NEET-PG 2015 - Pathology Practice Questions

Q: Which of the following is an oncogene?

RAS. ***RAS*** - RAS is an **oncogene**, not a tumor suppressor gene; it promotes cell proliferation and survival [1]. - Mutations in RAS lead to uncontrolled cell division, contributing to various cancers. *p53* - p53 is a crucial **tumor suppressor gene** responsible for regulating the cell cycle and preventing tumor formation [1,2]. - It functions by inducing apoptosis in cells with damaged DNA, preventing their proliferation [2]. *WT-1* - WT-1 is a **tumor suppressor gene** associated with Wilms' tumor and regulates kidney and gonadal development. - It plays a role in cell growth and differentiation, preventing tumorigenesis when functioning correctly. *Rb* - The Rb gene encodes the **retinoblastoma protein**, a key tumor suppressor that regulates the cell cycle by inhibiting cell division [1,2]. - Loss of Rb function is primarily associated with retinoblastoma and other cancers, indicating its critical role in tumor suppression [1,2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-301. [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. 227-228.

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: Which protein is defective in dilated cardiomyopathy?

Dystrophin. ***Dystrophin*** - **Dystrophin** is a crucial protein in the **muscle cell membrane** that anchors the cytoskeleton to the extracellular matrix. - Defects in dystrophin lead to sarcolemmal fragility, causing muscle damage and can result in **dilated cardiomyopathy**, especially in conditions like **Duchenne muscular dystrophy** [1]. *Myosin* - **Myosin** is a fundamental **motor protein** involved in muscle contraction, forming the thick filaments. - While mutations in myosin can cause various cardiac conditions, like hypertrophic cardiomyopathy, direct primary defects in myosin are not typically identified as the cause of dilated cardiomyopathy [2]. *Troponin* - **Troponin** is a protein complex that regulates muscle contraction by controlling the interaction between actin and myosin, particularly in response to calcium. - Although troponins are vital for cardiac function and are released during myocardial injury, their primary defect is not typically implicated in the etiology of dilated cardiomyopathy [2]. *Tropomyosin* - **Tropomyosin** is a protein that winds around actin filaments and, along with troponin, regulates the binding of myosin to actin. - While essential for muscle contraction, direct defects in tropomyosin are not a common genetic cause of dilated cardiomyopathy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.

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: Which of the following is a type of small vessel vasculitis?

Granulomatosis with polyangiitis (GPA). ***Granulomatosis with polyangiitis (GPA)*** - GPA is a prototypic **ANCA-associated small vessel vasculitis** characterized by necrotizing granulomas and vasculitis [1], [2]. - It commonly involves the **upper and lower respiratory tracts** and the **kidneys** with necrotizing granulomatous inflammation [1], [2]. - Classified as small vessel vasculitis according to the **Chapel Hill Consensus Conference** classification. *Classical PAN* - This refers to **Polyarteritis Nodosa (PAN)**, which is a **medium-sized vessel vasculitis**. - PAN is characterized by multifocal inflammatory and necrotizing lesions of medium-sized muscular arteries, **not small vessels**. *Giant cell arteritis* - **Giant cell arteritis (GCA)** is a **large vessel vasculitis** that primarily affects the aorta and its major branches, particularly the temporal artery [3]. - Symptoms include headache, jaw claudication, and visual disturbances, reflecting the involvement of larger blood vessels [3]. *None of the options* - This option is incorrect because Granulomatosis with polyangiitis (GPA) is a clear example of a small vessel vasculitis. - There is a correct answer among the provided choices. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516.

Q: Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?

Macrophages. ***Macrophages*** - **Macrophages** are increasingly recognized for their critical role in the pathogenesis and progression of **heart failure**, contributing to **cardiac remodeling**, chronic inflammation, and fibrosis - They infiltrate failing myocardium and play dual roles: promoting both **inflammation** and **tissue repair** - Their activation state (M1 vs M2 phenotypes) can significantly influence cardiac function and prognosis in heart failure patients - They secrete **cytokines**, **growth factors**, and **matrix metalloproteinases** that contribute to ventricular remodeling *Eosinophils* - **Eosinophils** are primarily involved in **allergic reactions** and defense against **parasitic infections** - While they can contribute to inflammation in specific cardiac conditions (e.g., **eosinophilic myocarditis**, **Loeffler endocarditis**), they are not primarily associated with the general pathophysiology of chronic heart failure *T cells* - **T cells** are central to **adaptive immunity**, including cell-mediated responses and modulation of immune reactions - Though T cells play a role in inflammatory processes in certain forms of heart disease, particularly **viral myocarditis**, they are not the predominant immune cell driving chronic cardiac remodeling in heart failure *B cells* - **B cells** are responsible for producing **antibodies** and are key players in humoral immunity - While B cells can contribute to autoimmune forms of heart disease and certain inflammatory processes, they are not typically the primary immune cell associated with the progression of chronic heart failure

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: Obliterative endarteritis in vasa vasorum is seen in -

Tertiary Syphilis. ***Tertiary Syphilis*** - **Obliterative endarteritis** of the **vasa vasorum** is a hallmark pathological finding in tertiary syphilis, particularly affecting the **aorta**. - This inflammation and occlusion of the small blood vessels supplying the aorta lead to **ischemic injury** of the aortic wall, causing **aneurysms** and **aortic regurgitation**. *Essential Hypertension* - While hypertension can lead to vascular changes like **arteriolosclerosis** and **hyperplastic arteriolosclerosis**, it does not typically involve obliterative endarteritis of the vasa vasorum. - The vascular damage in essential hypertension is more generalized to smaller arteries and arterioles, not specifically the vasa vasorum. *Systemic Lupus Erythematosus* - SLE is an **autoimmune disease** that can cause **vasculitis**, but the specific pattern of obliterative endarteritis of the vasa vasorum is not characteristic. - Vascular involvement in SLE is diverse, ranging from small vessel vasculitis to accelerated atherosclerosis, but distinct from syphilitic changes. *Pulmonary Tuberculosis* - Tuberculosis is primarily an **infectious granulomatous disease** affecting the lungs and other organs; it does not typically cause obliterative endarteritis of the vasa vasorum. - Although it can cause vascular complications like **aneurysms** (e.g., Rasmussen's aneurysm) due to erosion, the underlying mechanism is not the same as syphilitic changes.

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.

Question 1

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

Accepted Answer

Granulation tissue

Answer

Neoplasia

Answer

Hyperplasia

Answer

Fibrosis

Question 2

Which of the following is an oncogene?

Accepted Answer

RAS

Answer

WT-1

Answer

Rb

Answer

p53

Question 3

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

Accepted Answer

Metaplasia

Answer

Hypertrophy

Answer

Dysplasia

Answer

Hyperplasia

Question 4

Which protein is defective in dilated cardiomyopathy?

Accepted Answer

Dystrophin

Answer

Tropomyosin

Answer

Myosin

Answer

Troponin

Question 5

Lines of Zahn are LEAST likely to be seen in -

Accepted Answer

Lung

Answer

Liver

Answer

Kidney

Answer

Heart

Question 6

Which of the following is a type of small vessel vasculitis?

Accepted Answer

Granulomatosis with polyangiitis (GPA)

Answer

Classical PAN

Answer

Giant cell arteritis

Answer

None of the options

Question 7

Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?

Accepted Answer

Macrophages

Answer

Eosinophils

Answer

T cells

Answer

B cells

Question 8

Heart failure cells are seen in -

Accepted Answer

Pulmonary edema

Answer

Pulmonary infarction

Answer

Pulmonary abscess

Answer

Pulmonary tuberculosis

Question 9

Obliterative endarteritis in vasa vasorum is seen in -

Accepted Answer

Tertiary Syphilis

Answer

Essential Hypertension

Answer

Systemic Lupus Erythematosus

Answer

Pulmonary Tuberculosis

Question 10

Diabetic foot is associated with following type of gangrene -

Accepted Answer

Wet gangrene

Answer

Dry gangrene

Answer

Gas gangrene

Answer

Fournier's gangrene

NEET-PG 2015 — Pathology