General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1231: The term metaplasia refers to

A. Irregular, atypical proliferative changes in epithelial or mesenchymal cells
B. Loss of cell substance producing shrinkage of the cells
C. Replacement of one type of adult cell by another type of adult cell (Correct Answer)
D. None of the above

Explanation: **Explanation:** **Metaplasia** is a reversible change in which one differentiated (adult) cell type (epithelial or mesenchymal) is replaced by another adult cell type [1]. It is a protective adaptive response where the body replaces a sensitive cell type with one better suited to withstand a specific chronic irritation or stress [1], [2]. This change occurs via the **reprogramming of local stem cells** rather than the transformation of already differentiated cells. **Analysis of Options:** * **Option C (Correct):** This is the classic definition. A prime example is **Squamous Metaplasia** in the respiratory tract of smokers, where ciliated columnar epithelium is replaced by stratified squamous epithelium to survive the irritation of smoke [1], [2]. * **Option A (Incorrect):** This describes **Dysplasia**. Dysplasia is characterized by disordered growth, loss of cellular uniformity, and architectural orientation. While it can arise in metaplastic epithelium, it is considered a pre-neoplastic condition, not an adaptation. * **Option B (Incorrect):** This describes **Atrophy**. Atrophy is the reduction in the size of an organ or tissue due to a decrease in cell size and number [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Barrett’s Esophagus:** A critical example of **Columnar Metaplasia**, where squamous epithelium of the esophagus changes to columnar (intestinal) epithelium due to acid reflux [3]. It carries a risk of progression to Adenocarcinoma [3]. * **Connective Tissue Metaplasia:** Formation of bone in soft tissue (e.g., **Myositis Ossificans**) is a form of mesenchymal metaplasia. * **Vitamin A Deficiency:** Can induce squamous metaplasia in the respiratory tract and ducts of glands. * **Reversibility:** Metaplasia is reversible if the stimulus is removed; however, persistent irritation can lead to malignant transformation [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, p. 49. [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. 91-92. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349. [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, pp. 46-47.

Question 1232: Which of the following is an example of Type II hypersensitivity?

A. Blood transfusion reaction (Correct Answer)
B. Autoimmune hemolytic anemia
C. Allergic rhinitis
D. Glomerulonephritis

Explanation: **Explanation:** **Type II Hypersensitivity** (Cytotoxic Hypersensitivity) is mediated by **IgG or IgM** antibodies directed against antigens on specific cell surfaces or tissues [2]. This leads to cell destruction via the complement system, phagocytosis, or antibody-dependent cellular cytotoxicity (ADCC) [2]. **Why Option A is correct:** **Blood transfusion reactions** (specifically acute hemolytic reactions) occur when host antibodies bind to antigens on the donor’s red blood cells [1]. This triggers the complement cascade, leading to intravascular hemolysis [1]. This is a classic example of Type II hypersensitivity. **Analysis of Incorrect Options:** * **Option B (Autoimmune Hemolytic Anemia):** While this is *also* a Type II hypersensitivity reaction, in the context of this specific question, Blood Transfusion Reaction is the most traditional textbook example. (Note: In some exams, both A and B could be correct, but A is the primary prototype). * **Option C (Allergic Rhinitis):** This is a **Type I (Immediate)** hypersensitivity reaction mediated by **IgE** and mast cell degranulation. * **Option D (Glomerulonephritis):** Most forms (like Post-streptococcal GN) are **Type III** hypersensitivity reactions, involving the deposition of circulating **antigen-antibody complexes**. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Hypersensitivity (ACID):** **A**naphylactic (I), **C**ytotoxic (II), **I**mmune-Complex (III), **D**elayed-type (IV). * **Type II Examples:** Myasthenia Gravis, Graves' disease, Rheumatic fever, Goodpasture syndrome, and Erythroblastosis fetalis [2]. * **Key Distinction:** Type II involves antibodies binding to **fixed** cell-surface antigens, whereas Type III involves **soluble** antigens forming complexes that deposit in tissues [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 214.

Question 1233: Translocation between two acrocentric chromosomes occurs with breakpoints near the centromeres, resulting in very large and very small chromosomes. The smaller fragment is typically lost. What is this type of cytogenetic abnormality?

A. Deletion
B. Balanced translocation
C. Robertsonian translocation (Correct Answer)
D. Inversion

Explanation: ### Explanation **Correct Answer: C. Robertsonian translocation** **Why it is correct:** A Robertsonian translocation is a specific type of structural chromosomal abnormality involving **acrocentric chromosomes** (chromosomes 13, 14, 15, 21, and 22) [1]. It occurs when the long arms (q arms) of two acrocentric chromosomes fuse at the centromere, and the short arms (p arms) are lost. * **Mechanism:** Breakpoints occur at or near the centromeres [1]. The fusion creates one very large chromosome (containing the genetic material of both long arms) and a tiny fragment (containing the short arms). * **Outcome:** Because the short arms of acrocentric chromosomes contain redundant ribosomal RNA genes, their loss is clinically insignificant in the carrier. However, the total chromosome count reduces to **45**. **Why incorrect options are wrong:** * **A. Deletion:** This involves the loss of a segment of a single chromosome, not an exchange or fusion between two different chromosomes [2]. * **B. Balanced translocation:** While Robertsonian translocation is a form of translocation, "Balanced translocation" usually refers to reciprocal translocations where genetic material is exchanged between non-homologous chromosomes without the loss of a fragment or a change in chromosome number (remains 46) [2]. * **D. Inversion:** This occurs when a single chromosome undergoes two breaks, and the intervening segment is reinserted after being flipped 180 degrees [2]. It does not involve fusion between two different chromosomes. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Type:** The most frequent Robertsonian translocation involves chromosomes **14 and 21**. * **Clinical Significance:** Carriers are phenotypically normal but are at high risk of producing unbalanced gametes, leading to spontaneous abortions or **Down Syndrome (Trisomy 21)** [1]. * **Down Syndrome Etiology:** Approximately **4%** of Down Syndrome cases are due to Robertsonian translocation (unlike the 95% caused by meiotic non-disjunction). This type is **not** related to maternal age and carries a high recurrence risk in families [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 169-171. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 169-170.

Question 1234: What type of hypersensitivity reaction is the Arthus reaction?

A. Localized immune complex (Correct Answer)
B. Antigen-antibody reaction
C. Complement mediated
D. Antibody mediated

Explanation: **Explanation:** The **Arthus reaction** is a classic example of a **Type III Hypersensitivity reaction** [1], [2]. It is defined as a **localized** area of tissue necrosis resulting from acute immune complex vasculitis [3]. **Why the correct answer is right:** The reaction occurs when an antigen is injected into the skin of an individual who already has high levels of pre-formed circulating IgG antibodies [1]. These antibodies diffuse into the vessel walls, where they bind with the injected antigen to form **immune complexes** [2]. These complexes deposit in the local vessel walls, activating the complement system (C5a) and recruiting neutrophils [1]. The resulting release of lysosomal enzymes and reactive oxygen species causes focal fibrinoid necrosis and thrombosis. **Why the incorrect options are wrong:** * **Antigen-antibody reaction:** While this occurs, it is too vague. All hypersensitivity types (I, II, and III) involve antigen-antibody interactions. * **Complement mediated:** Complement activation is a *step* in the process, but it does not define the reaction type. Type II reactions can also be complement-mediated. * **Antibody mediated:** This usually refers to Type II hypersensitivity, where antibodies bind to antigens on specific cell surfaces or tissues (e.g., Myasthenia Gravis), rather than forming complexes in the circulation or vessel walls [2]. **High-Yield Facts for NEET-PG:** * **Time Frame:** Occurs within 4–10 hours (Intermediate) [1]. * **Morphology:** Characterized by **Fibrinoid Necrosis** of the vessels on histology. * **Clinical Example:** Swelling and pain at the injection site after a booster vaccination (e.g., Tetanus or Diphtheria) in a previously sensitized person [3]. * **Systemic vs. Local:** While the Arthus reaction is **localized**, Systemic Lupus Erythematosus (SLE) and Serum Sickness are examples of **systemic** Type III hypersensitivity [2], [3]. **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. 172-174. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216.

Question 1235: MIC-2 is a marker of which of the following?

A. Ewing sarcoma (Correct Answer)
B. Chronic lymphocytic leukemia
C. Mantle cell lymphoma
D. All of these

Explanation: **Explanation:** **MIC-2 (CD99)** is a cell surface glycoprotein encoded by the *MIC2* gene. It is the most sensitive immunohistochemical marker for the **Ewing Sarcoma/Primitive Neuroectodermal Tumor (PNET)** family of tumors. In Ewing sarcoma, CD99 typically shows a characteristic strong, diffuse, and continuous membranous staining pattern. This is a high-yield diagnostic feature used to differentiate Ewing sarcoma from other "small round blue cell tumors" of childhood. **Analysis of Options:** * **Ewing Sarcoma (Correct):** Over 95% of Ewing sarcoma cases express MIC-2. It is essential for diagnosis, especially when combined with the characteristic translocation t(11;22)(q24;q12). * **Chronic Lymphocytic Leukemia (CLL):** CLL is characterized by markers like CD5, CD19, CD20, and CD23 [1]. It is typically negative for MIC-2. * **Mantle Cell Lymphoma (MCL):** MCL is defined by the t(11;14) translocation and overexpression of Cyclin D1 [1]. While some lymphoblastic lymphomas can express CD99, MCL does not. **Clinical Pearls for NEET-PG:** 1. **Specificity Note:** While highly sensitive for Ewing sarcoma, CD99 is **not 100% specific**. It can also be positive in Lymphoblastic Lymphoma, Synovial Sarcoma, and Solitary Fibrous Tumors [2]. 2. **Genetics:** Ewing sarcoma is most commonly associated with the **EWS-FLI1** fusion gene. 3. **Radiology:** Look for the "onion-skin" periosteal reaction on X-ray. 4. **Homer-Wright Rosettes:** These may be seen in the PNET variant of the Ewing family of tumors. **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. 610-612. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 560-561.

Question 1236: Which of the following proteins contains a triple helix structure?

A. Cystine
B. Collagen (Correct Answer)
C. Pectin
D. DNA

Explanation: **Explanation:** **Collagen** is the correct answer because it is characterized by a unique **triple helix** quaternary structure (also known as a tropocollagen molecule). This structure consists of three polypeptide alpha-chains wound around each other. The stability of this helix is maintained by hydrogen bonds and the repetitive amino acid sequence **Gly-X-Y**, where Glycine (the smallest amino acid) fits into the restricted space of the helix core, and X and Y are typically Proline and Hydroxyproline. **Analysis of Incorrect Options:** * **Cystine (A):** This is a sulfur-containing amino acid formed by the oxidation of two cysteine molecules joined by a disulfide bond. It does not form a triple helix. * **Pectin (C):** This is a complex structural polysaccharide (carbohydrate) found in the primary cell walls of terrestrial plants. It is not a protein. * **DNA (D):** While DNA is a helical structure, it is a **double helix** composed of two polynucleotide strands, not a triple-stranded protein. **Clinical Pearls for NEET-PG:** * **Most Abundant Protein:** Collagen is the most abundant protein in the human body (approx. 25-30%). * **Vitamin C Role:** Vitamin C is a vital cofactor for the **hydroxylation** of proline and lysine residues; deficiency leads to **Scurvy** due to defective triple helix stabilization. * **Types to Remember:** * Type I: Bone, Skin, Tendon (90% of body collagen). * Type II: Cartilage. * Type III: Reticulin (Blood vessels, granulation tissue) [1]. * Type IV: Basement membrane ("4 is on the floor"). * **Genetic Disorders:** Osteogenesis Imperfecta (Type I defect) and Ehlers-Danlos Syndrome (Type III or V defects) are high-yield associations [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 154-156.

Question 1237: Increased blood volume in a tissue is known as which of the following?

A. Hyperemia (Correct Answer)
B. Edema
C. Congestion
D. Purpura

Explanation: **Explanation:** The correct answer is **Hyperemia**. Both hyperemia and congestion refer to an increase in blood volume within a specific tissue, but they differ significantly in their underlying mechanisms. **1. Why Hyperemia is correct:** Hyperemia is an **active process** resulting from arteriolar dilation, which leads to increased blood inflow into the capillary beds [1]. Because the tissue is perfused with oxygenated blood, it clinically appears **erythematous (red)** [2]. Common examples include skeletal muscle during exercise [1], sites of acute inflammation [2], or blushing. **2. Why the other options are incorrect:** * **Congestion (Option C):** While this also involves increased blood volume, it is a **passive process** resulting from impaired venous outflow (e.g., cardiac failure or venous obstruction). The tissue appears **cyanotic (blue-red)** due to the accumulation of deoxygenated hemoglobin [2]. * **Edema (Option B):** This refers to the accumulation of excess **fluid in the interstitial spaces** or body cavities, not an increase in blood volume within the vessels. * **Purpura (Option D):** This is a category of **hemorrhage** into the skin or mucous membranes (measuring 3-5 mm), representing blood that has escaped the vascular compartment. **NEET-PG High-Yield Pearls:** * **Nutmeg Liver:** Chronic passive congestion of the liver (often due to Right Heart Failure) leads to a characteristic "nutmeg" appearance due to centrilobular necrosis and congestion [2]. * **Heart Failure Cells:** These are hemosiderin-laden macrophages found in the alveoli during chronic pulmonary congestion [2]. * **Key Distinction:** Hyperemia = Active/Arterial/Red; Congestion = Passive/Venous/Blue [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. 185-187. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 126.

Question 1238: Schaumann bodies are seen in which condition?

A. Sarcoidosis (Correct Answer)
B. Chronic bronchitis
C. Asthma
D. Syphilis

Explanation: **Explanation:** **Sarcoidosis** is a multisystem disorder characterized by non-caseating granulomas [1]. Within these granulomas, specific microscopic inclusions are often found in the cytoplasm of multinucleated giant cells. **Schaumann bodies** are laminated, basophilic concretions composed of calcium and proteins. Along with **Asteroid bodies** (stellate-shaped inclusions), they are classic morphological hallmarks of Sarcoidosis, though they are not entirely pathognomonic [2]. **Analysis of Incorrect Options:** * **Chronic Bronchitis:** Characterized by goblet cell hyperplasia and an increased Reid Index; it does not feature granulomatous inflammation or Schaumann bodies. * **Asthma:** Associated with **Curschmann spirals** (mucus plugs) and **Charcot-Leyden crystals** (derived from eosinophils), but not Schaumann bodies. * **Syphilis:** Characterized by "Gumma" (a type of necrotic granuloma) and obliterative endarteritis. While it involves granulomatous inflammation, Schaumann bodies are not a feature. **NEET-PG High-Yield Pearls:** 1. **Schaumann Bodies:** Laminated calcified structures (Calcium + Protein). 2. **Asteroid Bodies:** Star-shaped eosinophilic inclusions in giant cells. 3. **Haman-Rich Syndrome:** Another name for Acute Interstitial Pneumonitis (often confused in pulmonary pathology). 4. **Kveim-Siltzbach Test:** A historical skin test used for Sarcoidosis diagnosis (now largely replaced by biopsy and imaging). 5. **Bilateral Hilar Lymphadenopathy:** The classic radiological presentation of Sarcoidosis [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. 198-200. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701.

Question 1239: Reversible loss of polarity with abnormality in size and shape of cells is known as?

A. Metaplasia
B. Dysplasia (Correct Answer)
C. Hyperplasia
D. Anaplasia

Explanation: **Explanation:** The correct answer is **Dysplasia**. **1. Why Dysplasia is correct:** Dysplasia (literally "bad growth") is a disordered proliferation characterized by a loss of architectural orientation and cellular uniformity [1]. The hallmark features include: * **Loss of Polarity:** Cells lose their normal arrangement and orientation relative to one another and the basement membrane [1]. * **Pleomorphism:** Variation in the **size and shape** of cells and nuclei. * **Nuclear Changes:** Increased nuclear-to-cytoplasmic (N:C) ratio, hyperchromasia, and increased mitotic figures. Crucially, dysplasia is considered a **pre-neoplastic** change that is **reversible** if the inciting stimulus is removed, provided it has not progressed to carcinoma in situ [1]. **2. Why other options are incorrect:** * **Metaplasia:** A reversible change where one adult cell type is replaced by another adult cell type (e.g., Squamous metaplasia in smokers) [1]. It involves a change in phenotype, not necessarily a loss of polarity or pleomorphism. * **Hyperplasia:** An increase in the *number* of cells in an organ or tissue. The cells remain morphologically normal and retain their polarity. * **Anaplasia:** This represents a total lack of differentiation and is a hallmark of **malignancy** [1]. Unlike dysplasia, anaplasia is **irreversible** and more severe, indicating a high-grade tumor. **NEET-PG High-Yield Pearls:** * **Dysplasia vs. Cancer:** Dysplasia does not involve the entire thickness of the epithelium and does not breach the basement membrane [1]. Once it breaches the basement membrane, it is called **Invasive Carcinoma**. * **Carcinoma in situ:** When dysplastic changes involve the full thickness of the epithelium but the basement membrane is intact [1]. * **Common Site:** The uterine cervix (CIN - Cervical Intraepithelial Neoplasia) is the classic example used in exams. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 278-280.

Question 1240: Foaming liver is seen in which of the following conditions?

A. Organophosphorus Poisoning
B. Actinomycosis
C. Gas gangrene (Correct Answer)
D. Anthrax

Explanation: **Explanation** **Correct Option: C. Gas gangrene** "Foaming liver" (also known as *foamy liver* or *liver emphysema*) is a classic post-mortem finding pathognomonic for infection by **Clostridium perfringens**, the primary causative agent of gas gangrene [1]. * **Mechanism:** *C. perfringens* is an anaerobic, gas-producing bacterium. In a septicemic state or post-mortem spread, the bacteria ferment carbohydrates (glycogen) in the liver tissue, leading to the production of gas bubbles (hydrogen and carbon dioxide). * **Gross Appearance:** On autopsy, the liver appears swollen, soft, and crepitant. The cut surface reveals multiple small, gas-filled cystic spaces, giving it a "Swiss cheese" or "foamy" appearance. **Analysis of Incorrect Options:** * **A. Organophosphorus Poisoning:** Characterized by features of cholinergic crisis (miosis, salivation, bradycardia). Pathologically, it may show non-specific fatty changes or congestion in the liver, but no gas formation. * **B. Actinomycosis:** Caused by *Actinomyces israelii*, it typically presents with "sulfur granules" and chronic abscesses with multiple draining sinuses. In the liver, it causes a "honeycomb" appearance due to multiple abscesses, not a foamy appearance. * **D. Anthrax:** Caused by *Bacillus anthracis*. It leads to hemorrhagic necrosis and significant edema (due to edema factor), but it is not a gas-forming infection [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Gas Gangrene:** Look for "crepitus" on physical exam and "gas under tissues" on X-ray [1]. * **Clostridium perfringens:** Produces **Alpha toxin** (Lecithinase), which causes massive hemolysis and tissue necrosis [2]. * **Nagler’s Reaction:** A biochemical test used to identify *C. perfringens* based on its lecithinase activity. * **Other "Liver" Gross Appearances:** * *Nutmeg Liver:* Chronic Passive Congestion (Right Heart Failure) [4]. * *Honeycomb Liver:* Actinomycosis. * *Frosted Liver (Zuckergussleber):* Perisplenitis/Perihepatitis (Serositis). **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. 103-104. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 390-391. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 374-375. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 401-402.

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