ratio < 2:1 in amniotic fluid indicates a high risk for RDS. * **Morphology:** The "Hyaline Membrane" is composed of fibrin mixed with cell debris from necrotic Type 1 pneumocytes [2]. * **Management:** Antenatal corticosteroids (e.g., Betamethasone) are given to the mother to accelerate fetal lung maturity by inducing surfactant synthesis in Type 2 cells [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 465-467. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 679-681.

Question 306: A 45-year-old, HIV-positive patient presents with features of pneumonia. What are the characteristic histopathological features suggesting Pneumocystis jirovecii pneumonia?

A. Prominent interstitial pneumonitis
B. Eosinophilic alveolar exudates (Correct Answer)
C. Prominent mononuclear cells in alveolar exudates
D. Neutrophilic infiltration of alveolar interstitium

Explanation: **Explanation:** *Pneumocystis jirovecii* pneumonia (PJP) is a classic opportunistic infection in immunocompromised patients, particularly those with HIV/AIDS (CD4 count <200 cells/µL) [1]. **1. Why Option B is Correct:** The hallmark histopathological finding of PJP is the presence of **intra-alveolar, foamy, eosinophilic (pink) exudates** [1]. This "cotton-candy" appearance is created by a mixture of the organisms (trophozoites and cysts), surfactant, and host proteins. Unlike typical bacterial pneumonia, the inflammatory response is minimal, and the exudate fills the alveolar spaces without significant cellular infiltration. **2. Why Other Options are Incorrect:** * **Option A:** While some thickening of the alveolar septa can occur, **interstitial pneumonitis** is more characteristic of viral infections (like CMV) or Mycoplasma [1]. In PJP, the primary pathology is intra-alveolar. * **Option C & D:** PJP is characterized by a **lack of a robust cellular response**. A prominent mononuclear (lymphocytic) or neutrophilic infiltrate suggests a pyogenic bacterial infection or a different fungal etiology. The "foamy" nature of PJP exudate is distinct because it is relatively acellular. **3. NEET-PG High-Yield Pearls:** * **Special Stains:** The cysts are best visualized using **Gomori Methenamine Silver (GMS)** stain, appearing as crushed ping-pong balls or "cup-and-saucer" shapes [1]. Periodic Acid-Schiff (PAS) can also be used. * **Diagnosis:** Bronchoalveolar lavage (BAL) is the gold standard for diagnosis. * **Radiology:** Classically presents with bilateral, perihilar "ground-glass" opacities. * **Treatment:** Trimethoprim-sulfamethoxazole (TMP-SMX) is the drug of choice for both treatment and prophylaxis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 318-319.

Question 307: Bronchiolitis obliterans with organizing pneumonia (BOOP) is characterized histologically in the lung by:

A. Asteroid bodies in giant cells within bronchioles
B. Loose fibrous tissue within bronchioles and alveoli (Correct Answer)
C. Multiple rheumatoid nodules within the interstitial tissue
D. Numerous eosinophils within the walls of the alveoli

Explanation: **Explanation:** **Bronchiolitis Obliterans Organizing Pneumonia (BOOP)**, now clinically referred to as **Cryptogenic Organizing Pneumonia (COP)**, is a clinicopathologic syndrome characterized by a specific reaction pattern to lung injury [1], [2]. **Why Option B is Correct:** The histological hallmark of BOOP is the presence of **Masson bodies**. These are polypoid plugs of **loose, organized connective tissue** (fibromyxoid stroma) found within the distal airways (bronchioles), alveolar ducts, and adjacent alveoli [2]. Unlike interstitial fibrosis, this process is intra-luminal and often reversible with corticosteroid therapy [2]. **Analysis of Incorrect Options:** * **Option A:** **Asteroid bodies** (star-shaped inclusions in giant cells) are characteristic of **Sarcoidosis**, not BOOP. * **Option C:** Multiple rheumatoid nodules in the lung periphery, especially when associated with coal worker's pneumoconiosis, define **Caplan Syndrome**. * **Option D:** Numerous eosinophils are the hallmark of **Eosinophilic Pneumonias** (e.g., Loeffler syndrome or Tropical Pulmonary Eosinophilia). While BOOP may have mild inflammation, eosinophils are not the primary diagnostic feature. **High-Yield NEET-PG Pearls:** * **Radiology:** Characterized by "patchy subpleural or peribronchial areas of consolidation" (often migratory) [2]. * **Masson Bodies:** The pathognomonic histological finding (loose whorls of collagen/fibroblasts). * **Clinical Presentation:** Patients typically present with a flu-like illness (cough, dyspnea, fever) that does not respond to antibiotics but shows a dramatic response to **steroids** [2]. * **Architecture:** Unlike Usual Interstitial Pneumonia (UIP), the underlying lung architecture in BOOP is generally preserved [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 693-695. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 330-331.

Question 308: A 53-year-old man presents with weakness, malaise, cough with bloody sputum, and night sweats. A chest X-ray shows bilateral apical densities, some cavitary. The patient has a history of documented exposure to Mycobacterium tuberculosis 20 years ago, and M. tuberculosis has been identified in his sputum. Which of the following best describes the expected lung pathology in this patient?

A. Dense fibrosis
B. Eosinophilic infiltration
C. Granulomas (Correct Answer)
D. Interstitial pneumonia

Explanation: **Explanation:** The clinical presentation of apical cavitary lesions, hemoptysis, and night sweats in a patient with a history of exposure 20 years ago is classic for **Secondary (Reactivation) Tuberculosis**. **1. Why the Correct Answer is Right:** The hallmark of *Mycobacterium tuberculosis* infection is **Granulomatous inflammation** [1]. This is a Type IV (delayed-type) hypersensitivity reaction. When alveolar macrophages cannot kill the bacilli, they present antigens to CD4+ T-cells (Th1). These T-cells secrete **Interferon-gamma (IFN-γ)**, which activates macrophages into **epithelioid histiocytes** [1]. These histiocytes fuse to form **Langhans giant cells** and aggregate to form granulomas, typically with central **caseous necrosis** [2]. **2. Why Incorrect Options are Wrong:** * **A. Dense fibrosis:** While healing of TB lesions involves fibrosis (fibrocalcific nodules) [3], the active, symptomatic disease described here is characterized by active granuloma formation and cavitation. * **B. Eosinophilic infiltration:** This is characteristic of parasitic infections or allergic conditions (e.g., Löffler syndrome or ABPA), not mycobacterial infections. * **D. Interstitial pneumonia:** This pattern is typical of viral infections (e.g., Influenza, CMV) or Mycoplasma, presenting with diffuse "ground-glass" opacities rather than localized apical cavities. **NEET-PG High-Yield Pearls:** * **Primary TB:** Characterized by the **Ghon Complex** (parenchymal lesion + involved lymph node), usually in the lower lobes. * **Secondary TB:** Typically involves the **apex of the lungs** due to high oxygen tension (M. tb is an obligate aerobe). * **Cytokine Key:** **TNF-α** is essential for maintaining granuloma integrity [1]. Patients starting Anti-TNF therapy (e.g., Infliximab) are at high risk for TB reactivation [1]. * **Stain:** Ziehl-Neelsen (Acid-fast) stain; **Auramine-Rhodamine** is the preferred screening fluorescent stain [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 380-381. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321.

Question 309: What pathological findings are revealed in status asthmaticus?

A. Suppurative endobronchial exudates
B. Mucous plugs in small bronchioles (Correct Answer)
C. Necrosis of bronchi
D. None of the above

Explanation: **Explanation:** **Status Asthmaticus** is a severe, life-threatening form of asthma that does not respond to standard bronchodilator therapy. The hallmark of this condition is severe airway obstruction. **Why Option B is Correct:** In status asthmaticus, the most characteristic gross finding is the presence of **thick, tenacious mucous plugs** that occlude the lumen of the small bronchi and bronchioles [1]. These plugs are formed due to goblet cell hyperplasia and excessive secretion. Microscopically, these plugs contain **Curschmann spirals** (coiled mucus strands) and **Charcot-Leyden crystals** (derived from eosinophil proteins). The lungs also appear over-distended (hyperinflated) due to air trapping [1]. **Why Other Options are Incorrect:** * **Option A (Suppurative endobronchial exudates):** This is characteristic of **Bronchiectasis** [2] or bacterial pneumonia, where there is pus formation. Asthma is an eosinophilic inflammatory process, not a purulent/suppurative one. * **Option C (Necrosis of bronchi):** Necrotizing inflammation is seen in conditions like **Necrotizing Pneumonia** or certain fungal infections (e.g., Aspergillus). Asthma involves mucosal edema and smooth muscle hypertrophy, but not tissue necrosis. **High-Yield NEET-PG Pearls:** * **Creola Bodies:** Desquamated clusters of bronchial epithelial cells found in the sputum of asthmatics. * **Airway Remodeling:** Long-term changes include thickening of the basement membrane (subepithelial fibrosis) and hypertrophy of the **bronchial smooth muscle** (the most striking feature) [1]. * **Eosinophils:** These are the predominant inflammatory cells in the bronchial walls [3]. * **Type I Hypersensitivity:** Most cases of extrinsic asthma are mediated by IgE and Mast cells [3]. **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. 690-691. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 688-689.

Question 310: Carcinoma of the lung is associated with exposure to which of the following?

A. Silica
B. Asbestosis (Correct Answer)
C. Coal
D. Cotton

Explanation: **Explanation:** **Correct Answer: B. Asbestosis** Asbestos exposure is a well-documented potent carcinogen for the respiratory tract [1]. It is associated with a 5-fold increase in the risk of **Bronchogenic Carcinoma** (the most common cancer in asbestos workers) and a massive 1000-fold increase in the risk of **Mesothelioma** [2]. When combined with cigarette smoking, the risk of bronchogenic carcinoma acts synergistically, increasing the risk by approximately 50 to 90 times [2]. The pathogenesis involves the generation of reactive oxygen species and chronic inflammation caused by the persistence of asbestos fibers in the lung parenchyma. **Incorrect Options:** * **A. Silica:** Exposure to crystalline silica (Silicosis) primarily causes a restrictive lung disease characterized by "eggshell calcification" of lymph nodes [1]. While some studies suggest a slight increase in lung cancer risk, it is not as strongly or classically associated as asbestos. * **C. Coal:** Coal Worker’s Pneumoconiosis (CWP) or "Black Lung Disease" is caused by the inhalation of coal dust. It leads to anthracosis and progressive massive fibrosis (PMF) but is **not** associated with an increased risk of lung carcinoma [1]. * **D. Cotton:** Exposure to cotton dust leads to **Byssinosis** ("Monday Morning Fever"). It is an occupational airway disease characterized by bronchoconstriction, not malignancy. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cancer in Asbestosis:** Bronchogenic Carcinoma (NOT Mesothelioma). * **Specific marker for Mesothelioma:** Calretinin (+ve), Cytokeratin 5/6 (+ve), and WT-1 (+ve). * **Asbestos bodies:** Golden-brown, fusiform/beaded rods with translucent centers (Ferruginous bodies) stained with Prussian Blue. * **Synergistic effect:** Smoking + Asbestos = Massive increase in Bronchogenic Carcinoma risk; however, smoking does **not** increase the risk of Mesothelioma [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 695. [2] 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. 221-222.

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