General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1071: Which of the following is a membrane receptor defect?

A. Thalassemia
B. Sickle cell disease
C. Familial hypercholesterolemia (Correct Answer)
D. Henoch Schonlein purpura

Explanation: **Explanation:** **Familial Hypercholesterolemia (FH)** is the classic example of a **membrane receptor defect** [1]. It is an autosomal dominant disorder caused by mutations in the gene encoding the **LDL receptor**. Under normal physiological conditions, these receptors are located on the cell membrane (primarily in the liver) and are responsible for the endocytosis of LDL-cholesterol [2]. A defect or deficiency in these receptors prevents the clearance of LDL from the plasma, leading to severe hypercholesterolemia and premature atherosclerosis [1]. **Analysis of Incorrect Options:** * **Thalassemia:** This is a **quantitative defect** in hemoglobin synthesis. It involves a decreased rate of synthesis of either alpha or beta-globin chains, leading to ineffective erythropoiesis and hemolysis. * **Sickle Cell Disease:** This is a **qualitative defect** of hemoglobin (HbS). It is caused by a point mutation in the beta-globin chain (glutamic acid replaced by valine at the 6th position), leading to hemoglobin polymerization under deoxygenated conditions. * **Henoch-Schönlein Purpura (HSP):** This is an **IgA-mediated systemic small-vessel vasculitis**. It is an immune-complex mediated (Type III hypersensitivity) disorder, not a receptor defect. **High-Yield Clinical Pearls for NEET-PG:** * **FH Genetics:** Most commonly involves the *LDLR* gene, but mutations in *APOB* or *PCSK9* can also cause similar phenotypes [1]. * **Clinical Triad:** Look for tendinous xanthomas (especially the Achilles tendon), xanthelasma, and premature coronary artery disease. * **Brown and Goldstein:** These scientists won the Nobel Prize for discovering the LDL receptor pathway through their work on FH. * **Statins:** These drugs work by inhibiting HMG-CoA reductase, which indirectly leads to an **upregulation of LDL receptors** on hepatocytes [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 151-152. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 156-157.

Question 1072: Reye's syndrome is diagnosed by using which stain?

A. Reticulin stain
B. Oil-red-O stain (Correct Answer)
C. PAS stain
D. Muci-carmine stain

Explanation: **Explanation:** **Reye’s Syndrome** is a rare but severe condition characterized by acute encephalopathy and fatty liver failure, typically following a viral illness (like Influenza or Varicella) in children treated with **Aspirin**. The hallmark pathological finding in the liver is **microvesicular steatosis** (small droplets of fat within hepatocytes). Because routine processing for H&E staining involves alcohol and xylene which dissolve lipids, fat appears as "clear vacuoles." To definitively demonstrate these lipid droplets, a **frozen section** must be used and stained with **Oil-red-O** or **Sudan Black**, which specifically stains neutral lipids bright red or black, respectively. **Analysis of Incorrect Options:** * **A. Reticulin stain:** Used to visualize Type III collagen fibers. It is helpful in diagnosing liver cirrhosis or identifying the architectural framework in tumors, but it does not stain lipids. * **C. PAS (Periodic Acid-Schiff) stain:** Used to highlight glycogen, mucopolysaccharides, and fungal elements. While it is a common liver stain (e.g., for Alpha-1 antitrypsin deficiency), it does not detect fat. * **D. Muci-carmine stain:** Specifically used to identify epithelial mucin (e.g., in adenocarcinomas) and the capsule of *Cryptococcus neoformans*. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Mitochondrial dysfunction leading to defective beta-oxidation of fatty acids. * **Electron Microscopy:** Shows characteristic "swelling and distortion of mitochondria" with loss of mitochondrial granules. * **Biochemical marker:** Elevated serum ammonia and transaminases with a normal or near-normal bilirubin. * **Aspirin Link:** Aspirin acts as a mitochondrial toxin in susceptible children; hence, Ibuprofen or Acetaminophen is preferred in pediatrics.

Question 1073: Calcitonin is a marker of which of the following?

A. Prostate cancer
B. Medullary carcinoma of the thyroid (Correct Answer)
C. Pheochromocytoma
D. Pancreatic cancer

Explanation: **Explanation:** **Medullary Carcinoma of the Thyroid (MTC)** arises from the **parafollicular C-cells** of the thyroid gland [3]. These cells are neuroendocrine in origin and their primary physiological function is the secretion of **Calcitonin**, a hormone involved in calcium homeostasis (though its clinical effect in humans is minimal) [1], [2]. In MTC, serum calcitonin levels are significantly elevated, making it a highly specific and sensitive **tumor marker** for diagnosis, monitoring treatment response, and detecting recurrence [1]. **Analysis of Incorrect Options:** * **Prostate Cancer:** The primary tumor marker is **Prostate-Specific Antigen (PSA)**. Acid phosphatase may also be elevated but is less specific. * **Pheochromocytoma:** This tumor of the adrenal medulla secretes catecholamines. Diagnosis relies on measuring urinary or plasma **metanephrines** and vanillylmandelic acid (VMA). * **Pancreatic Cancer:** The most common marker used is **CA 19-9**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Amyloid Stroma:** Histologically, MTC is characterized by nests of tumor cells in a prominent fibrovascular stroma containing **amyloid deposits** (formed by the precipitation of pro-calcitonin) [2]. 2. **Genetics:** Approximately 25% of MTC cases are familial, associated with **MEN 2A and 2B** syndromes due to mutations in the **RET proto-oncogene** [1], [3]. 3. **Staining:** On immunohistochemistry, MTC stains positive for Calcitonin, Chromogranin, and Synaptophysin. 4. **Congo Red:** The amyloid in MTC shows characteristic **apple-green birefringence** under polarized light. **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 1074: Which of the following statements about calcification is true?

A. Calcification is most commonly seen in the kidneys.
B. Serum calcium is normal in metastatic calcification.
C. Psammoma bodies are formed with dystrophic calcification. (Correct Answer)
D. Mitochondria are the rarest organelles affected in calcification.

Explanation: Pathologic calcification is the abnormal deposition of calcium salts in tissues. It is categorized into two types: **Dystrophic** and **Metastatic**. [1] **Why Option C is Correct:** Psammoma bodies are concentric, laminated calcified structures formed through **dystrophic calcification**. This occurs when calcium salts deposit in necrotic or degenerating tissues despite **normal serum calcium levels**. In certain tumors, single necrotic cells act as a seed (nidus) for calcium crystallization, which acquires lamellations over time. [1] * *High-yield examples:* **P**apillary carcinoma of thyroid, **S**erous cystadenocarcinoma of ovary, **M**eningioma, and **M**esothelioma (Mnemonic: **PSMM**). **Analysis of Incorrect Options:** * **Option A:** Calcification is not "most commonly" seen in the kidneys as a general rule. While nephrocalcinosis occurs in metastatic calcification, dystrophic calcification is far more frequent clinically (e.g., in atherosclerotic plaques or damaged heart valves). [1] * **Option B:** In **metastatic calcification**, serum calcium levels are **elevated** (hypercalcemia). [1] It occurs in normal tissues due to systemic metabolic derangements (e.g., hyperparathyroidism, bone destruction). [1] * **Option D:** Mitochondria are actually the **first** organelles to be affected in intracellular calcification, as they are the primary site for calcium accumulation during cell injury. [2] **NEET-PG Clinical Pearls:** 1. **Dystrophic Calcification:** Normal serum calcium; occurs in dead/dying tissue (e.g., Caseous necrosis in TB, Atheroma). [1] 2. **Metastatic Calcification:** High serum calcium; occurs in healthy tissues, especially those with an internal alkaline environment (Lungs, Gastric mucosa, Kidneys). [3] 3. **Monckeberg’s Arteriosclerosis:** A classic example of dystrophic calcification involving the tunica media of medium-sized muscular arteries. [4] **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. 134-135. [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. 53-55. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 76-77. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 655-656.

Question 1075: What is the most common tumor of the spleen?

A. Lymphoma (Correct Answer)
B. Sarcoma
C. Hemangioma
D. Metastasis

Explanation: **Explanation:** The spleen is a secondary lymphoid organ, making it a primary site for hematologic malignancies. **Lymphoma** is considered the most common tumor of the spleen [1]. It can involve the spleen either as a primary site (Primary Splenic Lymphoma) or, more frequently, as part of systemic dissemination (Secondary involvement) [2]. Among these, Non-Hodgkin Lymphoma (NHL) is the most prevalent subtype. **Analysis of Options:** * **A. Lymphoma (Correct):** Due to the abundance of lymphoid tissue in the white pulp, the spleen is frequently involved in lymphoproliferative disorders [1]. * **B. Sarcoma:** Primary splenic sarcomas (like angiosarcoma) are extremely rare, though they are highly aggressive when they occur. * **C. Hemangioma:** This is the most common **benign** primary tumor of the spleen. While frequently encountered as an incidental finding, it is less common overall than lymphomatous involvement. * **D. Metastasis:** While the spleen is highly vascular, it is a relatively uncommon site for solid tumor metastases (e.g., from breast or lung cancer) compared to the liver or lungs. This is attributed to the spleen’s high concentration of immune cells and the rhythmic contraction of its capsule. **NEET-PG High-Yield Pearls:** * **Most common benign tumor of spleen:** Hemangioma. * **Most common primary malignant tumor of spleen:** Angiosarcoma (rare, but the most common *non-lymphoid* primary malignancy). * **Most common cause of massive splenomegaly:** Chronic Myeloid Leukemia (CML) or Myelofibrosis (in India, also consider Visceral Leishmaniasis/Kala-azar). * **Gamna-Gandy Bodies:** Siderofibrotic nodules (calcium and iron deposits) seen in the spleen in conditions like portal hypertension or sickle cell anemia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 560-570. [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. 609-610.

Question 1076: Which of the following is associated with the RET proto-oncogene?

A. MEN1
B. Medullary carcinoma of thyroid (Correct Answer)
C. Small cell carcinoma of lung
D. Melanoma

Explanation: The **RET proto-oncogene** (located on chromosome 10q11) encodes a receptor tyrosine kinase essential for the development of neuroendocrine cells. Mutations in this gene lead to constitutive activation of the receptor, driving oncogenesis [1]. ### **Why Medullary Carcinoma of Thyroid (MTC) is Correct:** MTC is the hallmark malignancy associated with RET mutations [1]. * **Sporadic MTC:** Approximately 50% of sporadic cases harbor somatic RET mutations. * **Familial MTC:** Nearly 100% of hereditary cases (MEN 2A and 2B) are caused by germline RET mutations [1]. Prophylactic thyroidectomy is often indicated in children carrying these mutations. ### **Analysis of Incorrect Options:** * **A. MEN1:** This syndrome is caused by a mutation in the **MEN1 gene** (encoding the protein Menin) on chromosome 11 [2]. It is characterized by the "3 Ps": Pituitary, Parathyroid, and Pancreatic tumors. * **C. Small cell carcinoma of lung:** This is most commonly associated with **RB1** and **TP53** mutations, as well as **MYC** amplification. * **D. Melanoma:** The most frequent driver mutations in melanoma involve **BRAF** (V600E), **NRAS**, or **KIT**, rather than RET. ### **High-Yield Clinical Pearls for NEET-PG:** * **MEN 2A:** MTC + Pheochromocytoma + Parathyroid hyperplasia [1]. * **MEN 2B:** MTC + Pheochromocytoma + Mucosal neuromas + Marfanoid habitus [1]. * **Hirschsprung Disease:** While *gain-of-function* RET mutations cause cancer, *loss-of-function* mutations in the same gene are associated with Hirschsprung disease (congenital aganglionic megacolon). * **Papillary Thyroid Carcinoma:** Can also involve RET via chromosomal rearrangement (**RET/PTC rearrangement**), though MTC is the classic association for point mutations [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1137. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1139-1140. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1097-1098.

Question 1077: Hypertrophy is a type of

A. Cell injury
B. Cellular adaptation (Correct Answer)
C. Carcinoma
D. Cell aging

Explanation: **Explanation:** **1. Why Cellular Adaptation is Correct:** Cellular adaptation refers to the reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their environment [1]. **Hypertrophy** is a specific form of adaptation where there is an **increase in the size of cells**, leading to an increase in the size of the organ [2]. It occurs in cells that have a limited capacity to divide (e.g., cardiac and skeletal muscle), where the increased functional demand is met by synthesizing more structural proteins and organelles rather than by cell division [1]. **2. Why Other Options are Incorrect:** * **Cell Injury:** This occurs when the adaptive capability is exceeded or if the external stress is inherently harmful [1]. While prolonged hypertrophy (e.g., in the heart) can eventually lead to cell injury and heart failure, hypertrophy itself is a protective, adaptive response. * **Carcinoma:** This refers to malignant neoplasms arising from epithelial tissue. Carcinoma involves uncontrolled, irreversible cell proliferation (neoplasia), whereas hypertrophy is a controlled, reversible increase in cell size [2]. * **Cell Aging:** Also known as senescence, this involves a progressive decline in cellular function and viability over time, often characterized by the accumulation of metabolic damage (e.g., lipofuscin). **3. NEET-PG High-Yield Pearls:** * **Mechanism:** Hypertrophy is driven by the activation of phosphoinositide 3-kinase (PI3K/AKT) pathways and G-protein coupled receptors [1]. * **Physiological Example:** Uterine enlargement during pregnancy (combined hypertrophy and hyperplasia) [2] or skeletal muscle growth in athletes. * **Pathological Example:** Left Ventricular Hypertrophy (LVH) due to systemic hypertension [1]. * **Key Distinction:** Hypertrophy (size) vs. Hyperplasia (number) [2]. Permanent cells (cardiac/skeletal muscle/neurons) undergo **only** hypertrophy, not hyperplasia. **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. 45-46. [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. 85-88.

Question 1078: Gamma Gandy bodies contain hemosiderin and what other substance?

A. Sodium
B. Calcium (Correct Answer)
C. Magnesium
D. Calcium

Explanation: **Explanation:** **Gamma-Gandy bodies** (also known as Siderofibrotic nodules) are small, firm, brown-to-yellow nodules found in the spleen. They represent organized areas of focal hemorrhage that have undergone subsequent fibrosis and mineralization. **Why Calcium is the Correct Answer:** When focal hemorrhage occurs within the splenic parenchyma (often due to portal hypertension), the extravasated red blood cells break down [1]. This leads to the deposition of **Hemosiderin** (derived from iron) [1]. Over time, these areas undergo fibrous scarring. A key feature of this process is **dystrophic calcification**, where **Calcium** salts (along with iron) deposit onto the fibrous connective tissue and elastic fibers [2]. Under a microscope, they appear as golden-yellow or brown pigments that stain positive with Prussian blue (for iron) and Alizarin Red (for calcium). **Analysis of Incorrect Options:** * **A. Sodium:** Sodium is a primary extracellular cation involved in fluid balance but does not participate in the formation of organized mineralized nodules or dystrophic calcification. * **C. Magnesium:** While magnesium can sometimes be found in trace amounts in various physiological processes, it is not a diagnostic or characteristic component of Gamma-Gandy bodies. * **D. Calcium:** (Duplicate option provided in the prompt; Calcium is the definitive constituent). **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Cause:** Portal Hypertension (secondary to Cirrhosis). * **Other Causes:** Sickle Cell Anemia, Hemochromatosis, and Lymphoma. * **Imaging:** On MRI, Gamma-Gandy bodies appear as "signal voids" (dark spots) on T2*-weighted Gradient Echo (GRE) sequences due to the paramagnetic effect of iron. * **Staining:** They are characterized by the presence of **siderotic granules** and **incrustation of fibers** with iron and calcium. **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. 75-76. [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. 76-77.

Question 1079: Which organelle plays the most important role in apoptosis?

A. Smooth endoplasmic reticulum
B. Golgi complex
C. Mitochondria (Correct Answer)
D. Rough endoplasmic reticulum

Explanation: **Explanation:** The **mitochondria** are considered the "central executioners" of apoptosis, particularly in the **intrinsic (mitochondrial) pathway**, which is the major mechanism of programmed cell death in mammals [1], [2]. **Why Mitochondria is correct:** Apoptosis is triggered when mitochondrial membrane permeability increases due to the action of pro-apoptotic proteins (like **BAX and BAK**) [1], [3]. This leads to the leakage of **Cytochrome c** from the inner mitochondrial membrane into the cytosol [1]. Once in the cytosol, Cytochrome c binds to Apaf-1 to form the **apoptosome**, which activates **Caspase-9**, initiating the executioner phase of cell death [2]. Mitochondria also release other pro-apoptotic proteins like Smac/DIABLO, which neutralize endogenous inhibitors of apoptosis (IAPs). **Why other options are incorrect:** * **Smooth Endoplasmic Reticulum (SER):** Primarily involved in lipid synthesis, detoxification, and calcium storage. While ER stress can trigger apoptosis, it is not the primary executioner organelle. * **Golgi Complex:** Functions in protein packaging and modification; it does not play a direct regulatory role in the apoptotic signaling cascade. * **Rough Endoplasmic Reticulum (RER):** Responsible for protein synthesis. Like the SER, it is a site of cellular stress but not the central organelle governing the apoptotic pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Anti-apoptotic proteins:** BCL-2, BCL-XL (they maintain mitochondrial membrane integrity) [3]. * **Pro-apoptotic proteins:** BAX, BAK (they form pores in the mitochondrial membrane) [3]. * **Initiator Caspases:** Caspase-9 (Intrinsic pathway), Caspase-8 and 10 (Extrinsic pathway) [1]. * **Executioner Caspases:** Caspase-3 and 6. * **Marker of Apoptosis:** Annexin V (binds to phosphatidylserine flipped to the outer membrane). **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. 65-67. [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. 64-65. [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. 80-81.

Question 1080: Russell bodies are seen in which of the following cell types?

A. Lymphocytes
B. Neutrophils
C. Macrophages
D. None of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **None of the above** because Russell bodies are characteristic inclusions found specifically in **Plasma cells**. [1] **1. Understanding Russell Bodies:** Russell bodies are large, eosinophilic, homogeneous immunoglobulin inclusions. They represent an accumulation of newly synthesized immunoglobulins within the cisternae of the **Rough Endoplasmic Reticulum (RER)** of a plasma cell. This occurs when the rate of protein synthesis exceeds the cell's capacity to secrete them, often seen in chronic inflammatory states or Plasma Cell Dyscrasias (e.g., Multiple Myeloma). [1] **2. Analysis of Options:** * **Lymphocytes (A):** While plasma cells are derived from B-lymphocytes, the term "Russell bodies" is reserved for the secretory phase (plasma cells). * **Neutrophils (B):** Neutrophils contain primary (azurophilic) and secondary (specific) granules, but they do not produce immunoglobulins and thus do not form Russell bodies. * **Macrophages (C):** Macrophages may contain "tingible bodies" (debris from phagocytosed cells), but they do not synthesize the immunoglobulins required to form Russell bodies. [3] **3. High-Yield Clinical Pearls for NEET-PG:** * **Mott Cells:** A plasma cell containing multiple Russell bodies is referred to as a **Mott cell** (or grape cell). [1] * **Dutcher Bodies:** If the immunoglobulin inclusions are found within the **nucleus** (intranuclear) rather than the cytoplasm, they are called Dutcher bodies (commonly seen in Waldenström Macroglobulinemia). [2] * **Staining:** Russell bodies are PAS (Periodic Acid-Schiff) positive. * **Location:** They are a classic example of **intracellular protein accumulation**, a key concept in cellular adaptation and injury. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618. [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. 606-607. [3] 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, p. 606.

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Cell Injury and Cell Death

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Adaptations of Cellular Growth

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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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