General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1201: Lipoxins synthesized from arachidonic acid act by which of the following mechanisms?

A. Decreasing leucocyte migration, adhesion, and chemotaxis (Correct Answer)
B. Increasing leucocyte migration, adhesion, and chemotaxis
C. Promoting vasoconstriction
D. Increasing vascular permeability

Explanation: **Explanation:** **Lipoxins** are endogenous, anti-inflammatory derivatives of **arachidonic acid** metabolism [1]. Unlike most other eicosanoids (like leukotrienes and prostaglandins) which promote inflammation, lipoxins function as "stop signals" to resolve the inflammatory process. **1. Why Option A is Correct:** Lipoxins (specifically LXA4 and LXB4) are synthesized via the **lipoxygenase pathway** through a unique transcellular biosynthetic mechanism involving neutrophils and platelets [1]. Their primary role is to **inhibit inflammation** by: * **Decreasing neutrophil recruitment:** They inhibit the chemotaxis and adhesion of neutrophils to the endothelium. * **Promoting Resolution:** They stimulate the non-phlogistic recruitment of monocytes and the clearance of apoptotic debris by macrophages (efferocytosis). **2. Why the Other Options are Incorrect:** * **Option B:** This describes the action of **Leukotrienes (e.g., LTB4)** and Chemokines (e.g., IL-8), which are pro-inflammatory and actively recruit leukocytes to the site of injury [1]. * **Option C:** Lipoxins actually promote **vasodilation**, opposing the action of vasoconstrictors like Thromboxane A2 [1]. * **Option D:** Increasing vascular permeability is a hallmark of **Leukotrienes (LTC4, LTD4, LTE4)** and Histamine [1]. Lipoxins help stabilize the vascular barrier during the resolution phase. **High-Yield Clinical Pearls for NEET-PG:** * **Transcellular Biosynthesis:** Lipoxins require two cell types for synthesis (e.g., Neutrophils produce intermediates which are converted to Lipoxins by Platelets). * **Resolution of Inflammation:** The switch from pro-inflammatory leukotrienes to anti-inflammatory lipoxins is a key step in the resolution of acute inflammation. * **Aspirin-Triggered Lipoxins (ATLs):** Aspirin can acetylate COX-2, leading to the production of "15-epi-lipoxins," which have potent anti-inflammatory effects. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 95-96.

Question 1202: Histiocytosis X is seen in all of the following conditions except?

A. Hand-Schüller-Christian disease
B. Eosinophilic granuloma
C. Letterer-Siwe syndrome
D. Torres syndrome (Correct Answer)

Explanation: **Explanation:** **Histiocytosis X**, now more commonly known as **Langerhans Cell Histiocytosis (LCH)**, is a group of idiopathic disorders characterized by the abnormal proliferation of mature bone marrow-derived Langerhans cells [1]. These cells are identified by their characteristic "coffee-bean" nuclei and **Birbeck granules** (tennis-racket shaped) on electron microscopy [1]. **Why Option D is Correct:** **Torres syndrome** (also known as Muir-Torre syndrome) is a variant of Lynch syndrome. It is an autosomal dominant condition characterized by sebaceous gland tumors and internal malignancies (most commonly colorectal cancer). It is a disorder of DNA mismatch repair (MMR) genes and has no pathological association with Langerhans cell proliferation. **Why Other Options are Incorrect:** Langerhans Cell Histiocytosis traditionally presents in three clinical forms, all of which are included in the "Histiocytosis X" spectrum: * **Letterer-Siwe syndrome (Option C):** The acute disseminated form, typically seen in infants (<2 years). It involves multiple organs (skin, liver, spleen, bone marrow). * **Hand-Schüller-Christian disease (Option A):** The chronic disseminated form, characterized by the classic triad of **calvarial bone defects, exophthalmos, and diabetes insipidus**. * **Eosinophilic granuloma (Option B):** The benign, localized form, usually presenting as solitary or multiple bone lesions (most commonly in the skull, ribs, or femur). **High-Yield Clinical Pearls for NEET-PG:** * **Immunohistochemistry (IHC) Markers:** LCH cells are positive for **CD1a, S100, and CD207 (Langerin)** [1]. Langerin is the most specific marker. * **Electron Microscopy:** Look for **Birbeck granules** [1]. * **Radiology:** "Punched-out" lytic lesions in the skull are a classic finding. **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. 629-630.

Question 1203: Which of the following is NOT true about apoptosis?

A. Annexin V can be used as a marker.
B. Inflammation is typically present. (Correct Answer)
C. Cell shrinkage is a characteristic feature.
D. Clumping of chromatin is observed.

Explanation: **Explanation:** Apoptosis, or "programmed cell death," is a highly regulated pathway of cell death [1] that occurs without eliciting an inflammatory response [2]. **Why Option B is the correct answer:** Unlike necrosis, where the plasma membrane ruptures and releases intracellular contents into the surrounding tissue (triggering an inflammatory cascade), **apoptosis does not typically involve inflammation**. In apoptosis, the plasma membrane remains intact, and the cell breaks into membrane-bound "apoptotic bodies." These are rapidly cleared by professional phagocytes (macrophages) before their contents can leak, thus avoiding an inflammatory reaction [2]. **Analysis of Incorrect Options:** * **Option A (Annexin V):** In early apoptosis, the membrane phospholipid **phosphatidylserine** flips from the inner leaflet to the outer leaflet of the plasma membrane. Annexin V has a high affinity for phosphatidylserine and is used as a specific laboratory marker to identify apoptotic cells. * **Option C (Cell shrinkage):** This is a hallmark morphological feature. The cytoplasm becomes dense and the organelles become tightly packed, contrasting with the cell swelling (oncosis) seen in necrosis. * **Option D (Clumping of chromatin):** This is the most characteristic feature of apoptosis. The chromatin aggregates peripherally under the nuclear membrane, often leading to nuclear fragmentation (karyorrhexis). **High-Yield NEET-PG Pearls:** * **Caspases** are the executioner enzymes of apoptosis (Cysteine proteases that cleave after Aspartic acid) [3]. * **Intrinsic Pathway:** Mediated by Mitochondria and Cytochrome C release (Bcl-2 family) [3]. * **Extrinsic Pathway:** Mediated by Death Receptors (FAS/FAS-L or TNF-R) [4]. * **DNA Laddering:** On electrophoresis, apoptosis shows a "step-ladder" pattern (internucleosomal cleavage), whereas necrosis shows a "smear" pattern. **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. 63-64. [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. 67-69. [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. 64-65. [4] 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, p. 67.

Question 1204: Dystrophic calcification occurs in all of the following conditions except?

A. Rheumatic heart disease
B. Lymph node
C. Normal kidney (Correct Answer)
D. Aneurysm

Explanation: **Explanation:** The core concept tested here is the distinction between **Dystrophic** and **Metastatic calcification**. [1], [2] **1. Why "Normal kidney" is the correct answer:** Dystrophic calcification occurs in **dead, dying, or degenerated tissues** despite normal serum calcium levels. A **normal kidney** consists of healthy, viable tissue. For calcification to occur in a normal kidney [1], there must be an underlying metabolic derangement (hypercalcemia) [2], which leads to **Metastatic calcification** (specifically involving the interstitial tissue of the gastric mucosa, kidneys, and lungs) [1]. Therefore, calcification in a "normal" kidney is not dystrophic. **2. Analysis of incorrect options:** * **Rheumatic heart disease (A):** Chronic inflammation leads to scarring and damage of heart valves. Calcification of these damaged valves is a classic example of dystrophic calcification. * **Lymph node (B):** Healed or necrotic lymph nodes (commonly seen in old Tuberculosis/Ghon complex) undergo dystrophic calcification [3]. * **Aneurysm (D):** Atherosclerotic plaques within an aneurysm undergo necrosis and degeneration, providing a nidus for dystrophic calcification. **3. NEET-PG High-Yield Pearls:** * **Dystrophic Calcification:** Serum calcium is **Normal**. Occurs in: Atherosclerosis, Caseous necrosis (TB), Psammoma bodies (Papillary thyroid CA, Meningioma, Serous cystadenocarcinoma of ovary), and Monckeberg’s medial calcific sclerosis. * **Metastatic Calcification:** Serum calcium is **Elevated** [2]. Occurs in: Hyperparathyroidism, Vitamin D toxicity, and Bone destruction (Multiple Myeloma). * **Morphology:** On H&E stain, both appear as basophilic (blue-purple), amorphous granular clumps [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. 76-77. [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. 134-135. [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, p. 55.

Question 1205: What is the earliest and most common form of reversible cell injury?

A. Cloudy swelling
B. Cellular swelling
C. Albuminous degeneration
D. All of the above (Correct Answer)

Explanation: **Explanation:** The earliest and most common manifestation of reversible cell injury is **cellular swelling** (also known as hydropic change or vacuolar degeneration) [1]. This occurs due to the failure of energy-dependent membrane pumps (specifically the Na⁺-K⁺ ATPase pump) following injury [1]. When the pump fails, sodium accumulates inside the cell, leading to an obligatory iso-osmotic gain of water to maintain equilibrium, causing the cell to swell [1]. **Why "All of the above" is correct:** In pathology, the terms **Cellular swelling**, **Cloudy swelling**, and **Albuminous degeneration** are synonymous. * **Cloudy swelling:** Historically used because the affected organ appears pale and swollen, and the cytoplasm looks "cloudy" or granular under a light microscope due to the presence of small clear vacuoles (distended ER) [1]. * **Albuminous degeneration:** An older term referring to the proteinaceous/granular appearance of the cytoplasm in swollen cells. Since all three terms describe the same fundamental pathological process of acute intracellular edema, Option D is the correct choice. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Reduced ATP → Failure of Na⁺-K⁺ pump → Influx of Na⁺ and H₂O + Efflux of K⁺ → Cellular swelling [1]. * **Microscopic hallmark:** Small, clear vacuoles within the cytoplasm (Hydropic change) [1]. * **Ultrastructural changes (EM):** Blunting of microvilli, mitochondrial swelling, and detachment of ribosomes from the Rough ER [1]. * **Reversibility:** If the injurious stimulus (e.g., hypoxia) is removed, the cell can return to its normal homeostatic state [1]. If it persists, it may progress to irreversible injury (necrosis). **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. 49-55.

Question 1206: What is true about metaplasia?

A. Loss of polarity
B. Nucleus is smaller in size
C. It is a reversible change (Correct Answer)
D. Immature cells

Explanation: ### Explanation **Metaplasia** is a reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another differentiated cell type [1]. It is a protective adaptive response to chronic irritation or stress, where the original cells are replaced by cells better suited to withstand the adverse environment [2]. #### Why the Correct Answer is Right: * **Reversibility:** Metaplasia is a hallmark of **cellular adaptation**. If the chronic stimulus (e.g., smoking or acid reflux) is removed, the tissue can revert to its original cellular architecture. This distinguishes it from neoplasia, which is irreversible. #### Why the Other Options are Wrong: * **A. Loss of polarity:** This is a characteristic of **dysplasia** or malignancy (anaplasia). In metaplasia, the new cell type is fully mature and maintains its organized orientation. * **B. Nucleus is smaller in size:** Metaplastic cells are mature, differentiated cells; their nuclei typically appear normal for that specific cell type. Significant nuclear changes (like pleomorphism or increased N:C ratio) are features of **dysplasia**. * **C. Immature cells:** Metaplasia involves **mature** cells. The process occurs via the **reprogramming of stem cells** (reserve cells) to differentiate into a different mature lineage, rather than the transformation of already existing mature cells. #### High-Yield Clinical Pearls for NEET-PG: 1. **Most Common Type:** Squamous metaplasia (e.g., in the respiratory tract of smokers where columnar cells become squamous) [1]. 2. **Barrett’s Esophagus:** A classic example of **columnar metaplasia**, where squamous epithelium changes to columnar (intestinal) epithelium due to acid reflux [3]. 3. **Vitamin A Deficiency:** Can induce squamous metaplasia in the respiratory tract and ducts of glands. 4. **Pre-cancerous Potential:** While metaplasia is reversible, persistent irritation can lead to a progression from **Metaplasia → Dysplasia → Carcinoma** [2]. **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. 91-92. [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, p. 49. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349.

Question 1207: Which of the following is NOT a mutation associated with Down syndrome?

A. Mosaicism
B. Robertsonian translocation
C. Maternal nondisjunction
D. VNTRs (Correct Answer)

Explanation: **Explanation:** Down syndrome (Trisomy 21) is the most common chromosomal disorder and a frequent topic in NEET-PG [2]. The question asks for the option **NOT** associated with its pathogenesis. **Why VNTRs is the correct answer:** **VNTRs (Variable Number Tandem Repeats)** are short nucleotide sequences organized as tandem repeats, showing variations in length between individuals. They are used as genetic markers in **DNA fingerprinting** and linkage analysis. They are physiological variations in the non-coding regions of DNA and are not a causative mechanism for chromosomal aneuploidies like Down syndrome. **Analysis of Incorrect Options:** * **Maternal Nondisjunction (95%):** This is the most common cause [2]. It occurs due to the failure of homologous chromosomes to separate during Meiosis I (usually in the ovum). It is strongly associated with advanced maternal age [2]. * **Robertsonian Translocation (4%):** This involves the attachment of the long arm of chromosome 21 to another acrocentric chromosome (usually 14 or 22) [1]. This is significant because it can be inherited from a carrier parent, leading to **familial Down syndrome** [1]. * **Mosaicism (1%):** This occurs due to mitotic nondisjunction during early embryonic development [1]. These individuals have two cell lines (one normal, one trisomic) and often exhibit a milder phenotype [1]. **NEET-PG High-Yield Pearls:** * **Most common cause:** Meiotic nondisjunction (Maternal > Paternal). * **Cytogenetics:** 47, XX, +21 (Nondisjunction); 46, XX, der(14;21)(q10;q10), +21 (Translocation) [1]. * **Clinical Markers:** Simian crease, Brushfield spots, endocardial cushion defects (ASD/VSD), and increased risk of **Acute Leukemia** (AMKL in <5 years; ALL in >5 years) and early-onset **Alzheimer’s disease** (due to APP gene on Chromosome 21). * **Screening:** Low AFP, low Estriol, and high hCG/Inhibin A (Quadruple test). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 170-171. [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. 92-93.

Question 1208: Which of the following has a propensity to metastasize through lymph nodes?

A. Alveolar rhabdomyosarcoma (Correct Answer)
B. Osteosarcoma
C. Both
D. None

Explanation: **Explanation:** The standard rule in oncology is that **carcinomas** spread primarily via the lymphatic system, while **sarcomas** spread hematogenously (via the blood) [1]. However, there are specific exceptions to this rule that are frequently tested in the NEET-PG exam. **1. Why Alveolar Rhabdomyosarcoma is correct:** While most sarcomas avoid lymph nodes, a specific group known by the mnemonic **SCARE** (or **SRECC**) has a high propensity for lymphatic spread. **Alveolar rhabdomyosarcoma** is a classic member of this group [2]. It is a highly aggressive soft tissue sarcoma, and the presence of nodal involvement is a significant prognostic factor. **2. Why the other options are incorrect:** * **Osteosarcoma:** This is the most common primary malignant bone tumor. It follows the classic sarcoma rule and metastasizes almost exclusively via the **hematogenous route**, most commonly to the lungs [1]. Lymph node involvement is extremely rare (less than 3%). * **Options C & D:** Since only Alveolar rhabdomyosarcoma follows the lymphatic pattern, these options are incorrect. **High-Yield Clinical Pearls for NEET-PG:** To remember the sarcomas that spread via **Lymph Nodes**, use the mnemonic **"SCARE"**: * **S:** **S**ynovial sarcoma [3] * **C:** **C**lear cell sarcoma * **A:** **A**ngiosarcoma / **A**lveolar rhabdomyosarcoma * **R:** **R**habdomyosarcoma (specifically Alveolar subtype) * **E:** **E**pithelioid sarcoma (The most common sarcoma to involve lymph nodes) **Note:** Conversely, remember the **Carcinomas** that spread via **Blood** (Hematogenous): **F**ollicular thyroid carcinoma, **R**enal cell carcinoma (RCC), **H**epatocellular carcinoma (HCC), and **C**horiocarcinoma (**Mnemonic: FRHC**). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 282. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1224-1225. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1225-1226.

Question 1209: What is the mechanism of transmission for Alpha-1 antitrypsin deficiency?

A. Autosomal recessive (Correct Answer)
B. Autosomal dominant
C. X-linked recessive
D. X-linked dominant

Explanation: **Alpha-1 Antitrypsin (AAT) Deficiency** is a genetic disorder characterized by low levels of the AAT protein, which normally protects the lungs from damage by neutrophil elastase [1], [2]. **Why Autosomal Recessive is correct:** AAT deficiency follows an **autosomal recessive** pattern of inheritance [1]. The condition is governed by the *SERPINA1* gene on chromosome 14 [1], [3]. The alleles are co-dominant, meaning both alleles contribute to the phenotype. However, for the clinical disease to manifest (especially the severe form), an individual typically needs to inherit two deficient alleles (most commonly the **PiZZ** genotype) [1], [3]. Heterozygotes (PiMZ) are usually asymptomatic carriers but may have an increased risk of lung disease if they smoke. **Why other options are incorrect:** * **Autosomal Dominant:** While the alleles are co-dominant, the clinical syndrome of liver and lung involvement requires a homozygous state for significant pathology, fitting the recessive model in medical examinations. * **X-linked Recessive/Dominant:** The *SERPINA1* gene is located on **Chromosome 14** (an autosome), not on the sex chromosomes (X or Y) [3]. Therefore, it affects males and females equally. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Misfolded AAT proteins aggregate in the endoplasmic reticulum of hepatocytes, leading to liver cirrhosis [1]. The lack of AAT in the lungs leads to uninhibited elastase activity, causing **Panacinar Emphysema** (classically involving the lower lobes) [1], [2], [3]. * **Histology:** Characterized by **PAS-positive, diastase-resistant globules** in the periportal hepatocytes. * **Genotypes:** * **PiMM:** Normal. * **PiZZ:** Most severe clinical disease (lowest AAT levels) [3]. * **PiSZ:** Increased risk of emphysema. * **Clinical Presentation:** Neonatal cholestasis, juvenile cirrhosis, or early-onset emphysema in a non-smoker [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 856-858. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 152-153. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 683-684.

Question 1210: The sago spleen and lardaceous spleen are conditions seen in which of the following?

A. Congestive splenomegaly
B. Autosplenectomy
C. Secondaries in spleen
D. Amyloidosis of the spleen (Correct Answer)

Explanation: **Explanation:** The correct answer is **Amyloidosis of the spleen (Option D)**. Amyloidosis is characterized by the extracellular deposition of misfolded fibrillar proteins [1]. In the spleen, amyloid deposition occurs in two distinct macroscopic patterns depending on the site of involvement: 1. **Sago Spleen:** Amyloid is deposited primarily in the **splenic follicles (white pulp)**. On gross examination, these deposits appear as pale, translucent, grain-like granules resembling sago (tapioca) seeds. 2. **Lardaceous Spleen:** Amyloid is deposited in the **splenic sinuses and red pulp** (sparing the follicles). These deposits fuse to form large, map-like areas with a waxy, firm consistency resembling "lard" (pig fat). **Why other options are incorrect:** * **A. Congestive splenomegaly:** Typically seen in portal hypertension. It is characterized by "Gamna-Gandy bodies" (siderofibrotic nodules), not amyloid patterns. * **B. Autosplenectomy:** This refers to the shrunken, fibrotic, and calcified spleen seen in Sickle Cell Anemia due to repeated infarctions. * **C. Secondaries in spleen:** Splenic metastasis is relatively rare but presents as discrete neoplastic nodules, not diffuse amyloid patterns. **High-Yield Clinical Pearls for NEET-PG:** * **Staining:** Amyloid shows **Apple-green birefringence** under polarized light when stained with **Congo Red** [2]. * **Microscopy:** On H&E stain, amyloid appears as an amorphous, eosinophilic, hyaline-like extracellular substance [2]. * **Sago vs. Lardaceous:** Remember **S**ago = **S**plenic follicles (White pulp); **L**ardaceous = Red pulp. **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.

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Cell Injury and Cell Death

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Adaptations of Cellular Growth

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Hemodynamic Disorders

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Genetic Disorders

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