UPSC-CMS 2025 — Pathology

Q: 'Masson Bodies' formed due to proliferation of immature collagen are a characteristic histopathological finding seen in which of the following conditions?

Cryptogenic Organizing Pneumonia. ***Cryptogenic Organizing Pneumonia*** - **Masson bodies**, which are intraluminal plugs of organizing connective tissue composed of fibroblasts, myofibroblasts, and immature collagen, are the **hallmark histopathological feature** of cryptogenic organizing pneumonia (COP) [1]. - These plugs are found predominantly in the **alveolar ducts** and **bronchioles**, leading to a characteristic pattern of organizing pneumonia [1]. *Lymphocytic Interstitial Pneumonia* - Characterized by a **dense interstitial infiltrate** dominated by **lymphocytes**, plasma cells, and histiocytes, often forming germinal centers. - It is frequently associated with **immunodeficiency states** such as HIV infection or autoimmune diseases like Sjögren's syndrome. *Desquamative Interstitial Pneumonia* - Marked by the accumulation of a large number of **macrophages** within the alveolar spaces, with minimal interstitial inflammation or fibrosis. - Primarily seen in **smokers** and is thought to be a reaction to inhaled particulate matter. *Respiratory Bronchiolitis* - Characterized by **peribronchiolar inflammation** and fibrosis, with pigment-laden macrophages accumulating within the respiratory bronchioles. - This condition is also strongly associated with **cigarette smoking** and is considered a milder variant of interstitial lung disease. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 330-331. [Practice more Pathology PYQs on OnCourse]

Q: Melanosis coli, which occurs due to long term consumption of stimulant laxatives, presents as brown discolouration of colonic mucosa due to deposition of which one of the following pigments?

Lipofuscin. ***Lipofuscin*** - **Melanosis coli** is characterized by the accumulation of **lipofuscin** in macrophages within the lamina propria of the colon. - This accumulation is typically induced by the long-term use of **stimulant laxatives**, particularly those containing anthraquinones (e.g., senna, cascara). *Haemoglobin* - **Haemoglobin** is the protein in red blood cells responsible for oxygen transport and does not deposit in the colonic mucosa to cause brown discoloration in melanosis coli. - Its presence in stool typically indicates **gastrointestinal bleeding**, which is a distinct condition from melanosis coli. *Haemosiderin* - **Haemosiderin** is an iron-storage complex that can accumulate in tissues as a result of **hemorrhage** or increased iron load [1]. - While it can cause brown discoloration, it is not the pigment responsible for the characteristic appearance of melanosis coli. *Melanin* - **Melanin** is the pigment primarily responsible for skin and hair color, produced by melanocytes [1]. - It is not found in significant amounts in the colonic mucosa and is not involved in the pathogenesis of melanosis coli. **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. 75. [Practice more Pathology PYQs on OnCourse]

Q: Which of the following syndromes are caused due to genomic imprinting? I. Rubinstein Taybi syndrome II. Prader-Willi syndrome III. Angelman syndrome IV. Edward syndrome Select the correct answer using the code given below :

II and III. ***II and III (Correct Answer)*** - **Prader-Willi syndrome** and **Angelman syndrome** are classic examples of disorders caused by **genomic imprinting** defects on chromosome 15 [1]. - **Prader-Willi syndrome** results from the loss of paternal 15q11-q13 expression, while **Angelman syndrome** results from the loss of maternal 15q11-q13 expression [1]. - Both conditions demonstrate parent-of-origin effects, where the same chromosomal region causes different phenotypes depending on whether the mutation is inherited from the mother or father [1]. *II and IV (Incorrect)* - While Prader-Willi syndrome is linked to genomic imprinting, **Edward syndrome** (Trisomy 18) is caused by a chromosomal abnormality (an extra copy of chromosome 18), not genomic imprinting. - Edward syndrome presents with distinct clinical features like **micrognathia** and **rocker-bottom feet**, different from imprinting disorders. *I and IV (Incorrect)* - **Rubinstein-Taybi syndrome** is caused by mutations in the **CREBBP** gene or deletion of 16p13.3, which are not related to genomic imprinting. - **Edward syndrome** is a chromosomal aneuploidy (Trisomy 18), not a disorder of genomic imprinting. *I and III (Incorrect)* - **Rubinstein-Taybi syndrome** is a genetic disorder caused by mutations in the CREBBP or EP300 genes, and it is not associated with genomic imprinting. - Only **Angelman syndrome** among these two options is caused by genomic imprinting. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 181-182. [Practice more Pathology PYQs on OnCourse]

Q: Which of the following are the aetiological factors associated with a communicating hydrocephalus ? I. Post haemorrhagic II. Lesions within the ventricle III. CSF infection IV. Raised CSF protein Select the correct answer using the code given below :

I, III and IV. ***I, III and IV*** - **Communicating hydrocephalus** occurs when there is impaired CSF absorption in the **subarachnoid space** despite a patent ventricular system. - **Post-hemorrhagic**, **CSF infection** (meningitis), and **raised CSF protein** (e.g., from tumors or inflammation) can all obstruct the arachnoid villi, preventing proper CSF reabsorption [1]. *I, II and III* - While **post-hemorrhagic** and **CSF infection** are causes of communicating hydrocephalus, **lesions within the ventricle** typically cause **non-communicating (obstructive) hydrocephalus** by blocking CSF flow *within* the ventricular system itself [1]. - This option incorrectly includes an obstructive cause and omits **raised CSF protein**, which is a known cause of impaired CSF absorption. *II, III and IV* - This option incorrectly includes **lesions within the ventricle** as a cause of communicating hydrocephalus, which usually leads to **non-communicating hydrocephalus** [1]. - It correctly identifies **CSF infection** and **raised CSF protein** but omits **post-hemorrhagic** causes, which are a common etiology [1]. *I, II and IV* - This option incorrectly includes **lesions within the ventricle**, which typically cause **non-communicating hydrocephalus** [1]. - While **post-hemorrhagic** and **raised CSF protein** are valid causes, the inclusion of an obstructive cause makes this option incorrect for *communicating* hydrocephalus. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 703-704. [Practice more Pathology PYQs on OnCourse]

9 Previous Year Questions with Answers & Explanations

Questions

'Masson Bodies' formed due to proliferation of immature collagen are a characteristic histopathological finding seen in which of the following conditions?

Melanosis coli, which occurs due to long term consumption of stimulant laxatives, presents as brown discolouration of colonic mucosa due to deposition of which one of the following pigments?

Which of the following syndromes are caused due to genomic imprinting? I. Rubinstein Taybi syndrome II. Prader-Willi syndrome III. Angelman syndrome IV. Edward syndrome Select the correct answer using the code given below :

Which of the following are the malignancies associated with lymphoedema? I. Kaposi Sarcoma II. Squamous cell carcinoma III. Malignant melanoma IV. Leukaemia Select the correct answer using the code given below :

Which of the following are the aetiological factors associated with a communicating hydrocephalus ? I. Post haemorrhagic II. Lesions within the ventricle III. CSF infection IV. Raised CSF protein Select the correct answer using the code given below :

What is the most common type of tumour of Vermiform Appendix?

The earliest specific cystoscopic appearance of Bilharzial cystitis is :

Which of the following are poor prognostic factors in endometrial adenocarcinoma? I. Estrogen and progesterone receptor positivity II. HER-2/neu gene expression III. Histologic types papillary serous or clear cell carcinoma IV. Aneuploid tumours Select the correct answer using the code given below :

Which of the following hematological findings are seen in pregnant women with thalassemia trait?

UPSC-CMS 2025 - Pathology UPSC-CMS Practice Questions and MCQs

Question 1: 'Masson Bodies' formed due to proliferation of immature collagen are a characteristic histopathological finding seen in which of the following conditions?

A. Lymphocytic Interstitial Pneumonia
B. Desquamative Interstitial Pneumonia
C. Respiratory Bronchiolitis
D. Cryptogenic Organizing Pneumonia (Correct Answer)

Explanation: ***Cryptogenic Organizing Pneumonia*** - **Masson bodies**, which are intraluminal plugs of organizing connective tissue composed of fibroblasts, myofibroblasts, and immature collagen, are the **hallmark histopathological feature** of cryptogenic organizing pneumonia (COP) [1]. - These plugs are found predominantly in the **alveolar ducts** and **bronchioles**, leading to a characteristic pattern of organizing pneumonia [1]. *Lymphocytic Interstitial Pneumonia* - Characterized by a **dense interstitial infiltrate** dominated by **lymphocytes**, plasma cells, and histiocytes, often forming germinal centers. - It is frequently associated with **immunodeficiency states** such as HIV infection or autoimmune diseases like Sjögren's syndrome. *Desquamative Interstitial Pneumonia* - Marked by the accumulation of a large number of **macrophages** within the alveolar spaces, with minimal interstitial inflammation or fibrosis. - Primarily seen in **smokers** and is thought to be a reaction to inhaled particulate matter. *Respiratory Bronchiolitis* - Characterized by **peribronchiolar inflammation** and fibrosis, with pigment-laden macrophages accumulating within the respiratory bronchioles. - This condition is also strongly associated with **cigarette smoking** and is considered a milder variant of interstitial lung disease. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 330-331.

Question 2: Melanosis coli, which occurs due to long term consumption of stimulant laxatives, presents as brown discolouration of colonic mucosa due to deposition of which one of the following pigments?

A. Lipofuscin (Correct Answer)
B. Haemoglobin
C. Haemosiderin
D. Melanin

Explanation: ***Lipofuscin*** - **Melanosis coli** is characterized by the accumulation of **lipofuscin** in macrophages within the lamina propria of the colon. - This accumulation is typically induced by the long-term use of **stimulant laxatives**, particularly those containing anthraquinones (e.g., senna, cascara). *Haemoglobin* - **Haemoglobin** is the protein in red blood cells responsible for oxygen transport and does not deposit in the colonic mucosa to cause brown discoloration in melanosis coli. - Its presence in stool typically indicates **gastrointestinal bleeding**, which is a distinct condition from melanosis coli. *Haemosiderin* - **Haemosiderin** is an iron-storage complex that can accumulate in tissues as a result of **hemorrhage** or increased iron load [1]. - While it can cause brown discoloration, it is not the pigment responsible for the characteristic appearance of melanosis coli. *Melanin* - **Melanin** is the pigment primarily responsible for skin and hair color, produced by melanocytes [1]. - It is not found in significant amounts in the colonic mucosa and is not involved in the pathogenesis of melanosis coli. **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. 75.

Question 3: Which of the following syndromes are caused due to genomic imprinting? I. Rubinstein Taybi syndrome II. Prader-Willi syndrome III. Angelman syndrome IV. Edward syndrome Select the correct answer using the code given below :

A. II and IV
B. I and IV
C. I and III
D. II and III (Correct Answer)

Explanation: ***II and III (Correct Answer)*** - **Prader-Willi syndrome** and **Angelman syndrome** are classic examples of disorders caused by **genomic imprinting** defects on chromosome 15 [1]. - **Prader-Willi syndrome** results from the loss of paternal 15q11-q13 expression, while **Angelman syndrome** results from the loss of maternal 15q11-q13 expression [1]. - Both conditions demonstrate parent-of-origin effects, where the same chromosomal region causes different phenotypes depending on whether the mutation is inherited from the mother or father [1]. *II and IV (Incorrect)* - While Prader-Willi syndrome is linked to genomic imprinting, **Edward syndrome** (Trisomy 18) is caused by a chromosomal abnormality (an extra copy of chromosome 18), not genomic imprinting. - Edward syndrome presents with distinct clinical features like **micrognathia** and **rocker-bottom feet**, different from imprinting disorders. *I and IV (Incorrect)* - **Rubinstein-Taybi syndrome** is caused by mutations in the **CREBBP** gene or deletion of 16p13.3, which are not related to genomic imprinting. - **Edward syndrome** is a chromosomal aneuploidy (Trisomy 18), not a disorder of genomic imprinting. *I and III (Incorrect)* - **Rubinstein-Taybi syndrome** is a genetic disorder caused by mutations in the CREBBP or EP300 genes, and it is not associated with genomic imprinting. - Only **Angelman syndrome** among these two options is caused by genomic imprinting. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 181-182.

Question 4: Which of the following are the malignancies associated with lymphoedema? I. Kaposi Sarcoma II. Squamous cell carcinoma III. Malignant melanoma IV. Leukaemia Select the correct answer using the code given below :

A. I, II and IV (Correct Answer)
B. II, III and IV
C. I, III and IV
D. I, II and III

Explanation: ***I, II and IV*** - **Kaposi sarcoma** is a well-documented malignancy that can develop in chronically lymphoedematous limbs, particularly in classic and endemic forms. - **Squamous cell carcinoma** can arise as a complication of chronic lymphoedema, developing in areas of long-standing skin changes and inflammation [1]. - **Leukaemia** is included here as it can cause lymphadenopathy and secondary lymphoedema, representing a bidirectional relationship where leukemic infiltration leads to lymphatic obstruction. - **Note:** The most classic malignancy associated with chronic lymphoedema is **angiosarcoma (Stewart-Treves syndrome)**, though it is not listed among the options. *II, III and IV* - While this includes **squamous cell carcinoma** (correct) [1], it incorrectly includes **malignant melanoma**. - **Malignant melanoma** has no established association with lymphoedema as a predisposing condition, though melanoma can cause lymphoedema through nodal metastases [2]. *I, III and IV* - This incorrectly includes **malignant melanoma** and omits **squamous cell carcinoma**. - **Squamous cell carcinoma** is a more clearly established malignancy that can arise in chronic lymphoedema [1]. *I, II and III* - This correctly includes **Kaposi sarcoma** and **squamous cell carcinoma** but incorrectly includes **malignant melanoma**. - **Malignant melanoma** does not have a recognized causal relationship with pre-existing lymphoedema. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 643-644. [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. 234-235.

Question 5: Which of the following are the aetiological factors associated with a communicating hydrocephalus ? I. Post haemorrhagic II. Lesions within the ventricle III. CSF infection IV. Raised CSF protein Select the correct answer using the code given below :

A. I, II and III
B. II, III and IV
C. I, II and IV
D. I, III and IV (Correct Answer)

Explanation: ***I, III and IV*** - **Communicating hydrocephalus** occurs when there is impaired CSF absorption in the **subarachnoid space** despite a patent ventricular system. - **Post-hemorrhagic**, **CSF infection** (meningitis), and **raised CSF protein** (e.g., from tumors or inflammation) can all obstruct the arachnoid villi, preventing proper CSF reabsorption [1]. *I, II and III* - While **post-hemorrhagic** and **CSF infection** are causes of communicating hydrocephalus, **lesions within the ventricle** typically cause **non-communicating (obstructive) hydrocephalus** by blocking CSF flow *within* the ventricular system itself [1]. - This option incorrectly includes an obstructive cause and omits **raised CSF protein**, which is a known cause of impaired CSF absorption. *II, III and IV* - This option incorrectly includes **lesions within the ventricle** as a cause of communicating hydrocephalus, which usually leads to **non-communicating hydrocephalus** [1]. - It correctly identifies **CSF infection** and **raised CSF protein** but omits **post-hemorrhagic** causes, which are a common etiology [1]. *I, II and IV* - This option incorrectly includes **lesions within the ventricle**, which typically cause **non-communicating hydrocephalus** [1]. - While **post-hemorrhagic** and **raised CSF protein** are valid causes, the inclusion of an obstructive cause makes this option incorrect for *communicating* hydrocephalus. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 703-704.

Question 6: What is the most common type of tumour of Vermiform Appendix?

A. Germ cell tumour
B. Adenocarcinoma
C. Papillary cell tumour
D. Carcinoid tumour (Correct Answer)

Explanation: ***Carcinoid tumour*** - **Carcinoid tumors** (neuroendocrine tumors) are the **most common primary neoplasms of the appendix**, accounting for approximately 30-50% of all appendiceal tumors. [1] - They typically originate from the **enterochromaffin cells** in the appendiceal mucosa and are often discovered incidentally during appendectomy for suspected appendicitis. - Most appendiceal carcinoids are **small (<2 cm), benign, and located at the tip** of the appendix. [1] *Adenocarcinoma* - **Adenocarcinomas** are the second most common primary tumor of the appendix, representing about 10-20% of cases. - These **epithelial malignancies** include mucinous and non-mucinous subtypes and can present with symptoms mimicking acute appendicitis. - Mucinous adenocarcinomas may lead to **pseudomyxoma peritonei** if they rupture. *Germ cell tumour* - **Germ cell tumors** are exceptionally rare in the appendix and more commonly arise from the gonads (testes, ovaries) or midline structures. - These tumors originate from **pluripotent germ cells** and are not a significant consideration for appendiceal neoplasms. *Papillary cell tumour* - This term describes a **morphological growth pattern** (papillary architecture) rather than a specific primary tumor classification. - While some epithelial tumors may exhibit papillary features, this is **not a recognized primary tumor type** of the appendix. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 375-376.

Question 7: The earliest specific cystoscopic appearance of Bilharzial cystitis is :

A. Sandy patches (Correct Answer)
B. Pseudo tubercles
C. Nodules
D. Ulcers

Explanation: ***Sandy patches*** - **Sandy patches** are the **earliest and most characteristic** specific cystoscopic finding in Bilharzial cystitis (urinary schistosomiasis). [1] - They appear as fine, yellow-golden granules resembling grains of sand, visible through the bladder mucosa, representing **calcified *Schistosoma haematobium* eggs** deposited in the submucosa. - This pathognomonic finding typically appears in the trigone and posterior bladder wall and is the hallmark early sign during cystoscopy. *Pseudo tubercles* - **Pseudo tubercles (bilharzial tubercles)** represent a **later stage** of the disease, occurring after sandy patches. - They are organized granulomatous reactions (granulomas) that form around egg deposits within the bladder wall, appearing as small, whitish-yellow elevated lesions. [1] - While specific for schistosomiasis, they develop after the initial egg deposition phase marked by sandy patches. *Nodules* - **Nodules** represent more advanced inflammatory changes or can be associated with chronic schistosomiasis and potential neoplastic transformation. - They are non-specific and can occur in various bladder pathologies, not characteristic of early disease. *Ulcers* - **Ulcers** develop in advanced stages of Bilharzial cystitis due to chronic inflammation, tissue necrosis, or secondary bacterial infection. - They indicate significant mucosal damage and are not early manifestations of the disease. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 405-406.

Question 8: Which of the following are poor prognostic factors in endometrial adenocarcinoma? I. Estrogen and progesterone receptor positivity II. HER-2/neu gene expression III. Histologic types papillary serous or clear cell carcinoma IV. Aneuploid tumours Select the correct answer using the code given below :

A. II, III and IV (Correct Answer)
B. I, III and IV
C. I, II and IV
D. I, II and III

Explanation: ***II, III and IV*** - **HER-2/neu gene expression**, **papillary serous or clear cell histologic types**, and **aneuploid tumors** are all associated with a more aggressive disease course and worse outcomes in endometrial adenocarcinoma [1]. - These factors indicate less differentiated and often more resistant cancer, leading to higher recurrence rates and lower survival [1]. *I, III and IV* - This option incorrectly includes **estrogen and progesterone receptor positivity** as a poor prognostic factor, which is actually a favorable prognostic indicator. - **HER-2/neu gene expression** is a significant poor prognostic factor but is excluded from this option. *I, II and IV* - This option incorrectly includes **estrogen and progesterone receptor positivity** as a poor prognostic factor. - It also incorrectly excludes **histologic types papillary serous or clear cell carcinoma**, which are well-established poor prognostic factors [1]. *I, II and III* - This option incorrectly lists **estrogen and progesterone receptor positivity** as a poor prognostic factor. - It also incorrectly excludes **aneuploid tumors**, which are recognized indicators of poor prognosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1017-1024.

Question 9: Which of the following hematological findings are seen in pregnant women with thalassemia trait?

A. Raised HbA₂ and low MCV (Correct Answer)
B. Low serum total iron binding capacity
C. Low MCHC
D. Low HbA₂ and raised MCV

Explanation: ***Raised HbA₂ and low MCV*** - Beta-thalassemia trait is characterized by a **compensatory increase in HbA₂** (alpha2-delta2 globin chains) synthesis and **microcytic (low MCV)** red blood cells [1]. - This combination is a classic finding that helps differentiate thalassemia trait from iron deficiency anemia in pregnant women. *Low serum total iron binding capacity* - **Low total iron binding capacity (TIBC)** is typically seen in **anemia of chronic disease**, where iron stores are often adequate or high. - In thalassemia trait, iron stores are usually normal or increased, and TIBC is usually normal or slightly increased. *Low HbA₂ and raised MCV* - **Low HbA₂** is seen in alpha-thalassemia trait or iron deficiency anemia, not beta-thalassemia trait [2]. - **Raised MCV (macrocytosis)** is characteristic of conditions like **folate or B12 deficiency** or megaloblastic anemia, which is not associated with uncomplicated thalassemia trait [1]. *Low MCHC* - **Low MCHC (mean corpuscular hemoglobin concentration)** indicates hypochromic red blood cells and is found in various microcytic anemias, including **iron deficiency anemia** [1]. - While it can be present in thalassemia trait, it is not as specific as the combination of **raised HbA₂** and **low MCV** for distinguishing beta-thalassemia trait from other microcytic conditions [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 588-591. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 649-650.