General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 141: What is the Leiden factor?

A. Factor VI
B. Factor VIII
C. Factor IV
D. Factor V (Correct Answer)

Explanation: **Explanation:** **Factor V Leiden** is the most common inherited cause of hypercoagulability (thrombophilia) among Caucasians [1]. It is caused by a specific point mutation in the Factor V gene (G1691A), which results in the substitution of arginine by glutamine at position 506 [1]. **Why Option D is Correct:** Under normal physiological conditions, **Activated Protein C (APC)** inactivates Factor Va and Factor VIIIa to limit clot formation. In Factor V Leiden, the mutation alters the cleavage site on Factor V where Protein C normally binds. This renders Factor V resistant to inactivation by APC (**APC Resistance**) [1]. Consequently, Factor V remains active in the circulation for longer periods, leading to a prothrombotic state and increased risk of Venous Thromboembolism (VTE) [1]. **Why Other Options are Incorrect:** * **Factor VI:** This factor does not exist in the modern coagulation cascade (it was previously thought to be an activated form of Factor V). * **Factor VIII:** While Factor VIII is also inactivated by Protein C, the "Leiden" mutation specifically affects Factor V. Deficiencies in Factor VIII lead to Hemophilia A. * **Factor IV:** This refers to Calcium ions ($Ca^{2+}$), which are essential cofactors for several steps in the coagulation cascade but are not associated with the Leiden mutation. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant. * **Clinical Presentation:** Recurrent Deep Vein Thrombosis (DVT) and Pulmonary Embolism [1]. * **Diagnosis:** Suspect in patients with "Activated Protein C Resistance" on screening assays; confirmed by genetic testing (PCR). * **Key Association:** It is a major risk factor for cerebral venous thrombosis in women taking oral contraceptive pills (OCPs). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134.

Question 142: What is the half-life of C-reactive protein (CRP)?

A. 6 hours
B. 12 hours
C. 20 hours (Correct Answer)
D. 24 hours

Explanation: **Explanation:** **C-reactive protein (CRP)** is a classic acute-phase reactant synthesized by the liver in response to pro-inflammatory cytokines, primarily **Interleukin-6 (IL-6)** [1], [2]. It serves as a sensitive marker of systemic inflammation [1]. **Why 20 hours is correct:** The plasma half-life of CRP is remarkably constant at approximately **19–20 hours** under both physiological and pathological conditions. Because its half-life is fixed, the circulating concentration of CRP is determined solely by its **rate of production**. This makes it an excellent clinical surrogate for the intensity of the inflammatory stimulus; once the stimulus (e.g., infection or trauma) is removed, CRP levels fall rapidly at a predictable rate. **Analysis of Incorrect Options:** * **6 hours (A):** This is too short. While CRP levels begin to rise within 4–6 hours of an insult, the protein persists longer in the circulation. * **12 hours (B):** While closer, this underestimates the stability of the CRP molecule in plasma. * **24 hours (D):** Although CRP levels typically peak at 36–50 hours, the specific biological half-life is shorter than a full day. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** CRP acts as an opsonin; it binds to phosphocholine on bacterial surfaces and apoptotic cells, activating the **classical complement pathway** (via C1q) [1]. * **Kinetics:** Levels start rising at 4–6 hours, double every 8 hours, and peak at **36–50 hours**. * **hs-CRP:** High-sensitivity CRP is used as a marker for **cardiovascular risk stratification** (chronic low-grade inflammation) [1]. * **ESR vs. CRP:** CRP is a more sensitive and rapidly responding marker than ESR (Erythrocyte Sedimentation Rate), as ESR depends on fibrinogen levels which have a much longer half-life. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 501-502. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 111.

Question 143: Keratinizing metaplasia of salivary glands results due to the deficiency of which vitamin?

A. Vitamin A (Correct Answer)
B. Thiamine
C. Riboflavin
D. Vitamin E

Explanation: **Explanation:** **Vitamin A (Retinol)** is essential for the maintenance of specialized epithelia, particularly the differentiation of mucus-secreting columnar epithelium. When Vitamin A is deficient, these specialized cells undergo **squamous metaplasia**, transforming into a keratinizing stratified squamous epithelium [1]. This process occurs in the salivary glands, respiratory tract, and urinary tract [1]. In the salivary glands, the loss of mucus production and the buildup of keratin debris can lead to ductal obstruction and secondary infections. **Analysis of Incorrect Options:** * **Thiamine (Vitamin B1):** Deficiency primarily leads to Beriberi (Dry/Wet) and Wernicke-Korsakoff syndrome, affecting the cardiovascular and nervous systems, not epithelial differentiation. * **Riboflavin (Vitamin B2):** Deficiency is characterized by cheilosis, glossitis, and corneal neovascularization, but it does not cause keratinizing metaplasia. * **Vitamin E:** Acts as a potent antioxidant protecting cell membranes from lipid peroxidation. Deficiency leads to hemolytic anemia and neurological deficits (spinocerebellar ataxia). **NEET-PG High-Yield Pearls:** * **Metaplasia** is a reversible change where one adult cell type is replaced by another to withstand stress [1]. * **Vitamin A & the Eye:** Deficiency causes Xerophthalmia. The sequence is: Nyctalopia (Night blindness) → Conjunctival xerosis → **Bitot’s spots** (keratin plaques) → Corneal xerosis → Keratomalacia (corneal melting). * **Therapeutic use:** All-trans retinoic acid (ATRA) is used in Acute Promyelocytic Leukemia (M3) to induce cell differentiation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 49.

Question 144: In malignant hypertension, necrosis is of which type?

A. Caseous necrosis
B. Fibrinoid necrosis (Correct Answer)
C. Liquifactive necrosis
D. Coagulative necrosis

Explanation: ### Explanation **Correct Answer: B. Fibrinoid Necrosis** **Why it is correct:** Fibrinoid necrosis is a specialized form of cell death typically seen in immune-mediated vascular damage and severe hypertensive emergencies [2]. In **malignant hypertension**, the extreme elevation in blood pressure causes acute hemodynamic stress, leading to the leakage of plasma proteins (including **fibrinogen**) into the vessel wall [1]. These proteins, combined with the necrosis of smooth muscle cells in the tunica media, create a bright pink, amorphous, "fibrin-like" appearance under H&E staining [4]. This specific vascular lesion is often termed **arteriolosclerosis** (specifically hyperplastic or necrotizing arteriolitis). **Why other options are incorrect:** * **Caseous Necrosis:** Characterized by a "cheese-like" friable appearance, this is classically associated with **Tuberculosis** (granulomatous inflammation). * **Liquefactive Necrosis:** Occurs when enzymatic digestion transforms tissue into a liquid viscous mass. It is the hallmark of **CNS infarcts** (brain) and **abscesses** (bacterial/fungal infections). * **Coagulative Necrosis:** The most common pattern of necrosis, where cell outlines are preserved for a few days. It is typically seen in **ischemic infarcts** of solid organs (heart, kidney, spleen), except the brain. **NEET-PG High-Yield Pearls:** * **Malignant Hypertension:** Defined by BP >200/120 mmHg + papilledema [3]. * **Microscopic Hallmark:** "Onion-skinning" (hyperplastic arteriolosclerosis) and fibrinoid necrosis [1]. * **Kidney Involvement:** Known as **malignant nephrosclerosis**, it presents grossly as a **"flea-bitten kidney"** due to petechial hemorrhages. * **Other sites for Fibrinoid Necrosis:** Aschoff bodies (Rheumatic Heart Disease), Polyarteritis Nodosa (PAN), and Type III Hypersensitivity reactions (Arthus reaction). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 943-945. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 277-278. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 276-277. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499.

Question 145: NSAID drug-induced edema is primarily due to which of the following mechanisms?

A. Increased hydrostatic pressure (Correct Answer)
B. Protein-losing enteropathy
C. Endothelial damage due to IL-2
D. Low oncotic pressure

Explanation: **Explanation:** The primary mechanism of NSAID-induced edema is **increased hydrostatic pressure** resulting from renal effects [1]. NSAIDs inhibit the enzyme Cyclooxygenase (COX), leading to decreased synthesis of **Prostaglandins (PGE2 and PGI2)**. In the kidneys, these prostaglandins are essential for maintaining vasodilation of the afferent arterioles. Their inhibition leads to: 1. **Renal Vasoconstriction:** Reducing renal blood flow. 2. **Sodium and Water Retention:** Decreased perfusion triggers the Renin-Angiotensin-Aldosterone System (RAAS) and increases tubular reabsorption of sodium [2][3]. 3. **Increased Plasma Volume:** The resulting expansion of intravascular volume increases capillary hydrostatic pressure, forcing fluid into the interstitial space (edema) [1]. **Analysis of Incorrect Options:** * **Option B (Protein-losing enteropathy):** While NSAIDs can cause GI ulcers, they do not typically cause systemic edema via protein loss unless there is severe, chronic erosive gastritis/colitis leading to hypoproteinemia, which is not the primary mechanism. * **Option C (Endothelial damage due to IL-2):** This describes the mechanism of "Capillary Leak Syndrome," often seen in systemic inflammatory response syndromes or specific immunotherapy, not NSAID use. * **Option D (Low oncotic pressure):** This occurs in conditions like Nephrotic syndrome (protein loss) or Cirrhosis (decreased synthesis) [1]. NSAIDs cause fluid *gain* (hydrostatic) rather than protein *loss* (oncotic). **NEET-PG High-Yield Pearls:** * **Triple Whammy:** The dangerous combination of **NSAIDs + ACE Inhibitors + Diuretics** can precipitate acute kidney injury (AKI) by severely compromising glomerular filtration. * NSAIDs are a common cause of **secondary hypertension** and can exacerbate pre-existing Congestive Heart Failure (CHF) due to fluid retention [1][3]. * **Analgesic Nephropathy:** Chronic NSAID use is associated with **Renal Papillary Necrosis** and Chronic Interstitial Nephritis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 124. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 496-497. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 520-521.

Question 146: Granulomatous inflammatory reaction is caused by all of the following EXCEPT:

A. M. Tuberculosis
B. M. Leprae
C. Yersinia pestis
D. Mycoplasma (Correct Answer)

Explanation: **Explanation:** A **granuloma** is a localized collection of activated macrophages (epithelioid cells), often surrounded by a collar of lymphocytes and sometimes containing multinucleated giant cells [1], [2]. It is a form of chronic inflammation triggered by agents that are difficult to eradicate. **Why Mycoplasma is the Correct Answer:** * **Mycoplasma pneumoniae** typically causes **atypical pneumonia** characterized by interstitial inflammation. The histological hallmark is a peribronchial and perivascular infiltration of **lymphocytes and plasma cells**, rather than a granulomatous response. It lacks a cell wall and does not trigger the Type IV hypersensitivity reaction required for granuloma formation. **Analysis of Incorrect Options:** * **M. Tuberculosis:** The classic cause of granulomatous inflammation [1]. It produces **caseating granulomas** (central necrosis) due to the delayed-type hypersensitivity response to the bacterium's waxy cell wall (mycolic acid). * **M. Leprae:** Causes leprosy, characterized by either **tuberculoid granulomas** (well-formed) or **lepromatous lesions** (foamy macrophages), depending on the host's immune response. * **Yersinia pestis:** While primarily causing necrotizing inflammation in bubonic plague, certain species of Yersinia (like *Y. pseudotuberculosis* and *Y. enterocolitica*) are well-known causes of **sarcoid-like non-caseating granulomas** in mesenteric lymph nodes. **NEET-PG High-Yield Pearls:** 1. **Non-infectious causes of granulomas:** Sarcoidosis (non-caseating), Berylliosis, and Foreign body reaction (suture, talc) [2]. 2. **Stellate Granulomas:** Characteristically seen in **Cat Scratch Disease** (*Bartonella henselae*) and Lymphogranuloma venereum (LGV). 3. **Key Cytokine:** **IFN-gamma** (secreted by Th1 cells) is the most important cytokine for activating macrophages into epithelioid cells. 4. **TNF-alpha:** Essential for maintaining the structural integrity of a granuloma; TNF inhibitors can cause latent TB to reactivate. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360. [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. 196-200.

Question 147: Malignant cells characteristically

A. Have a shorter cell cycle than the normal cells in their parent tissue
B. Have the same DNA content as the normal cells in their parent tissue
C. Are contact inhibited in tissue culture
D. Take at least 30 doubling times before they become clinically detectable (Correct Answer)

Explanation: ### Explanation **1. Why Option D is Correct:** The growth of a tumor is determined by the **doubling time** of the cells. For a tumor to become clinically detectable (approximately **1 cm** in diameter or **1 gram** in weight), it must undergo at least **30 population doublings**. At this stage, the tumor contains roughly **$10^9$ (1 billion) cells**. It takes only 10 more doublings ($10^{12}$ cells) to reach a size that is usually incompatible with life (approx. 1 kg). **2. Why the Other Options are Incorrect:** * **Option A:** It is a common misconception that malignant cells divide faster. In reality, the **cell cycle time** of many cancer cells is actually **the same or even longer** than that of their normal counterparts [2]. Tumor growth occurs because the **growth fraction** (the proportion of cells in the replicative pool) is high and apoptosis is decreased, not because the cycle itself is shorter [2]. * **Option B:** Malignant cells are characterized by **genetic instability** [1]. They often exhibit **aneuploidy** (abnormal number of chromosomes) or polyploidy, meaning their DNA content is typically different (often higher) than normal diploid cells [1]. * **Option C:** Normal cells stop dividing when they come into contact with each other (contact inhibition). Malignant cells **lose contact inhibition**, allowing them to pile up and grow in a disorganized, multilayered fashion in culture [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Growth Fraction:** This is the most important determinant of drug susceptibility. Chemotherapy is most effective against tumors with a high growth fraction (e.g., Burkitt Lymphoma). * **Gompertzian Growth:** Tumor growth is not linear; it follows a sigmoid curve where the growth rate slows down as the tumor gets larger due to nutrient depletion and poor blood supply [2]. * **Smallest Detectable Mass:** 1 gram ($10^9$ cells) is the threshold for clinical detection via physical exam or imaging. **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. 212-213, 232-233. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 276-278.

Question 148: Clear cells are commonly seen in which of the following lesions?

A. Pleomorphic adenoma
B. Warthin's tumor
C. Mucoepidermoid carcinoma (Correct Answer)
D. Adenomatoid odontogenic tumor

Explanation: **Explanation:** **Mucoepidermoid Carcinoma (MEC)** is the most common malignant salivary gland tumor. It is histologically characterized by a mixture of three cell types: **mucous cells, epidermoid (squamous) cells, and intermediate cells.** [1] Clear cells are a recognized variant in MEC, often resulting from the accumulation of glycogen or as a fixation artifact in the cytoplasm. In high-grade variants or specific "clear cell" subtypes, these cells can be prominent, making MEC a classic differential for clear cell lesions of the head and neck. **Analysis of Incorrect Options:** * **Pleomorphic Adenoma:** Known as "mixed tumor," it features a combination of epithelial/myoepithelial cells and a mesenchymal-like stroma (myxoid, chondroid, or osteoid). While myoepithelial cells can occasionally appear clear, it is not the defining feature. * **Warthin’s Tumor (Papillary Cystadenoma Lymphomatosum):** Characterized by a pathognomonic **double layer of oncocytic cells** (eosinophilic, granular cytoplasm) resting on a dense lymphoid stroma with germinal centers. [1] * **Adenomatoid Odontogenic Tumor (AOT):** An odontogenic tumor characterized by duct-like structures lined by cuboidal or columnar cells and "rosette" patterns, rather than clear cell predominance. **NEET-PG High-Yield Pearls:** * **MEC Staining:** Mucous cells in MEC stain positive with **Mucicarmine**, PAS, and Alcian Blue. * **Clear Cell Differentials:** Other "clear cell" tumors in pathology include **Renal Cell Carcinoma (most common overall)**, Clear Cell Odontogenic Carcinoma, and Clear Cell Sarcoma. [2] * **Warthin’s Tumor Association:** Strongly associated with **smoking** and most commonly occurs in the tail of the parotid gland. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, p. 753. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 959.

Question 149: What are the chances of an offspring being affected when one parent is an autosomal dominant heterozygote?

A. 25%
B. 50% (Correct Answer)
C. 100%
D. None

Explanation: In **Autosomal Dominant (AD)** inheritance, the presence of a single mutant allele is sufficient to express the disease phenotype [1]. When one parent is a heterozygote (Aa) and the other is unaffected (aa), the offspring have a **50% probability** of inheriting the affected allele [1]. **1. Why 50% is correct:** Using a Punnett square (Aa !! aa), the possible genotypes for the offspring are: * **Aa** (Affected): 50% * **aa** (Unaffected): 50% Because the trait is dominant, every child who inherits the 'A' allele will manifest the disease. **2. Why other options are incorrect:** * **25%:** This is the recurrence risk for an **Autosomal Recessive** disorder when both parents are asymptomatic carriers (Aa !! Aa) [1]. * **100%:** This would only occur if one parent was a homozygote (AA) for the dominant trait, which is rare in clinical practice as many AD conditions are lethal in the homozygous state. * **None:** This is incorrect because the dominant allele is transmitted to half of the progeny on average. **High-Yield Clinical Pearls for NEET-PG:** * **Vertical Transmission:** AD disorders typically appear in every generation. * **Male = Female:** Both sexes are affected with equal frequency. * **Reduced Penetrance:** An individual may inherit the dominant gene but not express the phenotype (e.g., Retinoblastoma). * **Variable Expressivity:** Patients with the same genetic mutation show different clinical severities (e.g., Neurofibromatosis Type 1) [2]. * **Key Examples:** Marfan syndrome, Huntington disease, Achondroplasia, and Familial Hypercholesterolemia [2]. **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. 53-54. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 149-150.

Question 150: What is the term for physiologic programmed cell death?

A. Apoptosis (Correct Answer)
B. Lysis
C. Autolysis
D. Autopsy

Explanation: **Explanation:** **Apoptosis** is the correct answer because it is defined as a pathway of cell death induced by a tightly regulated intracellular program [1]. It is often referred to as "programmed cell death" or "cell suicide." Unlike necrosis, apoptosis can be a **physiologic process** (e.g., embryogenesis, endometrial breakdown during menses, or elimination of self-reactive lymphocytes) or a pathologic one (e.g., DNA damage or viral infections) [1], [3]. It is characterized by cell shrinkage, chromatin condensation [2], and the formation of apoptotic bodies without inciting an inflammatory response. **Why other options are incorrect:** * **Lysis:** Refers to the physical disintegration of a cell membrane, typically resulting in the release of cytoplasmic contents. It is a feature of necrosis or osmotic stress, not a programmed physiologic process. * **Autolysis:** This is the post-mortem degradation of cells by their own endogenous enzymes (lysosomal enzymes). It occurs after the death of the entire organism and is not a controlled cellular program. * **Autopsy:** This is a surgical procedure (post-mortem examination) performed on a corpse to determine the cause of death; it is not a cellular process. **High-Yield NEET-PG Pearls:** * **Morphological Hallmark:** The most characteristic feature of apoptosis is **chromatin condensation** (pyknosis) [2]. * **Key Enzymes:** **Caspases** (Cysteine-aspartic proteases) are the executioners of apoptosis [1]. * **DNA Pattern:** On gel electrophoresis, apoptosis shows a characteristic **"Step-ladder pattern"** due to internucleosomal DNA cleavage by endonucleases [2] (contrast this with the "smear pattern" seen in necrosis). * **Membrane Change:** Phosphatidylserine flips from the inner to the outer leaflet of the plasma membrane, serving as an "eat-me" signal for macrophages. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 63-65. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 740-741. [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. 80-81.

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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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