General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 781: Which one of the following disorders is autosomal recessive?

A. Tay-Sachs disease (Correct Answer)
B. Adult polycystic kidney disease
C. Marfan syndrome
D. Familial hypercholesterolemia

Explanation: **Explanation:** **Tay-Sachs disease** is the correct answer as it is a classic example of an **Autosomal Recessive (AR)** lysosomal storage disorder [1]. It is caused by a deficiency of the enzyme **Hexosaminidase A**, leading to the accumulation of GM2 gangliosides in the brain [3]. Most enzyme deficiencies and metabolic disorders follow an AR inheritance pattern [2]. **Analysis of Incorrect Options:** * **Adult Polycystic Kidney Disease (ADPKD):** As the name implies, this is an **Autosomal Dominant (AD)** condition, typically caused by mutations in the *PKD1* or *PKD2* genes. (Note: The infantile form is AR). * **Marfan Syndrome:** This is an **AD** disorder of connective tissue caused by a mutation in the *FBN1* gene on chromosome 15, which encodes **Fibrillin-1**. * **Familial Hypercholesterolemia:** This is one of the most common **AD** disorders, involving a mutation in the **LDL receptor gene**, leading to premature atherosclerosis and xanthomas. **High-Yield Clinical Pearls for NEET-PG:** * **Tay-Sachs Key Findings:** Look for "Cherry-red spot" on the macula (without hepatosplenomegaly) and "Onion-skin" appearance of lysosomes on electron microscopy [3]. * **Rule of Thumb:** Most structural protein defects (e.g., Marfan) and receptor defects (e.g., Familial Hypercholesterolemia) are **Autosomal Dominant**, whereas most enzyme deficiencies (e.g., Inborn errors of metabolism) are **Autosomal Recessive** [2]. * **Exception:** Hunter Syndrome and Fabry Disease are the two major lysosomal storage diseases that are **X-linked Recessive**, not AR. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 150-151. [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. 57-58. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 161.

Question 782: Oval stem cells are located in?

A. Canal of Schlemm
B. Canal of Herring (Correct Answer)
C. Space of Disse
D. Basal lamina of myotubules

Explanation: **Explanation:** The correct answer is **Canal of Hering** (Option B). **Why it is correct:** In the liver, when the regenerative capacity of mature hepatocytes is compromised (due to chronic injury or toxins), a population of facultative stem cells known as **Oval cells** is activated. These bipotential stem cells are located within the **Canals of Hering**, which are the terminal bile ductules that connect the bile canaliculi to the larger interlobular bile ducts [1]. Oval cells can differentiate into both hepatocytes and biliary epithelial cells (cholangiocytes), playing a crucial role in liver regeneration [2], [3]. **Why the other options are incorrect:** * **Canal of Schlemm:** Located in the eye, this structure is responsible for draining aqueous humor from the anterior chamber into the systemic circulation. Obstruction here leads to glaucoma. * **Space of Disse:** This is the perisinusoidal space in the liver between hepatocytes and sinusoids. It contains **Ito cells** (Stellate cells), which store Vitamin A and are responsible for fibrosis (collagen production) in liver cirrhosis. * **Basal lamina of myotubules:** This is the location of **Satellite cells**, which are the regenerative stem cells of skeletal muscle, not oval cells. **High-Yield Clinical Pearls for NEET-PG:** * **Oval Cells:** Bipotential stem cells in the liver (Hepatocytes + Cholangiocytes) [2]. * **Ito Cells (Stellate Cells):** Located in the Space of Disse; primary cells involved in hepatic fibrosis. * **Kupffer Cells:** Specialized macrophages located within the hepatic sinusoids. * **Regeneration Marker:** Alpha-fetoprotein (AFP) can sometimes be elevated during active oval cell proliferation. **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. 104-105. [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. 108-109. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 833-834.

Question 783: Which of the following is NOT an example of physiological apoptosis?

A. Organogenesis
B. Hormonal dependent apoptosis
C. Graft versus host disease (Correct Answer)
D. Selective death of lymphocytes

Explanation: **Explanation:** Apoptosis is programmed cell death, which can occur under both **physiological** (normal development/homeostasis) and **pathological** (disease/injury) conditions. **Why C is the Correct Answer:** **Graft-versus-host disease (GVHD)** is an example of **pathological apoptosis**. In GVHD, donor T-cells recognize the recipient's HLA antigens as foreign and mount an immune attack. This leads to cytotoxic T-lymphocyte (CTL) mediated apoptosis of host cells (commonly in the skin, liver, and GI tract) via the Perforin/Granzyme pathway. Since this is an immune-mediated injury resulting from a disease state, it is not physiological. **Analysis of Incorrect Options:** * **A. Organogenesis:** During embryonic development, apoptosis is essential for "sculpting" the body, such as the removal of interdigital webs to form fingers and the involution of the Müllerian/Wolffian ducts [1]. * **B. Hormonal dependent apoptosis:** This occurs during normal physiological cycles, such as the shedding of the endometrial lining during menstruation or the regression of the lactating mammary gland after weaning [2]. * **D. Selective death of lymphocytes:** This is a crucial homeostatic mechanism. It involves the elimination of self-reactive T and B cells (negative selection) and the death of lymphocytes that fail to express appropriate antigen receptors, preventing autoimmunity [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphological Hallmark:** The most characteristic feature of apoptosis is **chromatin condensation** (pyknosis). * **Key Enzyme:** **Caspases** (Cysteine-aspartic proteases) are the executioners of apoptosis [3]. * **Pathological Examples to Remember:** Viral infections (e.g., Councilman bodies in Hepatitis), DNA damage (p53 mediated), and atrophy of organs after duct obstruction. * **Difference from Necrosis:** Apoptosis involves **no inflammation** and the cell membrane remains intact (forming apoptotic bodies). **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. 81-82. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 63-64. [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.

Question 784: What is the most common source of embolism?

A. Deep vein thrombosis (DVT) (Correct Answer)
B. Trauma
C. Infection
D. Surgery

Explanation: **Explanation:** The most common source of embolism is a **thrombus** (thromboembolism) [3]. Specifically, over 95% of pulmonary emboli originate from **Deep Vein Thrombosis (DVT)** of the lower extremities [1], particularly from the proximal leg veins above the knee (e.g., popliteal, femoral, and iliac veins). These thrombi dislodge and travel through the venous circulation, passing through the right side of the heart to occlude the pulmonary arterial vasculature. **Analysis of Options:** * **B. Trauma:** While trauma can lead to embolism, it is typically associated with specific types like **Fat Embolism** (following long bone fractures) or **Air Embolism** [2]. It is statistically less frequent than DVT. * **C. Infection:** This leads to **Septic Embolism** (e.g., from vegetative endocarditis). While clinically significant, it represents a minority of total embolic events. * **D. Surgery:** Surgery is a major *risk factor* for developing DVT (due to stasis and hypercoagulability) [2], but the surgery itself is not the source; the resulting thrombus is. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site for DVT:** Deep veins of the calf (however, proximal leg veins are more likely to embolize). * **Virchow’s Triad:** The three factors contributing to thrombosis are endothelial injury, stasis, and hypercoagulability. * **Paradoxical Embolism:** An embolus that originates in the venous circulation but enters the systemic arterial circulation through a right-to-left shunt (e.g., Patent Foramen Ovale) [5]. * **Saddle Embolus:** A large embolus that straddles the bifurcation of the main pulmonary artery [4], often causing sudden death. **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. 143-144. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 705. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 135-136. [4] 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. 145-146. [5] 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. 144-145.

Question 785: Which cells are typically positive for CD16 and CD56 markers?

A. NK cells (Correct Answer)
B. B Lymphocytes
C. Helper T lymphocyte
D. Cytotoxic T lymphocyte

Explanation: **Explanation:** **NK (Natural Killer) cells** are large granular lymphocytes that form a critical part of the innate immune system [1]. They are characterized by the expression of two primary surface markers: 1. **CD16:** Also known as Fc̹RIII, it acts as a low-affinity receptor for the Fc portion of IgG, mediating **Antibody-Dependent Cellular Cytotoxicity (ADCC)**. 2. **CD56:** Also known as Neural Cell Adhesion Molecule (NCAM), it is the definitive marker used to identify NK cells in clinical pathology. **Analysis of Incorrect Options:** * **B Lymphocytes:** Characterized by markers **CD19, CD20, and CD21**. They also express MHC Class II and surface Immunoglobulins (sIg) [1]. * **Helper T Lymphocytes (Th):** These are defined by the presence of **CD3** (pan-T cell marker) and **CD4** [1]. * **Cytotoxic T Lymphocytes (Tc):** These are defined by **CD3** and **CD8** [1]. While some activated CD8+ T cells may occasionally express CD16, the combination of CD16 and CD56 is the classic signature for NK cells. **High-Yield Clinical Pearls for NEET-PG:** * **NK Cell Function:** They do not require prior sensitization and kill cells that show "missing self" (downregulation of MHC-I), a common tactic used by viruses and tumor cells [1]. * **CD56 Bright vs. Dim:** CD56^bright cells are primarily cytokine producers (IFN-̳), while CD56^dim cells (which are CD16+) are more potently cytotoxic. * **Chediak-Higashi Syndrome:** A high-yield association where NK cell function is impaired due to defective vesicle trafficking. * **Marker Tip:** If a question mentions **CD16, CD56, and CD3 negative**, it is definitively an NK cell. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 200-201.

Question 786: Which of the following occurs in ischemic cell injury?

A. Efflux of K+ and Na+
B. Influx of K+ and Ca++
C. Influx of K+ and H2O
D. Influx of Na+ and Ca++ (Correct Answer)

Explanation: **Explanation:** Ischemic cell injury begins with a decrease in oxidative phosphorylation, leading to a rapid decline in **ATP production** [1]. This ATP depletion is the primary driver of the electrolyte imbalances observed in the cell. **1. Why Option D is Correct:** The failure of the **ATP-dependent Na+/K+ pump** prevents the cell from pumping Sodium (Na+) out and Potassium (K+) in [1]. Consequently, **Na+ accumulates inside the cell** (Influx). This creates an osmotic gradient that draws water into the cell, leading to cellular swelling [1]. Simultaneously, the failure of Ca++ pumps (which normally maintain low cytosolic calcium) leads to an **influx of Calcium (Ca++)** from the extracellular space and its release from intracellular stores (mitochondria and ER) [1]. Increased cytosolic calcium is a critical "point of no return" as it activates various lytic enzymes (proteases, nucleases, and phospholipases) that cause irreversible damage [1]. **2. Why Other Options are Incorrect:** * **Option A & B:** In ischemia, there is an **efflux of K+** (leaking out) and an **influx of Na+** (leaking in). K+ does not influx; its intracellular concentration drops [1]. * **Option C:** While H2O does influx (causing hydropic change), **K+ does not**. K+ moves out of the cell down its concentration gradient because the pump that normally pulls it in is inactive [1]. **Clinical Pearls for NEET-PG:** * **Earliest change in ischemia:** Decreased ATP production [1]. * **First morphological sign of cell injury:** Cellular swelling (Hydropic change/Vacuolar degeneration) [1]. * **Irreversible injury markers:** Severe mitochondrial damage, profound membrane damage, and **massive Calcium influx** [1]. * **Anaerobic Glycolysis:** Ischemia leads to a switch to anaerobic metabolism, causing an accumulation of lactic acid and a **decrease in intracellular pH** (clumping of nuclear chromatin) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 49-62.

Question 787: Which of the following is not an example of fibrinoid necrosis?

A. Polyarteritis nodosa (PAN)
B. Rheumatoid arthritis
C. Pancreatitis (Correct Answer)
D. Rheumatic fever

Explanation: **Explanation:** The correct answer is **Pancreatitis** because it is the classic example of **Fat Necrosis**, not fibrinoid necrosis. In acute pancreatitis, activated pancreatic lipases are released into the peritoneal cavity, liquefying fat cell membranes and splitting triglyceride esters into fatty acids [2]. These fatty acids combine with calcium to form chalky white deposits, a process known as **saponification** [2]. **Understanding Fibrinoid Necrosis:** Fibrinoid necrosis is a specialized form of cell death usually seen in immune-mediated vascular damage. It is characterized by the deposition of immune complexes and leaking plasma proteins (like fibrin) into the vessel walls, appearing bright pink (eosinophilic) and "smudgy" on H&E stains. **Analysis of Incorrect Options:** * **Polyarteritis nodosa (PAN):** This is a systemic necrotizing vasculitis and the "textbook" example of fibrinoid necrosis in small-to-medium-sized arteries [1]. * **Rheumatoid arthritis:** Fibrinoid necrosis is found within the center of **Rheumatoid nodules** (subcutaneous nodules). * **Rheumatic fever:** It is characterized by the presence of **Aschoff bodies** in the myocardium, which contain a central area of fibrinoid necrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Malignant Hypertension:** Another high-yield example where fibrinoid necrosis occurs in the arterioles. * **Hyperacute Transplant Rejection:** Also shows fibrinoid necrosis due to antibody-mediated vessel wall damage. * **Fat Necrosis Tip:** Look for "shadowy outlines of necrotic adipocytes" and "basophilic calcium deposits" in pathology descriptions of the pancreas or breast tissue [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [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. 55.

Question 788: What is the hairpin-shaped eosinophilic structure present in a radicular cyst?

A. Rushton bodies (Correct Answer)
B. Russell bodies
C. Both of the above
D. None of the above

Explanation: **Explanation:** **Rushton bodies** (Option A) are the correct answer. These are unique, eosinophilic, calcified microscopic structures found within the epithelial lining of odontogenic cysts, most commonly the **Radicular cyst** [1]. They are characterized by their distinct morphology, often described as **hairpin-shaped**, linear, straight, or polycyclic. While their exact origin is debated, they are generally considered to be a secretory product of the odontogenic epithelium [1]. **Why other options are incorrect:** * **Russell bodies (Option B):** These are eosinophilic, large, homogeneous immunoglobulin-containing inclusions found in the cytoplasm of **plasma cells** undergoing excessive synthesis of antibodies. They are associated with chronic inflammation (e.g., Rhinoscleroma) but do not have a "hairpin" shape and are not specific to odontogenic cyst epithelium. * **Option C and D:** These are incorrect as Rushton bodies and Russell bodies are distinct entities with different origins and morphologies. **High-Yield Clinical Pearls for NEET-PG:** * **Radicular Cyst:** The most common inflammatory odontogenic cyst, typically found at the apex of a non-vital tooth [1]. * **Histology of Radicular Cyst:** Look for stratified squamous epithelial lining, **Rushton bodies**, and "Cholesterol clefts" with associated giant cells in the fibrous capsule [1]. * **Differentiating "Bodies":** * **Rushton:** Odontogenic cysts (Hairpin/Linear). * **Russell:** Plasma cells (Immunoglobulins). * **Negri:** Rabies (Intracytoplasmic in neurons). * **Psammoma:** Papillary thyroid CA, Meningioma, Mesothelioma, Serous cystadenocarcinoma of ovary (Laminated calcifications). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 741-742.

Question 789: Amyloid is stained with:

A. Lugol's iodine
B. Methyl violet
C. Congo red (Correct Answer)
D. Sudan black

Explanation: **Explanation:** **Amyloidosis** refers to the extracellular deposition of misfolded proteins in a cross-beta pleated sheet configuration [1]. **Congo red** is the gold standard diagnostic stain for amyloid. Under ordinary light, it stains amyloid **pinkish-red** [1]. However, its pathognomonic feature is seen under **polarized light**, where it exhibits a characteristic **apple-green birefringence** [1][2]. This occurs because the dye molecules align perfectly with the highly organized beta-pleated structure of the amyloid fibrils [1]. **Analysis of Incorrect Options:** * **A. Lugol’s Iodine:** Historically used for gross identification of amyloid (turning it mahogany brown), but it is not a definitive microscopic stain. It is more commonly used to identify starch or in the Schiller test for cervical cancer. * **B. Methyl Violet:** This is a metachromatic stain. While it can stain amyloid a rose-pink color (metachromasia), it is less specific than Congo red and is rarely used as the primary diagnostic tool today. * **C. Sudan Black:** This is a lipid-soluble stain used to identify neutral fats and phospholipids. It is a key stain in hematopathology to differentiate Acute Myeloid Leukemia (AML) from Acute Lymphoblastic Leukemia (ALL). **High-Yield NEET-PG Pearls:** * **Thioflavin T/S:** Fluorescent stains used for amyloid; highly sensitive but less specific than Congo red. * **H&E Appearance:** Amyloid appears as an amorphous, eosinophilic, hyaline extracellular substance [2]. * **Precursor Proteins:** AL (Light chain) is associated with Multiple Myeloma; AA (Serum Amyloid Associated) is associated with chronic inflammation (e.g., TB, RA). * **Organ Involvement:** The kidney is the most common and potentially most serious site of amyloid deposition [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 533-534.

Question 790: The mucin clot test is performed to detect which of the following?

A. Mucin in stool
B. Protein in cerebrospinal fluid
C. Hyaluronate in synovial fluid (Correct Answer)
D. Protein in pleural fluid

Explanation: ### Explanation **Correct Answer: C. Hyaluronate in synovial fluid** The **Mucin Clot Test** (also known as the Ropes test) is a biochemical assessment used to estimate the amount and quality of **hyaluronic acid (hyaluronate)** in synovial fluid [1]. **Mechanism:** When glacial acetic acid (2–5%) is added to normal synovial fluid, the hyaluronate (a glycosaminoglycan) reacts with the protein in the fluid to form a tight, ropy white clot surrounded by clear fluid. * **Good Clot:** Indicates high concentration and high polymerization of hyaluronate (Normal or Osteoarthritis). * **Poor/Friable Clot:** Indicates low concentration or degradation of hyaluronate by bacterial enzymes or inflammatory cells (seen in Septic or Rheumatoid arthritis). --- ### Why other options are incorrect: * **A. Mucin in stool:** Mucin in stool is usually assessed macroscopically or via microscopy (e.g., in cases of amoebic dysentery or mucous colitis), not by the mucin clot test. * **B. Protein in CSF:** Protein levels in CSF are measured using quantitative methods like the turbidimetric method (sulfosalicylic acid) or Pandy’s test (for globulins). * **D. Protein in pleural fluid:** Pleural fluid protein is measured to differentiate between transudates and exudates (Light’s Criteria) using standard biochemical analyzers, not acetic acid precipitation. --- ### NEET-PG High-Yield Pearls: * **Synovial Fluid Analysis:** Normal synovial fluid does not clot spontaneously because it lacks fibrinogen. If it clots spontaneously, it indicates severe inflammation (leakage of clotting factors). * **Viscosity:** The high viscosity of synovial fluid is solely due to **Hyaluronate** [1]. * **Rice Bodies:** These are collagen-encased tiny free-floating fragments found in synovial fluid, classically associated with **Rheumatoid Arthritis**. * **Polarizing Microscopy:** Essential for crystals—**Monosodium urate** (Gout) shows needle-shaped, strongly negative birefringence; **Calcium pyrophosphate** (Pseudogout) shows rhomboid, weakly positive birefringence. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1209-1210.

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