FMGE 2019 — Pathology
9 Previous Year Questions with Answers & Explanations
Which type of necrosis is seen in the brain?
Which of the following ions is important in irreversible cell injury?
Berry aneurysm most commonly occurs due to?
A patient has MCV <80, MCH <23. Which type of anaemia shall be classified?
Which patient has the best prognosis in breast cancer?
Which of the following has Autosomal Recessive inheritance?
Cellulitis is characterized as:
Which tumor arises from embryonic neural cells?
Acute graft rejection occurs within?
FMGE 2019 - Pathology FMGE Practice Questions and MCQs
Question 1: Which type of necrosis is seen in the brain?
- A. Coagulative
- B. Liquefactive (Correct Answer)
- C. Fat
- D. Fibrinoid
Explanation: ***Liquefactive*** - Liquefactive necrosis is characterized by the transformation of tissue into a **liquid viscous mass**, commonly seen in the brain after **ischemic injury**. - Often associated with brain **infarcts** or **abscess formation**, where cell death results in the accumulation of **neutrophils and pus**. [1] *Fibrinoid* - Fibrinoid necrosis is typically associated with **immune-mediated vascular damage**, not commonly seen in the brain. - This type of necrosis occurs in conditions like **polyarteritis nodosa** or **lupus**, where **fibrin-like protein** deposits are found in vessel walls. *Coagulative* - Coagulative necrosis usually occurs in **myocardial infarction** and is characterized by the preservation of cell outlines due to **denaturation of proteins**. - It is not typical in brain tissue, which undergoes liquefactive necrosis in cases of cell death. *Fat* - Fat necrosis is primarily associated with **enzymatic destruction of adipose tissue**, often related to pancreatic damage or trauma. - It is not relevant to brain necrosis, which does not characteristically present with fat necrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269.
Question 2: Which of the following ions is important in irreversible cell injury?
- A. Sodium
- B. Chloride
- C. Calcium (Correct Answer)
- D. Potassium
Explanation: ***Calcium*** - An increase in intracellular **calcium** concentration is a critical event in irreversible cell injury, activating various destructive enzymes like **phospholipases**, **proteases**, **endonucleases**, and ATPases [1]. - This influx of calcium can occur due to mitochondrial dysfunction (leading to impaired calcium sequestration) or damage to the plasma membrane [1]. *Sodium* - While important for maintaining **osmotic balance** and cell volume, dysregulation of sodium primarily contributes to **cellular swelling** (hydropic change), which is an early and often reversible sign of cell injury [1]. - Increased intracellular sodium typically leads to water influx, but its direct role in irreversible damage is secondary to calcium. *Chloride* - Changes in chloride ion distribution are often secondary to sodium dysregulation and play a role in maintaining **charge neutrality** and osmotic balance across the cell membrane. - It is not directly implicated as a primary mediator of the **enzyme activation cascade** that leads to irreversible cell damage. *Potassium* - **Potassium** is the major intracellular cation; its leakage out of the cell is a consequence of cell membrane damage, indicating loss of membrane integrity. - While significant **potassium efflux** is a sign of severe injury, it is not the initiator of the irreversible damage pathway, unlike calcium. **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. 57-62.
Question 3: Berry aneurysm most commonly occurs due to?
- A. Muscle and adventitial layer defect
- B. Medial layer and internal elastic lamina defect (Correct Answer)
- C. Endothelial injury of vessel due to HTN
- D. Adventitia defect
Explanation: ***Medial layer and internal elastic lamina defect*** - **Berry aneurysms** are most commonly saccular dilatations that occur at arterial bifurcations in the **Circle of Willis** [1]. - These aneurysms result from a congenital or acquired weakness in the **tunica media** and the **internal elastic lamina** at these bifurcation points, making the vessel wall susceptible to high pressures [1]. *Muscle and adventitial layer defect* - Defects primarily in the **muscle layer** (media) and **adventitia** are less commonly the primary cause of berry aneurysms. - While all layers contribute to vessel integrity, the specific absence in the medial and internal elastic lamina is key for berry aneurysms [1]. *Endothelial injury of vessel due to HTN* - While hypertension is a significant **risk factor** for aneurysm formation and rupture, it primarily exacerbates existing structural weaknesses rather than being the direct cause of the initial structural defect. - **Endothelial injury alone** is not the primary anatomical defect responsible for generating berry aneurysms; it contributes to atherosclerosis, which can lead to other types of aneurysms. *Adventitia defect* - A defect solely in the **adventitia** is not the primary predisposing factor for berry aneurysms. - The adventitia provides external support, but the integrity of the media and internal elastic lamina is crucial for maintaining the vessel's structural strength against intraluminal pressure [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1272-1273.
Question 4: A patient has MCV <80, MCH <23. Which type of anaemia shall be classified?
- A. Microcytic hypochromic (Correct Answer)
- B. Normocytic normochromic
- C. Normocytic hypochromic
- D. Hyperchromic macrocytic
Explanation: ***Microcytic hypochromic*** - A **Mean Corpuscular Volume (MCV)** less than **80 fL** indicates **microcytosis** (small red blood cells) [1]. - A **Mean Corpuscular Hemoglobin (MCH)** less than **23 pg** indicates **hypochromia** (pale red blood cells due to reduced hemoglobin content) [1]. *Normocytic normochromic* - This classification refers to red blood cells with **normal MCV (80-100 fL)** and **normal MCH (27-32 pg)**. - Examples include anemia of chronic disease or acute blood loss, which do not fit the given lab values. *Normocytic hypochromic* - While **hypochromia (MCH <23)** is present, the **MCV is less than 80 fL**, which makes it microcytic, not normocytic. - This combination is not a standard classification; hypochromia typically accompanies microcytosis [1]. *Hyperchromic macrocytic* - **Macrocytic anemia** is characterized by an **MCV >100 fL**, which is the opposite of the given MCV of <80. - The term "hyperchromic" is generally not used for anemia classification because red blood cells have a maximal hemoglobin concentration and cannot be truly hyperchromic. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591.
Question 5: Which patient has the best prognosis in breast cancer?
- A. Luminal B
- B. Luminal A (Correct Answer)
- C. Triple negative breast cancer
- D. HER2-positive breast cancer
Explanation: ***Luminal A*** - Luminal A breast cancer is characterized by **estrogen receptor (ER)-positive**, **progesterone receptor (PR)-positive**, and **HER2-negative** status, along with a **low Ki-67 index** [1]. - This subtype generally has the **best prognosis** among all breast cancer subtypes due to its hormone sensitivity and slower proliferation rate, making it highly responsive to endocrine therapy [1]. *Luminal B* - Luminal B breast cancer is typically **ER-positive**, **PR-negative or low**, and can be **HER2-positive or negative**, but notably has a **high Ki-67 index**, indicating rapid cell proliferation [1]. - Compared to Luminal A, it has a **worse prognosis** due to its more aggressive biological behavior, requiring more intensive treatment approaches. *HER2-positive breast cancer* - HER2-positive breast cancer is characterized by **overexpression or amplification of HER2 (human epidermal growth factor receptor 2)** [1]. - Although it was historically associated with poor prognosis, the introduction of **targeted HER2 therapy (trastuzumab, pertuzumab)** has significantly improved outcomes [2]. - However, it still has a **more aggressive course than Luminal A**, with higher proliferation rates and requires targeted therapy in addition to standard treatment. *Triple negative breast cancer* - Triple negative breast cancer is characterized by **ER-negative, PR-negative, and HER2-negative** status, lacking all three major hormone receptors [1]. - This subtype generally has the **worst prognosis** among breast cancer subtypes due to lack of targeted therapy options and more aggressive biological behavior with higher recurrence rates [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1066. [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. 258-259.
Question 6: Which of the following has Autosomal Recessive inheritance?
- A. Osteogenesis imperfecta
- B. Hereditary spherocytosis
- C. von Willebrand Disease Type 1
- D. Sickle cell anaemia (Correct Answer)
Explanation: **Sickle cell anaemia** - This condition is inherited in an **autosomal recessive** pattern [2], meaning an individual must inherit two copies of the defective gene (one from each parent) to manifest the disease [3]. - It is caused by a mutation in the **beta-globin gene** [1], leading to abnormal hemoglobin production and characteristic sickle-shaped red blood cells [1]. *Osteogenesis imperfecta* - This disorder is predominantly inherited in an **autosomal dominant** pattern, meaning only one copy of the mutated gene is sufficient to cause the condition. - It is characterized by **brittle bones** due to defects in type I collagen synthesis. *Hereditary spherocytosis* - The most common and severe forms of hereditary spherocytosis are inherited as an **autosomal dominant** trait, though rarer autosomal recessive forms exist. - It involves defects in red blood cell membrane proteins, leading to **spherocytes** and hemolytic anemia. *von Willebrand Disease Type 1* - This is the most common type of von Willebrand disease and is inherited in an **autosomal dominant** pattern. - It is characterized by a **partial quantitative deficiency** of von Willebrand factor. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 53-54. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 150-151.
Question 7: Cellulitis is characterized as:
- A. Suppurative and invasive
- B. Nonsuppurative and non-invasive
- C. Nonsuppurative and invasive (Correct Answer)
- D. Suppurative and non-invasive
Explanation: ***Nonsuppurative and invasive*** - Cellulitis is considered **nonsuppurative** as it typically lacks macroscopic pus formation, distinguishing it from abscesses. - It is **invasive** because it involves the dermal and subcutaneous tissues, spreading through fascial planes. *Suppurative and invasive* - This description is more indicative of conditions like an **abscess**, which involves localized collections of pus. - While abscesses are invasive, cellulitis characteristically lacks the discrete pus collection. *Nonsuppurative and non-invasive* - Conditions that are nonsuppurative and non-invasive might include self-limiting skin rashes or superficial inflammatory processes. - Cellulitis involves deeper tissue infection, which inherently makes it invasive. *Suppurative and non-invasive* - A condition that is suppurative but non-invasive would be rare and contradictory, as pus formation often indicates a tissue response that is at least locally invasive. - Superficial pustules might be considered suppurative and relatively non-invasive, but cellulitis clearly extends beyond such superficial lesions.
Question 8: Which tumor arises from embryonic neural cells?
- A. Medulloblastoma (Correct Answer)
- B. Fibrous astrocytoma
- C. Neuroglioma
- D. Ependymoma
Explanation: ***Medulloblastoma*** - This tumor arises from **embryonic neural cells** in the **cerebellum**. - It is a highly malignant **brain tumor** most commonly found in children [1]. *Fibrous astrocytoma* - This is a type of **glioma** that arises from **mature astrocytes**, not embryonic neural cells. - It typically occurs in adults and can be found in various locations within the brain. *Neuroglioma* - This is a broad term that refers to **tumors of neuroglial origin**, meaning they arise from glial cells. - It does not specifically refer to a tumor originating from embryonic neural cells. *Ependymoma* - This tumor arises from **ependymal cells**, which line the **ventricles** and **spinal canal**. - While these are technically neural cells, they are more differentiated than the embryonic neural cells that give rise to medulloblastoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1314-1315.
Question 9: Acute graft rejection occurs within?
- A. Few minutes
- B. 6-12 months
- C. Few hours
- D. < 6 months (Correct Answer)
Explanation: ***< 6 months*** - **Acute graft rejection** typically occurs within the first few **weeks to months** after transplantation due to a T-cell mediated immune response against the donor organ [1]. - While it can manifest at any time, the majority of cases occur within the **first 6 months** post-transplant, making this the most appropriate time frame [1]. *Few minutes* - Rejection presenting within minutes of transplantation is characteristic of **hyperacute rejection**, which is caused by pre-existing **donor-specific antibodies** [1]. - This rapid form of rejection is mediated by **complement activation** and leads to immediate graft failure [1]. *6-12 months* - Rejection occurring in this timeframe might still be acute, but the peak incidence is generally earlier. - Rejection presenting after 6 months is often categorized as **late acute rejection** or may start to transition towards signs of chronic rejection, which occurs over a longer period. *Few hours* - Rejection within a few hours could be a very early form of **acute rejection** or a delayed presentation of **hyperacute rejection** [1]. - However, the classic presentation of acute rejection is more prolonged than a few hours, usually developing over days to weeks. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 241-242.