NEET-PG 2015 - Pathology Practice Questions

Q: What does Ghon's focus indicate in the context of tuberculosis?

Primary complex. ***Primary complex*** - A **Ghon's focus** is the initial parenchymal lesion (typically subpleural) that develops during primary tuberculosis infection [1]. - The Ghon's focus, together with an enlarged regional lymph node (usually hilar or mediastinal), forms the **Ghon's complex** or **Primary complex** [2]. - When this complex undergoes calcification and healing, it is called a **Ranke complex**, which indicates past healed primary TB. *Post primary tuberculosis* - Also known as **reactivation tuberculosis** or **secondary tuberculosis**, this typically occurs years after the primary infection, usually in the apices of the lungs [2]. - It represents reactivation of dormant bacilli, not the initial primary infection lesion. - Characterized by cavitary lesions and often more severe pulmonary symptoms. *Miliary tuberculosis* - This is a form of progressive, widespread tuberculosis characterized by the presence of **tiny, millet-seed sized lesions** disseminated throughout the body via hematogenous spread [3]. - It indicates a severe and life-threatening form of TB resulting from massive lymphohematogenous dissemination. - Not related to the localized primary complex. *Tuberculous lymphadenitis* - This refers to **tuberculous infection of lymph nodes**, most commonly in the cervical region (scrofula). - While lymph node involvement is part of the primary complex, Ghon's focus specifically refers to the **parenchymal lung lesion**, not the lymph node component alone [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 379-380. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 319-320. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 320-321.

Q: First mediator of inflammation to be released is

Histamine. ***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.

Q: Structure of chromosomes is studied by?

G-banding. ***G-banding*** - G-banding is the most commonly used method for the **detailed examination of chromosomes**, allowing visualization of banding patterns [1][2]. - It facilitates the identification of **chromosomal abnormalities** and is essential in **cytogenetic studies** [1][2]. *Q-banding* - Q-banding reveals a different pattern that is primarily used for **detection of specific chromosome markers** but is less common than G-banding. - It is more useful for cases requiring **fluorescent bright bands** but not for overall structural analysis. *C-banding* - C-banding specifically highlights the **centromeric regions** of chromosomes, not the overall structure. - It is limited in scope compared to G-banding since it doesn't provide a complete picture of chromosome morphology. *Brd V-staining* - Brd V-staining focuses on specific **DNA regions** and is related to the **visualization of viral DNA** in infected cells rather than chromosome structure. - It does not offer insights into the **general structural characteristics** of chromosomes like G-banding does. **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. 54-55. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 167-168.

Q: Diabetic foot is associated with following type of gangrene -

Wet gangrene. ***Wet gangrene*** - Diabetic foot commonly leads to **ischemia** and **infection** [1], resulting in wet gangrene characterized by moist, necrotic tissue. - This type of gangrene is associated with **rapid progression** and can result in systemic toxicity, making prompt treatment essential. *Fournier's gangrene* - This type of gangrene specifically affects the **perineal** region and is not directly associated with diabetic foot. - It usually arises from infections related to **perineal trauma** or surgical procedures. *Gas gangrene* - Caused by **Clostridium** species and typically follows a traumatic injury or surgical procedure, not specifically related to diabetes. - Presents with **crepitus** and rapid systemic symptoms, different from the chronic nature of diabetic ulcers. *Dry gangrene* - Associated with **chronic ischemia** and necrosis, it occurs in conditions like peripheral arterial disease, not primarily with infections seen in diabetic foot [1]. - It usually develops gradually without the sudden onset of symptoms characteristic of wet gangrene.

Q: Lines of Zahn are LEAST likely to be seen in -

Lung. ***Lung*** - **Lines of Zahn are LEAST likely in the lungs** because most pulmonary thrombi are actually **emboli that formed elsewhere** (typically in deep leg veins) and then **lodged in pulmonary vessels**. - These pre-formed thrombi developed in **low-flow venous environments** and therefore **lack the characteristic layered appearance** of Lines of Zahn. - Even when thrombi form in situ in pulmonary vessels, the vascular bed characteristics make Lines of Zahn formation less common compared to other sites. *Heart* - **Mural thrombi** in heart chambers (especially post-MI in left ventricle or in atrial fibrillation) commonly show **Lines of Zahn**. - The **high-flow, turbulent environment** with continuous cardiac contractions creates ideal conditions for alternating platelet-fibrin and RBC layer deposition. - These are classic examples of antemortem thrombi with visible Lines of Zahn. *Liver* - **Portal vein thrombosis** and **hepatic vein thrombosis** (Budd-Chiari syndrome) can exhibit **Lines of Zahn**. - Despite being venous, these vessels have **sufficient flow velocity and turbulence** to allow layered thrombus formation. - Lines of Zahn indicate the thrombus formed during life with flowing blood. *Kidney* - **Renal artery thrombosis** and **renal vein thrombosis** frequently show **Lines of Zahn**. - Both arterial and venous renal circulation have adequate flow dynamics for layered thrombus formation. - These represent antemortem thrombi formed in vessels with active blood flow.

Q: What is a distinguishing feature of reticulocytes?

Presence of residual RNA and ribosomes. ***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.

Q: Heart failure cells are seen in -

Pulmonary edema. ***Pulmonary edema*** - Heart failure cells, or **hemosiderin-laden macrophages**, are typically found in the lungs during pulmonary edema due to left-sided heart failure [1]. - This condition leads to **increased pulmonary capillary pressure**, causing leakage of red blood cells into the alveoli, which macrophages then phagocytose [1]. *Pulmonary abscess* - Characterized by a **localized collection of pus** within the lung, typically due to infection, rather than heart failure. - Does not typically involve **hemosiderin-laden macrophages** indicative of chronic pulmonary congestion. *Pulmonary infarction* - Causes **tissue death** due to obstruction of blood flow, leading to necrosis rather than heart failure cells. - Typically presents with **infarcted lung tissue**, showing a different pathological process than seen in heart failure. *PulmonaryTB* - Primarily caused by **Mycobacterium tuberculosis**, leading to cavitary lesions and granulomatous inflammation, not heart failure cells. - The presence of **caseating granulomas** is characterized but does not indicate chronic pulmonary congestion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 536-538.

Q: Reversible change from one cell type to another is known as -

Metaplasia. ***Metaplesia*** - Refers to the **reversible change** from one cell type to another in response to chronic irritation or damage [1][2]. - It often occurs as an adaptive response in **epithelial tissues**, such as in the respiratory tract in smokers [1][2]. *Hypertrophy* - Represents an **increase in cell size** rather than a change in cell type [2]. - It is often a response to increased functional demand, as seen in **cardiac muscle** in athletes. *Hyperplesia* - Refers to an **increase in cell number** within a tissue or organ, not a change in cell type [2]. - Common in conditions such as **benign prostatic hyperplasia** but does not involve differentiation into other cell types. *Dysplasia* - Indicates an **abnormal growth or development** of cells, leading to disordered morphology rather than a transformation into another cell type. - It is often a precursor to cancer but does not signify the reversible nature of metaplasia. **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. 49. [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. 85-92.

Q: Fibrosis associated with liver cirrhosis is mediated by -

Transforming Growth Factor-beta (TGF-β). ***PDGF*** - Platelet-Derived Growth Factor (**PDGF**) is a critical mediator in the **fibrogenic response** associated with liver cirrhosis [1]. - It stimulates the **proliferation** and activation of hepatic stellate cells, leading to excessive **collagen deposition** and fibrosis [1][2]. *ICAM-1* - Intercellular Adhesion Molecule-1 (**ICAM-1**) primarily mediates **cell adhesion** and is involved in inflammatory processes, not directly in fibrosis. - While it may play a role in **leukocyte recruitment**, it does not contribute significantly to the fibrogenic pathway in liver cirrhosis. *PcAM-l* - **PCAM-1** (Platelet/endothelial cell adhesion molecule-1) is involved in **cell adhesion** and is primarily expressed on endothelial cells. - Its role is more associated with **angiogenesis** and inflammation, lacking direct involvement in the fibrogenic process of cirrhosis. *IFN-y* - Interferon-gamma (**IFN-y**) is a cytokine that predominantly has a role in **immune modulation** and does not directly induce fibroblast activation. - It may have regulatory effects on inflammation but does not lead to significant fibrosis associated with liver cirrhosis. **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. Liver and Gallbladder, pp. 830-832.

Question 1

What does Ghon's focus indicate in the context of tuberculosis?

Accepted Answer

Primary complex

Answer

Post primary tuberculosis

Answer

Miliary tuberculosis

Answer

Tuberculous lymphadenitis

Question 2

Which of the following is not considered an example of excess tissue growth?

Accepted Answer

Granulation tissue

Answer

Neoplasia

Answer

Hyperplasia

Answer

Fibrosis

Question 3

First mediator of inflammation to be released is

Accepted Answer

Histamine

Answer

Nitric oxide

Answer

PAF

Answer

IL-1

Question 4

Structure of chromosomes is studied by?

Accepted Answer

G-banding

Answer

C-banding

Answer

Q-banding

Answer

BrdU staining

Question 5

Diabetic foot is associated with following type of gangrene -

Accepted Answer

Wet gangrene

Answer

Dry gangrene

Answer

Gas gangrene

Answer

Fournier's gangrene

Question 6

Lines of Zahn are LEAST likely to be seen in -

Accepted Answer

Lung

Answer

Liver

Answer

Kidney

Answer

Heart

Question 7

What is a distinguishing feature of reticulocytes?

Accepted Answer

Presence of residual RNA and ribosomes

Answer

Slightly larger in size than RBCs

Answer

Mature in bone marrow

Answer

Constitute approximately 1% of the red cells

Question 8

Heart failure cells are seen in -

Accepted Answer

Pulmonary edema

Answer

Pulmonary infarction

Answer

Pulmonary abscess

Answer

Pulmonary tuberculosis

Question 9

Reversible change from one cell type to another is known as -

Accepted Answer

Metaplasia

Answer

Hypertrophy

Answer

Dysplasia

Answer

Hyperplasia

Question 10

Fibrosis associated with liver cirrhosis is mediated by -

Accepted Answer

Transforming Growth Factor-beta (TGF-β)

Answer

Platelet-Derived Growth Factor (PDGF)

Answer

Vascular Endothelial Growth Factor (VEGF)

Answer

Tumor Necrosis Factor-alpha (TNF-α)

NEET-PG 2015 — Pathology