General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 391: Time taken by tissue to develop frank necrosis is approximately:

A. 30 minutes
B. 1 hour
C. 2 hours
D. 4 hours (Correct Answer)

Explanation: ### Explanation The correct answer is **4 hours**. **1. Underlying Medical Concept** Necrosis is the morphological expression of cell death. It is important to distinguish between **biochemical cell death** and **morphological (frank) necrosis**. * **Biochemical death:** Occurs rapidly (e.g., in myocardial cells, irreversible injury occurs within 20–40 minutes) [1]. * **Frank Necrosis:** This refers to the structural changes visible under a light microscope (such as nuclear changes like pyknosis, karyorrhexis, and karyolysis). These changes require time to manifest because they depend on the leakage of lysosomal enzymes and the denaturation of proteins. In most tissues, including the heart, these light microscopic features take approximately **4 to 12 hours** to become evident [1]. Therefore, 4 hours is the earliest standard time frame for frank necrosis to develop. **2. Analysis of Incorrect Options** * **A (30 minutes) & B (1 hour):** At this stage, the injury may be irreversible at a biochemical level, but the tissue still appears histologically normal under a light microscope [1]. Only electron microscopy might show subtle changes like mitochondrial swelling. * **C (2 hours):** While enzymatic digestion has begun, the classic eosinophilic change and nuclear degradation are not yet distinct enough to be classified as "frank" necrosis [3]. **3. Clinical Pearls & High-Yield Facts for NEET-PG** * **Myocardial Infarction (MI) Timeline:** * **0–30 mins:** Reversible injury [1]. * **20–40 mins:** Irreversible injury begins (Biochemical death) [1]. * **1–4 hours:** Wavy fibers (earliest light microscopic change) [1]. * **4–12 hours:** Coagulative necrosis (Frank necrosis) begins [1]. * **Key Histological Hallmarks of Necrosis:** Increased eosinophilia (due to loss of cytoplasmic RNA) and nuclear changes (Pyknosis $\rightarrow$ Karyorrhexis $\rightarrow$ Karyolysis) [1]. * **Gold Standard for Early Detection:** Before 4 hours, necrosis cannot be seen by light microscopy; however, **TTC (Triphenyl Tetrazolium Chloride) staining** can identify infarcted areas macroscopically after 2–3 hours (the dead tissue remains unstained/pale) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 550.

Question 392: HER-2/NEU receptor gene mutation is seen in which cancer?

A. Squamous cell carcinoma
B. Breast cancer (Correct Answer)
C. Glioblastoma
D. All of the above

Explanation: **Explanation:** **HER-2/neu (ERBB2)** is a proto-oncogene located on chromosome **17q** [1]. It encodes a transmembrane glycoprotein with intrinsic tyrosine kinase activity, belonging to the Epidermal Growth Factor Receptor (EGFR) family. 1. **Breast Cancer (Correct):** Amplification or overexpression of the HER-2/neu gene occurs in approximately **15-25% of breast cancers** [1]. This leads to constitutive activation of downstream signaling pathways (like PI3K/AKT and MAPK), resulting in uncontrolled cell proliferation and increased tumor aggressiveness. It serves as both a **prognostic marker** (associated with poorer outcomes) and a **predictive marker** (predicts response to targeted therapies like Trastuzumab/Herceptin) [2]. 2. **Squamous Cell Carcinoma (Incorrect):** While EGFR (HER-1) is frequently mutated or overexpressed in squamous cell carcinomas (especially of the lung and head/neck), HER-2/neu is not a primary driver or diagnostic marker for this subtype. 3. **Glioblastoma (Incorrect):** Glioblastoma Multiforme (GBM) is more commonly associated with **EGFR amplification** (specifically the EGFRvIII mutation) and PTEN deletions, rather than HER-2/neu mutations. **High-Yield Clinical Pearls for NEET-PG:** * **Targeted Therapy:** Trastuzumab (Herceptin) is the monoclonal antibody used to treat HER-2 positive breast cancer [2]. * **Testing Methods:** Immunohistochemistry (IHC) is used for screening (protein expression), while **FISH (Fluorescence In Situ Hybridization)** is the gold standard for confirming gene amplification [1]. * **Other Associations:** Apart from breast cancer, HER-2/neu overexpression is also clinically significant in **Gastric and Gastroesophageal junction adenocarcinomas**. * **Chromosome:** Remember **17q21** for HER-2/neu [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1060. [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. 258-259.

Question 393: What is the characteristic finding of sweat chloride levels in patients with cystic fibrosis?

A. Decreased
B. Increased (Correct Answer)
C. No change
D. May increase or decrease

Explanation: **Explanation:** The correct answer is **B (Increased)**. **Pathophysiology:** Cystic Fibrosis (CF) is caused by a mutation in the **CFTR (Cystic Fibrosis Transmembrane Conductance Regulator)** gene. The CFTR protein functions differently depending on the tissue. In the **sweat glands**, its primary role is the **reabsorption** of chloride ions from the primary secretion back into the ductal cells [1]. Sodium follows chloride to maintain electrical neutrality. In CF patients, the defective CFTR channel cannot reabsorb chloride; consequently, chloride remains in the sweat, leading to an abnormally high concentration of salt (NaCl) on the skin surface [1]. **Analysis of Incorrect Options:** * **Option A (Decreased):** This is incorrect because the defect lies in the inability to *reabsorb* chloride from the lumen. Decreased levels are not seen in CF [1]. * **Option C & D (No change / May increase or decrease):** Sweat chloride levels are consistently elevated in classic CF, making these options clinically inaccurately. **High-Yield NEET-PG Pearls:** * **Gold Standard Diagnosis:** The **Pilocarpine Iontophoresis Sweat Test** is the diagnostic test of choice. A chloride concentration **>60 mmol/L** is diagnostic of CF. * **Tissue Paradox:** Remember the "CFTR Paradox"—in the **respiratory and GI tracts**, CFTR failure leads to decreased chloride *secretion* (causing thick, dehydrated mucus), whereas in **sweat glands**, it leads to decreased chloride *reabsorption* [1]. * **Genetics:** Most common mutation is **ΔF508** (Class II defect: protein misfolding and degradation). * **Clinical Sign:** Mothers often report that the infant "tastes salty" when kissed. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Lumen Of Sweat Duct, pp. 475-476.

Question 394: Myasthenia gravis is caused by dysfunction of -

A. Pineal gland
B. Thymus gland (Correct Answer)
C. Pituitary gland
D. Parathyroid gland

Explanation: **Explanation:** **Myasthenia Gravis (MG)** is an autoimmune neuromuscular disorder characterized by muscle weakness and fatigability. The correct answer is the **Thymus gland** because it plays a central role in the pathogenesis of the disease. In MG, the body produces autoantibodies against **acetylcholine receptors (AChR)** at the postsynaptic neuromuscular junction [1]. The thymus is believed to be the site where self-tolerance is lost; it contains "myoid cells" that express AChR on their surface, potentially triggering the production of these autoantibodies. Approximately 75% of MG patients have thymic abnormalities (65% **thymic hyperplasia** and 10% **thymoma**). **Analysis of Incorrect Options:** * **A. Pineal gland:** Responsible for melatonin secretion and circadian rhythm regulation; it has no role in neuromuscular transmission or MG. * **C. Pituitary gland:** The "master gland" regulating growth, metabolism, and reproduction; its dysfunction leads to conditions like acromegaly or Cushing’s disease, not MG. * **D. Parathyroid gland:** Regulates calcium and phosphate homeostasis. Dysfunction leads to hyper/hypocalcemia, which can cause muscle weakness, but via a different mechanism than the antibody-mediated blockade seen in MG. **High-Yield Clinical Pearls for NEET-PG:** * **Pathophysiology:** Type II Hypersensitivity reaction [2]. * **Clinical Presentation:** Ptosis and diplopia (extraocular muscles involved first) that worsens towards the end of the day. * **Diagnosis:** Edrophonium (Tensilon) test (briefly improves symptoms) and Ice pack test. * **Gold Standard Diagnosis:** Single-fiber electromyography (SFEMG) showing increased "jitter." * **Treatment:** Pyridostigmine (AChE inhibitor) and **Thymectomy**, which can lead to clinical remission even in the absence of a thymoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1237-1238. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214.

Question 395: What is the best prognostic type of Hodgkin's disease?

A. Lymphocyte predominant (Correct Answer)
B. Lymphocyte depletion
C. Mixed cellularity
D. Nodular sclerosis

Explanation: **Explanation:** Hodgkin Lymphoma (HL) is classified by the WHO into Classical HL and Nodular Lymphocyte Predominant HL (NLPHL). The prognosis of HL is inversely proportional to the number of Reed-Sternberg (RS) cells and directly proportional to the number of host lymphocytes. 1. **Lymphocyte Predominant (Option A):** This type has the **best prognosis** [1]. It is characterized by an abundance of reactive lymphocytes and very few RS cells (specifically the "Popcorn cell" or L&H variant) [1]. It usually presents in early stages (I or II) and has an excellent survival rate. 2. **Nodular Sclerosis (Option D):** This is the **most common** subtype overall. While it has a very good prognosis, it ranks second to the lymphocyte-predominant type [1]. It is characterized by lacunar cells and collagen bands. 3. **Mixed Cellularity (Option C):** This type has an intermediate prognosis [2]. It is frequently associated with the Epstein-Barr Virus (EBV) and presents with a diverse background of eosinophils, plasma cells, and macrophages [1]. 4. **Lymphocyte Depletion (Option B):** This is the **least common** and has the **worst prognosis** [2]. It is characterized by numerous pleomorphic RS cells and a paucity of lymphocytes [2]. It is often seen in elderly or HIV-positive patients. **High-Yield Pearls for NEET-PG:** * **Most Common Subtype:** Nodular Sclerosis. * **Best Prognosis:** Lymphocyte Predominant. * **Worst Prognosis:** Lymphocyte Depletion. * **Subtype most associated with EBV:** Mixed Cellularity (followed by Lymphocyte Depletion). * **RS Cell Markers:** Classical HL is **CD15+ and CD30+** (CD45-), whereas Lymphocyte Predominant HL is **CD20+ and CD45+** (CD15- and CD30-). **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. 616-618. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 559-560.

Question 396: What is the best investigation for diagnosing amyloidosis?

A. Rectal biopsy (Correct Answer)
B. Colonoscopy
C. CT scan
D. Upper GI endoscopy

Explanation: **Explanation:** Amyloidosis is a systemic disorder characterized by the extracellular deposition of misfolded proteins (amyloid) in various tissues [1]. For NEET-PG, it is crucial to distinguish between the "gold standard" for diagnosis and the "best initial/screening" investigations. **Why Rectal Biopsy is the Correct Answer:** Rectal biopsy is considered one of the most reliable and traditional sites for diagnosing systemic amyloidosis. The rectum has a rich submucosal vascular network, and amyloid has a high affinity for blood vessel walls. A deep rectal biopsy (including the submucosa) has a high diagnostic yield of approximately **75-80%**. While **Abdominal Fat Pad Aspiration** is now often the preferred initial screening test due to its non-invasive nature, rectal biopsy remains a definitive and high-yield diagnostic investigation among the provided options. **Analysis of Incorrect Options:** * **B. Colonoscopy:** This is a procedure used to visualize the colon. While a biopsy can be taken *during* a colonoscopy, the procedure itself is not a diagnostic test for amyloidosis. * **C. CT Scan:** Imaging modalities like CT scans may show organomegaly (e.g., hepatomegaly or splenomegaly), but they cannot detect microscopic amyloid deposits. * **D. Upper GI Endoscopy:** Similar to colonoscopy, this is a visualization tool. While gastric or duodenal biopsies can show amyloid, the yield is generally lower or less standardized than rectal or fat pad biopsies. **High-Yield Clinical Pearls for NEET-PG:** * **Staining:** The gold standard for identification is **Congo Red stain**, which shows **Apple-green birefringence** under polarized light [1]. * **Most Common Site for Biopsy:** Abdominal fat pad (easy, safe) followed by Rectal biopsy. * **Most Common Organ Involved:** Kidney (often presenting as Nephrotic Syndrome). * **Biopsy Site for Localized Amyloidosis:** Biopsy must be taken from the specific organ involved (e.g., Heart for senile systemic amyloidosis). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 264-269.

Question 397: Which of the following statements about amyloidosis is false?

A. It is made of proteins that calcify. (Correct Answer)
B. It can be a complication of chronic infections.
C. It is associated with extracellular eosinophilic hyaline material.
D. It shows apple-green birefringence under polarized light.

Explanation: ### **Explanation: Amyloidosis** **1. Why Option A is the Correct (False) Statement:** Amyloidosis is characterized by the extracellular deposition of **misfolded proteins** that aggregate into insoluble fibrils with a **cross-beta pleated sheet** configuration [1]. While amyloid deposits are dense and proteinaceous, they **do not typically undergo calcification**. Calcification (dystrophic) usually occurs in necrotic tissues or specific tumors (e.g., Psammoma bodies), whereas amyloid is defined by its unique physical structure and staining properties, not by mineral deposition. **2. Analysis of Other Options:** * **Option B (True):** Chronic infections (e.g., Tuberculosis, Bronchiectasis, Osteomyelitis) lead to the sustained release of Interleukin-1 and 6, which stimulates the liver to produce **Serum Amyloid A (SAA)** [4]. This results in **Secondary (AA) Amyloidosis** [5]. * **Option C (True):** On standard Hematoxylin and Eosin (H&E) staining, amyloid appears as an amorphous, **extracellular, eosinophilic (pink), hyaline material** [3]. * **Option D (True):** This is the diagnostic gold standard. When stained with **Congo Red**, amyloid exhibits a characteristic **apple-green birefringence** under polarized light due to the alignment of the beta-pleated sheets [2]. **3. NEET-PG High-Yield Pearls:** * **Stains:** Congo Red (most specific), Thioflavin T (fluorescent), and Crystal Violet (metachromatic). * **Most Common Type:** AL Amyloidosis (Primary), associated with Plasma Cell Dyscrasias (Light chains) [2]. * **Dialysis-associated:** $\beta_3$-microglobulin (often presents as Carpal Tunnel Syndrome) [4]. * **Alzheimer’s Disease:** $A\beta$ amyloid (derived from Amyloid Precursor Protein). * **Organ Involvement:** The **Kidney** is the most common and most serious organ involved (presents as Nephrotic Syndrome) [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] 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. [4] 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. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 267-268.

Question 398: Which of the following is NOT a characteristic of Turner syndrome?

A. Short stature
B. Webbed neck
C. Dysgenetic gonads
D. True hermaphrodism (Correct Answer)

Explanation: **Explanation:** **Turner Syndrome (45,X)** is the most common sex chromosome abnormality in females, characterized by the complete or partial absence of one X chromosome [1]. **Why "True Hermaphroditism" is the correct answer:** True Hermaphroditism (now termed **Ovotesticular Disorder of Sex Development**) is defined by the presence of both ovarian and testicular tissue in the same individual. Turner syndrome patients, however, do not possess testicular tissue. Instead, they have **"streak ovaries"** (dysgenetic gonads) where follicles are absent and replaced by fibrous stroma [1]. They are phenotypically female but remain sexually infantile. **Why the other options are incorrect:** * **Short Stature:** This is the most consistent clinical feature of Turner syndrome, primarily due to the haploinsufficiency of the **SHOX gene** located on the short arm of the X chromosome [1]. * **Webbed Neck (Cystic Hygroma/Pterygium colli):** This results from lymphatic obstruction during fetal development. Other related features include a low posterior hairline and a broad "shield-shaped" chest [1]. * **Dysgenetic Gonads:** As mentioned, accelerated oocyte loss leads to fibrous "streak" ovaries, resulting in primary amenorrhea and infertility. **High-Yield Clinical Pearls for NEET-PG:** * **Karyotype:** 45,X is the most common (50%), but mosaics (e.g., 45,X/46,XX) and structural abnormalities (Isochromosome Xq) also occur [1]. * **Cardiac Associations:** Bicuspid aortic valve (most common) and Coarctation of the aorta (pre-ductal). * **Renal Association:** Horseshoe kidney. * **Biochemical Markers:** Elevated LH and FSH levels (Hypergonadotropic hypogonadism) due to lack of feedback inhibition from estrogen. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 175-177.

Question 399: Amyloid deposits stain positively with all of the following reagents except?

A. Congo-red
B. Crystal violet
C. Methenamine silver (Correct Answer)
D. Thioflavin T

Explanation: **Explanation:** The correct answer is **Methenamine silver** because it is primarily used to stain fungi, basement membranes, and certain opportunistic pathogens (like *Pneumocystis jirovecii*), but it does not have an affinity for amyloid fibrils. **Why the other options are incorrect:** * **Congo Red:** This is the gold standard for amyloid staining. Under ordinary light, it stains amyloid pink-red [1]. Under polarized light, it demonstrates the pathognomonic **apple-green birefringence** due to the cross-beta-pleated sheet configuration of amyloid fibrils [1]. * **Crystal Violet (and Methyl Violet):** These are metachromatic stains. Amyloid reacts with these dyes to produce a rose-pink or reddish-violet color, contrasting with the blue/purple color of the dye itself. * **Thioflavin T (and S):** These are fluorescent dyes. When viewed under a fluorescence microscope, Thioflavin T gives a bright yellow-green fluorescence. This method is highly sensitive but less specific than Congo Red. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Type:** Systemic AL (Light chain) amyloidosis is the most common primary type; AA (Amyloid Associated) is secondary to chronic inflammation. * **Diagnosis:** Abdominal fat pad aspiration or rectal biopsy are the preferred initial screening sites (high sensitivity). * **H&E Appearance:** On standard Hematoxylin and Eosin stain, amyloid appears as an **extracellular, amorphous, eosinophilic (pink), hyaline** material [2]. * **Other Stains:** Sirius Red is another stain that can be used to demonstrate birefringence similar to Congo Red. **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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 580-581.

Question 400: Which of the following events occurs earliest in wound healing?

A. A thin continuous epithelial cover appears
B. Fibroblasts lay down collagen fibers
C. Granulation tissue fills the wound
D. Neutrophils line the wound edge (Correct Answer)

Explanation: ### Explanation Wound healing by primary intention follows a predictable chronological sequence of cellular and molecular events. **Why Option D is Correct:** The inflammatory phase is the first stage of wound healing. Within **24 hours**, neutrophils appear at the margins of the incision and move toward the fibrin clot [1]. They are the first cells to arrive (after platelets) to clear debris and prevent infection. This makes "neutrophils lining the wound edge" the earliest event among the choices provided. **Analysis of Incorrect Options:** * **Option A (Thin epithelial cover):** By **24 to 48 hours**, epithelial cells from both edges begin to migrate and proliferate along the dermis, meeting in the midline beneath the surface scab to yield a thin but continuous epithelial layer [2]. * **Option B (Fibroblasts laying collagen):** Fibroblasts enter the wound site around **day 3** and start secreting collagen fibers by **day 3 to 5** [2]. This marks the transition into the proliferative phase. * **Option C (Granulation tissue):** Granulation tissue (characterized by angiogenesis and fibroblast proliferation) typically peaks by **day 5**, filling the incisional space [1]. **High-Yield NEET-PG Pearls:** * **Chronology Summary:** * **0–24 hrs:** Neutrophils, fibrin clot. * **24–48 hrs:** Epithelial bridging. * **Day 3:** Macrophages replace neutrophils; granulation tissue starts [1]. * **Day 5:** Peak granulation tissue and maximal neovascularization [2]. * **Week 2:** Proliferation of fibroblasts and continued collagen accumulation. * **Month 2 onwards:** Scar formation and remodeling (Type III collagen replaced by Type I). * **Key Cell:** The **Macrophage** is considered the most essential cell for wound healing (orchestrates the transition from inflammation to repair) [1]. * **Tensile Strength:** At the end of 1 week, it is ~10%; it reaches ~70-80% by 3 months but rarely reaches 100% of pre-wound strength. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 115. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119.

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Cell Injury and Cell Death

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Adaptations of Cellular Growth

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Accumulations and Deposits

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Acute and Chronic Inflammation

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Tissue Repair and Wound Healing

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Hemodynamic Disorders

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Genetic Disorders

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Environmental Pathology

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Nutritional Diseases

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Molecular Basis of Disease

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