General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 31: Which chromosomal translocation is characteristic of Follicular lymphoma?

A. t(8;21)
B. t(8;14)
C. t(11;14)
D. t(14;18) (Correct Answer)

Explanation: **Explanation:** **Correct Answer: D. t(14;18)** Follicular Lymphoma (FL) is characterized by the translocation **t(14;18)(q32;q21)** [1], [2]. This translocation involves the **BCL-2 gene** on chromosome 18 and the **Immunoglobulin Heavy chain (IgH) locus** on chromosome 14 [1], [3]. * **Mechanism:** The BCL-2 gene is moved next to the highly active IgH promoter, leading to the **overexpression of BCL-2 protein** [2]. * **Pathophysiology:** BCL-2 is an anti-apoptotic protein. Its overexpression prevents programmed cell death in B-cells, leading to their accumulation and the formation of lymphoma [1], [3]. **Analysis of Incorrect Options:** * **A. t(8;21):** Characteristic of **Acute Myeloid Leukemia (AML-M2)**. It involves the RUNX1-RUNX1T1 fusion gene and is generally associated with a favorable prognosis. * **B. t(8;14):** Characteristic of **Burkitt Lymphoma**. It involves the **c-MYC** oncogene (Ch 8) and the IgH locus (Ch 14) [1], leading to rapid cellular proliferation (Starry-sky appearance). * **C. t(11;14):** Characteristic of **Mantle Cell Lymphoma**. It involves the **Cyclin D1 (PRAD-1)** gene (Ch 11) and the IgH locus (Ch 14), leading to cell cycle dysregulation. **High-Yield Clinical Pearls for NEET-PG:** * **BCL-2 Expression:** In normal lymph nodes, germinal centers are BCL-2 negative. In Follicular Lymphoma, the neoplastic follicles are **BCL-2 positive** (a key IHC diagnostic feature) [2], [3]. * **Clinical Course:** FL is an indolent (slow-growing) lymphoma but can transform into a more aggressive **Diffuse Large B-Cell Lymphoma (DLBCL)** (Richter’s-like transformation) [4]. * **Morphology:** Characterized by "Centrocytes" (cleaved cells) and "Centroblasts" (large non-cleaved cells) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 602-604. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 563-564.

Question 32: Which of the following proteins binds antiapoptotic proteins?

A. Bax (Correct Answer)
B. Bad
C. Bid
D. Bcl-2

Explanation: Apoptosis is regulated by the **Bcl-2 family of proteins**, which act as a rheostat to determine cell survival [1]. These proteins are categorized into three groups based on their function and BH (Bcl-2 Homology) domains. **Why Bax is the correct answer:** **Bax and Bak** are the primary **pro-apoptotic effectors**. Under cellular stress, Bax undergoes a conformational change, translocates to the outer mitochondrial membrane, and oligomerizes. Crucially, Bax acts by **binding to and neutralizing anti-apoptotic proteins** (like Bcl-2 and Bcl-xL) and by forming pores in the mitochondrial membrane (MAC - Mitochondrial Apoptosis-induced Channel) [2]. This leads to the release of Cytochrome *c* into the cytosol, triggering the caspase cascade [1]. **Analysis of Incorrect Options:** * **Bad and Bid (Options B & C):** These are **"BH3-only" proteins** (pro-apoptotic sensors). Their primary role is to sense cell stress and "activate" Bax/Bak or inhibit anti-apoptotic proteins. While they are part of the pathway, Bax is the definitive effector that directly counters the anti-apoptotic proteins to facilitate membrane permeabilization. * **Bcl-2 (Option D):** This is the prototype **anti-apoptotic protein** [2]. It prevents apoptosis by stabilizing the mitochondrial membrane and inhibiting Bax/Bak. It does not bind anti-apoptotic proteins; it *is* one. **NEET-PG High-Yield Pearls:** * **Pro-apoptotic (Effectors):** Bax, Bak. * **Pro-apoptotic (Sensors/BH3-only):** Bad, Bid, Bim, Puma, Noxa. * **Anti-apoptotic:** Bcl-2, Bcl-xL, MCL-1 [2]. * **Follicular Lymphoma Connection:** A translocation **t(14;18)** leads to overexpression of **Bcl-2**, resulting in decreased apoptosis and prolonged B-cell survival [3]. **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. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311.

Question 33: What is the maximum incidence of ABO isoimmunization?

A. O-positive mother to A-positive child (Correct Answer)
B. O-positive mother to B-positive child
C. A-positive mother to O-positive child
D. B-positive mother to O-positive child

Explanation: ### Explanation **Underlying Medical Concept** ABO isoimmunization (Hemolytic Disease of the Newborn) occurs when maternal antibodies cross the placenta and attack fetal red blood cells [1]. This typically occurs in **Group O mothers** because they naturally possess high titers of **IgG anti-A and anti-B antibodies** [3]. Unlike the IgM antibodies found in Group A or B individuals, IgG can cross the placental barrier [1]. The incidence is highest in **O-positive mothers with A-positive children** because the **A-antigen is more immunogenic** than the B-antigen. Furthermore, the A1 subgroup specifically has a high density of antigenic sites, leading to a more frequent immune response compared to B-antigens. **Analysis of Options** * **Option A (Correct):** Group O mothers have IgG antibodies; the A-antigen is the most common and potent target for these antibodies in the fetus. * **Option B (Incorrect):** While O-to-B isoimmunization does occur, it is statistically less frequent than O-to-A because the B-antigen is less prevalent in many populations and generally less immunogenic. * **Options C & D (Incorrect):** Mothers with blood groups A or B primarily produce **IgM** antibodies (anti-B and anti-A, respectively) [3]. Since IgM cannot cross the placenta, isoimmunization in these scenarios is clinically rare [1]. **NEET-PG High-Yield Pearls** * **Most Common Cause of HDN:** ABO incompatibility is now more common than Rh incompatibility (due to widespread use of Rhogam). * **Severity:** ABO HDN is usually **milder** than Rh HDN because fetal tissues and placental cells also express A and B antigens, which "buffer" or soak up the maternal antibodies before they reach fetal RBCs. * **Direct Coombs Test (DCT):** Often weakly positive or even negative in ABO HDN, unlike the strongly positive result seen in Rh incompatibility [2]. * **First Pregnancy:** Unlike Rh disease, ABO isoimmunization **can occur in the first pregnancy** because anti-A and anti-B antibodies are pre-formed [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 603-604. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.

Question 34: Which tumor marker is associated with breast cancer?

A. CA 15-3 (Correct Answer)
B. CA 19-9
C. CA 125
D. CEA

Explanation: ### Explanation **Correct Option: A. CA 15-3** Cancer Antigen 15-3 (CA 15-3) is a glycoprotein derived from the MUC1 gene. It is the most widely used serum tumor marker for **breast cancer**, particularly for monitoring treatment response and detecting recurrence in metastatic disease. While it lacks the sensitivity and specificity required for initial screening, rising levels are highly suggestive of disease progression. Another marker frequently associated with breast cancer is **CA 27-29**. [1] **Analysis of Incorrect Options:** * **B. CA 19-9:** This is the primary marker for **Pancreatic Adenocarcinoma**. It is also elevated in cholangiocarcinoma and other hepatobiliary malignancies. * **C. CA 125:** This is the classic marker for **Serous Ovarian Cancer**. It is also used to monitor endometriosis and pelvic inflammatory disease, though it is less specific in premenopausal women. * **D. CEA (Carcinoembryonic Antigen):** While CEA can be elevated in breast cancer, it is the gold-standard marker for **Colorectal Carcinoma**. It is also associated with cancers of the pancreas, lung, and stomach. **NEET-PG High-Yield Pearls:** * **Breast Cancer:** CA 15-3, CA 27-29, and CEA (for monitoring). [1] * **Ovarian Cancer:** CA 125 (Surface epithelial), AFP/hCG (Germ cell tumors). * **Pancreatic Cancer:** CA 19-9. * **Hepatocellular Carcinoma (HCC) & Yolk Sac Tumor:** AFP (Alpha-fetoprotein). * **Medullary Carcinoma of Thyroid:** Calcitonin. * **Prostate Cancer:** PSA (Prostate-Specific Antigen). * **Trophoblastic Tumors (Choriocarcinoma):** beta-hCG. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1066.

Question 35: The gene for Wilson's disease is located on which chromosome?

A. 7
B. 10
C. 13 (Correct Answer)
D. 17

Explanation: **Explanation:** **Wilson’s Disease (Hepatolenticular Degeneration)** is an autosomal recessive disorder of copper metabolism [1]. The correct answer is **Chromosome 13** because the **ATP7B gene**, which encodes a copper-transporting P-type ATPase, is located on the long arm of this chromosome (**13q14.3**). The underlying pathophysiology involves a defect in this ATPase, leading to impaired biliary excretion of copper and failure to incorporate copper into ceruloplasmin [1]. This results in toxic copper accumulation primarily in the **liver, brain (basal ganglia), and cornea** [2]. **Analysis of Incorrect Options:** * **Option A (Chromosome 7):** This is the location of the **CFTR gene**, which is mutated in **Cystic Fibrosis**. * **Option B (Chromosome 10):** Associated with the **RET proto-oncogene**, linked to **MEN 2A and 2B** syndromes. * **Option D (Chromosome 17):** This is a high-yield chromosome housing the **TP53** tumor suppressor gene and the **NF1** (Neurofibromatosis type 1) gene. **Clinical Pearls for NEET-PG:** * **Diagnosis:** Characterized by **decreased serum ceruloplasmin**, increased urinary copper excretion, and increased hepatic copper content on biopsy [2]. * **Kayser-Fleischer (KF) Rings:** Copper deposition in the **Descemet’s membrane** of the cornea (best seen on slit-lamp exam) [1]. * **Morphology:** Liver biopsy may show steatosis, chronic hepatitis, or cirrhosis [1]. Brain involvement often shows atrophy of the **putamen**. * **Treatment:** Copper chelators like **D-penicillamine** or Trientine, and Zinc (which inhibits intestinal copper absorption). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 855-856. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 394-395.

Question 36: Which of the following components is a potent neutrophil chemotactic agent?

A. C1
B. C2
C. C5a (Correct Answer)
D. C7, 8, 9 complex

Explanation: **Explanation:** **C5a** is the correct answer because it is one of the most potent **chemotactic factors** for neutrophils, monocytes, eosinophils, and basophils [1]. In the complement cascade, C5a acts as an **anaphylatoxin**, increasing vascular permeability and inducing degranulation of mast cells [1]. More importantly, it activates the lipoxygenase pathway of arachidonic acid metabolism in neutrophils, leading to the release of further inflammatory mediators. **Analysis of Incorrect Options:** * **C1:** This is the first component of the classical pathway. Its primary role is the initiation of the complement cascade upon binding to antigen-antibody complexes (IgG or IgM); it has no chemotactic properties. * **C2:** This is a plasma protein cleaved into C2a and C2b. C2b (prokinin) can influence vascular permeability, but it does not attract inflammatory cells. * **C7, 8, 9 complex:** These components, along with C5b and C6, form the **Membrane Attack Complex (MAC)**. The MAC’s primary function is to create pores in the lipid bilayer of target cells, leading to osmotic lysis, rather than cell signaling or chemotaxis. **High-Yield Clinical Pearls for NEET-PG:** * **Other potent neutrophil chemoattractants:** Leukotriene B4 (LTB4), Interleukin-8 (IL-8), and Bacterial products (N-formyl methionine peptides). * **Opsonization:** C3b is the primary complement component responsible for opsonization (tagging pathogens for phagocytosis). * **Anaphylatoxins:** C3a, C4a, and C5a (ranked by potency: C5a > C3a > C4a) [1]. * **Deficiency:** Deficiency of C5-C9 (MAC) predisposes individuals to recurrent *Neisseria* infections. **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. 163-164.

Question 37: If both parents are carriers of the beta-thalassemia gene, what is the chance of having a child with thalassemia major in each pregnancy?

A. 25% (Correct Answer)
B. 50%
C. 75%
D. 100%

Explanation: **Explanation:** The correct answer is **25%**. This question tests the understanding of **Autosomal Recessive (AR)** inheritance patterns, which is the mode of inheritance for Beta-thalassemia. **1. Why 25% is Correct:** Beta-thalassemia occurs due to mutations in the HBB gene on chromosome 11. When both parents are carriers (Thalassemia Minor/Trait), they each possess one normal allele (A) and one mutated allele (a). According to the Punnett Square for an AR disorder (Aa x Aa): * **25% (AA):** Unaffected/Normal. * **50% (Aa):** Carriers (Thalassemia Minor). * **25% (aa):** Affected (Thalassemia Major) [2]. Therefore, in every pregnancy, there is a 1 in 4 (25%) chance of the child inheriting both mutated alleles and developing Thalassemia Major. **2. Why Other Options are Incorrect:** * **50%:** This represents the probability of a child being a **carrier** (Thalassemia Minor), not having the disease (Major). * **75%:** This represents the probability of a child being **either** a carrier or affected (total risk of inheriting at least one mutated gene). * **100%:** This would only occur if both parents had Thalassemia Major (aa x aa), which is clinically rare due to the severity of the disease. **NEET-PG High-Yield Pearls:** * **Molecular Basis:** Most commonly caused by **point mutations** (unlike Alpha-thalassemia, which is usually due to gene deletions) [1]. * **Diagnosis:** Gold standard is **Hb Electrophoresis** or HPLC. In carriers (Minor), expect **HbA2 > 3.5%**. * **Microscopy:** Peripheral smear shows microcytic hypochromic anemia with characteristic **Target cells** and basophilic stippling. * **Radiology:** Chronic hemolysis leads to marrow expansion, appearing as a **"Crew-cut" appearance** on skull X-ray [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 646-649. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 600-601.

Question 38: Cell injury occurs due to which of the following?

A. Decreased cellular ATP generation (Correct Answer)
B. Cytosolic Ca++
C. Membrane damage
D. Intracellular K+

Explanation: The fundamental mechanism underlying cell injury, particularly in ischemic and hypoxic states, is the **depletion of ATP** [1]. ATP is critical for nearly all synthetic and degradative processes within the cell. When ATP levels fall below 5–10% of normal, it triggers a cascade of events: failure of the Na+/K+-ATPase pump leads to intracellular sodium accumulation and cellular swelling; failure of the Ca++ pump leads to calcium influx; and a switch to anaerobic glycolysis results in lactic acid accumulation and decreased intracellular pH [1]. Therefore, decreased ATP generation is the **primary trigger** that initiates the injury process. **Analysis of Options:** * **Option A (Correct):** Decreased ATP is the "master switch" for cell injury, leading to the failure of vital metabolic pathways [1]. * **Option B (Incorrect):** While an increase in **cytosolic Ca++** is a major mediator of cell injury (by activating enzymes like phospholipases and proteases), it is typically a *consequence* of ATP depletion or membrane damage, not the initial cause itself in this context [1]. * **Option C (Incorrect):** **Membrane damage** is a hallmark of *irreversible* cell injury [1]. While it is a critical component of the pathology, it usually follows the initial metabolic insult (like ATP loss or ROS production). * **Option D (Incorrect):** Cell injury is characterized by an **efflux of K+** (decreased intracellular K+) and an influx of Na+ and Ca++ [1]. High intracellular K+ is actually the normal physiological state. **NEET-PG High-Yield Pearls:** * **Earliest morphological change** in cell injury: Cellular swelling (hydropic change) [1]. * **Point of Irreversibility:** Marked by severe mitochondrial dysfunction (vacuolization) and profound membrane damage [1]. * **Mitochondrial Permeability Transition Pore (MPTP):** Its opening leads to the loss of mitochondrial membrane potential and failure of oxidative phosphorylation [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. 49-62.

Question 39: Which of the following statements about transposons is NOT true?

A. They are popularly known as jumping genes.
B. They are mobile genetic elements.
C. They are implicated in gene regulation and chromatin organization.
D. They modulate the translation of target messenger RNAs into their corresponding proteins. (Correct Answer)

Explanation: ### Explanation **Transposons** (also known as "jumping genes") are mobile genetic elements that make up approximately 45% of the human genome [1]. The correct answer is **D** because the description provided refers to the function of **MicroRNAs (miRNAs)**, not transposons [2]. #### Why Option D is the Correct Answer (The "False" Statement) Transposons function at the **DNA level** by moving or copying themselves within the genome. They do not directly modulate the translation of target mRNAs into proteins; that is the specific regulatory role of non-coding RNAs like **miRNAs** and **siRNAs**, which cause post-transcriptional gene silencing by binding to mRNA [2], [3]. #### Analysis of Other Options * **Options A & B:** These are true. Transposons are defined as **mobile genetic elements** that can shift positions within the genome (transposition), earning them the moniker **"jumping genes"** (discovered by Barbara McClintock) [1]. * **Option C:** This is true. While once dismissed as "junk DNA," we now know transposons play a vital role in **gene regulation** and **chromatin organization** [1]. They can act as promoters or enhancers and influence the folding of DNA within the nucleus. #### NEET-PG High-Yield Pearls * **Barbara McClintock:** Won the Nobel Prize for discovering transposons in maize. * **Mechanism:** They move via a "cut-and-paste" (DNA transposons) or "copy-and-paste" (Retrotransposons) mechanism. * **Clinical Significance:** Transposons are a major cause of **genetic variation** and can cause diseases (e.g., Hemophilia A) if they insert themselves into functional genes (insertional mutagenesis) [1]. * **Contrast with miRNA:** Remember, **miRNAs** regulate gene expression **post-transcriptionally**, whereas **transposons** alter the **genomic structure** itself [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 14-15. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 16-17. [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. 230-231.

Question 40: Which of the following statements is false regarding apoptosis?

A. Cell size is shrunken
B. Plasma membrane remains intact
C. It is always pathological (Correct Answer)
D. Does not elicit inflammation

Explanation: ### Explanation **Correct Answer: C. It is always pathological** **Why Option C is the correct (False) statement:** Apoptosis, often referred to as "programmed cell death," can be both **physiological and pathological** [2]. Unlike necrosis, which is always a result of irreversible cell injury (pathological), apoptosis is a highly regulated process used by the body to eliminate unwanted or potentially harmful cells without damaging the surrounding tissue. * **Physiological examples:** Embryogenesis (e.g., removal of interdigital webs), hormone-dependent involution (e.g., endometrial breakdown during menses) [2], and elimination of self-reactive lymphocytes. * **Pathological examples:** DNA damage (radiation/chemotherapy) [1], accumulation of misfolded proteins (ER stress), and certain viral infections (e.g., viral hepatitis). **Analysis of Incorrect Options:** * **A. Cell size is shrunken:** This is a hallmark of apoptosis. The cytoplasm condenses and organelles become more tightly packed. In contrast, necrosis involves cell swelling (oncosis). * **B. Plasma membrane remains intact:** In apoptosis, the membrane structure is preserved but its lipid orientation is altered (e.g., translocation of phosphatidylserine to the outer leaflet). This prevents the leakage of cellular contents. * **D. Does not elicit inflammation:** Because the plasma membrane remains intact and the resulting "apoptotic bodies" are rapidly phagocytosed by macrophages before they can leak enzymes, there is no inflammatory response. **High-Yield NEET-PG Pearls:** * **Morphological Hallmark:** Chromatin condensation (pyknosis) is the most characteristic feature. * **Biochemical Hallmark:** DNA fragmentation by Ca²⁺/Mg²⁺ dependent endonucleases, creating a **"Step-ladder pattern"** on gel electrophoresis. * **Key Enzymes:** **Caspases** (Cysteine aspartate-specific proteases) [2]. Initiator caspases are 8 and 9; Executioner caspases are 3, 6, and 7. * **Eat-me signal:** Presence of **Phosphatidylserine** on the outer layer of the plasma membrane. **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. 101-102. [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. 63-65.

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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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