FMGE 2018 - Pathology Practice Questions

Q: Pheochromocytoma produces all except?

Secretin. Secretin - **Secretin** is a hormone primarily produced by **S cells in the duodenum and jejunum** [3] in response to acidic chyme, stimulating pancreatic bicarbonate secretion. - Pheochromocytomas originate from **chromaffin cells** of the adrenal medulla and are known for producing catecholamines [2], not secretin. *Vasoactive intestinal polypeptide* - **Vasoactive intestinal polypeptide (VIP)** can be produced by some **neuroendocrine tumors** [1], including pheochromocytomas, though it's more commonly associated with VIPomas. - VIP acts as a **vasodilator** and can contribute to symptoms like flushing and diarrhea in rare cases of VIP-producing pheochromocytomas. *Calcitonin* - While calcitonin is primarily associated with **medullary thyroid carcinoma**, it can rarely be produced ectopically by **neuroendocrine tumors**, including some pheochromocytomas. - This ectopic production is part of the broader concept of **paraneoplastic syndromes** seen in various malignancies. *Norepinephrine* - **Norepinephrine** is a major catecholamine produced by pheochromocytomas, leading to classic symptoms such as **hypertension, palpitations, and sweating** [2]. - The tumor cells (chromaffin cells) are specialized to synthesize and release **catecholamines**, including norepinephrine and epinephrine [2].

Q: What is the histopathological finding 12 hours after ischemic injury to heart?

Hyper-eosinophilia of myocytes. ***Hyper-eosinophilia of myocytes*** - Within **4-12 hours** of myocardial ischemia, the most characteristic histological finding is the development of **hypereosinophilia** in the sarcoplasm of myocardial cells [1]. - This is due to the loss of **glycogen** and an increase in **cytoplasmic protein binding** to eosin, indicating early irreversible cell injury [1], [2]. *Neocapillary invasion of myocytes* - **Neocapillary invasion** is a feature of **healing** and **repair** processes, usually observed much later, typically days to weeks after the initial injury, to facilitate scar formation [1]. - This process involves the growth of **new blood vessels** into the damaged tissue. *Karyorrhexis of myocytes* - **Karyorrhexis**, the fragmentation of the cell nucleus, is a later stage of necrosis, usually becoming apparent **12-24 hours post-infarction** [1]. - In the initial 12 hours, nuclear changes like **pyknosis** (nuclear shrinkage and increased basophilia) might be observed, but karyorrhexis is not prominent [1]. *Coagulation necrosis of myocytes* - While myocardial infarction is characterized by **coagulation necrosis**, the classic histological signs of full-blown coagulation necrosis, such as loss of striations and nuclear changes, become prominent at **12-24 hours and beyond** [1]. - In the first 12 hours, **hypereosinophilia** is the primary early indicator of this necrotic process, preceding the more overt classical features [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 548-550.

Q: Which of the following is true about Anaplasia?

Loss of differentiation. ***Loss of differentiation*** - **Anaplasia** is defined as the loss of structural and functional differentiation in cells, indicating a reversal to a more primitive state [1]. - It is a hallmark feature of **malignancy** and is associated with increased proliferative capacity and aggressiveness of tumors [1]. *Benign and fully reversible* - **Anaplasia** is a characteristic of **malignant tumors** and is generally not reversible without treatment [1]. - Benign cellular changes are typically reversible and maintain their differentiation features [1]. *Loss of cohesion between cells* - While loss of cohesion can occur in some aggressive tumors, it is more specifically related to changes in cell adhesion molecules and is not the primary definition of **anaplasia**. - **Anaplasia** refers to the loss of differentiation, not solely the physical separation of cells [1]. *Change of epithelium type* - This description refers to **metaplasia**, which is the reversible change of one differentiated cell type to another differentiated cell type [1]. - **Anaplasia** involves a loss of differentiation, not merely a change to a different, still differentiated, cell type [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 276-280.

Q: Heart failure cells are:-

Pigmented alveolar macrophages. ***Pigmented alveolar macrophages*** - **Heart failure cells** are **alveolar macrophages** that have phagocytosed **hemosiderin** [1], which is derived from extravasated red blood cells. - This occurs in conditions causing **pulmonary congestion** and **hemorrhage**, most notably in chronic left-sided heart failure [2]. *Lipofuscin granules in cardiac cells* - **Lipofuscin** is a "wear-and-tear" pigment that accumulates in various aging cells, including **cardiac myocytes** [3]. - While present in heart cells, **lipofuscin granules** do not represent the classic "heart failure cells" which are found in the lung [3]. *Pigmented cells in pancreas* - **Pigmented cells in the pancreas** are not a recognized pathological entity described as "heart failure cells." - This option is medically irrelevant in the context of heart failure pathophysiology. *Pigmented hepatocytes* - **Pigmented hepatocytes** can be seen in various conditions, such as **hemochromatosis** (iron overload) or certain drug-induced liver injuries. - However, they are not referred to as "heart failure cells," which specifically refers to hemosiderin-laden macrophages in the lungs. **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. 75-76. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 536-537. [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, p. 75.

Question 1

Pheochromocytoma produces all except?

Accepted Answer

Secretin

Answer

Vasoactive intestinal polypeptide

Answer

Norepinephrine

Answer

Calcitonin

Question 2

What is the histopathological finding 12 hours after ischemic injury to heart?

Accepted Answer

Hyper-eosinophilia of myocytes

Answer

Neocapillary invasion of myocytes

Answer

Karyorrhexis of myocytes

Answer

Coagulation necrosis of myocytes

Question 3

Which of the following is true about Anaplasia?

Accepted Answer

Loss of differentiation

Answer

Benign and fully reversible

Answer

Loss of cohesion between cells

Answer

Change of epithelium type

Question 4

What is the mechanism of secondary healing?

Accepted Answer

Granulation tissue

Answer

Neovascularization

Answer

Scab formation

Answer

Granuloma formation

Question 5

Heart failure cells are:-

Accepted Answer

Pigmented alveolar macrophages

Answer

Lipofuscin granules in cardiac cells

Answer

Pigmented cells in pancreas

Answer

Pigmented hepatocytes

Question 6

Virchow's triad includes all except:-

Accepted Answer

Platelet thrombus

Answer

Stasis of blood flow

Answer

Endothelial injury

Answer

Hypercoagulability

FMGE 2018 — Pathology