General Pathology — MCQs

A couple is referred to the physician because their first three pregnancies have ended in spontaneous abortion. Chromosomal analysis reveals that the wife has two cell lines in her blood, one with a missing X chromosome (45,X) and the other normal (46,XX). Her chromosomal constitution can be described as?

Q589Easy

Secondary amyloidosis complicates which of the following?

Q590Easy

Amyloid protein in human beings is:

General Pathology Indian Medical PG Practice Questions and MCQs

Question 581: Which type of necrosis is typically seen in acute pancreatitis?

A. Coagulative necrosis
B. Fat necrosis (Correct Answer)
C. Liquefactive necrosis
D. Fibrinoid necrosis

Explanation: **Explanation:** **Fat necrosis** is the hallmark of acute pancreatitis [1]. This process occurs due to the premature activation of pancreatic enzymes, specifically **lipases**, which are released into the peripancreatic tissue and the peritoneal cavity. These enzymes break down triglycerides into free fatty acids. These fatty acids then combine with calcium ions in a process called **saponification**, forming chalky white, soap-like deposits that are macroscopically visible [1]. **Analysis of Incorrect Options:** * **Coagulative necrosis:** This is the most common type of necrosis, typically seen in hypoxic/ischemic injury in solid organs (e.g., myocardial infarction), except the brain. It preserves the basic structural outline of the tissue for a few days. * **Liquefactive necrosis:** Characterized by the digestion of dead cells into a liquid viscous mass. It is typically seen in bacterial/fungal infections and **ischaemic injury to the brain**. (Note: While the pancreatic parenchyma itself may undergo liquefaction, "Fat Necrosis" is the classic descriptor for the condition). * **Fibrinoid necrosis:** Usually seen in immune-mediated vascular damage (e.g., Polyarteritis Nodosa or malignant hypertension) where complexes of antigens and antibodies are deposited in arterial walls. **High-Yield Clinical Pearls for NEET-PG:** * **Microscopic appearance:** Fat necrosis shows shadowy outlines of necrotic adipocytes with basophilic (bluish) calcium deposits [1]. * **Saponification:** The "chalky white" appearance is a classic gross pathology description [1]. * **Clinical Correlation:** In acute pancreatitis, the degree of **hypocalcemia** (due to calcium being "consumed" during saponification) is a key prognostic indicator used in Ranson’s Criteria. **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. 55.

Question 582: What is a reason for tissue analysis in surgery?

A. Repeated Fine Needle Aspiration Cytology (FNAC)
B. To confirm a suspected or established clinical diagnosis for prognosis and treatment planning (Correct Answer)
C. To confirm radiological findings
D. For data recording purposes

Explanation: **Explanation:** Tissue analysis (Histopathology) remains the **"Gold Standard"** in surgical pathology [5]. The primary objective is to provide a definitive diagnosis that guides the entire clinical management of the patient [4]. 1. **Why Option B is Correct:** Histopathological examination allows for the identification of specific disease processes (e.g., distinguishing between benign and malignant tumors) [5]. Beyond diagnosis, it provides critical information for **prognosis** (such as tumor grading, depth of invasion, and lymphovascular invasion) [1], [3] and **treatment planning** (such as identifying hormone receptor status in breast cancer or surgical margins) [1], [2]. 2. **Why Other Options are Incorrect:** * **Option A:** FNAC is a cytological screening tool used *before* surgery. Tissue analysis (biopsy/resection) is more definitive than FNAC because it preserves tissue architecture [2]. * **Option C:** While pathology often correlates with radiology, the goal of surgery is not merely to "confirm" imaging but to provide a tissue-level diagnosis which imaging cannot definitively provide [5]. * **Option D:** Data recording and tumor registries are secondary administrative benefits, not the primary clinical reason for performing surgery and tissue analysis. **High-Yield Clinical Pearls for NEET-PG:** * **Frozen Section:** A form of rapid tissue analysis performed *intraoperatively* to determine surgical margins or the nature of a mass (benign vs. malignant) to decide the extent of surgery. * **Fixative of Choice:** 10% Neutral Buffered Formalin is the standard for routine histopathology. * **Biopsy Types:** **Incisional** (part of the lesion) vs. **Excisional** (entire lesion removed). Excisional biopsy is both diagnostic and therapeutic. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 344-346. [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. 256-257. [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. 236-237. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 443-444. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 340-341.

Question 583: All of the following mediators of acute inflammation are derived from cells except?

A. Kinins (Correct Answer)
B. Cytokines
C. Histamine
D. Leukotrienes

Explanation: Chemical mediators of acute inflammation are classified into two broad categories based on their source: **Cell-derived** and **Plasma-derived** [1]. ### 1. Why Kinins is the Correct Answer **Kinins (e.g., Bradykinin)** are **plasma-derived mediators** [2]. They are produced by the proteolytic cleavage of high-molecular-weight kininogen (HMWK) in the plasma, a process triggered by the activation of **Hageman Factor (Factor XII)** [2]. Because they circulate in the blood as inactive precursors and are not synthesized within cells for storage or immediate release, they are the exception in this list. ### 2. Why the Other Options are Incorrect * **Histamine:** This is a **cell-derived** vasoactive amine [1]. It is pre-formed and stored in the granules of **mast cells**, basophils, and platelets, from which it is released during the early phase of inflammation [4]. * **Cytokines:** These are **cell-derived** proteins (e.g., TNF, IL-1) produced primarily by activated macrophages, lymphocytes, and endothelial cells [1]. * **Leukotrienes:** These are **cell-derived** lipid mediators synthesized de novo from **arachidonic acid** via the lipoxygenase pathway in leukocytes (neutrophils and macrophages) [4]. ### Clinical Pearls for NEET-PG * **Factor XII (Hageman Factor)** is the "master switch" that links four systems: Kinin system, Clotting system, Fibrinolytic system, and Complement system [2]. * **Plasma-derived mediators** include the Complement system, Kinins, and Coagulation/Fibrinolytic proteins [2]. * **Cell-derived mediators** include Vasoactive amines (Histamine/Serotonin), Arachidonic acid metabolites (Prostaglandins/Leukotrienes), Cytokines, and Nitric Oxide [1]. * **Bradykinin** is responsible for inducing **pain** (along with Prostaglandin E2) and increasing vascular permeability [3][5]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94. [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. 189-190. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 100-101. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 94-95. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 584: Tooth discolouration due to high bilirubin secretion is seen in which condition?

A. Pink tooth of Mummery
B. Ochronosis
C. Chlorodontia (Correct Answer)
D. Leong teeth

Explanation: **Explanation:** **Correct Answer: C. Chlorodontia** Chlorodontia (green teeth) is a rare clinical manifestation of **hyperbilirubinemia** occurring during the period of tooth development [1]. In neonates or infants with prolonged jaundice (e.g., Biliary Atresia or Erythroblastosis Fetalis), high levels of circulating **conjugated bilirubin** are deposited in the dental hard tissues (dentin and enamel) [1], [2]. Because teeth are non-remodeling tissues, the pigment becomes permanently trapped, resulting in a characteristic green or yellowish-green discoloration. **Analysis of Incorrect Options:** * **A. Pink tooth of Mummery:** This refers to a pinkish discoloration caused by **internal resorption** of the tooth. The color is due to the highly vascularized granulation tissue within the pulp chamber shining through the thinned-out dentin and enamel. * **B. Ochronosis:** Associated with **Alkaptonuria** (deficiency of homogentisic acid oxidase). It results in the accumulation of homogentisic acid, causing dark blue-black pigmentation of connective tissues, cartilages (like the pinna), and joints, but is not the primary cause of neonatal green teeth. * **D. Leong teeth:** Also known as *Dens Evaginatus*, this is a developmental anomaly characterized by an accessory cusp-like elevation on the occlusal surface, typically seen in premolars. It is a structural anomaly, not a pigmentary one. **NEET-PG High-Yield Pearls:** * **Tetracycline staining:** Causes yellowish-brown discoloration and fluorescence under UV light; occurs if taken during tooth calcification. * **Congenital Erythropoietic Porphyria (Gunther disease):** Causes **reddish-brown** discoloration of teeth (Erythrodontia) due to porphyrin deposition. * **Fluorosis:** Causes "mottled enamel" with chalky white patches or brownish staining due to excessive fluoride intake (>1.5 mg/L). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 860-864. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 603-604.

Question 585: Which of the following is seen in both apoptosis and necrosis?

A. Both may be physiological
B. Both may be pathological (Correct Answer)
C. Inflammation
D. Intact cell membrane

Explanation: **Explanation:** Cell death occurs via two primary pathways: **Necrosis** and **Apoptosis**. Understanding their fundamental differences is a high-yield topic for NEET-PG [1]. **1. Why "Both may be pathological" is correct:** * **Necrosis** is *always* a pathological process resulting from irreversible cell injury (e.g., ischemia, toxins, or infections) [1]. It is never physiological. * **Apoptosis** can be either physiological (e.g., embryogenesis, endometrial shedding) [1] or **pathological**. Pathological apoptosis occurs when cells are damaged beyond repair, such as DNA damage (radiation/cytotoxic drugs) [2], accumulation of misfolded proteins (ER stress), or certain viral infections (e.g., viral hepatitis forming Councilman bodies). Therefore, being "pathological" is the common denominator. **2. Analysis of Incorrect Options:** * **A. Both may be physiological:** Incorrect. Necrosis is strictly pathological; it never occurs in healthy physiological states [1]. * **C. Inflammation:** Incorrect. Necrosis is characterized by the leakage of cellular contents, triggering an acute inflammatory response [1]. Apoptosis is "silent"; the cell membrane remains intact, and apoptotic bodies are phagocytosed without releasing pro-inflammatory mediators. * **D. Intact cell membrane:** Incorrect. In necrosis, the hallmark is the **loss of membrane integrity**, leading to enzymatic leakage [1]. In apoptosis, the membrane remains structurally intact (though altered) until phagocytosis occurs. **Clinical Pearls for NEET-PG:** * **Gold Standard for Apoptosis detection:** DNA Laddering (Step-ladder pattern on electrophoresis) due to internucleosomal cleavage by endonucleases. * **Necrosis Pattern:** Smear pattern on electrophoresis (random DNA degradation). * **Caspases:** The executioners of apoptosis (Cysteine proteases). * **Mitochondria:** Play a central role in the intrinsic pathway of apoptosis (release of Cytochrome C) [1]. **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. 49-64. [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. 101-103.

Question 586: Histologic sections of the thymus that reveal reactive follicles with germinal centers are diagnostic of what condition?

A. Acute inflammation
B. Chronic inflammation
C. Thymic hyperplasia (Correct Answer)
D. Thymic hypoplasia

Explanation: **Thymic Hyperplasia (Follicular Hyperplasia)** is characterized by the presence of lymphoid follicles with active germinal centers within the thymic medulla [1]. Normally, the thymus does not contain germinal centers; their presence indicates a B-cell mediated immune response within the T-cell dominant organ. * **Why Option C is Correct:** In pathology, "Thymic Hyperplasia" specifically refers to **lymphoid follicular hyperplasia** [1]. This is most famously associated with **Myasthenia Gravis (MG)**, where it is seen in approximately 65-75% of patients [1], [2]. These germinal centers contain B-cells that are involved in the production of autoantibodies against acetylcholine receptors (AChR) [3]. * **Why Option A & B are Incorrect:** While germinal centers are a feature of chronic inflammation in other tissues, in the context of the thymus, this specific histologic finding is the diagnostic hallmark of hyperplasia. Acute inflammation would show neutrophilic infiltration and necrosis, which is not the description provided. * **Why Option D is Incorrect:** Thymic hypoplasia (e.g., DiGeorge Syndrome) refers to the underdevelopment or absence of the gland, leading to T-cell deficiency, not the formation of reactive follicles. **NEET-PG High-Yield Pearls:** 1. **Association:** Always link Thymic Follicular Hyperplasia with **Myasthenia Gravis** [2]. 2. **Thymoma vs. Hyperplasia:** Thymoma is a true neoplasm of thymic epithelial cells; Hyperplasia is a reactive lymphoid process [1]. 3. **Treatment:** Thymectomy often improves symptoms in MG patients with thymic hyperplasia. 4. **Histology:** Look for **Hassall’s corpuscles** (normal thymic finding) [2] vs. **Germinal Centers** (diagnostic of hyperplasia) [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 571-572. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 634. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 213-214.

Question 587: Which of the following types of hypersensitivity reactions is associated with the given condition?

A. Anaphylactic type
B. Cytotoxic type (Correct Answer)
C. Type III hypersensitivity
D. Cell-mediated hypersensitivity

Explanation: ***Cytotoxic type*** - **Type II hypersensitivity** involves **IgG/IgM antibodies** binding to cell-surface or extracellular matrix antigens, leading to **complement activation** and **cell destruction**. - Classic example is **pemphigus vulgaris** where antibodies target **desmoglein proteins** in desmosomes, causing **acantholysis** and blister formation. *Anaphylactic type* - **Type I hypersensitivity** is mediated by **IgE antibodies** and **mast cell degranulation**, causing immediate reactions like **anaphylaxis**. - Involves **histamine release** and **vasodilation**, not direct cellular destruction by antibodies against structural proteins. *Type III hypersensitivity* - **Immune complex-mediated** reaction involving **antigen-antibody complexes** depositing in tissues, causing **inflammation**. - Examples include **serum sickness** and **lupus nephritis**, not autoantibodies targeting specific cell adhesion molecules. *Cell-mediated hypersensitivity* - **Type IV hypersensitivity** involves **T-cells** and **delayed-type reactions**, typically occurring **48-72 hours** after exposure. - Examples include **contact dermatitis** and **tuberculin skin test**, not antibody-mediated cellular damage.

Question 588: A couple is referred to the physician because their first three pregnancies have ended in spontaneous abortion. Chromosomal analysis reveals that the wife has two cell lines in her blood, one with a missing X chromosome (45,X) and the other normal (46,XX). Her chromosomal constitution can be described as?

A. Chimeric
B. Monoploid
C. Trisomic
D. Mosaic (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Mosaic** **Mosaicism** is defined as the presence of two or more populations of cells with different genotypes in one individual who has developed from a **single fertilized egg (zygote)** [1]. In this case, the wife has two cell lines (45,X and 46,XX) originating from the same zygote. This typically occurs due to **post-zygotic mitotic non-disjunction** or anaphase lag during early embryonic development [1]. Mosaic Turner syndrome (45,X/46,XX) often presents with a milder phenotype than classic Turner syndrome (45,X), allowing for secondary sexual characteristics and, occasionally, the ability to conceive, though it is a known cause of recurrent spontaneous abortions. **Why Incorrect Options are Wrong:** * **A. Chimeric:** Chimerism involves two or more cell lines derived from **different zygotes** (e.g., the fusion of two embryos or exchange of cells between twins in utero). * **B. Monoploid:** This refers to a cell or organism having a single set of chromosomes (n). In humans, only gametes are monoploid. * **C. Trisomic:** This refers to the presence of an extra chromosome (e.g., Trisomy 21). The patient in the question has a cell line with a missing chromosome (monosomy), not an extra one. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Mosaicism results from **post-zygotic** errors; Chimerism results from **fusion** of different zygotes. * **Germline Mosaicism:** If a mutation occurs in a germ cell precursor, the individual is phenotypically normal but can pass the mutation to multiple offspring (e.g., Osteogenesis Imperfecta, Duchenne Muscular Dystrophy). * **Turner Syndrome:** 45,X/46,XX is the most common mosaic pattern in Turner syndrome [1]. These patients have a higher risk of premature ovarian failure and recurrent pregnancy loss. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169.

Question 589: Secondary amyloidosis complicates which of the following?

A. Pneumonia
B. Chronic glomerulonephritis
C. Osteosarcoma
D. Chronic osteomyelitis (Correct Answer)

Explanation: **Secondary (AA) Amyloidosis** occurs due to the deposition of **Amyloid Associated (AA) protein**, which is derived from the precursor protein **Serum Amyloid A (SAA)** [3]. SAA is an acute-phase reactant synthesized by the liver in response to chronic inflammatory states [1]. 1. **Why Chronic Osteomyelitis is Correct:** Secondary amyloidosis is a complication of **long-standing chronic inflammation** [3]. Chronic osteomyelitis involves persistent infection and inflammation of the bone, leading to sustained high levels of SAA [1]. Over time, this protein undergoes limited proteolysis to form AA amyloid fibrils, which deposit in organs like the kidneys, liver, and spleen [1]. Other classic causes include Rheumatoid Arthritis (most common in the West), Tuberculosis, and Bronchiectasis [3]. 2. **Why Other Options are Incorrect:** * **Pneumonia:** This is typically an **acute** infection. Secondary amyloidosis requires months or years of persistent inflammation to develop. * **Chronic Glomerulonephritis:** While this is a chronic condition, it is a **consequence** (end-stage) of various renal insults rather than a primary driver of systemic SAA production. In fact, amyloidosis itself often *causes* nephrotic syndrome and subsequent renal failure [1]. * **Osteosarcoma:** This is a malignancy. While some cancers (like Hodgkin lymphoma) can cause AA amyloidosis, osteosarcoma is not a recognized classic precursor. Primary amyloidosis (AL type) is more commonly associated with plasma cell dyscrasias [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Stain of choice:** Congo Red (shows **Apple-green birefringence** under polarized light). * **Most common organ involved:** Kidney (presents as Nephrotic Syndrome). * **Precursor protein:** SAA (Acute phase reactant) [1]. * **Most common cause worldwide:** Rheumatoid Arthritis [3]. * **Most common cause in developing countries:** Tuberculosis/Chronic infections [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. 136-140. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267. [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. 195-196.

Question 590: Amyloid protein in human beings is:

A. A naturally present protein in normal individuals
B. Selectively involves blood vessels
C. Visible to the naked eye as whitish cheesy material
D. A material that gets deposited in extracellular spaces (Correct Answer)

Explanation: **Explanation:** **Amyloidosis** refers to a group of disorders characterized by the **extracellular** deposition of misfolded, insoluble fibrillar proteins [1]. 1. **Why Option D is Correct:** Amyloid is fundamentally an **extracellular** deposit [1]. These proteins aggregate into a characteristic β-pleated sheet configuration, which makes them resistant to proteolysis [4]. They accumulate in the interstitial spaces of various tissues and organs, eventually causing pressure atrophy and functional impairment of the parenchymal cells [4]. 2. **Why Other Options are Incorrect:** * **Option A:** Amyloid is **never** present in normal individuals. It is a pathological protein product resulting from abnormal folding of precursor proteins (like AL or AA) [1]. * **Option B:** While amyloid often involves blood vessel walls (causing fragility and hemorrhage), it is **not selective** to them [3]. It involves various sites including the basement membranes of viscera, nerves, and connective tissue. * **Option C:** Macroscopically, amyloid-involved organs are typically enlarged, firm, and have a **waxy, gray-tan, or translucent appearance** [2]. "Whitish cheesy material" is characteristic of **caseous necrosis** (e.g., Tuberculosis), not amyloid. **High-Yield Clinical Pearls for NEET-PG:** * **Staining:** The gold standard is **Congo Red**, which shows **apple-green birefringence** under polarized light [4]. * **Structure:** All amyloid types share a common **non-branching, linear fibril** structure (7.5–10 nm diameter) and a **cross-̢-pleated sheet** conformation on X-ray crystallography [4]. * **Composition:** 95% fibril proteins + 5% P-component (glycoprotein) [1]. * **Common Types:** **AL** (Primary, from light chains), **AA** (Secondary, from SAA protein in chronic inflammation), and **A̢** (found in Alzheimer’s disease) [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-266. [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. 135-136. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 533-534. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269.

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Cell Injury and Cell Death

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Adaptations of Cellular Growth

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Hemodynamic Disorders

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Genetic Disorders

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