What is the histopathological finding 12 hours after ischemic injury to heart?
Which of the following is true about Anaplasia?
What is the mechanism of secondary healing?
Heart failure cells are:-
Virchow's triad includes all except:-
FMGE 2018 - Pathology FMGE Practice Questions and MCQs
Question 11: What is the histopathological finding 12 hours after ischemic injury to heart?
- A. Neocapillary invasion of myocytes
- B. Hyper-eosinophilia of myocytes (Correct Answer)
- C. Karyorrhexis of myocytes
- D. Coagulation necrosis of myocytes
Explanation: ***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.
Question 12: Which of the following is true about Anaplasia?
- A. Benign and fully reversible
- B. Loss of cohesion between cells
- C. Change of epithelium type
- D. Loss of differentiation (Correct Answer)
Explanation: ***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.
Question 13: What is the mechanism of secondary healing?
- A. Neovascularization
- B. Scab formation
- C. Granuloma formation
- D. Granulation tissue (Correct Answer)
Explanation: ***Granulation tissue*** - **Secondary intention healing** involves the formation of abundant **granulation tissue** to fill the tissue defect [1]. - Granulation tissue consists of new **capillaries**, **fibroblasts**, and inflammatory cells, which lay the groundwork for wound closure [2]. *Neovascularization* - **Neovascularization** is the specific process of forming new blood vessels within the wound, which is a component of granulation tissue formation, but not the overall healing mechanism [2]. - While essential for delivering nutrients and oxygen, it's a sub-process rather than the primary mechanism for secondary healing itself. *Scab formation* - **Scab formation** is an initial protective mechanism, primarily associated with superficial wounds and not the intrinsic mechanism of tissue repair and closure in secondary healing. - A scab primarily protects the underlying wound from infection and desiccation while healing occurs beneath it. *Granuloma formation* - **Granuloma formation** is a specific type of chronic inflammatory response characterized by collections of macrophages, often seen in persistent infections or foreign body reactions, not typical secondary wound healing [2]. - It indicates a **cell-mediated immune response** to a non-degradable stimulus, aiming to wall off the offending agent. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [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. 105-107.
Question 14: Heart failure cells are:-
- A. Pigmented alveolar macrophages (Correct Answer)
- B. Lipofuscin granules in cardiac cells
- C. Pigmented cells in pancreas
- D. Pigmented hepatocytes
Explanation: ***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 15: Virchow's triad includes all except:-
- A. Stasis of blood flow
- B. Endothelial injury
- C. Platelet thrombus (Correct Answer)
- D. Hypercoagulability
Explanation: ***Platelet thrombus*** - Virchow's triad describes the three primary categories of factors that are thought to contribute to **thrombosis**, but it does not specifically include a formed **thrombus** itself. [1] - While **platelet thrombus** formation is an outcome of an imbalance in these factors, it is not one of the predisposing conditions identified by Virchow's triad. *Stasis of blood flow* - **Stasis** refers to a reduction in the rate of blood flow, which allows clotting factors to accumulate and endothelial cells to become hypoxic, increasing the risk of **thrombosis**. [1] - This is a well-established component of Virchow's triad, explaining why factors like immobility or venous insufficiency predispose to clot formation. *Endothelial injury* - **Endothelial injury** or dysfunction exposes the subendothelial collagen, leading to platelet adhesion and activation, and the initiation of the coagulation cascade. [1] - It is a critical component of Virchow's triad, often seen in conditions like **atherosclerosis** or trauma, which directly promotes thrombus formation. [2] *Hypercoagulability* - **Hypercoagulability**, or thrombophilia, refers to an increased propensity for coagulation due to genetic or acquired abnormalities in clotting factors. [1] - This imbalance in the coagulation system is a central part of Virchow's triad, leading to an exaggerated thrombotic response even in the absence of significant stasis or injury. [2] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 132-133. [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. 142-143.