FMGE 2023 — Pathology
14 Previous Year Questions with Answers & Explanations
A 65-year-old man dies due to myocardial infarction. Which stains can be used to see the infarct in the heart while conducting an autopsy?
Which of the following is implicated in the pathogenesis of rheumatoid arthritis?
Asbestos exposure may be associated with which of the following malignancies?
An 8-year-old boy presents with progressive muscle weakness and walking difficulties. On examination, pseudohypertrophy of calf muscles was noted. Which of the following is true regarding this condition?
Which of the following is a feature of hemolytic anemia?
Tamm-Horsfall mucoprotein is a major component of which of the following?
A three-year-old boy has been observed by his parents to be increasingly clumsy for the past 6 months. On a physical examination, there is a cauliflower-like growth in the left eye, leukocoria, and an absent red reflex. The microscopic appearance of the specimen shows Flexner-Wintersteiner rosettes. Which gene is involved in the given condition?
The given inclusion bodies are characteristic of which of the following organisms? 
A 70-year-old male comes with complaints of hip pain. An X-ray of the hip shows lytic lesions and elevated serum calcium levels. Bone marrow plasma cells are 42%, and the cells seen are given in the image below. What is the most likely diagnosis? 
The following picture shows a lymph node biopsy of a 30-year-old male with cervical lymphadenopathy. The diagnosis is
FMGE 2023 - Pathology FMGE Practice Questions and MCQs
Question 1: A 65-year-old man dies due to myocardial infarction. Which stains can be used to see the infarct in the heart while conducting an autopsy?
- A. Oil red O
- B. Triphenyl tetrazolium chloride (Correct Answer)
- C. Sudan black B
- D. Masson trichrome
Explanation: ***Triphenyl tetrazolium chloride***- This stain is used to macroscopically identify **acute myocardial infarction** during autopsy, typically within the first few hours up to 2 weeks post-infarct [1].- It detects the activity of **dehydrogenase enzymes** (like LDH); viable myocardium reacts with TTC to form a **brick red** color, while the necrotic (infarcted) tissue lacks these enzymes and remains **pale** or *gray-yellow* [1].*Oil red O*- **Oil red O** is a lipid stain primarily used to demonstrate neutral lipids and **triglycerides**, often used for conditions like steatosis or fat emboli.- It is not specific for the cellular necrosis defining an acute infarct and is generally used on frozen sections.*Sudan black B*- **Sudan black B** is a lipid stain used to visualize phospholipids, neutral lipids, and lipoproteins.- It is more commonly employed in hematopathology (e.g., staining **myeloblasts**) or for demonstrating specific lipid storage, not for defining the boundaries of an acute myocardial infarct in gross pathology examination.*Masson trichrome*- This is a differential stain used to distinguish between muscle (red) and **collagen** (blue or green), used to highlight **fibrosis**.- While crucial for identifying **old, healed myocardial infarcts** (scar tissue), it is ineffective for rapid visualization of a fresh, acute infarct where significant collagen deposition has not yet taken place [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554.
Question 2: Which of the following is implicated in the pathogenesis of rheumatoid arthritis?
- A. Defective cellular and humoral immunity
- B. Autoimmunity (Correct Answer)
- C. Chronic microbial infections
- D. IgE mediated
Explanation: ***Autoimmunity*** - **Rheumatoid arthritis (RA)** is fundamentally a chronic, systemic **autoimmune disease** where the immune system attacks the synovium and joint structures [1].- The pathogenesis involves the loss of **self-tolerance**, leading to the production of autoantibodies (like **RF** and **Anti-CCP**) and T-cell mediated chronic inflammation [2]. *IgE mediated*- **IgE mediated** reactions define Type I (Immediate) Hypersensitivity, which is the mechanism behind allergic reactions like **anaphylaxis** and asthma.- RA is primarily driven by Type III (immune complex) and Type IV (T-cell mediated) hypersensitivity mechanisms, not IgE-mediated mast cell degranulation.*Defective cellular and humoral immunity*- RA is characterized by an **overactive and misdirected** immune response against self-antigens, not a broad deficiency in the immune system.- Conditions resulting from defective immunity are classified as **immunodeficiency syndromes**, typically leading to recurrent, severe opportunistic infections.*Chronic microbial infections*- While certain infections may act as an environmental trigger in genetically susceptible individuals (**molecular mimicry**), the persistence of RA is due to established **autoimmunity**, not ongoing microbial proliferation.- Diseases caused by chronic microbial infections, such as **tuberculosis** or **leprosy**, resolve upon successful eradication of the pathogen, unlike RA which requires continuous immunosuppression. **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. 175-176. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1212.
Question 3: Asbestos exposure may be associated with which of the following malignancies?
- A. Hepatic angiosarcoma
- B. Skin carcinoma
- C. Acute myeloid leukemia
- D. Mesothelioma (Correct Answer)
Explanation: ***Mesothelioma***- The definitive and most recognized malignancy strongly linked to inhalation of **asbestos fibers** is **malignant mesothelioma**, primarily affecting the pleura or less commonly the peritoneum [1], [2].- Exposure typically involves a long latent period, often 20 to 50 years, after the initial exposure to asbestos minerals like **chrysotile** or **amphibole** [3].*Acute myeloid leukemia*- **Acute myeloid leukemia (AML)** is often linked to exposure to **benzene** or therapeutic **alkylating agents**, but not typically associated with asbestos inhalation [2].- AML is a malignancy of the **bone marrow** affecting myeloid precursors, distinct from the fibrotic and solid tumors caused by asbestos.*Hepatic angiosarcoma*- **Hepatic angiosarcoma** is a rare vascular tumor of the liver typically associated with chemical carcinogens such as **vinyl chloride monomer**, **arsenic**, or **thorium dioxide (Thorotrast)**.- There is no established primary association between asbestos exposure and the development of hepatic angiosarcoma.*Skin carcinoma*- **Skin carcinoma** (e.g., basal or squamous cell carcinoma) is overwhelmingly linked to chronic exposure to **ultraviolet (UV) radiation**.- While asbestos is a potent carcinogen associated with lung and pleural malignancies, it is not a recognized major risk factor for typical cutaneous carcinomas. **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. 221-222. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 286. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 339-340.
Question 4: An 8-year-old boy presents with progressive muscle weakness and walking difficulties. On examination, pseudohypertrophy of calf muscles was noted. Which of the following is true regarding this condition?
- A. Defective fibrillin
- B. Abnormal collagen
- C. Absent dystrophin (Correct Answer)
- D. Expansions of CTG triplet repeats
Explanation: ***Absent dystrophin***- Duchenne Muscular Dystrophy (DMD) is caused by mutations in the *DMD* gene located on the X-chromosome, leading to the complete or near-complete absence of the muscle stabilizing protein, **dystrophin** [1].- The resulting muscle fiber instability and necrosis cause the progressive weakness and **pseudohypertrophy** (replacement of muscle tissue with fat and connective tissue) observed in this young boy [1].*Abnormal collagen*- Abnormalities in collagen, such as Type I or V defects, are typically associated with disorders like **Osteogenesis Imperfecta** (brittle bone disease) or **Ehlers-Danlos Syndrome**, which involves skin and joint hyperlaxity [2].- Connective tissue disorders usually do not present with the characteristic **calf pseudohypertrophy** seen in DMD.*Expansions of CTG triplet repeats*- This genetic abnormality is the underlying cause of **Myotonic Dystrophy Type 1 (DM1)**, not DMD [3].- DM1 symptoms include **myotonia** (inability to quickly relax muscles), cataracts, frontal balding, and typically have a later or more variable onset pattern [4].*Defective fibrillin*- Defective **fibrillin-1** is the causative factor in **Marfan Syndrome**, an autosomal dominant disorder of connective tissue.- Marfan Syndrome primarily involves the skeletal, ocular (**ectopia lentis**), and cardiovascular systems (**aortic root dilation**), which is distinct from the primary myopathy seen in DMD. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 154-155. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 732-733. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1245-1246.
Question 5: Which of the following is a feature of hemolytic anemia?
- A. Neutropenia
- B. Reticulocytopenia
- C. Decreased haptoglobin (Correct Answer)
- D. All of the above
Explanation: ***Decreased haptoglobin***- Hemolytic anemia involves the rapid breakdown of red blood cells, which releases **free hemoglobin** into the blood plasma. [1]- **Haptoglobin** rapidly binds to this free hemoglobin and is subsequently cleared by the **reticuloendothelial system**, leading to significantly reduced or absent plasma haptoglobin levels. [1]*All of the options given below*- This option is incorrect because both **neutropenia** and **reticulocytopenia** are generally *not* features of uncomplicated hemolytic anemia.*Neutropenia*- **Neutropenia** (low neutrophil count) is not typically associated with hemolytic anemia, which primarily affects the **red cell line**.- It is usually seen in conditions involving bone marrow failure (e.g., **aplastic anemia**) or destruction of white cells, not premature RBC destruction.*Reticulocytopenia*- Uncomplicated hemolytic anemia stimulates the bone marrow to produce new RBCs, resulting in **reticulocytosis** (increased reticulocytes) as a compensatory mechanism. [1]- **Reticulocytopenia** (low reticulocytes) is seen when the bone marrow cannot respond, such as during an **aplastic crisis** (often due to **Parvovirus B19** infection) or when the anemia is caused by true bone marrow failure. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 638-640.
Question 6: Tamm-Horsfall mucoprotein is a major component of which of the following?
- A. Bence-Jones proteins
- B. Renal casts (Correct Answer)
- C. Mural thrombi
- D. Curschmann spirals
Explanation: ***Renal casts*** - **Tamm-Horsfall mucoprotein (THP)**, or **uromodulin**, is a glycoprotein synthesized by the tubular epithelial cells of the **thick ascending limb of the loop of Henle** and the distal tubule. - It forms the fundamental matrix of virtually all **renal casts** (hyaline, granular, waxy, fatty, etc.) when it precipitates in the concentrated, acidic environment of the distal nephron [1]. *Mural thrombi* - These are formed within blood vessels or the heart chambers and consist primarily of aggregated **platelets**, **fibrin**, and entrapped red blood cells. - Mural thrombi are related to circulatory pathology (e.g., atrial fibrillation, myocardial infarction) and are distinct from urinary tract components. *Curschmann spirals* - These spiral-shaped mucoid structures are found in the sputum of patients with conditions like severe bronchial **asthma** or chronic bronchitis. - They represent casts of small bronchi or bronchioles composed mainly of **mucus**, glycoproteins, and cellular debris produced by goblet cells and mucous glands. *Bence-Jones proteins* - These are **free monoclonal light chains** (kappa or lambda) of immunoglobulins that appear in the urine due to overproduction by pathologically proliferating plasma cells, most commonly in **multiple myeloma** [1]. - Bence-Jones proteins are filtered plasma proteins and are distinct from Tamm-Horsfall protein which is secreted by the renal tubular cells [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 942-943.
Question 7: A three-year-old boy has been observed by his parents to be increasingly clumsy for the past 6 months. On a physical examination, there is a cauliflower-like growth in the left eye, leukocoria, and an absent red reflex. The microscopic appearance of the specimen shows Flexner-Wintersteiner rosettes. Which gene is involved in the given condition?
- A. Rb gene (Correct Answer)
- B. Rhodopsin gene
- C. FBN 1 gene
- D. ATP 7B gene
Explanation: ***Rb gene***- The constellation of leukocoria, absent red reflex, and the microscopic finding of **Flexner-Wintersteiner rosettes** are pathognomonic for **retinoblastoma** [1, 3]. - The **Rb gene** (Retinoblastoma gene) is a critical **tumor suppressor gene** located on chromosome 13q14, and its inactivation leads to the development of this malignancy [1, 2]. *ATP 7B gene* - This gene is responsible for **Wilson disease**, an autosomal recessive disorder causing excessive **copper accumulation** in the liver, brain, and cornea (Kayser-Fleischer rings). - It is not associated with primary malignant retinal tumors like retinoblastoma. *Rhodopsin gene* - Mutations in the **rhodopsin gene** are the most common cause of **autosomal dominant retinitis pigmentosa**, which presents with progressive night blindness and visual field loss. - This condition involves retinal degeneration and does not cause a mass-forming neoplasm with leukocoria. *FBN 1 gene* - The **FBN1 gene** codes for **Fibrillin-1** and is mutated in **Marfan syndrome**, a connective tissue disorder. - While Marfan syndrome often causes ocular issues like **ectopia lentis** (lens dislocation), it does not cause retinoblastoma. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 737-738. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 300. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Eye, p. 1342.
Question 8: The given inclusion bodies are characteristic of which of the following organisms? 
- A. Epstein-Barr virus
- B. Herpes simplex virus
- C. Cytomegalovirus (Correct Answer)
- D. Human papillomavirus
Explanation: ***Cytomegalovirus*** - The image displays cells with marked enlargement (**cytomegaly**) and large, basophilic intranuclear inclusion bodies surrounded by a clear halo, which is the classic **"owl's eye"** appearance pathognomonic for Cytomegalovirus (CMV) infection [1]. - These inclusions are composed of viral particles and are typically seen in various tissues, such as the lungs, kidneys, and gastrointestinal tract, especially in **immunocompromised** patients [1]. *Human papillomavirus* - HPV infection is histologically characterized by **koilocytes**, which are squamous epithelial cells with a non-staining perinuclear halo and a wrinkled, hyperchromatic nucleus. - These changes are typically seen in cervical smears (Pap smears) or skin warts and are distinct from the large intranuclear inclusions of CMV. *Epstein-Barr virus* - EBV infection, particularly in infectious mononucleosis, is identified by the presence of **atypical lymphocytes** (Downey cells) in the peripheral blood, which have abundant cytoplasm and indented nuclei. - EBV does not produce the characteristic "owl's eye" intranuclear inclusions seen in the provided image. *Herpes simplex virus* - HSV infection is characterized by **multinucleated giant cells** with molded nuclei and eosinophilic intranuclear inclusions known as **Cowdry type A bodies**. - While both are herpesviruses, the inclusions in HSV typically give a **"ground-glass"** appearance to the nucleus, which is different from the distinct, haloed "owl's eye" inclusion of CMV. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 367-368.
Question 9: A 70-year-old male comes with complaints of hip pain. An X-ray of the hip shows lytic lesions and elevated serum calcium levels. Bone marrow plasma cells are 42%, and the cells seen are given in the image below. What is the most likely diagnosis? 
- A. Multiple myeloma (Correct Answer)
- B. ALL
- C. CML
- D. CLL
Explanation: ***Multiple myeloma*** - The patient's presentation with bone pain, **lytic bone lesions** on X-ray, **hypercalcemia**, and age >60 years is classic for multiple myeloma [1]. The diagnosis is confirmed by the bone marrow biopsy showing >10% clonal plasma cells (42% in this case) [2]. - The image displays a bone marrow aspirate with extensive infiltration by **plasma cells**, characterized by their eccentric nuclei, abundant basophilic cytoplasm, and a perinuclear halo (hof) [2]. Some binucleated forms are also visible, which can be seen in neoplastic plasmacytosis [2]. *CLL* - Chronic Lymphocytic Leukemia (CLL) is a malignancy of mature B-lymphocytes, not plasma cells. The characteristic finding on a peripheral smear would be **lymphocytosis** with many **smudge cells**. - While bone marrow infiltration occurs, it consists of small, mature-appearing lymphocytes with scant cytoplasm, which is morphologically distinct from the cells shown. *ALL* - Acute Lymphoblastic Leukemia (ALL) is a cancer of immature lymphoid cells called **lymphoblasts**. These cells typically have scant cytoplasm, a high nuclear-to-cytoplasmic ratio, and fine, dispersed chromatin. - ALL is most common in **children**, and while it can cause bone pain, the specific combination of lytic lesions, hypercalcemia, and mature plasma cell morphology is not characteristic. *CML* - Chronic Myeloid Leukemia (CML) is a myeloproliferative disorder involving the excessive production of **granulocytes** (neutrophils, eosinophils, basophils). The bone marrow would show granulocytic hyperplasia. - CML is genetically defined by the presence of the **Philadelphia chromosome** (BCR-ABL1 fusion gene) and clinically presents with marked leukocytosis and often massive splenomegaly, which are not features of this case. **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, p. 608. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-619.
Question 10: The following picture shows a lymph node biopsy of a 30-year-old male with cervical lymphadenopathy. The diagnosis is
- A. Hodgkin disease (Correct Answer)
- B. Chronic lymphocytic leukemia (CLL)
- C. Human papillomavirus (HPV)
- D. Acute myeloid leukemia (AML)
Explanation: ***Hodgkin disease*** - The image displays a classic **Reed-Sternberg cell**, a large, often binucleated cell with prominent, eosinophilic nucleoli giving it an "owl's eye" appearance [1]. This finding is pathognomonic for Hodgkin disease [3]. - The clinical presentation of a young adult male with painless cervical lymphadenopathy is a typical initial sign of Hodgkin lymphoma, particularly the nodular sclerosis subtype [1], [2]. *Acute myeloid leukemia (AML)* - AML is a malignancy of myeloid precursors in the bone marrow. A lymph node biopsy would show infiltration by **myeloblasts**, which lack the characteristic binucleation and prominent eosinophilic nucleoli of Reed-Sternberg cells. - Key diagnostic features for AML include the presence of **Auer rods** (cytoplasmic inclusions) in blasts and positive staining for **myeloperoxidase (MPO)**. *Human papillomavirus (HPV)* - HPV is a virus associated with squamous cell carcinomas. Its characteristic cellular finding is the **koilocyte**, a squamous epithelial cell with a wrinkled, hyperchromatic nucleus and a perinuclear halo. - While HPV-related oropharyngeal cancer can metastasize to cervical lymph nodes, the biopsy would show nests of malignant squamous cells, not the distinct cellular morphology seen here. *Chronic lymphocytic leukemia (CLL)* - CLL is a proliferation of small, mature-appearing B-lymphocytes. A lymph node biopsy in CLL would show a diffuse infiltration of these small, monotonous lymphocytes, completely different from the large, atypical cell shown. - The peripheral blood smear is more characteristic for CLL, often showing numerous small lymphocytes and pathognomonic **smudge cells**. **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. 614-616. [2] 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. 616-618. [3] 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, p. 616.