General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 671: PAS stains the following, except:

A. Glycogen
B. Lipids
C. Fungal cell wall
D. Basement membrane of bacteria (Correct Answer)

Explanation: **Explanation:** The **Periodic Acid-Schiff (PAS)** stain is a histochemical technique used to detect structures rich in **polysaccharides** (like glycogen), **mucopolysaccharides**, **glycoproteins**, and **glycolipids**. The mechanism involves the oxidation of carbon-carbon bonds by periodic acid to form aldehydes, which then react with the Schiff reagent to produce a characteristic **magenta/bright pink** color. [1] **Why Option D is the Correct Answer:** Bacteria do not possess a "basement membrane." They have a cell wall composed of peptidoglycan. While some bacteria (like *Tropheryma whipplei*) are PAS-positive, the term "basement membrane of bacteria" is anatomically incorrect and a distractor. PAS is classically used to stain the **human glomerular basement membrane (GBM)** and tubular basement membranes in the kidney. [2] **Analysis of Incorrect Options:** * **A. Glycogen:** This is the most common substance stained by PAS. It is highly concentrated in the liver and muscles. (Note: Diastase digestion can be used to differentiate glycogen from other PAS-positive substances). * **B. Lipids:** While pure neutral lipids are not PAS-positive, **glycolipids** and **phospholipids** (found in myelin or certain storage diseases) do react with PAS. * **C. Fungal cell wall:** The cell walls of fungi contain high amounts of chitin and glucans (polysaccharides), making PAS an excellent stain for identifying organisms like *Candida* or *Histoplasma*. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Whipple’s Disease:** Characterized by PAS-positive macrophages in the lamina propria of the small intestine. * **Alpha-1 Antitrypsin Deficiency:** Shows PAS-positive, diastase-resistant globules in hepatocytes. * **Ewing’s Sarcoma:** Tumor cells are PAS-positive due to high glycogen content. * **Amniotic Fluid Embolism:** PAS stain is used to identify fetal squames and mucin in maternal pulmonary vessels. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 362. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 526-527.

Question 672: Which of the following cell types is a CD8 cell?

A. T-cells (Correct Answer)
B. B-cells
C. Null cells
D. Macrophages

Explanation: **Explanation:** The correct answer is **A. T-cells**. **Understanding the Concept:** Lymphocytes are categorized into two main lineages: T-cells and B-cells [2]. T-cells are further divided based on their surface glycoproteins (Cluster of Differentiation or CD markers). **CD8+ T-cells**, also known as **Cytotoxic T-lymphocytes (CTLs)**, are responsible for direct cell-mediated killing of virus-infected cells and tumor cells by recognizing antigens presented on **MHC Class I** molecules [1]. In contrast, CD4+ T-cells are "Helper" cells that interact with MHC Class II [1], [4]. **Analysis of Incorrect Options:** * **B-cells:** These are characterized by surface markers such as **CD19, CD20, and CD21**. Their primary function is humoral immunity (antibody production), not cytotoxic activity associated with CD8 [2], [3]. * **Null cells:** These are lymphocytes that lack the conventional markers of T-cells (CD3) or B-cells (CD19/20). The most common example is **Natural Killer (NK) cells** [2]. While some NK cells can express CD8, they are defined by **CD16 and CD56**. * **Macrophages:** These are myeloid lineage cells, not lymphoid. Their characteristic markers include **CD14 and CD68**. They act as professional antigen-presenting cells (APCs). **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 8:** CD**4** x MHC **II** = 8; CD**8** x MHC **I** = 8. * **CD3:** The definitive marker for *all* T-cells (part of the T-cell receptor complex) [4]. * **Normal CD4:CD8 Ratio:** Approximately **2:1**. This ratio is famously inverted (becomes <1.0) in **HIV/AIDS** due to the depletion of CD4+ cells. * **Mantle Cell Lymphoma:** Look for **CD5** expression on B-cells (an unusual T-cell marker on a B-cell). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 240. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 579-580. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 198-199.

Question 673: Fibrosis is primarily due to which of the following growth factors?

A. Transforming growth factor-beta (TGF-β) (Correct Answer)
B. Tumor necrosis factor-alpha (TNF-α)
C. Interleukin-7 (IL-7)
D. Interleukin-10 (IL-10)

Explanation: **Explanation:** **Transforming Growth Factor-beta (TGF-β)** is the most important cytokine involved in the process of fibrosis and chronic inflammation [1]. It acts as a potent fibrogenic agent by: 1. **Stimulating fibroblast chemotaxis and proliferation** [1]. 2. **Increasing the synthesis of collagen** and other extracellular matrix (ECM) proteins [1]. 3. **Decreasing ECM degradation** by inhibiting metalloproteinases (MMPs) and increasing the activity of tissue inhibitors of metalloproteinases (TIMPs). In chronic injury, persistent TGF-β signaling leads to excessive collagen deposition, resulting in organ fibrosis (e.g., liver cirrhosis, pulmonary fibrosis) [1]. **Analysis of Incorrect Options:** * **TNF-α:** A potent pro-inflammatory cytokine primarily involved in acute inflammation, recruitment of leukocytes, and the formation of granulomas. While it can influence repair, it is not the primary driver of fibrosis. * **IL-7:** A cytokine essential for B and T cell development (lymphopoiesis) in the bone marrow and thymus. It has no direct role in collagen synthesis or fibrosis. * **IL-10:** An anti-inflammatory cytokine that limits the immune response and inhibits macrophage activation. It generally acts to *dampen* the inflammatory process rather than promote fibrosis. **High-Yield Clinical Pearls for NEET-PG:** * **TGF-β Dual Role:** In early stages of cancer, it acts as a tumor suppressor; in late stages, it promotes epithelial-mesenchymal transition (EMT) and metastasis. * **Mnemonic:** Remember **"TGF-β = Total Growth of Fibrosis."** * **Other Fibrogenic Factors:** PDGF (Platelet-derived growth factor) and FGF (Fibroblast growth factor) also contribute [2], but TGF-β is the "master regulator." **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 115-116. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 31-32.

Question 674: What is the normal ratio of Kappa to Lambda free light chains in serum?

A. 7:3
B. 6:4
C. 4:6 (Correct Answer)
D. 3:7

Explanation: The correct answer is **C (4:6)**. In human serum, immunoglobulins are composed of heavy chains and light chains (Kappa and Lambda). While B-cells produce slightly more Kappa light chains than Lambda light chains (a production ratio of approximately **2:1**), their serum concentrations are determined by their respective **clearance rates** through the kidneys. Kappa light chains exist primarily as **monomers**, making them smaller and more easily filtered by the renal glomeruli (shorter half-life). Lambda light chains tend to form **dimers**, increasing their molecular weight and slowing their renal clearance (longer half-life). Consequently, the steady-state concentration in normal serum results in a Kappa to Lambda ratio of approximately **0.66**, which is represented by the ratio **4:6** (or 2:3). **Analysis of Incorrect Options:** * **A (7:3) & B (6:4):** These options incorrectly suggest a predominance of Kappa chains in the serum. While Kappa production is higher, its rapid renal excretion prevents it from reaching these levels in a healthy individual. * **D (3:7):** This suggests an even lower ratio than normal, which does not align with physiological clearance patterns. **NEET-PG High-Yield Pearls:** 1. **Production Ratio:** The ratio of Kappa to Lambda *producing* cells in lymph nodes is **2:1**. 2. **Monoclonality:** A significant deviation in the Kappa:Lambda ratio (e.g., >3:1 or <1:3) is a hallmark of **monoclonal gammopathies** like Multiple Myeloma [1]. 3. **Bence-Jones Proteins:** These are free light chains found in urine; they precipitate at 40–60°C and redissolve at 100°C [1]. 4. **AL Amyloidosis:** This condition is more commonly associated with an overproduction of **Lambda** light chains [2]. **References:** [1] 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, pp. 608-609. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267.

Question 675: What is the conventional site for taking a biopsy in secondary amyloidosis?

A. Liver
B. Kidney
C. Rectum
D. Abdominal fat aspirate (Correct Answer)

Explanation: **Explanation:** In secondary (AA) amyloidosis, amyloid fibrils are deposited systemically in the extracellular matrix of various organs. While the kidney and liver are common sites of involvement [2], they are not the "conventional" or preferred initial sites for biopsy due to the risk of complications. **Why Abdominal Fat Aspirate is the Correct Answer:** Abdominal fat pad aspiration is currently the **initial procedure of choice** for diagnosing systemic amyloidosis. It is preferred because: * **High Sensitivity:** It has a sensitivity of approximately 70–90% for detecting systemic amyloid deposits. * **Safety:** It is a minimally invasive, bedside procedure with a significantly lower risk of bleeding compared to visceral biopsies. * **Staining:** The aspirated fat is stained with **Congo red**, which shows characteristic **apple-green birefringence** under polarized light [1]. **Analysis of Incorrect Options:** * **Rectum (Option C):** Historically, rectal biopsy was the gold standard (sensitivity ~75–80%). However, it is more invasive and uncomfortable for the patient than a fat aspirate, making it a secondary choice today. * **Kidney (Option B) & Liver (Option A):** These are the organs most frequently involved clinically in AA amyloidosis [2]. While a biopsy of these organs is highly definitive, it carries a **high risk of hemorrhage** because amyloid deposits in blood vessel walls increase capillary fragility and prevent effective vasoconstriction. They are usually reserved for cases where less invasive tests (fat/rectal) are negative but clinical suspicion remains high. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site of involvement (AA):** Kidney (presents as nephrotic syndrome). * **Most common cause of death:** Cardiac involvement (more common in AL amyloidosis). * **Stain of choice:** Congo Red (Apple-green birefringence) [1]. * **Gold Standard for subtyping:** Mass spectrometry-based proteomics. * **Secondary Amyloidosis (AA):** Associated with chronic inflammation (e.g., RA, TB, Osteomyelitis) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [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. 136-140.

Question 676: Which of the following is an antigen-presenting cell?

A. Langerhans cell (Correct Answer)
B. Macrophage
C. Cytotoxic T cell
D. Helper T cell

Explanation: Antigen-presenting cells (APCs) are specialized immune cells that capture antigens, process them into peptides, and present them via MHC molecules to T cells to initiate an adaptive immune response [2]. **1. Why Langerhans Cell is the Correct Answer:** Langerhans cells are specialized **dendritic cells** located in the stratum spinosum of the epidermis [1]. They are considered the most potent "professional" APCs [2]. Upon capturing an antigen in the skin, they migrate to regional lymph nodes, mature, and present the antigen to naive T cells [1]. Their hallmark ultrastructural feature is the **Birbeck granule** (tennis-racket shaped). **2. Analysis of Incorrect Options:** * **Macrophage (Option B):** While macrophages *can* act as APCs, in the context of standardized exams like NEET-PG, if both a specialized dendritic cell (Langerhans) and a macrophage are listed, the dendritic cell is the superior answer as it is the primary initiator of T-cell responses [1], [2]. * **Cytotoxic T cell (Option C):** These are effector cells (CD8+) that recognize antigens presented by MHC Class I molecules to kill virally infected or tumor cells [2]. They do not present antigens to other cells. * **Helper T cell (Option D):** These are coordinator cells (CD4+) that recognize antigens presented by APCs to secrete cytokines [3]. They are the "receivers" of the antigen presentation, not the presenters. **High-Yield Clinical Pearls for NEET-PG:** * **Professional APCs:** Dendritic cells (most potent), Macrophages, and B-lymphocytes [2]. * **MHC Association:** APCs present exogenous antigens via **MHC Class II** to CD4+ Helper T cells. * **Langerhans Cell Histiocytosis (LCH):** A proliferative disorder where cells stain positive for **CD1a, S100, and Langerin (CD207).** * **Follicular Dendritic Cells:** Found in germinal centers of lymph nodes; they present antigens to B cells (unlike regular dendritic cells which target T cells). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 200. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 207-208. [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. 157-158.

Question 677: Congo red staining for amyloid under polarized light shows what characteristic birefringence?

A. Silver birefringence
B. Golden birefringence
C. Blue birefringence
D. Green birefringence (Correct Answer)

Explanation: **Explanation:** **1. Why the Correct Answer is Right:** Amyloid is a pathological proteinaceous substance deposited in the extracellular space. Its defining physical characteristic is a **cross-beta pleated sheet** configuration [2]. When tissues containing amyloid are stained with **Congo red** dye and viewed under **polarized light**, the dye molecules align themselves along these beta-pleated sheets [2]. This specific alignment causes the light to split (birefringence), resulting in a characteristic **apple-green birefringence** [1], [2]. This is considered the "gold standard" for the histological diagnosis of amyloidosis. **2. Why the Incorrect Options are Wrong:** * **A. Silver birefringence:** Silver stains (like GMS or Jones) are typically used to highlight basement membranes, fungi, or reticulin fibers, but they do not produce birefringence under polarized light. * **B. Golden birefringence:** While Congo red-stained amyloid appears orange-red under ordinary light (the "pinkish-red" hue), it does not show golden birefringence under polarization [2]. * **C. Blue birefringence:** This is not a characteristic finding for amyloid. Some crystals (like calcium pyrophosphate) may show different colors under polarized light, but not amyloid [3]. **3. NEET-PG High-Yield Pearls:** * **Staining Properties:** Under ordinary light, Congo red gives amyloid a pink or red color [2]. Under UV light, it shows **thioflavin T/S fluorescence**. * **H&E Appearance:** On standard H&E stain, amyloid appears as an **extracellular, amorphous, eosinophilic (pink)** material [3]. * **Most Common Type:** Systemic AL (Light chain) amyloidosis is the most common primary form, while AA (Amyloid Associated) is seen in chronic inflammatory conditions. * **Organ Involvement:** The kidney is the most common and potentially most serious organ involved in systemic amyloidosis [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 580-581. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [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.

Question 678: Cloudy swelling is due to which of the following mechanisms?

A. Accumulation of water intracellularly (Correct Answer)
B. Lysozyme degeneration
C. Fat accumulation intracellularly
D. Glycogen accumulation

Explanation: **Explanation:** **Cloudy swelling** (also known as hydropic change or vacuolar degeneration) is the earliest and most common form of **reversible cell injury** [1]. **1. Why Option A is correct:** The primary mechanism is the failure of energy-dependent metabolic processes. When a cell is injured (e.g., by hypoxia or toxins), there is a decrease in ATP production [1]. This leads to the failure of the **Naⁱ-Kⁱ ATPase pump** on the plasma membrane. As a result, sodium accumulates inside the cell, creating an osmotic gradient that draws **water into the cytoplasm** [1]. This causes the cell to swell and the cytoplasm to appear granular or "cloudy" under a light microscope. **2. Why other options are incorrect:** * **Option B (Lysozyme degeneration):** This refers to autolysis or heterolysis seen in irreversible injury/necrosis, not the initial swelling phase [1]. * **Option C (Fat accumulation):** This is known as **Steatosis** (fatty change). While also a form of reversible injury, it involves the abnormal accumulation of triglycerides, commonly seen in the liver [1]. * **Option D (Glycogen accumulation):** This occurs in metabolic disorders like Diabetes Mellitus or Glycogen Storage Diseases, not as a general acute response to cellular injury. **NEET-PG High-Yield Pearls:** * **Earliest Light Microscopic Change:** Cloudy swelling is the first sign of cell injury visible under LM [1]. * **Ultrastructural Changes:** On electron microscopy, the first sign of cell injury is the **swelling of the endoplasmic reticulum**, followed by mitochondrial swelling. * **Gross Appearance:** Affected organs (liver, kidney, heart) appear enlarged, pale, and heavy with rounded margins. * **Reversibility:** If the injurious stimulus is removed, the Naⁱ-Kⁱ pump resumes function, and the cell returns to its normal state [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. 49-53, 60-61.

Question 679: Which of the following mutations in a tumor suppressor gene causes breast carcinoma?

A. p43
B. p53 (Correct Answer)
C. p73
D. p83

Explanation: **Explanation:** **Correct Option: B (p53)** The **TP53 gene**, located on chromosome **17p13.1**, is the most frequently mutated gene in human cancers, including breast carcinoma [1]. Known as the **"Guardian of the Genome,"** p53 encodes a protein that regulates the cell cycle, DNA repair, and apoptosis [2]. When DNA damage occurs, p53 triggers cell cycle arrest (via p21) to allow for repair or initiates apoptosis (via BAX) if the damage is irreparable [2], [3]. Loss-of-function mutations in p53 allow cells with damaged DNA to proliferate, leading to malignancy [1]. In breast cancer, p53 mutations are particularly common in the "Triple Negative" and "HER2-enriched" subtypes. **Incorrect Options:** * **A, C, and D (p43, p73, p83):** While p73 is a structural homolog of p53 and can induce apoptosis, it is rarely mutated in primary human breast cancers. p43 and p83 are not standard designations for primary tumor suppressor genes associated with breast carcinogenesis in the context of high-yield pathology. **High-Yield Clinical Pearls for NEET-PG:** * **Li-Fraumeni Syndrome:** A germline mutation in TP53 that predisposes individuals to a wide spectrum of tumors, most notably **S**arcomas, **B**reast cancer, **L**eukemia, and **A**drenal cortical carcinoma (Mnemonic: **SBLA**) [1]. * **Most common mutation in p53:** Missense mutation. * **Degradation:** p53 levels are normally kept low by **MDM2**, which facilitates its degradation. * **Other Breast Cancer Genes:** While p53 is a general tumor suppressor, **BRCA1 (17q)** and **BRCA2 (13q)** are the most specific genes associated with hereditary breast and ovarian cancer syndromes. **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. 227-228. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 303-304.

Question 680: Oedema is caused by a fall in plasma proteins below what percentage?

A. 0.5%
B. 5%
C. 15%
D. 50% (Correct Answer)

Explanation: **Explanation:** The development of edema is governed by **Starling’s Law**, which describes the balance between hydrostatic pressure (pushing fluid out of vessels) and plasma colloid osmotic pressure (pulling fluid into vessels). **1. Why 50% is correct:** Plasma proteins, primarily **albumin**, are responsible for maintaining the colloid osmotic pressure (oncotic pressure) [1]. The normal total plasma protein level is approximately **6–8 g/dL**. Edema typically manifests clinically when the total plasma protein level falls below **4 g/dL** or when the albumin level drops below **2.5 g/dL**. A drop from 8 g/dL to 4 g/dL represents a **50% reduction** in plasma protein concentration. At this threshold, the oncotic pressure can no longer counteract the hydrostatic pressure, leading to the leakage of fluid into the interstitial space [1]. **2. Why other options are incorrect:** * **0.5% and 5%:** These represent negligible decreases. The body has significant compensatory mechanisms (such as increased lymphatic drainage) that prevent edema until a substantial deficit occurs. * **15%:** While a 15% drop indicates mild hypoproteinemia, it is usually insufficient to overcome the "safety factor" of the interstitium and cause visible edema. **3. NEET-PG High-Yield Pearls:** * **Most important protein:** Albumin is the primary contributor to oncotic pressure due to its high concentration and small molecular weight [1]. * **Common Causes:** Hypoproteinemic edema is classically seen in **Nephrotic Syndrome** (excessive loss), **Cirrhosis** (decreased synthesis), and **Protein-Losing Enteropathy** or **Kwashiorkor** (malnutrition) [1]. * **Clinical Sign:** Edema caused by low plasma proteins is typically **pitting** and **generalized** (anasarca), often appearing first in areas with loose connective tissue, such as the eyelids (periorbital edema). **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.

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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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Environmental Pathology

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Molecular Basis of Disease

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