General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1221: Which of the following types of necrosis is most commonly associated with ischemic injury?

A. Coagulative necrosis (Correct Answer)
B. Casseous necrosis
C. Liquifactive necrosis
D. Fat necrosis

Explanation: **Explanation:** **Correct Answer: A. Coagulative Necrosis** Coagulative necrosis is the most common pattern of necrosis resulting from **ischemia (hypoxia)** in all solid organs except the brain [1]. The underlying mechanism involves the denaturation of structural proteins and enzymes (including lysosomal enzymes). This prevents proteolysis of the dead cells, resulting in the characteristic preservation of the basic **cellular outline and tissue architecture** for several days, even though the cells are dead (often described as "tombstone" appearance) [1]. **Incorrect Options:** * **B. Caseous Necrosis:** This is a "cheese-like" friable necrosis characteristic of granulomatous inflammation, most classically seen in **Tuberculosis**. It is a combination of coagulative and liquefactive necrosis. * **C. Liquefactive Necrosis:** This occurs when enzymatic digestion of dead cells prevails. It is characteristic of **bacterial/fungal infections** (abscess formation) and, importantly, **ischemic injury to the Central Nervous System (Brain)** [2]. * **D. Fat Necrosis:** This refers to focal areas of fat destruction, typically resulting from the release of activated pancreatic lipases (as seen in **Acute Pancreatitis**) or following trauma to breast tissue. **NEET-PG High-Yield Pearls:** * **Exception Rule:** Ischemia in the **Brain** leads to Liquefactive necrosis, not Coagulative [2]. * **Microscopic Hallmark:** Coagulative necrosis shows increased eosinophilia (pinkness) and loss of nuclei (pyknosis, karyorrhexis, and karyolysis) [1]. * **Gangrenous Necrosis:** This is not a distinct pattern but a clinical term usually applied to a limb that has lost blood supply and undergone coagulative necrosis (Dry gangrene) [2]. If bacterial infection is superimposed, it becomes liquefactive (Wet gangrene). **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. 51-55. [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. 148-149.

Question 1222: Metastatic calcification is most commonly seen in which of the following locations?

A. Cornea
B. Extensor tendons
C. Brain
D. Renal tubules (Correct Answer)

Explanation: **Explanation:** **Metastatic calcification** occurs when calcium salts are deposited in normal (viable) tissues due to hypercalcemia [1], [2]. This process typically affects tissues that have an **internal alkaline environment**, which favors the precipitation of calcium salts [1]. **Why Renal Tubules are the Correct Answer:** The kidneys are a primary site for metastatic calcification because they excrete acid (hydrogen ions). The secretion of acid into the tubular lumen creates a relative **alkalinity** within the renal tubular epithelial cells and the interstitium [1]. This high pH environment promotes the deposition of calcium, often leading to **nephrocalcinosis** [1]. Other common sites include the gastric mucosa, lungs, and systemic arteries, all of which lose acid (CO₂ or H⁺) and maintain an alkaline milieu [1]. **Analysis of Incorrect Options:** * **A. Cornea:** While calcification can occur here (e.g., Band Keratopathy), it is less common than renal involvement and often associated with chronic local inflammation (dystrophic) or specific metabolic states. * **B. Extensor tendons:** These are more commonly associated with **xanthomas** (lipid deposits) or **calcinosis cutis**, but they are not a primary or "most common" site for systemic metastatic calcification [2]. * **C. Brain:** Calcification in the brain (e.g., basal ganglia) is usually **dystrophic** (secondary to injury/Fahr’s syndrome) rather than a classic presentation of metastatic calcification. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Sites:** "Lungs, Kidneys, Stomach" (All lose acid, creating an alkaline environment) [1]. * **Dystrophic vs. Metastatic:** Dystrophic occurs in **dead/dying** tissue with **normal** serum calcium; Metastatic occurs in **living** tissue with **elevated** serum calcium [2]. * **Common Causes:** Hyperparathyroidism (most common), Vitamin D toxicity, and Bone resorption (Multiple Myeloma) [2]. * **Morphology:** Calcium salts appear as **basophilic (blue-purple)** amorphous deposits on H&E stain [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. 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.

Question 1223: What happens in hypertrophy?

A. Increase in the number of cells
B. Increase in the size of cells (Correct Answer)
C. Increase in protein within cells
D. Decrease in cell number

Explanation: **Explanation:** **Hypertrophy** is defined as an increase in the **size of cells**, which subsequently leads to an increase in the size of the affected organ [1]. This occurs because of an increased synthesis of structural proteins and organelles within the cell, rather than an increase in fluid (edema) [3]. It occurs in cells that have a limited capacity to divide (permanent cells), such as cardiac and skeletal muscle [2]. **Analysis of Options:** * **Option A (Incorrect):** An increase in the *number* of cells is called **Hyperplasia** [1]. While hypertrophy and hyperplasia often occur together (e.g., the pregnant uterus), they are distinct cellular adaptations [2]. * **Option B (Correct):** Hypertrophy specifically refers to cellular enlargement [2]. * **Option C (Incorrect):** While an increase in protein synthesis is the *mechanism* behind hypertrophy, the definition of the adaptation itself is the resulting increase in cell size [3]. * **Option D (Incorrect):** A decrease in cell number (and size) is termed **Atrophy**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Triggers:** Hypertrophy is triggered by increased workload (mechanical) or growth factors/hormones (e.g., AgII, TGF-β). 2. **Physiological Example:** Enlargement of skeletal muscle in bodybuilders or the uterus during pregnancy (both hypertrophy and hyperplasia) [3]. 3. **Pathological Example:** **Left Ventricular Hypertrophy (LVH)** due to systemic hypertension or aortic stenosis [4]. 4. **Key Molecular Shift:** In cardiac hypertrophy, there is often a "fetal gene program" switch, where adult hemoglobin or contractile proteins (α-myosin heavy chain) are replaced by fetal forms (β-myosin heavy chain) to economize energy. **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. 87-88. [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. 85-87. [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. 45-46. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536.

Question 1224: Turner syndrome is characterized by which chromosomal abnormality?

A. 45, XO (Correct Answer)
B. 47, XXY
C. Trisomy 13
D. Trisomy 18

Explanation: **Explanation:** **Turner Syndrome (45, XO)** is the most common sex chromosome abnormality in females, resulting from complete or partial monosomy of the X chromosome [1]. In approximately 50% of cases, there is a complete loss of one X chromosome (45, XO), often due to nondisjunction during paternal meiosis [2]. The lack of the second X chromosome leads to accelerated attrition of germ cells, resulting in "streak ovaries" and subsequent primary amenorrhea and infertility. **Analysis of Incorrect Options:** * **47, XXY (Option B):** This represents **Klinefelter Syndrome**, the most common cause of male hypogonadism [3]. It is characterized by testicular atrophy, gynecomastia, and a eunuchoid body habitus. * **Trisomy 13 (Option C):** This is **Patau Syndrome**. Clinical features include midline defects like holoprosencephaly, cleft lip/palate, polydactyly, and microphthalmia [2]. * **Trisomy 18 (Option D):** This is **Edwards Syndrome**. Key features include "rocker-bottom feet," clenched fists with overlapping fingers, micrognathia, and low-set ears. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiac Association:** Bicuspid aortic valve (most common) and Coarctation of the aorta (pre-ductal). * **Renal Association:** Horseshoe kidney. * **Physical Findings:** Short stature (due to *SHOX* gene deficiency), webbed neck (cystic hygroma/lymphatic obstruction), and widely spaced nipples (shield chest) [1]. * **Laboratory:** Elevated LH and FSH (Hypergonadotropic hypogonadism) due to ovarian failure. * **Note:** Turner syndrome is **not** associated with advanced maternal age. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 175-177. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 174-175.

Question 1225: Which of the following conditions is inherited in an autosomal recessive pattern?

A. Sickle cell anemia (Correct Answer)
B. Hemophilia
C. Hereditary spherocytosis
D. Glucose 6-phosphate dehydrogenase deficiency

Explanation: **Explanation:** **Correct Answer: A. Sickle cell anemia** Sickle cell anemia is a classic example of an **autosomal recessive (AR)** disorder [2]. It results from a point mutation in the $\beta$-globin gene on chromosome 11, where glutamic acid is replaced by valine at the 6th position [1]. For the disease to manifest clinically (HbSS), an individual must inherit two copies of the mutated gene (one from each parent) [3]. Heterozygotes (HbAS) carry the sickle cell trait and are generally asymptomatic [1]. **Analysis of Incorrect Options:** * **B. Hemophilia:** Both Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency) are **X-linked recessive** disorders. They primarily affect males, while females act as carriers. * **C. Hereditary spherocytosis:** This is most commonly inherited in an **autosomal dominant (AD)** pattern (approx. 75% of cases). it involves mutations in red cell membrane proteins like ankyrin, spectrin, or band 3. * **D. Glucose 6-phosphate dehydrogenase (G6PD) deficiency:** This is an **X-linked recessive** enzymopathy. It leads to episodic hemolysis triggered by oxidative stress (e.g., fava beans, infections, or drugs like primaquine). **High-Yield NEET-PG Pearls:** * **Mnemonic for AR disorders:** "ABCDE" – **A**lbinism, **B**artter syndrome, **C**ystic fibrosis/Congenital adrenal hyperplasia, **D**eafness (sensorineural), **E**nzymopathies (most inborn errors of metabolism) [2]. * **Sickle Cell Fact:** The mutation provides a selective survival advantage against *Plasmodium falciparum* malaria. * **Diagnostic Test:** Solubility test is used for screening; **Hemoglobin Electrophoresis** (showing HbS) is the gold standard for diagnosis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 150-151. [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. 53-54.

Question 1226: The APC gene exerts its effect in combination with which of the following?

A. Beta-catenin (Correct Answer)
B. E-cadherin
C. Alpha-catenin
D. BCAP31

Explanation: The **APC (Adenomatous Polyposis Coli)** gene is a critical tumor suppressor gene that functions as a key negative regulator of the **Wnt signaling pathway**. [1] ### **Mechanism of Action** In a resting cell (without Wnt signaling), the APC protein forms a "destruction complex" with Axin and GSK-3β. This complex binds to **Beta-catenin**, phosphorylating it and marking it for ubiquitination and proteasomal degradation. [1] * **When APC is mutated/lost:** Beta-catenin is not degraded. It translocates to the nucleus, where it binds to TCF (T-cell factor) transcription factors, promoting the expression of genes like *MYC* and *Cyclin D1*, leading to uncontrolled cell proliferation. [1], [2] ### **Analysis of Incorrect Options** * **B. E-cadherin:** While Beta-catenin binds to the cytoplasmic tail of E-cadherin to maintain cell-cell adhesion, the APC gene specifically regulates the *cytosolic pool* of Beta-catenin involved in signaling, not E-cadherin directly. * **C. Alpha-catenin:** This protein links the E-cadherin/Beta-catenin complex to the actin cytoskeleton. It is not the primary target regulated by the APC destruction complex. * **D. BCAP31:** This is an endoplasmic reticulum membrane protein involved in transport and apoptosis; it has no established role in the APC/Wnt signaling pathway. ### **High-Yield Clinical Pearls for NEET-PG** * **FAP (Familial Adenomatous Polyposis):** Caused by a germline mutation in the APC gene (Chromosome **5q21**). * **Vogelstein Model:** APC mutation is typically the **earliest event** ("first hit") in the adenoma-carcinoma sequence of colorectal cancer. [2] * **Turcot Syndrome:** Association of FAP with CNS tumors (Medulloblastoma). * **Gardner Syndrome:** FAP associated with osteomas, desmoid tumors, and epidermal cysts. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 304-305. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 819.

Question 1227: Which of the following is a metastasis suppressor gene in relation to prostate cancer?

A. KAI-1 (Correct Answer)
B. NM 23
C. KISS
D. p53

Explanation: **Explanation:** Metastasis suppressor genes are a distinct class of genes that inhibit the spread of cancer cells without necessarily affecting the growth of the primary tumor. **A. KAI-1 (CD82):** This is the correct answer. Located on chromosome 11p11.2, KAI-1 encodes a cell surface glycoprotein (tetraspanin) that promotes cell-cell adhesion and suppresses tumor cell migration. Its expression is significantly downregulated during the progression of **prostate cancer**, making it a specific marker for metastatic potential in this malignancy. **B. NM 23:** While this was the first metastasis suppressor gene discovered, it is most classically associated with **breast cancer** and melanomas. It functions as a nucleoside diphosphate kinase. **C. KISS-1:** This gene encodes the protein kisspeptin. It acts as a metastasis suppressor primarily in **melanoma** and breast cancer by signaling through G-protein coupled receptors to inhibit chemotaxis and invasion. **D. p53:** This is a classic **Tumor Suppressor Gene** (the "Guardian of the Genome"). While its loss certainly leads to advanced cancer and eventual metastasis, it primarily functions by regulating the cell cycle, DNA repair, and apoptosis at the primary site, rather than being classified specifically as a "metastasis suppressor gene." **High-Yield Clinical Pearls for NEET-PG:** * **KAI-1** = Prostate Cancer. * **NM 23** = Breast Cancer. * **BRMS1** = Breast Cancer Metastasis Suppressor. * **MKK4** = Ovarian Cancer. * **E-Cadherin** loss is a hallmark of the Epithelial-Mesenchymal Transition (EMT), a critical step in the metastatic cascade.

Question 1228: N-MYC amplification is associated with which of the following conditions?

A. Burkitt lymphoma
B. Squamous cell carcinoma of the lung
C. Astrocytoma
D. Neuroblastoma (Correct Answer)

Explanation: **Explanation:** The **MYC family of proto-oncogenes** (C-MYC, N-MYC, and L-MYC) encodes transcription factors that play a pivotal role in cell growth and proliferation. **N-MYC amplification** is a classic example of gene amplification in human tumors, where the gene is replicated many times, appearing as "Double Minutes" (extrachromosomal fragments) or "Homogeneously Staining Regions" (HSRs) on karyotyping. **Why Neuroblastoma is correct:** N-MYC amplification occurs in approximately 25–30% of **Neuroblastomas** [1]. It is the most significant prognostic indicator for this childhood tumor; its presence signifies an aggressive clinical course, rapid tumor progression, and a poor prognosis, regardless of the clinical stage [1]. **Analysis of Incorrect Options:** * **A. Burkitt Lymphoma:** This is associated with the **translocation t(8;14)**, which leads to the overexpression of **C-MYC**, not N-MYC [2]. * **B. Squamous Cell Carcinoma of the Lung:** While various mutations occur, **L-MYC** amplification is more specifically associated with Small Cell Carcinoma of the lung. * **C. Astrocytoma:** High-grade gliomas (like Glioblastoma) are more commonly associated with **EGFR amplification** or PTEN mutations rather than N-MYC. **High-Yield Clinical Pearls for NEET-PG:** * **C-MYC:** Burkitt Lymphoma (t(8;14)) [2]. * **N-MYC:** Neuroblastoma (Poor prognosis) [1]. * **L-MYC:** Small Cell Carcinoma of the Lung. * **Double Minutes/HSRs:** These are the cytogenetic hallmarks of gene amplification (commonly seen with N-MYC in Neuroblastoma and ERBB2 in Breast Cancer). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 486-487. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.

Question 1229: Fenton reaction leads to free radical generation when:

A. Radiant energy is absorbed by water
B. H2O2 is formed by myeloperoxidase
C. Ferrous ion is converted to ferric ion (Correct Answer)
D. Nitric oxide is converted to peroxynitrite

Explanation: ### Explanation The **Fenton reaction** is a critical mechanism in cellular pathology where transition metals catalyze the formation of highly reactive free radicals [1]. **1. Why Option C is Correct:** The Fenton reaction specifically involves the oxidation of **Ferrous iron (Fe²⁺)** to **Ferric iron (Fe³⁺)** in the presence of hydrogen peroxide ($H_2O_2$) [1]. This process results in the generation of the **Hydroxyl radical (•OH)**, which is the most reactive and damaging free radical in biological systems [1]. * **Equation:** $Fe^{2+} + H_2O_2 \rightarrow Fe^{3+} + \bullet OH + OH^-$ * *Note:* The reverse process (reducing $Fe^{3+}$ back to $Fe^{2+}$) is often facilitated by the superoxide radical ($O_2^{\bullet-}$), a process known as the **Haber-Weiss reaction** [1]. **2. Why Other Options are Incorrect:** * **Option A:** Absorption of radiant energy (like X-rays) by water causes **radiolysis**, which splits water directly into $\bullet H$ and $\bullet OH$ radicals [1]. This is a physical process, not the Fenton reaction. * **Option B:** Myeloperoxidase (MPO) is found in neutrophil granules. It converts $H_2O_2$ and chloride ions ($Cl^-$) into **Hypochlorous acid (HOCl)**, a potent bactericidal agent. * **Option D:** Nitric oxide ($NO$) reacts with superoxide ($O_2^{\bullet-}$) to form **Peroxynitrite ($ONOO^-$)** [1]. This is a reactive nitrogen species (RNS) rather than a product of iron-catalyzed Fenton chemistry. **3. NEET-PG High-Yield Pearls:** * **Most Reactive Radical:** The Hydroxyl radical ($\bullet OH$) produced by the Fenton reaction is the most potent inducer of lipid peroxidation [2]. * **Iron Overload:** In diseases like **Hemochromatosis** or **Thalassemia** (frequent transfusions), excess free iron leads to tissue damage (liver cirrhosis, heart failure) primarily via the Fenton reaction [2]. * **Protective Mechanisms:** The body prevents the Fenton reaction by sequestering iron in storage proteins like **Ferritin** and transport proteins like **Transferrin**. **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, p. 59. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 854.

Question 1230: Which of the following is false regarding Gaucher's disease?

A. Beta-glucocerebrosidase is defective
B. Cherry red spots are seen on fundoscopy
C. Erlenmeyer's flask deformity is present
D. Tartrate-resistant acid phosphatase is negative (Correct Answer)

Explanation: **Explanation:** Gaucher’s disease is the most common lysosomal storage disorder, characterized by an autosomal recessive deficiency of the enzyme **glucocerebrosidase** (also known as beta-glucosidase) [1]. **Why Option D is the correct (False) statement:** In Gaucher’s disease, the characteristic "Gaucher cells" (lipid-laden macrophages with a "wrinkled tissue paper" appearance) are metabolically active and secrete high levels of **Tartrate-Resistant Acid Phosphatase (TRAP)** [1]. Therefore, TRAP is **positive** in Gaucher’s disease, making the statement that it is negative false. TRAP positivity is also a classic marker for Hairy Cell Leukemia. **Analysis of Incorrect Options:** * **Option A:** This is a true statement. The primary defect is a deficiency of **beta-glucocerebrosidase**, leading to the accumulation of glucocerebroside in the reticuloendothelial system [1]. * **Option B:** This is true. While most commonly associated with Tay-Sachs and Niemann-Pick disease, **cherry-red spots** on the macula can be seen in Type 1 (rarely) and Type 2 Gaucher’s disease [2]. * **Option C:** This is true. **Erlenmeyer flask deformity** refers to the characteristic remodeling of the distal femur (flaring of the metaphysis) due to the expansion of the marrow by Gaucher cells [1], [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Gaucher Cells:** Pathognomonic macrophages with fibrillary, "crumpled tissue paper" cytoplasm and displaced nuclei [1]. * **Clinical Triad:** Hepatosplenomegaly (massive), bone pain/crises, and cytopenias [1], [2]. * **Type 1:** Most common, non-neuronopathic, seen in Ashkenazi Jews [1]. * **Treatment:** Enzyme Replacement Therapy (ERT) with **Imiglucerase** [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 162-163. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 161-162. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1188-1189. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 159.

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