General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 231: Which of the following is associated with chronic granulomatous disease?

A. Associated with formation of multiple granulomas (Correct Answer)
B. A benign neoplastic process
C. A parasitic disease
D. Acquired leukocyte function defect

Explanation: **Explanation:** **Chronic Granulomatous Disease (CGD)** is a primary immunodeficiency disorder caused by a genetic defect in the **NADPH oxidase enzyme complex**. This enzyme is responsible for the "respiratory burst," which generates reactive oxygen species (ROS) like superoxide radicals to kill phagocytosed pathogens. 1. **Why Option A is correct:** In CGD, phagocytes (neutrophils and macrophages) can ingest bacteria but cannot kill them due to the lack of ROS. To contain these persistent intracellular pathogens, the body mounts a T-cell mediated immune response, leading to the **formation of multiple granulomas** (collections of activated macrophages/epithelioid cells) throughout the body, particularly in the skin, liver, and lymph nodes [1]. 2. **Why Option B is incorrect:** CGD is an **immunodeficiency/inflammatory disorder**, not a neoplastic (cancerous) process. 3. **Why Option C is incorrect:** It is a **genetic (hereditary) disorder**, most commonly inherited in an **X-linked recessive** pattern (CYBB gene mutation), though autosomal recessive forms exist. It is not caused by parasites. 4. **Why Option D is incorrect:** CGD is a **congenital (inherited)** leukocyte function defect, not an acquired one. **High-Yield Clinical Pearls for NEET-PG:** * **Organisms:** Patients are highly susceptible to **Catalase-positive organisms** (e.g., *Staphylococcus aureus, Aspergillus, Nocardia, Serratia marcescens, and Burkholderia cepacia*). Catalase-positive bacteria neutralize their own $H_2O_2$, leaving the CGD-affected cell with no oxidative tools for killing. * **Gold Standard Diagnosis:** **Dihydrorhodamine (DHR) 123 flow cytometry** (more sensitive). * **Classic Test:** **Nitroblue Tetrazolium (NBT) dye test** (Negative/Colorless in CGD; Positive/Blue in normal cells). * **Treatment:** Prophylactic antibiotics, IFN-gamma, and Bone Marrow Transplant (curative). **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. 198-200.

Question 232: Which cation is found in extremely high concentrations in cells that have undergone coagulative necrosis?

A. Potassium
B. Calcium (Correct Answer)
C. Iron
D. Cobalt

Explanation: **Explanation:** The correct answer is **Calcium (B)**. **Why Calcium is correct:** Coagulative necrosis is typically caused by ischemia (except in the brain) [1]. When a cell is deprived of oxygen, ATP production fails, leading to the dysfunction of ATP-dependent membrane pumps (like the $Ca^{2+}$-ATPase). This results in a massive influx of extracellular calcium into the cytosol [2]. Furthermore, damage to the mitochondria and endoplasmic reticulum releases sequestered calcium into the cytoplasm [3]. This high concentration of intracellular calcium is a "point of no return" in cell injury as it activates various degradative enzymes (phospholipases, proteases, endonucleases, and ATPases), leading to irreversible membrane damage and nuclear chromatin destruction [2]. In later stages, this calcium can precipitate as calcium phosphate, a process known as **dystrophic calcification** [1]. **Why the other options are incorrect:** * **Potassium (A):** Potassium is the primary *intracellular* cation in healthy cells. During necrosis, membrane integrity is lost, causing potassium to leak **out** of the cell into the extracellular space (hyperkalemia), rather than accumulating within the necrotic cell. * **Iron (C):** While iron can cause oxidative stress via the Fenton reaction, it does not characteristically accumulate in extremely high concentrations as a hallmark of coagulative necrosis. Its accumulation is more specific to conditions like hemochromatosis or hemosiderosis. * **Cobalt (D):** Cobalt is a trace element and is not involved in the standard pathophysiology of cell death or necrotic morphology. **High-Yield NEET-PG Pearls:** * **Coagulative Necrosis:** The most common type of necrosis; the characteristic feature is the preservation of the basic structural outline of the cell/tissue for several days ("tombstone appearance") [1]. * **Dystrophic Calcification:** Occurs in necrotic/dead tissues with **normal** serum calcium levels. * **Enzyme Activation:** Remember that $Ca^{2+}$ is the key activator of **Phospholipase** (membrane damage) and **Endonuclease** (nuclear fragmentation/karyorrhexis) [2]. **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] 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. 102-103.

Question 233: Which of the following is a growth factor oncogene?

A. myc
B. fos
C. sis (Correct Answer)
D. jun

Explanation: **Explanation:** To understand oncogenes, it is essential to categorize them based on their role in the cell signaling pathway: growth factors, growth factor receptors, signal transducers, and nuclear transcription factors [2]. **Why 'sis' is correct:** The **v-sis** oncogene (derived from the Simian Sarcoma Virus) encodes a protein that is nearly identical to the **Platelet-Derived Growth Factor (PDGF-β chain)**. When this oncogene is activated, the cell overproduces PDGF, which then acts in an autocrine fashion on the cell's own PDGF receptors [1]. This continuous stimulation leads to uncontrolled cell proliferation, commonly seen in **astrocytomas** and **osteosarcomas** [1]. **Why the other options are incorrect:** * **A, B, and D (myc, fos, jun):** These are all **Nuclear Transcription Factors**. They act at the end of the signaling cascade. Once activated, they bind to DNA to initiate the transcription of genes required for the cell cycle (like Cyclin D). * **c-myc** is famously associated with Burkitt Lymphoma [t(8;14)]. * **N-myc** is associated with Neuroblastoma. * **L-myc** is associated with Small Cell Carcinoma of the Lung. **High-Yield Clinical Pearls for NEET-PG:** * **Growth Factor Oncogenes:** *sis* (PDGF-β), *int-2* (FGF) [1]. * **Growth Factor Receptor Oncogenes:** *ERBB1* (EGFR in Squamous cell CA of lung), *ERBB2/neu* (HER2 in Breast CA), *RET* (MEN 2A/2B) [1]. * **Signal Transducers:** *RAS* (GTP-binding protein; most common oncogene in human tumors), *ABL* (Tyrosine kinase; CML). * **Mnemonic for Transcription Factors:** "My Fos-Jun" (myc, fos, jun). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 292. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 292-293.

Question 234: Which syndrome is characterized by Trisomy 13?

A. Edward Syndrome
B. Patau Syndrome (Correct Answer)
C. Down Syndrome
D. Turner Syndrome

Explanation: **Explanation:** **Patau Syndrome (Trisomy 13)** is a severe chromosomal abnormality caused by the presence of an extra copy of chromosome 13 [1]. It is the least common and most severe of the three viable autosomal trisomies. The clinical presentation is characterized by defects in the fusion of midline structures. High-yield clinical features include the "classic triad": **Microphthalmia** (small eyes), **Cleft lip/palate**, and **Polydactyly** (extra fingers/toes) [1]. Other common findings include holoprosencephaly, "rocker-bottom" feet, and cutis aplasia (localized skin defects on the scalp). **Analysis of Incorrect Options:** * **Edward Syndrome (Trisomy 18):** Characterized by "PRINCE" features: **P**rominent occiput, **R**ocker-bottom feet, **I**ntellectual disability, **N**ondisjunction, **C**lenched fists (with overlapping fingers), and **E**ars (low-set) [1]. * **Down Syndrome (Trisomy 21):** The most common autosomal trisomy [1]. Key features include flat facies, epicanthal folds, Simian crease, and an increased risk of Alzheimer’s disease and ALL/AML. * **Turner Syndrome (45, XO):** A sex chromosome monosomy (not a trisomy). It presents in females with short stature, webbed neck, streak ovaries, and coarctation of the aorta. **NEET-PG High-Yield Pearls:** 1. **Maternal Age:** The risk for all three autosomal trisomies (13, 18, 21) increases with advanced maternal age due to meiotic nondisjunction. 2. **Survival:** Most infants with Patau Syndrome die within the first few days or months of life; survival beyond one year is rare (<10%) [1]. 3. **First Trimester Screening:** Patau syndrome typically shows decreased serum β-hCG and decreased PAPP-A. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 171-172.

Question 235: Amyloid-like stroma is seen in which of the following tumors?

A. Papillary tumor
B. Follicular tumor
C. Medullary tumor (Correct Answer)
D. Anaplastic tumor

Explanation: **Explanation:** **Medullary Thyroid Carcinoma (MTC)** is the correct answer because it is a neuroendocrine tumor derived from the **parafollicular C-cells** of the thyroid [2]. These cells secrete excessive amounts of **calcitonin** [3]. The characteristic "amyloid-like stroma" is formed by the deposition of procalcitonin molecules that undergo misfolding and aggregate into insoluble fibrils. On histology, this appears as an acellular, eosinophilic material that shows **apple-green birefringence** under polarized light when stained with **Congo Red** [2]. **Why other options are incorrect:** * **Papillary Thyroid Carcinoma:** Characterized by "Orphan Annie eye" nuclei, Psammoma bodies (dystrophic calcification), and nuclear grooves. It does not typically feature amyloid stroma. * **Follicular Thyroid Carcinoma:** Identified by capsular or vascular invasion [2]. The stroma is usually fibrous, not amyloidogenic. * **Anaplastic Thyroid Carcinoma:** A highly aggressive tumor showing pleomorphic giant cells and spindle cells with extensive necrosis and hemorrhage, but lacking specific amyloid deposition [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Association:** Approximately 25% of MTC cases are familial, associated with **RET proto-oncogene** mutations (MEN 2A and 2B syndromes) [1]. * **Tumor Marker:** Serum **Calcitonin** is used for both diagnosis and monitoring recurrence. * **Histology:** Look for a "nesting" (Zellballen) pattern or organoid arrangement of cells. * **Staining:** Positive for neuroendocrine markers like **Chromogranin A** and **Synaptophysin**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1102-1103. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 430-431. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 428-429.

Question 236: The activation of caspases is likely to lead to what?

A. Apoptotic cell death (Correct Answer)
B. Blood coagulation
C. Mitotic cell division
D. G1 to S phase of cell cycle

Explanation: ### Explanation **Correct Answer: A. Apoptotic cell death** Caspases (**C**ysteine-aspartic **asp**erity-specific prote**ases**) are the central executioners of **Apoptosis** (programmed cell death) [1]. They exist as inactive zymogens (pro-caspases) and, once activated, initiate a proteolytic cascade [1]. * **Initiator Caspases:** Caspase-8 and 9 (Intrinsic/Extrinsic pathways) [1]. * **Executioner Caspases:** Caspase-3, 6, and 7. These cleave structural proteins and activate DNAses, leading to the characteristic DNA fragmentation and cell shrinkage seen in apoptosis [1]. **Why the other options are incorrect:** * **B. Blood coagulation:** This process is mediated by the **coagulation cascade** involving clotting factors (like Thrombin and Fibrinogen), not caspases. * **C & D. Mitotic cell division / G1 to S phase:** These are stages of the **Cell Cycle**. Progression through the cell cycle is regulated by **Cyclins** and **Cyclin-Dependent Kinases (CDKs)**. Caspases actually inhibit the cell cycle by cleaving proteins necessary for its progression when a cell is marked for death. --- ### NEET-PG High-Yield Pearls * **Caspase-3** is the most important "Executioner Caspase" common to both intrinsic and extrinsic pathways. * **Intrinsic Pathway (Mitochondrial):** Triggered by the release of **Cytochrome c**, which binds to APAF-1 to form the **Apoptosome**, activating **Caspase-9** [1]. * **Extrinsic Pathway (Death Receptor):** Involves Fas-FasL or TNF-TNFR1 binding, leading to the activation of **Caspase-8** [1]. * **Marker for Apoptosis:** Annexin V (binds to Phosphatidylserine on the outer membrane) and DNA laddering on electrophoresis. * **Inflammation:** While most caspases are apoptotic, **Caspase-1** is involved in forming the "Inflammasome" and processing IL-1β (Pyroptosis). **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. 64-67.

Question 237: Pyrimidine dimers are a characteristic feature in which condition?

A. Xeroderma pigmentosum (Correct Answer)
B. Alkylating agents
C. X-rays
D. Gamma rays

Explanation: Explanation: 1. Why Xeroderma Pigmentosum (XP) is correct: Pyrimidine dimers (specifically thymine dimers) are the hallmark DNA lesion caused by Ultraviolet (UV) radiation [1]. In healthy individuals, these dimers are repaired via the Nucleotide Excision Repair (NER) pathway. Xeroderma pigmentosum is an autosomal recessive disorder characterized by a genetic deficiency in the enzymes required for NER (most commonly UV-specific endonucleases) [1]. Consequently, pyrimidine dimers accumulate, leading to mutations in proto-oncogenes and tumor suppressor genes, which manifests as extreme photosensitivity and a 2000-fold increased risk of skin cancers (BCC, SCC, and Melanoma) [1]. 2. Why other options are incorrect: * Alkylating agents (Option B): These are chemical mutagens that typically cause the cross-linking of DNA strands or the addition of methyl/ethyl groups to bases (e.g., O6-methylguanine), rather than pyrimidine dimers. * X-rays and Gamma rays (Options C & D): These represent ionizing radiation [1]. Unlike UV light, ionizing radiation causes cell injury by generating free radicals (indirect action) or by causing single and double-strand DNA breaks and particulate damage [1]. They do not specifically produce pyrimidine dimers. High-Yield Clinical Pearls for NEET-PG: * NER Pathway: Remember the mnemonic "NER is for UV"—Nucleotide Excision Repair fixes UV damage [1]. * Clinical Triad of XP: Severe sunburn on minimal exposure, "parchment-like" skin (xeroderma), and hyperpigmented macules (freckling). * Associated Cancers: XP patients often develop skin malignancies before the age of 10 [1]. * Other Repair Defects: Contrast XP with Lynch Syndrome (Mismatch Repair defect) and Ataxia-Telangiectasia (defect in repair of double-strand breaks caused by ionizing radiation) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-323.

Question 238: Myoglobinuria is associated with which of the following?

A. Tumours
B. Electrical injury
C. Crush injury (Correct Answer)
D. All of the above

Explanation: **Explanation:** **Myoglobinuria** refers to the presence of myoglobin in the urine, which occurs following **rhabdomyolysis** [1] (the breakdown of skeletal muscle fibers). **1. Why Crush Injury is the Correct Answer:** Crush injury is the classic cause of traumatic rhabdomyolysis. When muscle tissue is subjected to prolonged pressure or physical trauma, the sarcolemma (muscle cell membrane) is damaged. This leads to the massive release of **myoglobin**, a heme-containing protein, into the systemic circulation. Because myoglobin is a small molecule, it is easily filtered by the glomerulus, resulting in myoglobinuria. This is clinically significant as it can lead to **Acute Tubular Necrosis (ATN)** and subsequent acute kidney injury. **2. Analysis of Other Options:** * **Electrical Injury:** While severe high-voltage electrical burns can cause muscle necrosis and myoglobinuria, it is less common than crush injuries in a general clinical context. However, in many standardized exams, if "All of the above" is not the intended answer, "Crush injury" remains the most definitive and classic association. * **Tumours:** Generally, tumors do not cause the acute, massive skeletal muscle lysis required to produce significant myoglobinuria. Lysis of tumor cells (Tumor Lysis Syndrome) releases intracellular ions and nucleic acids [2], but not myoglobin. **3. High-Yield Clinical Pearls for NEET-PG:** * **The "Dipstick" Paradox:** In myoglobinuria, the urine dipstick is **positive for blood** (due to the peroxidase activity of the heme group), but microscopy reveals **no RBCs**. * **Color of Urine:** Myoglobinuria typically presents as **dark, tea-colored, or cola-colored urine**. * **Complication:** The primary concern is **Acute Kidney Injury (AKI)** caused by the direct toxic effect of myoglobin on renal tubular cells and the formation of intratubular casts (pigment nephropathy). * **Other Causes:** Strenuous exercise (marathons), statin-induced myopathy, and McArdle disease [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1246-1247. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 941-942.

Question 239: Which type of cells are most dependent on IFN-γ?

A. IFN-γ (Correct Answer)
B. IL-4
C. IL-5
D. IL-6

Explanation: **Explanation:** The correct answer is **IFN-γ**. This question focuses on the cytokine profile of Helper T-cells (Th1 vs. Th2) and their specific roles in the immune response. **Why IFN-γ is correct:** Interferon-gamma (IFN-γ) is the signature cytokine produced by **Th1 cells** [3]. Its primary function is the **activation of macrophages**, enhancing their ability to kill intracellular pathogens (like *M. tuberculosis*) through the production of reactive oxygen species (ROS) and nitric oxide [4]. IFN-γ also stimulates B-cells to undergo class switching to IgG, which opsonizes microbes for phagocytosis. In a feedback loop, IFN-γ further promotes the differentiation of naive T-cells into Th1 cells, making the Th1 response highly dependent on its presence. **Why other options are incorrect:** * **IL-4:** This is the signature cytokine of **Th2 cells**. It induces B-cell class switching to **IgE**, which is essential for mast cell degranulation and allergic responses [4]. * **IL-5:** Also produced by **Th2 cells**, its primary role is the activation and recruitment of **eosinophils**, crucial for defending against helminthic (parasitic) infections. * **IL-6:** This is a pro-inflammatory cytokine produced by macrophages and dendritic cells. It plays a key role in the **acute phase response** (inducing CRP from the liver) and the differentiation of Th17 cells. **High-Yield Clinical Pearls for NEET-PG:** * **Th1 Response:** Driven by IL-12; produces IFN-γ; activates macrophages (Cell-mediated immunity) [2]. * **Th2 Response:** Driven by IL-4; produces IL-4, IL-5, and IL-13; activates eosinophils and IgE (Humoral/Allergic immunity). * **Granuloma Formation:** IFN-γ is the most critical cytokine for granuloma formation as it transforms macrophages into epithelioid cells [1]. * **Deficiency:** Mutations in the IFN-γ receptor lead to increased susceptibility to atypical mycobacterial infections (Mendelian Susceptibility to Mycobacterial Disease - MSMD). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 380-381. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 380. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 206. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 105-106.

Question 240: What is the characteristic histological finding of Leser-Trélat sign?

A. Seborrheic keratosis (Correct Answer)
B. Actinic keratosis
C. Basal cell carcinoma
D. Squamous cell carcinoma

Explanation: **Explanation:** The **Leser-Trlat sign** is a classic paraneoplastic syndrome characterized by the sudden appearance or rapid increase in the number and size of multiple **seborrheic keratoses**. Histologically, these lesions are identical to sporadic seborrheic keratoses, showing hyperkeratosis, acanthosis, and characteristic **horn cysts** (keratin-filled cysts) [1]. **Why Option A is correct:** The sign is most commonly associated with underlying visceral malignancies, particularly **gastric adenocarcinoma**. The sudden eruption is thought to be mediated by the systemic release of growth factors, such as **Transforming Growth Factor-alpha (TGF-α)**, from the tumor cells, which stimulates epidermal proliferation. **Why the other options are incorrect:** * **B. Actinic keratosis:** These are premalignant lesions caused by UV damage, characterized by cytologic atypia in the lower epidermis; they are not part of the Leser-Trlat sign [2]. * **C. Basal cell carcinoma:** This is a common skin malignancy, but it presents as pearly papules with telangiectasia, not as a sudden eruptive sign of internal cancer. * **D. Squamous cell carcinoma:** While SCC can be a primary skin cancer or an internal malignancy, the specific cutaneous marker for Leser-Trlat is the benign seborrheic keratosis, not the malignant SCC itself [1], [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common association:** Gastric Adenocarcinoma (GI tract). * **Pathogenesis:** Overproduction of TGF-α and EGF (Epidermal Growth Factor). * **Differential Diagnosis:** Do not confuse with "Pseudo-Leser-Trlat sign," which can occur in inflammatory conditions like erythrodermic psoriasis [3]. * **Key Histology:** "Stuck-on" appearance, basaloid cells, and keratin-filled horn cysts [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 642-643. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 644-645. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 640-641.

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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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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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