General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 341: Which cytokine possesses pyrogenic activity?

A. IL-6 (Correct Answer)
B. IL-8
C. TGF beta
D. IL-3

Explanation: **Explanation:** **Correct Option: A (IL-6)** Fever (pyrexia) is mediated by **pyrogens**. Cytokines such as **IL-1, TNF-̑, and IL-6** act as endogenous pyrogens [1]. When released (primarily by macrophages), these cytokines travel via the bloodstream to the anterior hypothalamus. Here, they induce the enzyme **cyclooxygenase (COX)**, which converts arachidonic acid into **Prostaglandin E2 (PGE2)** [1]. PGE2 resets the hypothalamic thermostat to a higher level, resulting in fever. Among the options provided, IL-6 is a potent inducer of the acute-phase response and pyrogenesis [1]. **Incorrect Options:** * **B. IL-8:** This is a potent **chemotactic factor** for neutrophils. Its primary role is "recruitment" rather than systemic thermoregulation. * **C. TGF-beta:** This is an **anti-inflammatory** and profibrotic cytokine. It helps in wound healing and limits the immune response; it does not induce fever. * **D. IL-3:** This is a hematopoietic growth factor (multilineage colony-stimulating factor) that stimulates the differentiation of stem cells in the bone marrow [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Major Endogenous Pyrogens:** IL-1 (most potent), TNF, and IL-6. * **Acute Phase Reactants:** IL-6 is the primary stimulator for the hepatic synthesis of acute-phase proteins like **CRP** and Fibrinogen [1]. * **Mechanism of NSAIDs:** Drugs like Paracetamol and Aspirin reduce fever by inhibiting COX, thereby blocking the synthesis of PGE2 in the hypothalamus. * **IL-8 Mnemonic:** "Clean up on aisle 8"—IL-8 recruits neutrophils to clean up the site of inflammation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 111.

Question 342: Which of the following statements is NOT true regarding cystic fibrosis?

A. The defective gene encodes for the membrane protein called cystic fibrosis transmembrane conductance regulator.
B. Normal CFTR is an ion channel specific for calcium. (Correct Answer)
C. It is an autosomal recessive disorder.
D. Altered pH of the surface secretions decreases bactericidal activity.

Explanation: ### Explanation **1. Why Option B is the Correct Answer (The False Statement):** The **Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)** is a cAMP-activated **chloride (Cl⁻) channel** [1], not a calcium channel. Its primary function is to regulate the transport of chloride ions across epithelial membranes. In the lungs and GI tract, it pumps chloride *out* of cells; in sweat glands, it reabsorbs chloride *from* the primary sweat [1]. Calcium signaling is not the primary mechanism of the CFTR protein. **2. Analysis of Other Options:** * **Option A:** This is true. The *CFTR* gene is located on **Chromosome 7 (7q31.2)**. The most common mutation is the **ΔF508** (deletion of phenylalanine at position 508), leading to protein misfolding and degradation. * **Option C:** This is true. Cystic Fibrosis is the most common lethal **autosomal recessive** disorder in Caucasian populations [3]. * **Option D:** This is true. Defective chloride transport leads to an abnormally acidic pH in surface secretions [2]. This **low pH** impairs the function of antimicrobial peptides (defensins) and decreases the overall bactericidal activity, predisposing patients to chronic infections (e.g., *Pseudomonas aeruginosa*) [4]. ### High-Yield Clinical Pearls for NEET-PG: * **Sweat Gland Paradox:** Unlike other tissues, sweat glands in CF cannot reabsorb chloride, leading to **high salt content in sweat** (Diagnostic: Sweat Chloride Test >60 mEq/L) [1]. * **Lungs:** Thick, viscid mucus leads to bronchiectasis and recurrent infections [4]. * **Pancreas:** Exocrine insufficiency, malabsorption, and "Steatorrhea" [2]. * **Reproductive System:** 95% of males are infertile due to **Congenital Bilateral Absence of Vas Deferens (CBAVD)**. * **Meconium Ileus:** A classic presentation in newborns [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Lumen Of Sweat Duct, pp. 475-476. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 789. [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. 120-122. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, p. 478.

Question 343: What is the most common aneuploidy compatible with life?

A. Down syndrome (Correct Answer)
B. Turner syndrome
C. Klinefelter's syndrome
D. Patau syndrome

Explanation: **Explanation:** **Aneuploidy** refers to an abnormal number of chromosomes (extra or missing). The correct answer is **Down syndrome (Trisomy 21)** because it is the most common autosomal aneuploidy and the most common chromosomal disorder compatible with long-term survival [1],[2]. Chromosome 21 is relatively small and gene-poor compared to other autosomes, allowing the fetus to survive to term and into adulthood despite the genetic imbalance [2]. **Analysis of Options:** * **Down Syndrome (Trisomy 21):** The most common live-born trisomy with an incidence of approximately 1 in 700 to 1.4 per 1000 births [1],[3]. While many cases result in spontaneous abortion, it remains the most prevalent aneuploidy in the general population. * **Turner Syndrome (45, X):** This is the most common sex chromosome aneuploidy in *conception*, but it has a very high intrauterine lethality rate (approx. 99% of 45,X fetuses are miscarried). Therefore, it is less common in live births than Down syndrome. * **Klinefelter’s Syndrome (47, XXY):** A common sex chromosome aneuploidy affecting males. While frequent, its prevalence in the general population is lower than that of Down syndrome [3]. * **Patau Syndrome (Trisomy 13):** An autosomal trisomy characterized by severe malformations (holoprosencephaly, polydactyly). Most infants die within the first days or months of life, making it far less "compatible with life" than Trisomy 21 [1],[2]. **NEET-PG High-Yield Pearls:** * **Most common cause of Down Syndrome:** Meiotic non-disjunction (95%), strongly associated with advanced maternal age [1]. * **Most common chromosomal cause of spontaneous abortion:** Trisomy (specifically Trisomy 16 is the most common trisomy found in miscarriages, but it is never seen in live births) [2]. * **Most common sex chromosome abnormality:** Klinefelter’s syndrome (1 in 500-1000 male births). * **Edward Syndrome:** Trisomy 18 (clenched fists, rocker-bottom feet) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 171-172. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169. [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. 92-93.

Question 344: A patient presented with chest pain to the emergency room and dies within 12 hours of arrival. Autopsy performed 5 days later shows necrosis in the myocardium. What is the type of necrosis?

A. Fibrinoid
B. Coagulative (Correct Answer)
C. Caseous
D. Liquefactive

Explanation: **Explanation:** The correct answer is **Coagulative Necrosis**. **Why Coagulative Necrosis is correct:** Coagulative necrosis is the characteristic pattern of cell death seen in **hypoxic/ischemic injury** in all solid organs except the brain. In this case, the patient presented with chest pain (suggestive of Myocardial Infarction) and died within 12 hours [1]. Even though the autopsy was delayed, the underlying process of myocardial infarction triggers protein denaturation. This denaturation inactivates lysosomal enzymes, preventing immediate proteolysis. Consequently, the **basic structural outline of the dead tissue is preserved** for several days, giving it a firm texture [1]. **Why other options are incorrect:** * **Fibrinoid Necrosis:** Typically seen in immune-mediated vascular damage (e.g., Polyarteritis Nodosa) or malignant hypertension, characterized by the deposition of immune complexes and fibrin in arterial walls. * **Caseous Necrosis:** A "cheese-like" friable necrosis characteristic of **Tuberculosis** (granulomatous inflammation). It represents a complete loss of tissue architecture. * **Liquefactive Necrosis:** Characterized by the digestion of dead cells into a liquid viscous mass. It is seen in **focal bacterial/fungal infections** and, uniquely, in **ischemic injury to the Central Nervous System (Brain)**. **High-Yield Clinical Pearls for NEET-PG:** * **Heart:** Ischemia → Coagulative Necrosis [2]. * **Brain:** Ischemia → Liquefactive Necrosis. * **Microscopic Hallmark:** Coagulative necrosis is characterized by **"Tombstone cells"** or "Ghost cells"—cells that have lost their nuclei (karyolysis) but retain their cellular shape and cytoplasmic borders [1]. * **Timeline:** In MI, the first gross change (mottling) usually appears between 12–24 hours, but the microscopic process of coagulative necrosis begins within 4–12 hours [1]. **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, p. 550.

Question 345: Enzyme levels increase in tissue injury due to which of the following mechanisms?

A. Lysis of cells (Correct Answer)
B. Enzyme secretion
C. Absence of inhibitors in serum
D. All of the above

Explanation: **Explanation:** **1. Why "Lysis of cells" is correct:** The fundamental mechanism behind elevated serum enzyme levels in tissue injury is the **loss of membrane integrity**. Most enzymes are intracellular proteins localized within the cytoplasm, mitochondria, or lysosomes. When a cell undergoes injury (especially irreversible injury leading to necrosis), the plasma membrane becomes permeable or ruptures (lysis) [1]. This allows the intracellular contents, including enzymes, to leak into the extracellular fluid and subsequently into the bloodstream [1]. This principle forms the basis of diagnostic enzymology. **2. Why other options are incorrect:** * **Enzyme secretion:** Secretion is an active, physiological process (e.g., digestive enzymes from the pancreas). In tissue injury, the release is passive and pathological, not a controlled secretory process. * **Absence of inhibitors in serum:** While serum inhibitors (like $\alpha$1-antitrypsin) regulate enzyme activity, their absence does not cause an *increase* in the release of enzymes from tissues; it only affects the degradation or activity of enzymes already present. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Marker of Irreversible Injury:** Significant enzyme leakage typically signifies **necrosis** (irreversible injury) [1] rather than reversible injury, where membrane blebbing occurs but rupture is absent [1]. * **Specific Markers:** * **Myocardial Infarction:** Troponins (most specific), CK-MB. * **Liver Injury:** ALT (more specific for hepatocytes) and AST. * **Acute Pancreatitis:** Serum Amylase and Lipase (Lipase is more specific). * **Prostate Cancer:** Acid Phosphatase (PSA is a protease, not an enzyme in the traditional sense, but used similarly). * **Mitochondrial Enzymes:** The presence of mitochondrial enzymes (e.g., Mitochondrial AST) in serum usually indicates more severe, deep-seated cellular damage [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. 49-61.

Question 346: A translocation is called 'balanced' if:

A. There is an excess of genetic material.
B. There is deficient genetic material.
C. There is no break in any chromosome.
D. No loss or gain of genetic material occurs. (Correct Answer)

Explanation: ### Explanation **1. Why Option D is Correct:** A **balanced translocation** occurs when there is an exchange of chromosomal segments between non-homologous chromosomes without any net loss or gain of genetic material. Because the full complement of genes is still present (just in a different location), the individual is typically **phenotypically normal**. However, they carry a high risk of producing "unbalanced" gametes, leading to spontaneous abortions or offspring with birth defects [1]. **2. Why Other Options are Incorrect:** * **Options A & B:** If there is an excess (duplication) or deficiency (deletion) of genetic material, the translocation is termed **unbalanced**. Unbalanced translocations usually result in clinical abnormalities, intellectual disabilities, or non-viable pregnancies. * **Option C:** This is biologically impossible for a translocation. By definition, a translocation requires a **double-strand break** in at least two chromosomes followed by the reciprocal exchange of the broken segments [2]. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Robertsonian Translocation:** A specific type of balanced translocation involving **acrocentric chromosomes** (13, 14, 15, 21, 22). The short arms (p) are lost, and the long arms (q) fuse. Since the p-arms contain redundant rRNA genes, the individual remains phenotypically normal [1]. * **Down Syndrome Risk:** A carrier of a balanced Robertsonian translocation involving chromosome 21 [e.g., 45,XX,der(14;21)(q10;q10)] has a significantly higher recurrence risk of having a child with Down Syndrome compared to trisomy 21 caused by non-disjunction [1]. * **Philadelphia Chromosome:** A classic example of a reciprocal balanced translocation **t(9;22)**, creating the *BCR-ABL* fusion gene seen in Chronic Myeloid Leukemia (CML) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 170-171. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.

Question 347: The Nitroblue tetrazolium test is used for which of the following?

A. Phagocytes (Correct Answer)
B. Complement
C. T cell
D. B cell

Explanation: The **Nitroblue Tetrazolium (NBT) test** is a functional assay used to evaluate the metabolic activity of **phagocytes** (specifically neutrophils and macrophages) [1]. It assesses the "respiratory burst" or "oxidative burst" mechanism, which is essential for killing ingested microorganisms [2]. 1. **Why Phagocytes is Correct:** During phagocytosis, the enzyme **NADPH oxidase** reduces oxygen to superoxide radicals [2]. In the NBT test, the colorless, water-soluble NBT dye is added to the patient's neutrophils. If NADPH oxidase is functional, it reduces the NBT into **formazan**, an insoluble **blue-black precipitate** visible under a microscope. A positive NBT test (blue cells) indicates normal phagocytic function [1]. 2. **Why other options are incorrect:** * **Complement:** Evaluated using the CH50 assay (classical pathway) or AH50 (alternative pathway). * **T cells:** Assessed via flow cytometry (CD3, CD4, CD8 counts) or delayed-type hypersensitivity (DTH) skin tests. * **B cells:** Evaluated by measuring serum immunoglobulin levels or flow cytometry (CD19, CD20). **High-Yield Clinical Pearls for NEET-PG:** * **Chronic Granulomatous Disease (CGD):** This is the classic condition where the NBT test is **negative** (cells remain colorless/pale) due to a deficiency in NADPH oxidase. * **Modern Gold Standard:** While NBT was the traditional test, the **Dihydrorhodamine (DHR) flow cytometry test** is now the preferred, more sensitive method for diagnosing CGD. * **Inheritance:** The most common form of CGD is **X-linked recessive** (mutations in the *gp91phox* subunit). * **Infections:** CGD patients are highly susceptible to **catalase-positive organisms** (e.g., *S. aureus, Aspergillus, Nocardia, Serratia*). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 89-91. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 91.

Question 348: Benzopyrene is changed to a carcinogen in animals due to all of the following mechanisms EXCEPT:

A. Epoxide formation
B. p53 activation
C. Cytochrome C activation (Correct Answer)
D. Induction of metabolism by cytochrome P450

Explanation: **Explanation:** **Benzopyrene** (specifically Benzo[a]pyrene) is a potent polycyclic aromatic hydrocarbon found in cigarette smoke and grilled meats [2]. It is a **pro-carcinogen**, meaning it requires metabolic activation to become a "direct-acting" carcinogen [4]. **Why Option C is the Correct Answer:** **Cytochrome C** is a component of the electron transport chain in mitochondria and is primarily associated with the intrinsic pathway of **apoptosis** (programmed cell death) when released into the cytosol. It plays no role in the metabolic activation of chemical carcinogens. Therefore, it is the "Except" option. **Analysis of Incorrect Options:** * **Option D (Induction of metabolism by CYP450):** This is the primary mechanism of activation. Benzo[a]pyrene is metabolized by the **Cytochrome P450** enzyme system (specifically CYP1A1) in the liver and lungs [1]. * **Option A (Epoxide formation):** During metabolism by CYP450, Benzo[a]pyrene is converted into a highly reactive intermediate called **7,8-dihydrodiol-9,10-epoxide** [1]. This epoxide is the "ultimate carcinogen" that binds covalently to DNA. * **Option B (p53 activation):** Once the epoxide forms DNA adducts (specifically at Guanine residues), it causes mutations. If these mutations occur in the **TP53 gene**, it leads to the loss of cell cycle control [3]. In the context of the question, the metabolic process leads to the eventual "activation" or involvement of p53 pathways due to DNA damage. **High-Yield NEET-PG Pearls:** * **Ultimate Carcinogen:** The reactive form of a pro-carcinogen that reacts with DNA (e.g., Epoxides). * **Aflatoxin B1:** Another pro-carcinogen (from *Aspergillus flavus*) activated by CYP450 into an epoxide, leading to Hepatocellular Carcinoma via a specific mutation in **codon 249 of p53** [3]. * **Ames Test:** Used to determine the mutagenic potential of a chemical; it often uses liver extract to provide the necessary CYP450 enzymes for activation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 423-424. [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. 217-218. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 331-332. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 330-331.

Question 349: Basal cell carcinoma commonly spreads by which route?

A. Lymphatics
B. Haematogenous
C. Direct spread (Correct Answer)
D. All the above

Explanation: **Explanation:** **Basal Cell Carcinoma (BCC)** is the most common skin cancer globally [1]. Its biological behavior is characterized by being **locally invasive but rarely metastatic** [1]. 1. **Why Direct Spread is Correct:** BCC is often referred to as a **"Rodent Ulcer"** because of its tendency to invade deeply into local tissues, including the dermis, subcutaneous fat, and even underlying muscle or bone if left untreated. It spreads by continuity and contiguity. The tumor cells are highly dependent on their specialized stroma (growth factors and matrix); once they enter the lymphatic or vascular systems, they usually fail to survive without this microenvironment support, making direct extension the primary mode of progression. 2. **Why Other Options are Incorrect:** * **Lymphatic & Haematogenous Spread:** Metastasis in BCC is exceptionally rare (incidence <0.1%) [1]. While it can theoretically occur to regional lymph nodes or lungs, it is not the "common" route. If a skin lesion shows significant lymphatic spread, **Squamous Cell Carcinoma (SCC)** or **Melanoma** should be suspected instead [2]. 3. **High-Yield NEET-PG Pearls:** * **Origin:** Derived from the basal layer of the epidermis or hair follicles. * **Risk Factor:** Chronic exposure to UV light (UVB) is the most significant factor [3]. * **Classic Appearance:** Pearly papule with telangiectasia and rolled-out borders [1]. * **Histology:** Characterized by **Peripheral Palisading** (nuclei at the edge of clusters align in a parallel fashion) and **Clefting artifacts** (retraction of stroma from tumor nests) [1]. * **Genetics:** Associated with mutations in the **PTCH1 gene** (Hedgehog signaling pathway), often seen in **Gorlin Syndrome** (Basal Cell Nevus Syndrome) [1][3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1160-1162. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 644-645. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 643-644.

Question 350: Mitochondrial DNA (mt-DNA) is known for all except:

A. Maternal inheritance
B. Heteroplasmy
C. Leber hereditary optic neuropathy is the prototype
D. Nemaline myopathy results due to mutations in mtDNA (Correct Answer)

Explanation: **Explanation:** The correct answer is **D**. **Nemaline myopathy** is a congenital neuromuscular disorder characterized by the presence of "nemaline rods" in muscle fibers. Crucially, it is caused by mutations in **nuclear DNA** (most commonly the *NEB* and *ACTA1* genes) which follow Mendelian inheritance (Autosomal Dominant or Recessive), not mitochondrial DNA mutations [3]. **Analysis of other options:** * **A. Maternal inheritance:** During fertilization, the zygote receives almost all its cytoplasm and organelles from the ovum. Therefore, mtDNA is inherited exclusively from the mother [1]. * **B. Heteroplasmy:** This refers to the presence of a mixture of more than one type of organellar genome (mutated and wild-type mtDNA) within a single cell [1]. The severity of mitochondrial diseases depends on the proportion of mutated mtDNA reaching a threshold. * **C. Leber Hereditary Optic Neuropathy (LHON):** This is the classic prototype of mitochondrial inheritance [2]. It leads to bilateral loss of central vision due to mutations in genes encoding the NADH dehydrogenase protein [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mitochondrial DNA (mtDNA):** It is double-stranded, circular, and lacks histones. It encodes 13 proteins of the respiratory chain, 22 tRNAs, and 2 rRNAs. * **Threshold Effect:** A minimum number of mutated mtDNA copies must be present before oxidative phosphorylation is sufficiently compromised to cause clinical symptoms [1]. * **Common Mitochondrial Disorders:** Remember the mnemonics **MELAS** (Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like episodes) and **MERRF** (Myoclonic Epilepsy with Ragged Red Fibers) [4]. * **Gomori Trichrome Stain:** Used to identify "Ragged Red Fibers," which are a hallmark of mitochondrial myopathies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 181. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 177. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1247-1248. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1305-1306.

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