General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1011: Which stain is used to detect lipids in tissue?

A. Oil Red O (Correct Answer)
B. Mucicarmine
C. PAS
D. Myeloperoxidase

Explanation: **Explanation:** **Correct Answer: A. Oil Red O** Lipids are typically dissolved out of tissues during routine processing (dehydration with alcohol and clearing with xylene). To detect them, tissues must be processed using **frozen sections**. **Oil Red O** is a lysochrome (fat-soluble dye) that works on the principle of physical solubility. The dye is more soluble in the lipid droplets than in the solvent, causing it to move into the fat and stain it a brilliant red. Other common lipid stains include **Sudan Black B** and **Sudan IV**. [2] **Analysis of Incorrect Options:** * **B. Mucicarmine:** This is a specific stain used to identify **acid mucopolysaccharides (mucin)**. It is classically used to identify *Cryptococcus neoformans* (staining its capsule red) and adenocarcinomas. * **C. PAS (Periodic Acid-Schiff):** This stain detects **glycogen** and complex carbohydrates. [1] It is used for basement membranes, fungal walls, and identifying glycogen storage diseases. * **D. Myeloperoxidase (MPO):** This is an enzyme histochemical stain (or IHC marker) used to identify cells of **myeloid lineage**. It is the gold standard for differentiating Acute Myeloid Leukemia (AML) from Acute Lymphoblastic Leukemia (ALL). **High-Yield Clinical Pearls for NEET-PG:** * **Frozen Section is mandatory:** You cannot use paraffin-embedded sections for lipid staining because the processing solvents remove the fat. * **Fat Embolism:** Oil Red O is the stain of choice to demonstrate fat globules in the microvasculature (e.g., in the lungs or brain) following long bone fractures. * **Osmium Tetroxide:** This is another lipid stain that turns fat **black** and is unique because it also acts as a fixative for electron microscopy. **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. 75. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 161-162.

Question 1012: A patient, two months post-renal transplant, presents with difficulty in breathing. Chest X-ray reveals bilateral diffuse interstitial infiltrates, predominantly in the perihilar region. What is the most probable etiologic agent?

A. Cytomegalovirus (CMV)
B. Mycobacterium tuberculosis
C. Staphylococcus aureus
D. Pneumocystis jirovecii (Correct Answer)

Explanation: **Explanation:** The clinical presentation of a post-renal transplant patient with bilateral diffuse interstitial infiltrates, particularly in the perihilar region, is classic for **Pneumocystis jirovecii pneumonia (PJP)**. [1] **1. Why Pneumocystis jirovecii is correct:** PJP is a common opportunistic fungal infection in immunocompromised individuals (especially those on post-transplant immunosuppression or with HIV). [1] The hallmark radiological finding is **bilateral, symmetrical, "ground-glass" opacities** or interstitial infiltrates starting from the perihilar region and spreading peripherally. The timing (two months post-transplant) coincides with the period of maximal immunosuppression. **2. Why the other options are incorrect:** * **Cytomegalovirus (CMV):** While CMV is a major post-transplant pathogen, it typically presents with more systemic symptoms (fever, leukopenia) and, if causing pneumonia, often shows nodular or patchy infiltrates rather than the classic perihilar interstitial pattern. [1] * **Mycobacterium tuberculosis:** TB usually presents with focal consolidations, cavitary lesions (upper lobes), or miliary patterns, rather than diffuse perihilar interstitial infiltrates. * **Staphylococcus aureus:** This causes acute, necrotizing pyogenic pneumonia characterized by lobar consolidation, abscess formation, or pneumatoceles, not a diffuse interstitial pattern. **3. NEET-PG High-Yield Pearls:** * **Diagnosis:** Silver stains (Gomori Methenamine Silver - GMS) show characteristic **"crushed ping-pong ball"** or "cup-and-saucer" shaped cysts. [1] * **Investigation of Choice:** Bronchoalveolar Lavage (BAL) is the most sensitive diagnostic method. * **Prophylaxis:** Trimethoprim-sulfamethoxazole (TMP-SMX) is the standard drug for both prophylaxis and treatment. * **Biomarker:** Elevated serum **Beta-D-Glucan** is a sensitive but non-specific marker for PJP. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 318-319.

Question 1013: Which anticoagulant is best suited for the osmotic fragility test?

A. Heparin (Correct Answer)
B. EDTA
C. Trisodium citrate
D. Potassium oxalate

Explanation: The **Osmotic Fragility Test (OFT)** measures the resistance of red blood cells (RBCs) to hemolysis when exposed to varying concentrations of hypotonic saline. The choice of anticoagulant is critical because any alteration in the ionic concentration or volume of the RBCs can lead to false results. **1. Why Heparin is the Correct Answer:** Heparin is the preferred anticoagulant for OFT because it is a **pharmacological anticoagulant** that works by activating antithrombin III [1]. Unlike other agents, it **does not alter the size or shape of the RBCs**, nor does it interfere with the electrolyte balance of the plasma. This ensures that the baseline osmotic state of the cell remains physiological before the test begins. **2. Why Other Options are Incorrect:** * **EDTA (Ethylenediaminetetraacetic acid):** While excellent for routine morphology (CBC), EDTA is a chelating agent that removes calcium. It can cause slight shrinkage of RBCs and introduces additional salts into the sample, which can artificially alter the osmotic gradient. * **Trisodium Citrate:** This is a liquid anticoagulant (used in 1:9 or 1:4 ratios). It **dilutes the blood sample** and significantly alters the tonicity of the plasma, making it unsuitable for fragility studies. * **Potassium Oxalate:** Oxalates work by precipitating calcium. They cause **fluid to shift out of the RBCs**, leading to cell shrinkage (crenation), which falsely increases their resistance to lysis. **Clinical Pearls for NEET-PG:** * **Increased OFT:** Seen in **Hereditary Spherocytosis** [2], [3] (Spherocytes have a low surface-area-to-volume ratio and burst easily [4]). * **Decreased OFT:** Seen in **Thalassemia** [5], Sickle Cell Anemia, and Iron Deficiency Anemia (Target cells have a high surface-area-to-volume ratio). * **Incubated OFT:** Increasing the incubation time (24 hours at 37°C) makes the test more sensitive for mild cases of Hereditary Spherocytosis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 583-584. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602.

Question 1014: Intracellular calcification begins in which organelle?

A. Mitochondria (Correct Answer)
B. Golgi body
C. Nucleus
D. Endoplasmic reticulum

Explanation: **Explanation:** **1. Why Mitochondria is the Correct Answer:** Intracellular calcification is a hallmark of cell injury. In **dystrophic calcification**, the process begins with the accumulation of calcium in the **mitochondria** of dying cells [1]. This occurs because injured cells lose their ability to regulate cytosolic calcium levels [2]. Mitochondria, which normally function as a reservoir, become overloaded. The high concentration of phosphate (from ATP breakdown) within the mitochondria reacts with this excess calcium to form **hydroxyapatite crystals**, which serve as the nidus for further mineral deposition [1]. **2. Why Other Options are Incorrect:** * **Golgi Body:** While involved in protein modification and trafficking, it does not play a primary role in the initiation of mineral crystallization during cell injury. * **Nucleus:** Although DNA can bind calcium in late-stage necrosis, it is not the site of initiation. * **Endoplasmic Reticulum (ER):** The ER is a major storage site for intracellular calcium in healthy cells (via the SERCA pump). However, during the pathological process of calcification, the actual formation of crystalline mineral deposits begins in the mitochondria, not the ER [2]. **3. NEET-PG High-Yield Pearls:** * **Dystrophic Calcification:** Occurs in dead/dying tissues with **normal** serum calcium levels (e.g., Atherosclerosis, Monckeberg’s sclerosis, Psammoma bodies). * **Metastatic Calcification:** Occurs in normal tissues due to **hypercalcemia** (e.g., Hyperparathyroidism, Vitamin D toxicity). It primarily affects "acid-excreting" organs like the gastric mucosa, kidneys, and lungs [3]. * **Morphology:** On H&E stain, calcification appears as **basophilic** (blue-purple), amorphous, granular clumps. * **Psammoma Bodies:** These are laminated, concentric calcifications seen in Papillary thyroid carcinoma, Serous cystadenocarcinoma of the ovary, and Meningioma. **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. 53-55. [2] 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. 57-59. [3] 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. 76-77.

Question 1015: Diffuse proliferative glomerulonephritis in Lupus nephritis falls under which class?

A. Class II
B. Class III
C. Class IV (Correct Answer)
D. Class V

Explanation: **Explanation:** The classification of Lupus Nephritis is based on the **ISN/RPS (International Society of Nephrology/Renal Pathology Society)** criteria, which is a high-yield topic for NEET-PG. **Correct Option: C (Class IV)** **Class IV (Diffuse Proliferative Glomerulonephritis)** is the most common and most severe form of lupus nephritis [1]. It is characterized by involvement of **≥ 50% of glomeruli** [1]. Pathologically, it shows global or segmental endocapillary proliferation, "wire-loop" lesions (due to subendothelial immune complex deposits), and often presents with nephritic syndrome or rapidly progressive renal failure [1]. **Analysis of Incorrect Options:** * **Class II (Mesangial Proliferative LN):** Characterized by purely mesangial hypercellularity and matrix expansion with mesangial immune deposits. * **Class III (Focal Proliferative LN):** Similar to Class IV but involves **< 50% of glomeruli** [1]. It is the focal counterpart of the diffuse form. * **Class V (Membranous LN):** Characterized by diffuse thickening of the glomerular basement membrane due to **subepithelial** deposits. It typically presents with nephrotic-range proteinuria. **NEET-PG High-Yield Pearls:** * **Most common class:** Class IV [1]. * **Most severe/worst prognosis:** Class IV [1]. * **Wire-loop lesions:** Characteristic of Class IV (subendothelial deposits) [1]. * **Spikes and Domes:** Characteristic of Class V (subepithelial deposits). * **Full House Pattern:** Immunofluorescence showing IgG, IgA, IgM, C3, and C1q positivity is classic for Lupus Nephritis. * **Class VI:** Advanced Sclerotic LN (>90% sclerosed glomeruli). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 230-232.

Question 1016: Which of the following is an example of immune complex-mediated (Type III) hypersensitivity?

A. Anaphylaxis
B. Autoimmune hemolytic anemia
C. Systemic lupus erythematosus (Correct Answer)
D. Type 1 diabetes

Explanation: ### Explanation **Correct Answer: C. Systemic lupus erythematosus (SLE)** **Mechanism of Type III Hypersensitivity:** Type III hypersensitivity is mediated by **immune complexes** (antigen-antibody aggregates) [1]. In SLE, autoantibodies (like anti-dsDNA) bind to circulating antigens [1]. These complexes are not efficiently cleared and instead deposit in small blood vessels, joints, and renal glomeruli [1]. This deposition activates the **complement system** (classical pathway), leading to the recruitment of neutrophils, release of lysosomal enzymes, and subsequent tissue damage (vasculitis, arthritis, or glomerulonephritis) [1], [2]. **Analysis of Incorrect Options:** * **A. Anaphylaxis:** This is a **Type I (Immediate)** hypersensitivity reaction. It is mediated by **IgE** antibodies binding to mast cells and basophils, leading to the degranulation of vasoactive amines like histamine. * **B. Autoimmune hemolytic anemia:** This is a **Type II (Cytotoxic)** hypersensitivity reaction. Here, antibodies (IgG or IgM) bind directly to antigens on the **surface of specific cells** (RBCs), leading to their destruction via opsonization or complement-mediated lysis. * **D. Type 1 diabetes:** This is primarily a **Type IV (Cell-mediated)** hypersensitivity reaction. It involves T-cell-mediated destruction of pancreatic beta cells, rather than antibody-mediated damage. **NEET-PG High-Yield Pearls:** * **Mnemonic for Hypersensitivity (ACID):** **A**naphyalctic (I), **C**ytotoxic (II), **I**mmune-Complex (III), **D**elayed-type (IV). * **Key Type III Examples:** SLE, Post-streptococcal glomerulonephritis (PSGN), Rheumatoid Arthritis, Serum Sickness, and Arthus Reaction [1]. * **Complement levels:** In active Type III reactions like SLE, serum C3 and C4 levels are typically **decreased** due to excessive consumption during the inflammatory process. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216. [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. 172-173.

Question 1017: Tigered effect in tissues is due to accumulation of:

A. Calcium
B. Fat (Correct Answer)
C. Fibrin
D. Copper

Explanation: **Explanation:** The **"Tigered effect"** (also known as *Tigroid heart* or *Tabby cat heart*) refers to a specific macroscopic pattern of **fatty change (steatosis)** in the myocardium. **1. Why Fat is the Correct Answer:** This effect occurs due to prolonged, moderate **hypoxia** (often seen in profound anemia). In the heart, hypoxia prevents the proper oxidation of fatty acids, leading to the accumulation of intracellular lipid vacuoles [1]. These fatty deposits appear as yellow bands or streaks. Because the subendocardial layers are most sensitive to hypoxia, they alternate with bands of normal, reddish-brown myocardium, creating a striped appearance reminiscent of a tiger’s skin or a tabby cat. **2. Why Other Options are Incorrect:** * **A. Calcium:** Accumulation of calcium leads to *calcification* (Dystrophic or Metastatic). Macroscopically, this appears as gritty, white, hard deposits, not a striped pattern. * **C. Fibrin:** Fibrin is an inflammatory exudate. In the heart, it causes "Bread and Butter" pericarditis, characterized by a shaggy, irregular surface. * **D. Copper:** Excess copper accumulation is characteristic of *Wilson’s Disease*, primarily affecting the liver (cirrhosis) and basal ganglia, and causing Kayser-Fleischer rings in the cornea. **3. High-Yield Clinical Pearls for NEET-PG:** * **Tigered Effect vs. Diffuse Steatosis:** While *hypoxia* causes the striped Tigered effect, *toxins* (like Diphtheria or Phosphorus) cause a uniform, diffuse fatty change throughout the myocardium [1]. * **Most Common Site of Fatty Change:** The **Liver** is the most common organ involved in fatty change because it is the central organ of lipid metabolism [2]. * **Stains for Fat:** To demonstrate fat in histopathology, use **Frozen Sections** (as routine processing with alcohol/xylene dissolves fat) and stains like **Sudan IV, Sudan Black, or Oil Red O.** **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 579-580. [2] 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. 73.

Question 1018: What is true about metastatic calcification?

A. Serum calcium level is normal
B. Occurs in dead or dying tissue
C. Occurs in damaged heart valves
D. Principally affects the kidneys, lungs, and gastric mucosa (Correct Answer)

Explanation: **Explanation:** Pathologic calcification is divided into two types: **Dystrophic** and **Metastatic**. Understanding the distinction between them is high-yield for NEET-PG. **Why Option D is Correct:** Metastatic calcification occurs in **normal tissues** whenever there is **hypercalcemia** (elevated serum calcium) [2]. It preferentially affects tissues that lose acid, creating an internal **alkaline environment**, which favors the precipitation of calcium salts [1]. The most common sites are: 1. **Gastric mucosa:** Excretes HCl [1]. 2. **Kidneys:** Excretes acid (ammonium chloride) [1]. 3. **Lungs:** Excretes $CO_2$ [1]. 4. **Systemic arteries and pulmonary veins.** **Analysis of Incorrect Options:** * **Option A:** In metastatic calcification, serum calcium levels are **elevated** (due to hyperparathyroidism, bone resorption, Vitamin D toxicity, or renal failure) [2]. Normal serum calcium is characteristic of *dystrophic* calcification. * **Option B & C:** These describe **Dystrophic Calcification**. Dystrophic calcification occurs in dead, dying, or degenerate tissues (like necrotic centers or damaged heart valves) despite having **normal** serum calcium levels. **NEET-PG High-Yield Pearls:** * **Morphology:** On H&E stain, both types appear as basophilic (blue-purple), amorphous granular clumps [1]. * **Psammoma Bodies:** These are laminated, concentric calcifications seen in Dystrophic calcification (e.g., Papillary thyroid carcinoma, Meningioma, Serous cystadenocarcinoma of the ovary) [2]. * **Milk-Alkali Syndrome:** A classic cause of metastatic calcification due to excessive ingestion of calcium and absorbable antacids. * **Reversibility:** Metastatic calcification is generally reversible if the underlying hypercalcemia is corrected, whereas dystrophic calcification is usually permanent. **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. 76-77. [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. 134-135.

Question 1019: All the following organs likely undergo coagulative necrosis except?

A. Spleen
B. Heart
C. Kidney
D. Brain (Correct Answer)

Explanation: **Explanation:** The core concept tested here is the pattern of tissue death following ischemia. **Coagulative necrosis** is the most common pattern of necrosis, typically seen in all solid visceral organs following hypoxic/ischemic injury (infarction). **Why Brain is the Correct Answer:** The **Brain** is the notable exception to the rule of coagulative necrosis. Ischemic injury to the central nervous system (CNS) results in **Liquefactive necrosis** [1]. This occurs because the brain has a high lipid content and a high concentration of lysosomal enzymes (hydrolases) within microglial cells. These enzymes rapidly digest the dead tissue, turning it into a liquid, viscous mass, eventually forming a cystic space [1]. **Analysis of Incorrect Options:** * **Heart (Myocardium):** Ischemic injury (Myocardial Infarction) is the classic example of coagulative necrosis. The cell proteins and enzymes are denatured, preserving the basic structural outline of the "tombstone" cells for several days. * **Kidney:** Renal infarcts (often wedge-shaped) undergo coagulative necrosis due to the denaturation of structural proteins. * **Spleen:** Splenic infarcts also follow the coagulative pattern, maintaining the tissue architecture while losing cellular detail. **NEET-PG High-Yield Pearls:** * **Coagulative Necrosis:** Characteristic of all solid organ infarcts **except the brain**. * **Liquefactive Necrosis:** Seen in **Brain infarcts** and **Abscesses** (due to bacterial/fungal infections) [1]. * **Caseous Necrosis:** "Cheese-like" appearance, characteristic of **Tuberculosis**. * **Fat Necrosis:** Seen in **Acute Pancreatitis** (enzymatic) and breast trauma (non-enzymatic). * **Fibridoid Necrosis:** Seen in immune-mediated vascular damage (e.g., Polyarteritis Nodosa, Malignant Hypertension). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269.

Question 1020: Chediak-Higashi syndrome is characterized by the following findings, except?

A. It is an autosomal recessive disorder.
B. It involves mutation in the LYST gene.
C. It is associated with oculocutaneous albinism.
D. It results in effective phagolysosome formation. (Correct Answer)

Explanation: ### Explanation **Chediak-Higashi Syndrome (CHS)** is a rare autosomal recessive primary immunodeficiency disorder characterized by a defect in **intracellular protein trafficking** [1]. **1. Why Option D is the Correct Answer:** The hallmark of CHS is a defect in the **LYST gene** (Lysosomal Trafficking Regulator), which governs the fusion of vesicles. In this condition, there is a **failure of phagosomes to fuse with lysosomes**, resulting in **ineffective phagolysosome formation** [1]. This leads to impaired intracellular killing of bacteria, making patients highly susceptible to recurrent pyogenic infections [1]. **2. Analysis of Other Options:** * **Option A:** CHS is indeed an **autosomal recessive** disorder, typically presenting in early childhood [1]. * **Option B:** The molecular basis is a mutation in the **LYST gene** (also known as CHS1), located on chromosome 1q42. * **Option C:** **Oculocutaneous albinism** is a classic feature. It occurs because melanocytes cannot properly transfer melanin-containing melanosomes to keratinocytes due to the trafficking defect [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Giant Granules:** The pathognomonic finding is the presence of **giant peroxidase-positive lysosomal granules** in neutrophils and precursors on a peripheral blood smear [1]. * **Clinical Tetrad:** 1. Recurrent pyogenic infections (Staphylococcal/Streptococcal) [1]. 2. Partial oculocutaneous albinism [1]. 3. Progressive neurological abnormalities (ataxia, neuropathy) [1]. 4. Bleeding tendencies (due to dense body deficiency in platelets) [1]. * **Accelerated Phase:** Most patients eventually enter a "lymphoma-like" accelerated phase characterized by hemophagocytic lymphohistiocytosis (HLH), hepatosplenomegaly, and pancytopenia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246.

Practice by Chapter

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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