What is a distinguishing feature of reticulocytes?
Caseating necrosis most commonly occurs in
Liquefactive necrosis is seen in:
Which type of necrosis is most commonly associated with the spread of infection?
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?
Which substance plays a significant role in the tumor metastasis cascade?
Most common cause of idiopathic interstitial pneumonia is
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 51: What is a distinguishing feature of reticulocytes?
- A. Slightly larger in size than RBCs
- B. Presence of residual RNA and ribosomes (Correct Answer)
- C. Mature in bone marrow
- D. Constitute approximately 1% of the red cells
Explanation: ***Presence of residual RNA and ribosomes*** - This is the **defining and most distinguishing feature** of reticulocytes that differentiates them from mature red blood cells. - Reticulocytes contain residual **ribosomal RNA** and other organelles that are lost when they mature into erythrocytes. - This residual RNA forms a **reticular (network-like) pattern** when stained with supravital stains like **new methylene blue** or **brilliant cresyl blue**, which is the basis for their name and identification. - The presence of RNA allows for **reticulocyte counting**, an important marker of bone marrow erythropoietic activity. *Slightly larger in size than RBCs* - While reticulocytes may be slightly larger (polychromatophilic appearance), size variation is **not specific** and overlaps significantly with mature RBCs. - Size is not a reliable distinguishing feature and is not used for identification or counting. *Mature in bone marrow* - Reticulocytes are **released from the bone marrow** as immature red cells and complete their maturation in the **peripheral circulation** over 24-48 hours. - They do not fully mature in the bone marrow; their presence in peripheral blood is normal. *Constitute approximately 1% of the red cells* - Normal reticulocyte count is **0.5-2%** (or approximately 1%) of total red blood cells in healthy adults. - This is a **population characteristic** indicating normal erythropoietic activity, not a distinguishing cellular feature.
Question 52: Caseating necrosis most commonly occurs in
- A. Brain
- B. Liver
- C. Kidney
- D. Lung (Correct Answer)
Explanation: ***lung*** - **Caseating necrosis** is classically associated with **tuberculosis**, which primarily affects the lungs [1]. - It is characterized by the presence of **granulomatous inflammation**, often leading to the formation of cavities in pulmonary tissue. *Brain* - While certain infections can lead to necrosis in the brain, they typically do not present as **caseating necrosis**, which is specific to certain conditions like tuberculosis. - The brain may show **liquefactive necrosis** or other types of necrosis, rather than **caseation**. *liver* - The liver usually shows **macrovesicular steatosis** or **apoptosis** in conditions like hepatitis, not caseating necrosis. - **Granulomatous hepatitis** can occur, but it does not typically result in **caseating** type necrosis associated with lung pathology. *kidney* - The kidneys can experience necrosis from various causes, but caseating necrosis is not typical; they are more often involved in **focal segmental glomerulosclerosis** or **acute tubular necrosis**. - Chronic kidney conditions may involve granulomas, but they usually are not characterized by **caseation** similar to that seen in pulmonary tissue. **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, p. 55.
Question 53: Liquefactive necrosis is seen in:
- A. Brain (Correct Answer)
- B. Cardiac tissue
- C. Pulmonary tissue
- D. Splenic tissue
Explanation: ***Brain*** - **Liquefactive necrosis** primarily occurs in the **brain** due to the high fat content and the process of enzymatic degradation of tissue after a cerebral infarction [1]. - This type of necrosis results in the transformation of tissue into a liquid viscous mass, often observed during **abscess formation** or ischemic damage [1]. *Spleen* - Commonly undergoes **caseous necrosis** in conditions like tuberculosis, not liquefactive necrosis. - **Hematopoietic tissue** destruction can occur, but it generally results in a differing necrotic pattern. *Heart* - Typically exhibits **coagulative necrosis** following myocardial infarction due to ischemic damage. - This results in the preservation of tissue architecture, differing from the liquid consistency seen in liquefactive necrosis. *Lungs* - Usually experiences **caseous necrosis** in the context of pulmonary tuberculosis, or **hemorrhagic necrosis** after certain infections, but not liquefactive necrosis. - The predominant necrotic process in the lungs is often related to **inflammatory responses** rather than liquefactive changes. **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 54: Which type of necrosis is most commonly associated with the spread of infection?
- A. Fibrinoid necrosis
- B. Fat necrosis
- C. Liquefactive necrosis (Correct Answer)
- D. Coagulative necrosis
Explanation: ***Liquifactive necrosis*** - Caused by the enzymatic digestion of tissue, leading to the formation of liquid pus, typically associated with bacterial infections [1]. - Commonly occurs in the **brain** and in a tissue impacted by **pyogenic bacteria** [1], demonstrating how infection can lead to tissue damage. *Fat necrosis* - Primarily related to inflammation of fat tissue, often seen in pancreatitis or trauma to fat areas. - It is not directly caused by infections but rather by fat cell damage and necrosis, leading to **saponification**. *Fibrinoid necrosis* - Associated with **immune-mediated vascular injury**, seen in conditions like **vasculitis** or **malignant hypertension** [2]. - Characterized by the deposition of **fibrin-like protein** [2], not directly related to infectious processes. *Coagulative necrosis* - Typically occurs in ischemic conditions like myocardial infarction, where tissue architecture is preserved despite cell death. - It is not directly linked to infection spread, as it relates more to loss of blood supply rather than infectious agents. **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. 193-194. [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. 103-104.
Question 55: 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 56: 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 57: 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 58: 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 59: Which substance plays a significant role in the tumor metastasis cascade?
- A. TNF-alpha
- B. CD99
- C. NM23
- D. MMP-2 (Matrix Metalloproteinase-2) (Correct Answer)
Explanation: ***Collagenase IV*** - Collagenase IV is involved in the **degradation of extracellular matrix**, facilitating tumor invasion and metastasis [1,2]. - It plays a crucial role in breaking down **type IV collagen**, a major component of the **basement membrane**, allowing cancer cells to migrate [2]. *TNF-alpha* - While TNF-alpha is a cytokine that can promote **tumor growth**, it is not directly involved in the **metastatic cascade** like collagenase IV [3,4]. - It primarily functions in **inflammation** and immune response, affecting tumor microenvironment rather than directly facilitating invasion. *NM23* - NM23 is noted for its potential role as a **tumor suppressor**, and lower levels are associated with metastasis. - However, it does not play a direct role in the *metastatic cascade* itself [3,4], as it primarily influences **tumor progression** rather than matrix degradation. *CD99* - CD99 is a cell adhesion molecule implicated in **cell migration**, but it is not a significant factor in the **enzymatic breakdown** of tissue during metastasis [1,2]. - Its expression has more to do with **cell adhesion characteristics**, rather than directly promoting invasive capabilities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 315-316. [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. 232-233. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 314-315. [4] 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. 233-234.
Question 60: Most common cause of idiopathic interstitial pneumonia is
- A. Idiopathic pulmonary fibrosis (Correct Answer)
- B. Organizing pneumonia
- C. Sarcoidosis
- D. Lipoid pneumonia
Explanation: ***Idiopathic pulmonary fibrosis (IPF)*** - This is the **most common** form of idiopathic interstitial pneumonia, accounting for approximately **50-60% of all IIP cases** - Represents the **most severe** IIP subtype with poor prognosis - Characterized by progressive **usual interstitial pneumonia (UIP) pattern** with fibroblastic foci and honeycombing - Presents with progressive dyspnea, dry cough, and restrictive lung disease *Organizing pneumonia* - While **Cryptogenic Organizing Pneumonia (COP)** is a form of idiopathic interstitial pneumonia, it is **much less common than IPF** [1] - Characterized by **intra-alveolar granulation tissue (Masson bodies)** [1] - Better prognosis and steroid-responsive compared to IPF [1] *Sarcoidosis* - This is **NOT classified as an idiopathic interstitial pneumonia** - It is a separate **multisystem granulomatous disease** with **non-caseating granulomas** - Has a distinct etiology related to altered immune response - Does not belong to the IIP classification system *Lipoid pneumonia* - This is **NOT an idiopathic interstitial pneumonia** - Results from **aspiration of lipid substances** causing exogenous lipoid pneumonia - Has a **known extrinsic cause**, therefore not "idiopathic" - Not part of the IIP classification **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 330-331.