What type of necrosis is associated with Myocardial Infarction (MI)?
Which of the following is not considered an example of excess tissue growth?
First mediator of inflammation to be released is
Rolling of leucocytes on endothelial cells is mediated by which of the following?
What is the characteristic feature of neuropraxia?
Which of the following is derived from fibroblast cells?
Post-streptococcal glomerulonephritis (PSGN) is an example of which type of hypersensitivity?
What is the number of antigens typically evaluated in comprehensive HLA matching for organ transplantation?
What is the most common type of graft rejection?
What is the initial event in serum sickness?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 11: What type of necrosis is associated with Myocardial Infarction (MI)?
- A. Coagulative necrosis (Correct Answer)
- B. Liquefactive necrosis
- C. Caseous necrosis
- D. Fat necrosis
Explanation: ***Coagulative necrosis*** - Myocardial infarction (MI) typically results in **coagulative necrosis**, characterized by the preservation of the outline of the tissue despite cellular death [1]. - It is often associated with **ischemia**, where blood supply is obstructed, leading to cell death while maintaining tissue architecture for a time [1]. *Fat necrosis* - Fat necrosis is typically associated with **trauma** or **inflammation** in fat tissue, often seen in conditions like pancreatitis. - It is characterized by the presence of **necrotic adipocytes** and does not involve the myocardium directly or predominantly. *Caseous necrosis* - Caseous necrosis is often associated with **tuberculosis** infections, where tissue becomes crumbly and cheese-like. - It is not relevant to myocardial infarction, which does not present with the classical **granulomatous inflammation** of caseous necrosis. *Liquefactive necrosis* - Liquefactive necrosis typically occurs in conditions such as **brain infarcts** or bacterial infections leading to **pus formation**, not in MI. - It involves the transformation of tissue into a **liquid viscous mass**, which is not characteristic of myocardial tissue affected by infarction. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.
Question 12: Which of the following is not considered an example of excess tissue growth?
- A. Granulation tissue (Correct Answer)
- B. Neoplasia
- C. Hyperplasia
- D. Fibrosis
Explanation: ***Granulation tissue*** - Granulation tissue is a normal part of the healing process and does not represent an **excessive growth** of tissue [3]. - It consists mainly of **new connective tissue** and blood vessels formed during healing, rather than a pathological proliferation [3]. *Hyperplasia* - Hyperplasia is characterized by an **increase in the number** of cells in a tissue, leading to tissue enlargement [1][2]. - This process is often a response to a stimulus, such as hormonal changes or injury, indicating **excess tissue growth** [2]. *Neoplasia* - Neoplasia refers to the **abnormal proliferation** of cells, forming a neoplasm or tumor, which can be benign or malignant. - This is a clear example of **excess tissue growth**, as it involves uncontrolled cell division. *Fibrosis* - Fibrosis implies the formation of excess **fibrous connective tissue**, leading to a stiff or thickened tissue, signifying abnormal tissue growth [4]. - It often results from chronic inflammation or injury, again reflecting **excessive tissue** formation [4]. **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. 87-88. [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. 85-87. [3] 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. 105-106. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 111-112.
Question 13: First mediator of inflammation to be released is
- A. Nitric oxide
- B. PAF
- C. Histamine (Correct Answer)
- D. IL-1
Explanation: ***Histamine*** - Histamine is the **first mediator of inflammation released** by mast cells and basophils during an allergic or inflammatory response [1][3]. - It promotes **vasodilation** and increased vascular permeability, leading to typical symptoms of inflammation [1][2]. *PAF* - Platelet-activating factor (PAF) is released later in the inflammatory process and is primarily involved in **amplifying** the response rather than initiating it. - It plays a role in **platelet aggregation** and acting on vascular smooth muscle but is not the first released mediator. *Nitric oxide* - Nitric oxide is produced by endothelial cells and plays a role in **vascular relaxation and inflammation**, but it is not among the first mediators released. - It is involved in more **regulatory functions** in the inflammatory response rather than the initial trigger. *IL-1* - Interleukin-1 (IL-1) is a cytokine that is important for the **inflammatory response**, but it is produced after the initial release of mediators like histamine [2]. - It is primarily secreted by **activated macrophages** and contributes to the **amplification** of the immune response [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 84-85. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 93-94.
Question 14: Rolling of leucocytes on endothelial cells is mediated by which of the following?
- A. ICAM-1
- B. Integrin
- C. IL-8
- D. P-selectin (Correct Answer)
Explanation: ***P- selectin*** - P-selectin is a **cell adhesion molecule** crucial for the **rolling** of leukocytes on endothelial cells during the inflammatory response [1]. - It is expressed on activated endothelial cells and binds to **sialylated carbohydrates** on leukocytes, facilitating their transient adhesion [1]. *IL-8* - IL-8 is a **chemokine** that primarily acts as a chemotactic factor for neutrophils rather than mediating rolling on endothelium. - While it attracts leukocytes to sites of inflammation, it does not play a role in the initial contact or rolling process. *ICAM-1* - ICAM-1 is an **intercellular adhesion molecule** that facilitates **firm adhesion** rather than rolling of leukocytes. - It primarily interacts with **integrins** on leukocytes to stabilize their adhesion after rolling has occurred. *(3, integrin* - Integrins play a significant role in **firm adhesion** and not the rolling phase, interacting with receptors like ICAM-1. - The binding of integrins to their ligands occurs after leukocytes have initially rolled on the endothelium. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.
Question 15: What is the characteristic feature of neuropraxia?
- A. Damage to the endoneurium
- B. Damage to the epineurium
- C. No structural damage to the nerve (Correct Answer)
- D. Damage to the axon
Explanation: ***No structural damage to the nerve*** - **Neuropraxia** is the mildest form of nerve injury, characterized by a **temporary block in nerve conduction** without structural damage to the axon or surrounding connective tissues. - This typically results in **temporary sensory and/or motor deficits** that fully resolve within weeks to months. *Damage to the endoneurium* - Damage to the **endoneurium** would indicate a more severe injury, such as **axonotmesis**, where the axon is damaged but the connective tissue sheaths are preserved. - This level of injury suggests that wallerian degeneration would occur distal to the lesion, leading to **slower and incomplete recovery**. *Damage to the epineurium* - Damage to the **epineurium**, along with the endoneurium and perineurium, signifies **neurotmesis**, the most severe nerve injury. - This involves a **complete transection of the nerve**, requiring surgical intervention for any chance of functional recovery. *Damage to the axon* - Damage to the **axon** itself, often alongside preserved connective tissues, is characteristic of **axonotmesis**. - While recovery is possible through axonal regeneration, it is **slower and less complete** than in neuropraxia.
Question 16: Which of the following is derived from fibroblast cells?
- A. MMP2
- B. Collagen (Correct Answer)
- C. Angiopoietin
- D. TGF-β
Explanation: ***Collagen*** - Collagen is a structural protein that is predominantly produced by **fibroblast cells** in the extracellular matrix [1][2]. - It provides tensile strength and structural support to various tissues, playing a crucial role in wound healing and tissue repair [2]. *TGF-13* - Transforming Growth Factor-beta 1 (TGF-β1) is primarily produced by **immune cells** and is involved in cell growth and differentiation, not primarily by fibroblasts. - It plays a role in **fibrosis** and inflammation, but is not directly synthesized by fibroblast cells themselves. *MMP2* - Matrix Metalloproteinase-2 (MMP-2) is produced by various cell types, including **endothelial and epithelial cells**, but not predominantly by fibroblasts. - It is involved in the degradation of **extracellular matrix** components rather than being a product of fibroblast synthesis. *Angiopoietin* - Angiopoietin is primarily secreted by **endothelial cells** and plays a significant role in blood vessel formation and maturation. - It is not derived from fibroblast cells and is unrelated to their primary function of producing the extracellular matrix. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 31-32. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 34-35.
Question 17: Post-streptococcal glomerulonephritis (PSGN) is an example of which type of hypersensitivity?
- A. Type -1 hypersensitivity
- B. Type -2 hypersensitivity
- C. Type -3 hypersensitivity (Correct Answer)
- D. Type -4 hypersensitivity
Explanation: ***Type -3 hypersensitivity*** - Post-streptococcal glomerulonephritis (PSGN) is caused by **immune complex deposition**, a hallmark of type III hypersensitivity reactions [1][2][3]. - It involves the formation of **antigen-antibody complexes** following a streptococcal infection, leading to inflammation in the kidneys [1][2]. *Type -1 hypersensitivity* - Characterized by **IgE-mediated** reactions, such as allergies and anaphylaxis, which do not apply to PSGN. - It typically involves **mast cells** and histamine release, notably absent in PSGN cases. *Type -4 hypersensitivity* - Involves **T-cell mediated** responses and is related to delayed-type reactions, not applicable to PSGN. - Common examples include **contact dermatitis** and graft-versus-host disease, differing fundamentally from PSGN's mechanism. *Type -2 hypersensitivity* - Characterized by **antibody-mediated cytotoxicity**, such as in hemolytic anemia, unrelated to immune complexes in PSGN. - Typically involves direct damage to cells, contrasting with the immune complex mechanism observed in PSGN [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216.
Question 18: What is the number of antigens typically evaluated in comprehensive HLA matching for organ transplantation?
- A. 10 (Correct Answer)
- B. 4
- C. 16
- D. 22
Explanation: ***10*** - The **number of criteria for HLA matching** in organ transplantation is typically 10, consisting of 6 class I and 4 class II antigens. - Proper HLA matching is critical for minimizing the risk of **graft rejection** and ensuring **recipient compatibility** [1]. *16* - While there are various HLA antigens, a total of **16** criteria is not a standard number used for matching purposes. - This number may include other factors but does not represent the core criteria for **HLA matching**. *4* - HLA matching involves more than **4 criteria**, inadequate for reliable transplantation outcomes. - This number does not encompass the essential **class I and class II antigens** that are necessary for effective matching. *22* - A total of **22 criteria** exceeds the conventional standard for HLA matching, which is not practical or necessary. - This figure may relate to overall HLA typing but is not applicable for the matching process itself. **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. 179-180.
Question 19: What is the most common type of graft rejection?
- A. Hyperacute
- B. Acute (Correct Answer)
- C. Chronic
- D. Acute on chronic
Explanation: ***Acute*** - **Acute rejection** is the most common type of graft rejection, occurring in **10-40% of transplant recipients**. [1] - It typically occurs **days to weeks to months** after transplantation (most commonly within the first 6 months). [1] - Mediated primarily by **T-lymphocytes** (cellular rejection) or **antibodies** (antibody-mediated rejection) reacting against donor antigens. [1] - Usually **responsive to immunosuppressive therapy** when detected early. *Hyperacute* - **Hyperacute rejection** is rare (occurs in <1% of cases) due to routine **pre-transplant cross-matching**. - Occurs within **minutes to hours** after transplantation due to **pre-existing circulating antibodies** against donor antigens. [1] - Results in immediate thrombosis and graft necrosis, requiring **immediate graft removal**. [1] *Chronic* - **Chronic rejection** (chronic allograft dysfunction) develops **months to years** after transplantation. - It is the **most common cause of late graft failure**, but not the most common type of rejection episode. - Characterized by **gradual, progressive loss of graft function** with vascular and fibrotic changes. - **Largely irreversible** and poorly responsive to treatment. *Acute on chronic* - This is **not a primary category** of graft rejection but represents an **acute rejection episode superimposed** on a graft already undergoing chronic changes. - Reflects exacerbation in a chronically rejecting graft. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-242.
Question 20: What is the initial event in serum sickness?
- A. It is associated with hypocomplementemia.
- B. It is a type III hypersensitivity reaction.
- C. It occurs due to exposure to heterologous antigens. (Correct Answer)
- D. It can lead to leukocytoclastic vasculitis.
Explanation: ***Can lead to leukocytoclastic vasculitis*** - Serum sickness is characterized by the formation of **immune complexes**, which can trigger **leukocytoclastic vasculitis** affecting the blood vessels [1][2]. - Symptoms can include **rash, fever, and arthralgia**, typically occurring 1-3 weeks after exposure to the offending antigen [2]. *Can occur due to homologous antigen* - Serum sickness is usually a reaction to **heterologous** antigens, such as those from animal serum, not **homologous** ones. - Homologous antigens do not typically elicit the immune response seen in serum sickness; hence, this statement is incorrect. *Type 2 hypersensitivity* - Serum sickness is classified as a **Type III hypersensitivity** reaction due to the immune complex formation, not Type II [1]. - Type II is characterized by antibody-mediated destruction of **target cells**, which does not apply here. *Hypercomplementemia* - Serum sickness is associated with **hypocomplementemia** due to complement consumption from immune complex formation, not hypercomplementemia. - This can lead to **decreased complement levels** during the response, making this statement incorrect. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216. [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. 172-173.