NEET-PG 2013 Practice Questions

Q: Superior wall of middle ear is formed by ?

Tegmen tympani. ***Tegmen tympani*** - The **tegmen tympani** is a thin plate of **petrous temporal bone** that forms the roof or superior wall of the middle ear cavity. - This structure separates the middle ear from the **middle cranial fossa** and its contents, including the **temporal lobe of the brain**. *Jugular bulb* - The **jugular bulb** is the dilated superior portion of the **internal jugular vein** and forms part of the **floor (inferior wall)** of the middle ear cavity, not the superior wall. - Its close proximity to the middle ear makes it vulnerable to injury during otologic surgery. *Tympanic membrane* - The **tympanic membrane** (eardrum) forms the **lateral wall** of the middle ear cavity, separating it from the external auditory canal. - It is crucial for **sound transmission** by vibrating in response to sound waves. *Carotid wall* - The **carotid wall** forms the **anterior wall** of the middle ear cavity and is related to the **internal carotid artery** as it narrows through the carotid canal. - This wall is not the superior boundary of the middle ear.

Q: Which type of RNA is primarily involved in gene silencing?

miRNA. ***miRNA*** - **miRNA** (microRNA) is a small non-coding RNA molecule that plays a crucial role in **post-transcriptional regulation of gene expression**. - It functions by binding to complementary messenger RNA (mRNA) molecules, leading to **mRNA degradation** or **inhibition of translation**, thereby silencing genes. - miRNA is the primary RNA type involved in **gene silencing** through the RNA interference (RNAi) pathway. *rRNA* - **rRNA** (ribosomal RNA) is a primary component of **ribosomes**, the cellular machinery responsible for protein synthesis. - Its main function is to **catalyze peptide bond formation** and provide structural integrity to the ribosome, not gene silencing. *tRNA* - **tRNA** (transfer RNA) is responsible for carrying specific **amino acids** to the ribosome during protein synthesis. - It acts as an adapter molecule, translating the **genetic code** in mRNA into an amino acid sequence. *mRNA* - **mRNA** (messenger RNA) carries genetic information from **DNA to ribosomes** for protein synthesis. - While mRNA can be targeted by gene silencing mechanisms (like miRNA), it is not the RNA type that performs the silencing function itself.

Q: Which cytokine activates macrophages?

IFN-γ. ***IFN-γ (Interferon-gamma)*** - **IFN-γ is the classic macrophage-activating cytokine**, enhancing phagocytic and antimicrobial functions - Promotes expression of **MHC class I and II molecules**, increasing antigen presentation capacity - Produced mainly by **Th1 cells and NK cells** during cell-mediated immunity - Key cytokine in defense against **intracellular pathogens** (mycobacteria, viruses) *IL-8* - **IL-8 is a chemokine** (cytokine subfamily) primarily involved in **neutrophil chemotaxis** - Recruits neutrophils to sites of infection or inflammation - Does not directly activate macrophages like IFN-γ - Important in acute inflammatory responses *PAF (Platelet-Activating Factor)* - **Not a cytokine** - it is a **phospholipid mediator** - Involved in allergic and inflammatory responses - Functions include **platelet aggregation**, **vasodilation**, and **bronchoconstriction** - While it affects immune responses, it doesn't function as a macrophage-activating cytokine *Leukotriene B4* - **Not a cytokine** - it is a **lipid mediator** (eicosanoid) derived from arachidonic acid - Primarily acts as a **chemoattractant for neutrophils** - Promotes neutrophil and monocyte adhesion and migration to inflammatory sites - Does not directly activate macrophages

Q: What is a hamartoma?

Developmental malformation. ***Development malformation*** - A **hamartoma** is a type of **benign tumor** that consists of an overgrowth of mature cells, representing a **developmental malformation** [1]. - It is formed from tissues that are normally present in the affected organ but are disorganized, leading to a characteristic appearance. *Malignant tumor* - Hamartomas are classified as **benign tumors** [1], not malignant, as they do not invade surrounding tissues or metastasize. - Despite being a growth, they do not exhibit the aggressive characteristics of malignant tumors. *Hemorrhage in vessel* - Hemorrhage refers to bleeding within a vessel and is unrelated to the definition or nature of a **hamartoma**. - Hamartomas do not consist of blood or bleeding; instead, they involve disorganized tissue growth. *Metastatic tissue* - Metastatic tissue refers to cancerous cells that have spread from their original site, which contrasts with the **non-cancerous** nature of hamartomas [1]. - Hamartomas do not involve the spread of cancer cells, but rather a **local abnormality** in tissue arrangement. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 481-482.

Q: What is the primary mechanism involved in the pathogenesis of acute proliferative glomerulonephritis?

Immune complex mediated. ***Immune complex mediated*** - The pathogenesis of **acute proliferative glomerulonephritis** is primarily caused by **immune complexes** that deposit in the glomeruli, leading to inflammation [1]. - This is typically associated with **post-streptococcal infections**, where the body's immune response generates complexes that affect kidney function [1]. *Cytotoxic T-cell mediated* - This mechanism involves T-cells directly damaging cells, which is not the primary cause of **acute proliferative glomerulonephritis**. - It is more relevant in conditions like **viral infections** or **transplant rejection**, rather than immune complex diseases. *Antibody mediated* - While antibodies play a role in various diseases, acute proliferative glomerulonephritis is primarily mediated by **immune complexes**, not just antibodies alone [1]. - This oes not account for the presence of **complexes formed from antigens**, which is crucial in the pathogenesis [1]. *Cell-mediated (Type IV)* - Type IV hypersensitivity involves delayed-type hypersensitivity, typically seen in **tuberculosis** or **contact dermatitis**, not in acute glomerulonephritis. - The inflammation in this case is due to **immune complexes**, rather than a purely cell-mediated response [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-916.

Q: Fibrinoid necrosis with neutrophilic infiltration is seen in ?

Polyarteritis Nodosa (PAN). ***PAN*** - **Fibrinoid necrosis** with **neutrophilic infiltration** is characteristic of Polyarteritis Nodosa (PAN), which primarily affects medium-sized arteries [1]. - The necrosis is often seen in the context of **systemic vasculitis**, where it leads to damage and inflammation of vessel walls [3]. *Takayasu arteritis* - Primarily affects **large vessels** like the aorta and its major branches, typically presenting with **pulselessness** or **claudication**. - It shows **granulomatous inflammation** rather than fibrinoid necrosis with neutrophilic infiltration. *Giant cell arteritis* - Predominantly affects large and medium arteries, especially the **temporal artery**, often leading to headaches and visual disturbances. - It is associated with **giant cells** and lymphocytic infiltration rather than fibrinoid necrosis. *Wegener's granulomatosis* - Characterized by **granulomatous inflammation** and vasculitis affecting small to medium vessels, particularly in the lungs and kidneys. - It does not typically present with **fibrinoid necrosis**; instead, it shows necrotizing granulomas [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 687-688.

Q: All are true about non-bacterial thrombotic endocarditis, except?

Vegetation > 5 mm. ***Vegetation > 5 mm*** - Non-bacterial thrombotic endocarditis (NBTE) typically features **small vegetations**, often less than 5 mm, associated with conditions like **cancer** or **hypercoagulable states** [1]. - The presence of larger vegetations is more characteristic of **infective endocarditis**, making this statement false regarding NBTE. *Cause emboli* - NBTE is known to cause **embolic phenomena** due to small vegetations that dislodge, leading to **ischemia** in distant organs. - It is associated with conditions such as **adenocarcinoma**, contributing to possible embolic events. *No inflammatory reaction* - Although inflammatory cells are sparse, NBTE can produce a **minimal inflammatory response** in the tissues. - The presence of fibrin deposits and small vegetations has implications for **thrombus formation**, suggesting a mild inflammatory component. *Locally nondestructive* - NBTE vegetations are primarily **nondestructive** to the underlying valves [1], contrasting with infected vegetations that can cause significant **valvular damage**. - However, this characteristic still does not undermine that these vegetations can lead to systemic embolism despite being locally nondestructive. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568.

Q: Macrophages are converted to epithelioid cells by which cytokine?

IFN-γ. ***IFN-γ: A cytokine involved in classical macrophage activation*** - **Interferon-gamma (IFN-γ)** is a key cytokine produced by activated T cells and NK cells that plays a crucial role in activating macrophages and converting them into **epithelioid cells** [1]. - This conversion is essential for the formation of **granulomas**, a hallmark of chronic inflammatory responses, particularly in infections like tuberculosis [1]. *TNF-α: A cytokine involved in granuloma maintenance* - **Tumor Necrosis Factor-alpha (TNF-α)** is vital for the **formation and maintenance** of granulomas, but it is not directly responsible for the initial conversion of macrophages to epithelioid cells. - While TNF-α helps to **organize and contain** the infection within the granuloma, IFN-γ drives the phenotypic change of macrophages. *TGF-β: A cytokine involved in tissue remodeling* - **Transforming Growth Factor-beta (TGF-β)** is predominantly involved in **tissue repair, fibrosis, and immune regulation**, promoting extracellular matrix production. - It does not primarily induce the differentiation of macrophages into epithelioid cells; rather, it often plays a role in the later stages of granuloma development, contributing to **fibrotic encapsulation** [1]. *IL-4: A cytokine involved in alternative macrophage activation* - **Interleukin-4 (IL-4)** is a characteristic cytokine that drives **alternative macrophage activation (M2 pathway)**, leading to roles in allergic responses and tissue repair [1]. - The M2 phenotype is distinct from the classically activated (M1) phenotype associated with epithelioid cell formation, which is driven by IFN-γ. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.

Q: Which mediators are involved in the resolution of inflammation?

Resolvins, protectins, and lipoxins. ***Resolvins, protectins, and lipoxins*** - These are **specialized pro-resolving mediators (SPMs)** derived from omega-3 and omega-6 polyunsaturated fatty acids that actively promote the resolution phase of inflammation. - **Lipoxins** (from arachidonic acid) inhibit neutrophil chemotaxis and promote macrophage-mediated clearance of apoptotic cells. - **Resolvins** (from EPA and DHA) actively terminate inflammatory signals, reduce neutrophil infiltration, and enhance bacterial clearance. - **Protectins** promote resolution by limiting neutrophil recruitment and enhancing clearance of inflammatory debris. - These mediators represent the **endogenous "stop signals"** that actively resolve inflammation rather than simply suppressing it. *IL-10, IL-1 receptor antagonist, and TGF-β* - While these have **anti-inflammatory** effects, they are not classified as primary resolution mediators. - **IL-10** inhibits pro-inflammatory cytokine synthesis and suppresses immune responses (immunosuppressive rather than pro-resolving). - **IL-1 receptor antagonist (IL-1Ra)** blocks IL-1 signaling, preventing inflammation amplification. - **TGF-β** promotes tissue repair and has immunosuppressive functions. - These are **anti-inflammatory mediators** that prevent or dampen inflammation, distinct from specialized pro-resolving mediators that actively orchestrate the resolution process. *TNF-alpha, IL-1, and CRP* - **TNF-alpha** and **IL-1** are classic **pro-inflammatory cytokines** that initiate and amplify inflammation. - **CRP (C-reactive protein)** is an acute-phase reactant and biomarker of inflammation, not a mediator of resolution. *Interferon-gamma and IL-12* - **IFN-γ** and **IL-12** promote **Th1 immune responses** and cellular immunity. - These are pro-inflammatory mediators involved in host defense against intracellular pathogens, not resolution of inflammation.

Q: Which of the following statements is true about red muscle fibers?

Exhibit more oxidative capacity. ***Exhibit more oxidative capacity*** - **Red muscle fibers**, also known as **slow-twitch fibers**, are rich in **mitochondria** and enzymes for aerobic respiration, allowing for sustained contractions and high oxidative capacity. - Their high oxidative capacity is crucial for activities requiring **endurance**, such as long-distance running or maintaining posture through efficient **ATP production** via the **electron transport chain**. *Contain fewer mitochondria than white muscle fibers* - **Red muscle fibers** contain **more mitochondria** than white muscle fibers to support their greater reliance on **aerobic metabolism** for sustained energy production. - **Mitochondria** are the primary sites of **oxidative phosphorylation**, which is essential for the continuous ATP supply needed by these endurance specialized fibers. *Utilize glycolytic metabolism* - While red fibers can perform some glycolysis, their primary metabolic pathway is **oxidative phosphorylation**, utilizing **fatty acids** and **glucose** aerobically. - **Glycolytic metabolism** is more characteristic of **white muscle fibers (fast-twitch)**, which rely on anaerobic pathways for rapid, high-intensity contractions. *Have less myoglobin than white muscle fibers* - **Red muscle fibers** are characterized by a **high content of myoglobin**, which gives them their characteristic red color and high oxygen storage capacity. - **Myoglobin** is crucial for oxygen delivery to the mitochondria, supporting the sustained aerobic metabolism of these fibers, in contrast to white fibers which have less myoglobin.

Question 1

Superior wall of middle ear is formed by ?

Accepted Answer

Tegmen tympani

Answer

Jugular bulb

Answer

Tympanic membrane

Answer

Carotid wall

Question 2

Which type of RNA is primarily involved in gene silencing?

Accepted Answer

miRNA

Answer

rRNA

Answer

tRNA

Answer

mRNA

Question 3

Which cytokine activates macrophages?

Accepted Answer

IFN-γ

Answer

Leukotriene B4

Answer

IL-8

Answer

PAF

Question 4

What is a hamartoma?

Accepted Answer

Developmental malformation

Answer

Malignant tumor

Answer

Metastatic tissue

Answer

Hemorrhage in vessel

Question 5

What is the primary mechanism involved in the pathogenesis of acute proliferative glomerulonephritis?

Accepted Answer

Immune complex mediated

Answer

T-cell mediated cytotoxicity

Answer

Direct antibody-mediated injury

Answer

Type IV hypersensitivity reaction

Question 6

Fibrinoid necrosis with neutrophilic infiltration is seen in ?

Accepted Answer

Polyarteritis Nodosa (PAN)

Answer

Giant Cell Arteritis

Answer

Takayasu Arteritis

Answer

Wegener's Granulomatosis

Question 7

All are true about non-bacterial thrombotic endocarditis, except?

Accepted Answer

Vegetation > 5 mm

Answer

No inflammatory reaction

Answer

Locally nondestructive

Answer

Cause emboli

Question 8

Macrophages are converted to epithelioid cells by which cytokine?

Accepted Answer

IFN-γ

Answer

TNF-α

Answer

TGF-β

Answer

IL-4

Question 9

Which mediators are involved in the resolution of inflammation?

Accepted Answer

Resolvins, protectins, and lipoxins

Answer

TNF Alfa, IL-1, and CRP

Answer

IL-10, IL-1 receptor antagonist, and TGF-β

Answer

Interferon-gamma and IL-12

Question 10

Which of the following statements is true about red muscle fibers?

Accepted Answer

Exhibit more oxidative capacity

Answer

Contain fewer mitochondria than white muscle fibers

Answer

Have less myoglobin than white muscle fibers

Answer

Utilize glycolytic metabolism

NEET-PG 2013

Anatomy

Biochemistry

Microbiology

Pathology

Physiology