General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 181: Cachexin is:

A. IL-2
B. IL-12
C. INF-gamma
D. TNF (Correct Answer)

Explanation: **Explanation:** The correct answer is **TNF (Tumor Necrosis Factor)**, specifically TNF-alpha. **Why TNF is the correct answer:** TNF-alpha was historically named **"Cachexin"** because of its pivotal role in causing **cachexia**—a syndrome characterized by progressive weight loss, muscle wasting, and anorexia seen in chronic infections and malignancies. TNF-alpha promotes cachexia by [1]: 1. **Suppressing appetite** via its action on the hypothalamus. 2. **Inhibiting lipoprotein lipase (LPL)**, which prevents the uptake of fatty acids from circulating lipoproteins into adipose tissue. 3. **Promoting proteolysis** and lipolysis, leading to the breakdown of skeletal muscle and fat stores. **Analysis of Incorrect Options:** * **A. IL-2:** Primarily functions as a T-cell growth factor. It is essential for the proliferation of T-lymphocytes and NK cell activation but does not cause systemic wasting. * **B. IL-12:** Produced by macrophages and dendritic cells, its main role is to stimulate the differentiation of naive T cells into Th1 cells and induce IFN-gamma production. * **C. INF-gamma:** A key cytokine for activating macrophages (classical pathway) and promoting Th1 responses. While it contributes to inflammation, it is not the primary mediator known as cachexin. **NEET-PG High-Yield Pearls:** * **Primary Source:** TNF-alpha is mainly produced by activated **macrophages**. * **Dual Role:** In small amounts, it mediates acute inflammation; in large amounts, it causes **septic shock** [1] (via systemic vasodilation and DIC) and cachexia. * **Other Mediators:** While TNF is the chief "cachexin," **IL-1 and IL-6** also contribute to the wasting process in chronic diseases. * **Inhibitor:** TNF-alpha is a key target in treating autoimmune diseases like Rheumatoid Arthritis (e.g., Etanercept, Infliximab). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 110-111.

Question 182: Edema is caused by all of the following mechanisms, EXCEPT:

A. Increased vascular permeability
B. Obstruction to lymphatic flow
C. Sodium retention
D. Increased plasma proteins (Correct Answer)

Explanation: **Explanation:** Edema is defined as the accumulation of excess fluid in the interstitial spaces. According to **Starling’s Law**, fluid movement between the intravascular and interstitial compartments is governed by the balance of hydrostatic and oncotic pressures [2]. **Why "Increased plasma proteins" is the correct answer:** Plasma proteins (primarily albumin) are the main determinants of **Plasma Colloid Oncotic Pressure**. This pressure acts as a "suction force" that keeps fluid inside the blood vessels. Therefore, an *increase* in plasma proteins would actually prevent edema by drawing fluid back into the circulation [1]. Edema is caused by a **decrease** in plasma proteins (hypoproteinemia), as seen in Nephrotic syndrome or Liver cirrhosis [1]. **Analysis of incorrect options:** * **Increased vascular permeability:** In inflammation, chemical mediators cause endothelial gaps, allowing fluid and proteins to leak into the interstitium (Exudate), leading to inflammatory edema [2], [4]. * **Obstruction to lymphatic flow:** Lymphatics normally drain the small amount of residual interstitial fluid. Obstruction (e.g., Filariasis or post-surgical scarring) leads to lymphedema [3]. * **Sodium retention:** Sodium is osmotically active. Retention of sodium (and consequently water) increases hydrostatic pressure and dilutes oncotic pressure, leading to generalized edema (e.g., Congestive Heart Failure or Renal failure) [3]. **NEET-PG High-Yield Pearls:** * **Transudate vs. Exudate:** Transudate is protein-poor (seen in CHF/Cirrhosis); Exudate is protein-rich (seen in Inflammation). * **Dependent Edema:** Edema of the lower limbs (influenced by gravity), characteristic of Right Heart Failure [3]. * **Anasarca:** Severe, generalized edema with profound subcutaneous tissue swelling. * **Pitting Edema:** Characteristic of low protein states or cardiac failure; non-pitting edema is typically seen in lymphatic obstruction (Myxedema/Filariasis) [3]. **References:** [1] 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. 126-127. [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. 186-187. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 124-126. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 85-86.

Question 183: Which intermediate filament is characteristic of fibroblasts?

A. Lamin A
B. Vimentin (Correct Answer)
C. Desmin
D. Cytokeratin

Explanation: **Explanation:** Intermediate filaments (IFs) are crucial components of the cytoskeleton that provide mechanical strength to cells. They are highly tissue-specific, making them excellent immunohistochemical (IHC) markers in diagnostic pathology. **Why Vimentin is correct:** **Vimentin** is the characteristic intermediate filament of **mesenchymal cells**. Since fibroblasts are the prototypical cells of mesenchymal origin (connective tissue), they express vimentin. In tumor pathology, Vimentin is used as a primary marker for **sarcomas** (malignancies of mesenchymal origin). **Analysis of Incorrect Options:** * **Lamin A:** These are nuclear intermediate filaments found in the **nuclear lamina** (inner lining of the nuclear envelope) of most differentiated somatic cells, not specific to the cytoplasmic cytoskeleton of fibroblasts. * **Desmin:** This is the marker for **muscle cells** (skeletal, cardiac, and smooth muscle). It is used clinically to identify tumors like rhabdomyosarcomas or leiomyosarcomas. * **Cytokeratin:** This is the characteristic marker for **epithelial cells**. It is the primary IHC marker used to diagnose **carcinomas**. **NEET-PG High-Yield Pearls:** * **Vimentin** is also positive in Melanoma, Renal Cell Carcinoma (RCC), and Endometrial Carcinoma (exceptions where epithelial tumors show vimentin). * **Glial Fibrillary Acidic Protein (GFAP):** Marker for astrocytes and ependymal cells (Glial tumors/Gliomas). * **Neurofilaments:** Marker for neurons and neural tumors (e.g., Neuroblastoma). * **Synaptophysin/Chromogranin:** Markers for neuroendocrine tumors.

Question 184: Haemorrhagic infarction is seen in which of the following?

A. Venous thrombosis
B. Thrombosis
C. Embolism
D. Central venous thrombosis (Correct Answer)

Explanation: **Explanation:** **Infarction** refers to an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage. Infarcts are classified based on their color into **White (Anemic)** and **Red (Haemorrhagic)** [1]. **Why the correct answer is right:** **Haemorrhagic (Red) infarcts** occur in tissues where blood can collect in the infarcted zone. A classic cause is **venous occlusion** (e.g., Central Venous Sinus Thrombosis or Ovarian Torsion) [1]. When the venous drainage is blocked, the tissue becomes intensely congested; the resulting pressure prevents arterial inflow, leading to ischemia. Because the vessels are engorged and damaged, blood leaks into the necrotic tissue, giving it a red/haemorrhagic appearance. **Analysis of Incorrect Options:** * **B & C (Thrombosis/Embolism):** These are general mechanisms of vascular occlusion. While they can cause red infarcts in specific organs (like the lung), they more commonly cause **White (Anemic) infarcts** in solid organs with end-arterial circulation, such as the heart (MI), spleen, and kidney [1]. * **A (Venous thrombosis):** While technically correct in a general sense, **Central Venous Thrombosis** (Option D) is the more specific clinical entity provided in the options that consistently results in haemorrhagic infarction of the brain parenchyma. **High-Yield Clinical Pearls for NEET-PG:** * **Red Infarcts occur in:** 1. **Loose tissues** (e.g., Lung) [1]. 2. **Tissues with dual circulation** (e.g., Lung, Liver, Small Intestine) [1]. 3. **Tissues previously congested** by sluggish venous outflow [1]. 4. **Reperfusion injury** (when flow is restored to a site of previous arterial occlusion) [1]. * **White Infarcts occur in:** Solid organs with **end-arterial circulation** (Heart, Spleen, Kidney) [1]. * **Morphology:** All infarcts (except the brain) typically show **Coagulative Necrosis**. The brain undergoes **Liquefactive Necrosis**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140.

Question 185: A 55-year-old male presented with dry mouth and rheumatoid arthritis with high titers of anti-SS-A and anti-SS-B antibodies. He was diagnosed with a minor salivary gland tumor. What is the earliest histologic finding in this condition?

A. Endothelial cells
B. Basophils
C. Lymphocytes (Correct Answer)
D. Eosinophils

Explanation: ### Explanation The clinical presentation of dry mouth (xerostomia), rheumatoid arthritis, and the presence of **anti-SS-A (Ro)** and **anti-SS-B (La)** antibodies is diagnostic of **Sjögren Syndrome** [3]. This is a chronic autoimmune disorder characterized by the lymphocytic destruction of exocrine glands, primarily the lacrimal and salivary glands [4]. **Why Lymphocytes are the Correct Answer:** The hallmark of Sjögren Syndrome is the **periductal lymphocytic infiltration** of the exocrine glands [1]. In the early stages, CD4+ T-helper cells and some B cells aggregate around small ducts [3]. As the disease progresses, these lymphocytic infiltrates form lymphoid follicles with germinal centers, eventually leading to the destruction of the glandular acini and fibrosis. A lip biopsy (minor salivary gland biopsy) is the gold standard for diagnosis, where a "focus score" (aggregates of ≥50 lymphocytes) is calculated. **Why Other Options are Incorrect:** * **Endothelial cells:** While angiogenesis occurs in chronic inflammation, endothelial cell proliferation is not the primary or earliest diagnostic histologic feature of this autoimmune process. * **Basophils:** These are involved in Type I hypersensitivity and systemic allergic reactions; they do not play a primary role in the glandular destruction of Sjögren Syndrome. * **Eosinophils:** These are typically associated with parasitic infections or allergic conditions (e.g., Churg-Strauss or asthma) and are not a characteristic finding in Sjögren’s. **High-Yield Clinical Pearls for NEET-PG:** * **Triad:** Keratoconjunctivitis sicca (dry eyes), xerostomia (dry mouth), and an associated autoimmune disease (most commonly Rheumatoid Arthritis) [2]. * **Antibodies:** Anti-Ro (SS-A) and Anti-La (SS-B) are highly specific. Note: Anti-Ro can cross the placenta, causing **neonatal lupus** and congenital heart block. * **Malignancy Risk:** Patients have a **40-fold increased risk** of developing **MALT Lymphoma** (Marginal Zone B-cell Lymphoma) due to chronic B-cell stimulation [4]. * **Diagnostic Test:** Schirmer’s test (to measure tear production). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 749-750. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 678-679. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 234-235. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 236.

Question 186: Supernumerary tooth, described as a 'tooth within a tooth', is most commonly seen in which of the following dental anomalies?

A. Maxillary lateral incisors (Correct Answer)
B. Mandibular second premolar
C. Mandibular incisors
D. Maxillary central and lateral incisors

Explanation: **Explanation:** The condition described as a "tooth within a tooth" is clinically known as **Dens invaginatus** (or *Dens in dente*). It is a developmental malformation resulting from an invagination of the enamel organ into the dental papilla during odontogenesis, before calcification occurs. **Why Maxillary Lateral Incisors are correct:** The **maxillary lateral incisor** is the most frequently affected tooth (over 90% of cases). This anomaly typically occurs in the lingual pit area. Because the invagination is lined by enamel, it creates a pocket that traps plaque and bacteria, often leading to early dental caries [1], pulpitis, and periapical lesions even in the absence of visible decay. **Analysis of Incorrect Options:** * **B & C (Mandibular teeth):** Dens invaginatus is significantly rarer in the mandible compared to the maxilla. Mandibular premolars and incisors are seldom involved in this specific developmental anomaly. * **D (Maxillary central incisors):** While the maxillary central incisor is the second most common site, the **lateral incisor** remains the classic and most frequent "high-yield" answer for examinations. **NEET-PG High-Yield Pearls:** * **Dens Evaginatus:** The opposite of *dens in dente*; it is an accessory cusp (Leong’s tubercle) most commonly seen in **Mandibular Premolars**. * **Taurodontism:** "Bull-like" teeth with enlarged pulp chambers and apically displaced furcations, often associated with **Klinefelter Syndrome**. * **Mesiodens:** The most common supernumerary tooth, typically located between the two maxillary central incisors. * **Radiographic Appearance:** Dens invaginatus appears as a pear-shaped radiopaque outline of enamel within the pulp chamber [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 343-344. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, p. 741.

Question 187: Which of the following is a predisposing factor for arterial thrombosis?

A. Antithrombin III deficiency
B. Protein S deficiency
C. Protein C deficiency
D. Homocysteinemia (Correct Answer)

Explanation: **Explanation:** The formation of a thrombus is governed by **Virchow’s Triad**: endothelial injury, stasis or turbulent blood flow, and hypercoagulability [1]. **Why Homocysteinemia is correct:** Elevated levels of homocysteine (Homocysteinemia) contribute to **arterial thrombosis** primarily by causing **endothelial cell injury** [2]. It promotes the production of reactive oxygen species, leading to vascular inflammation and the activation of pro-coagulant factors. Unlike many other hypercoagulable states that primarily affect the low-pressure venous system, endothelial damage is a prerequisite for thrombosis in high-pressure, high-flow arteries [1]. **Why the other options are incorrect:** * **Options A, B, and C (Antithrombin III, Protein S, and Protein C deficiencies):** These are classic inherited hypercoagulable states (thrombophilias). These deficiencies result in a failure to inhibit the coagulation cascade (specifically factors Va, VIIIa, and Thrombin). While they are potent risk factors for **Venous Thromboembolism (VTE)**, such as Deep Vein Thrombosis (DVT) and Pulmonary Embolism, they are rarely associated with isolated arterial thrombosis. **High-Yield Pearls for NEET-PG:** * **Arterial Thrombi:** Usually occur at sites of endothelial injury (e.g., atherosclerosis) or turbulence [3]. They are often "pale" or "white" thrombi (rich in platelets) [1]. * **Venous Thrombi:** Usually occur at sites of stasis. They are "red" or "stasis" thrombi (rich in RBCs). * **Lines of Zahn:** Gross and microscopic laminations (pale platelet/fibrin layers vs. dark RBC layers) that signify a thrombus formed in **flowing blood**, helping distinguish a pre-mortem thrombus from a post-mortem clot. * **Homocysteinemia Causes:** Can be hereditary (Cystathionine β-synthase deficiency) or acquired (deficiency of Vitamin B12, B6, or Folate). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 132-133. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 502-503. [3] 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. 142-143.

Question 188: Which of the following is not considered a precancerous lesion?

A. Lichen planus
B. Verrucous carcinoma (Correct Answer)
C. Submucous fibrosis
D. Leukoplakia

Explanation: **Explanation** The distinction between a **precancerous lesion** (premalignant) and a **malignant lesion** is a frequent high-yield topic in NEET-PG. 1. **Why Verrucous Carcinoma is the correct answer:** Verrucous carcinoma (Ackerman’s tumor) is a **well-differentiated variant of squamous cell carcinoma**. By definition, it is already a **malignant neoplasm**, not a precursor to one. Although it is slow-growing and rarely metastasizes, it is locally invasive and characterized by a "pushing" border. Therefore, it cannot be classified as a "precancerous" lesion because the transition to malignancy has already occurred. 2. **Analysis of Incorrect Options (Precancerous Lesions):** * **Leukoplakia:** This is the most common precancerous lesion of the oral cavity [1]. It is a clinical term for a white patch that cannot be characterized clinically or pathologically as any other disease [1], [2]. * **Oral Submucous Fibrosis (OSMF):** A chronic, progressive condition strongly associated with areca nut chewing [1]. It carries a high risk of malignant transformation due to epithelial atrophy and chronic inflammation. * **Lichen Planus:** Specifically the erosive and atrophic forms of oral lichen planus are recognized as having a small but significant potential for malignant transformation into squamous cell carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **Precancerous Lesion:** A morphologically altered tissue in which cancer is more likely to occur than its normal counterpart (e.g., Leukoplakia, Erythroplakia). * **Precancerous Condition:** A generalized state associated with a significantly increased risk of cancer (e.g., Xeroderma pigmentosum, Syphilitic glossitis). * **Erythroplakia** has a much higher malignant transformation rate than Leukoplakia. * **Verrucous Carcinoma** is often associated with "snuff dipper's" tobacco use and typically presents as a cauliflower-like growth. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 344-345. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 737-738.

Question 189: In wound healing, what is the correct sequence of cell appearance?

A. Macrophage -> Platelet -> Neutrophils -> Fibroblast
B. Neutrophils -> Macrophages -> Platelet -> Fibroblast
C. Platelet -> Neutrophils -> Macrophages -> Fibroblast (Correct Answer)
D. Platelet -> Macrophages -> Neutrophils -> Fibroblast

Explanation: **Explanation:** The correct sequence of cell appearance in wound healing follows the physiological phases of repair: **Hemostasis → Inflammation → Proliferation → Remodeling.** 1. **Platelets (Hemostasis):** Immediately upon injury, platelets are the first to arrive. They form a hemostatic plug and release growth factors (like PDGF and TGF-̢) that act as chemoattractants for subsequent inflammatory cells. 2. **Neutrophils (Early Inflammation):** Within 24 hours, neutrophils are the first leukocytes to reach the site [1]. Their primary role is to clear bacteria and debris via phagocytosis. 3. **Macrophages (Late Inflammation):** Appearing around 48–72 hours, macrophages are the "master regulators" of wound healing [3]. They replace neutrophils, continue phagocytosis, and secrete cytokines that stimulate the proliferative phase [2]. 4. **Fibroblasts (Proliferation):** Starting from day 3 to 5, fibroblasts migrate to the wound site to synthesize collagen and extracellular matrix, forming granulation tissue [3]. **Analysis of Incorrect Options:** * **Options A & B:** Incorrect because they place macrophages or neutrophils before platelets. Without the initial platelet plug and chemical signaling, the inflammatory cascade cannot be efficiently initiated. * **Option D:** Incorrect because it places macrophages before neutrophils. In the standard inflammatory timeline, the acute response (neutrophils) always precedes the chronic/regulatory response (macrophages) [1]. **NEET-PG High-Yield Pearls:** * **Type III Collagen** is synthesized first in granulation tissue, which is later replaced by **Type I Collagen** (stronger) during remodeling. * **Zinc deficiency** and **Vitamin C deficiency** are common causes of delayed wound healing (impaired collagen synthesis). * **Macrophages** are essential for the transition from the inflammatory phase to the proliferative phase [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 89. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 115.

Question 190: Compared to fresh blood, stored blood has:

A. More 2,3-DPG
B. High extracellular K+ (Correct Answer)
C. High extracellular Hb
D. Increased platelets

Explanation: **Explanation:** The storage of blood leads to a series of biochemical and morphological changes collectively known as the **"Storage Lesion."** **Why High Extracellular K+ is Correct:** The Na+/K+ ATPase pump on the red blood cell (RBC) membrane is temperature-dependent. During storage at 1–6°C, this pump becomes inactive. Consequently, potassium (K+) leaks out of the RBCs into the plasma (extracellular fluid), while sodium enters the cells. This results in a progressive increase in extracellular potassium levels over time, which can pose a risk of hyperkalemia during massive or pediatric transfusions. **Analysis of Incorrect Options:** * **A. More 2,3-DPG:** Levels of **2,3-Diphosphoglycerate (2,3-DPG) decrease** significantly during storage. This increases the affinity of hemoglobin for oxygen, causing a **left shift** in the oxygen dissociation curve and reducing oxygen delivery to tissues. * **C. High extracellular Hb:** While some hemolysis occurs, significant free hemoglobin is not a standard feature of properly stored blood unless the unit is expired or damaged. The increase in K+ is a much more consistent and clinically significant biochemical marker. * **D. Increased platelets:** Platelets are highly unstable at 1–6°C. Their viability and count decrease rapidly in stored whole blood; they lose function within 48–72 hours. **High-Yield Clinical Pearls for NEET-PG:** * **pH Changes:** Stored blood becomes more **acidic** due to the accumulation of lactate and pyruvate (anaerobic glycolysis). * **Clotting Factors:** Levels of labile factors (**Factor V and Factor VIII**) decrease significantly during storage. * **Storage Lesion Summary:** ↓ pH, ↓ 2,3-DPG, ↓ ATP, ↓ Glucose, **↑ Potassium**, and ↑ Lactate. * **Massive Transfusion Risk:** Can lead to hypocalcemia (citrate toxicity) and hyperkalemia.

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Cell Injury and Cell Death

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Adaptations of Cellular Growth

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Accumulations and Deposits

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Acute and Chronic Inflammation

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Tissue Repair and Wound Healing

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Hemodynamic Disorders

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Genetic Disorders

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Environmental Pathology

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Nutritional Diseases

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Molecular Basis of Disease

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