NEET-PG 2015 Practice Questions

Q: B cells are located in which region of lymph nodes?

Cortical follicles. ***Cortical follicles*** - **B cells** are predominantly found within the **cortical follicles** of lymph nodes, where they mature and become activated upon encountering antigens [2]. - These follicles can be primary (inactive) or secondary (active, containing **germinal centers** for B cell proliferation and differentiation). *Paracortical region* - The **paracortical region** is primarily occupied by **T cells** and is the site where T cells interact with antigen-presenting cells [1]. - While it's adjacent to B cell areas, it's not the primary location for B cells. *Medullary sinuses* - **Medullary sinuses** are channels in the medulla of the lymph node, containing macrophages and plasma cells, which are *differentiated B cells*. - They are not the primary residence for undifferentiated B cells. *Subcapsular region* - **Subcapsular region** is the space immediately beneath the capsule of the lymph node where lymph initially enters. - It contains macrophages and dendritic cells that sample antigens but is not a primary B cell zone.

Q: Chymotrypsinogen is activated into chymotrypsin by:

Trypsin. ***Activation of Chymotrypsinogen by Trypsin*** - **Trypsin** is the primary enzyme responsible for the activation of **chymotrypsinogen** into its active form, **chymotrypsin**, by cleaving a specific peptide bond. - This activation is part of a cascade of proteolytic enzyme activations in the **pancreatic juice**, crucial for protein digestion in the small intestine. *Pepsin* - **Pepsin** is a protease active in the **stomach**, requiring an acidic environment for its activity, and is involved in the initial breakdown of proteins. - It does not play a role in the activation of pancreatic zymogens like chymotrypsinogen; its primary function is protein digestion in the gastric lumen. *Renin* - **Renin** is an enzyme primarily involved in the **renin-angiotensin-aldosterone system** (RAAS), which regulates blood pressure and fluid balance. - Its action involves cleaving **angiotensinogen** to form angiotensin I, and it has no role in the activation of digestive enzymes like chymotrypsinogen. *HCl* - **Hydrochloric acid (HCl)** is produced in the stomach and is essential for providing the acidic environment required for **pepsin's activity** and for denaturing proteins. - While HCl is crucial for digestion, it does not directly activate chymotrypsinogen; this activation is an enzymatic process carried out by another protease.

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: Which of the following does not predispose to leukemia?

Alcohol. ***Alcohol*** - Alcohol consumption does not have a well-established association with an increased risk of leukemia compared to other factors. - While excessive alcohol can impact overall health, it is not considered a primary risk factor for developing leukemia. *Chemical exposure* - Certain chemicals, such as **benzene** and **formaldehyde**, are known to be **leukemogenic** and can increase the risk of leukemia. [1] - Occupational exposure to these chemicals has been linked to **acute myeloid leukemia (AML)** and other types of leukemia. [1] *Smoking* - Smoking has been clearly associated with an increased risk of **acute myeloid leukemia (AML)** and other hematologic malignancies. [1] - The toxins in tobacco smoke can cause **DNA damage**, contributing to the development of leukemia. *Genetic disorder* - Certain genetic disorders, like **Down syndrome** and **Fanconi anemia**, are associated with an increased risk of leukemia. - Individuals with these genetic predispositions have a higher likelihood of developing various forms of leukemia.

Q: Which sympathomimetic drug is primarily known to increase heart rate?

Isoprenaline. ***Isoprenaline*** - **Isoprenaline** (isoproterenol) is a non-selective beta-adrenergic agonist, with a strong affinity for **β1 and β2 receptors** [1]. - Its activation of **β1 receptors** in the heart leads to a significant increase in **heart rate (positive chronotropy)** and contractility (positive inotropy) [1]. - It is the **most potent chronotropic agent** among sympathomimetics and is primarily known for increasing heart rate [2]. *Phenylephrine* - **Phenylephrine** is a selective **α1 adrenergic agonist** that causes vasoconstriction [4]. - It increases blood pressure but typically causes **reflex bradycardia** (decreased heart rate) due to baroreceptor activation. - Does NOT directly increase heart rate. *Noradrenaline* - **Noradrenaline** (norepinephrine) primarily acts on **α1 receptors** causing vasoconstriction, and to a lesser extent on **β1 receptors** [3]. - While it can stimulate β1 receptors, its predominant effect is to increase **mean arterial pressure** through vasoconstriction, often causing **reflex bradycardia** [3]. *Adrenaline* - **Adrenaline** (epinephrine) acts on **α1, β1, and β2 receptors** [4]. While it does increase heart rate via **β1 receptor** stimulation, it also causes significant **vasoconstriction** (via α1) and **vasodilation** (via β2). - Its cardiovascular effects are more complex and dose-dependent compared to isoprenaline's specific chronotropic action.

Q: What is the primary process involved in Wallerian degeneration?

Nerve degeneration. ***Nerve degeneration*** - **Wallerian degeneration** specifically refers to the process of **axon degeneration** that occurs distal to the site of injury when a nerve fiber is severed [2]. - This process involves the breakdown of the **axon** and its myelin sheath, leading to loss of function [1]. *Muscle degeneration* - While prolonged nerve degeneration can lead to muscle **atrophy** due to denervation, **muscle degeneration itself** is not the primary process of Wallerian degeneration. - Wallerian degeneration focuses on the **nerve itself**, not the target tissue. *Nerve regeneration* - **Nerve regeneration** is the process where damaged nerves attempt to regrow and re-establish connections [2]. - This is a subsequent, and not always successful, event that can occur *after* Wallerian degeneration has cleared the debris [1]. *Muscle regeneration* - **Muscle regeneration** refers to the repair and regrowth of damaged muscle tissue, typically involving satellite cells. - It is unrelated to Wallerian degeneration, which is a process affecting the **nerve**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698. [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. 109-110.

Q: Mechanism of secretion of ammonia in distal tubule is?

Passive diffusion. ***Passive diffusion*** - Ammonia (NH3) is a **lipid-soluble molecule** that can readily cross cell membranes, including those of the distal tubule and collecting duct, down its **concentration gradient**. - This process is crucial for regulating **acid-base balance**, as NH3 traps H+ ions to form NH4+, which is then excreted. *Primary active transport* - This mechanism involves the direct use of **ATP hydrolysis** to move ions against their concentration gradient, which is not the primary way ammonia is secreted in the distal tubule. - While NH4+ can be secreted via active transport in some segments (e.g., substituting for K+ on the Na-K-2Cl cotransporter in the thick ascending limb), free ammonia diffusion is distinct. *Symport* - **Symport** involves the co-transport of two or more different molecules or ions in the same direction across a cell membrane, powered by an electrochemical gradient. - This mechanism is not typically involved in the secretion of uncharged, lipid-soluble ammonia. *Antiport* - **Antiport** is a type of coupled transport where two different ions or molecules move in opposite directions across a membrane. - While antiport systems are essential for various renal functions (e.g., Na+/H+ exchanger), they are not the primary mechanism for the secretion of free ammonia in the distal tubule.

Q: Vibrations are detected by which types of receptors?

Rapidly adapting. ***Rapidly adapting*** - **Rapidly adapting mechanoreceptors**, such as **Pacinian corpuscles** and **Meissner's corpuscles**, are highly sensitive to changes in pressure and movement. - They fire at the **onset and offset of a stimulus**, making them ideal for detecting vibrations, which are rhythmic changes in pressure. *Slowly adapting* - **Slowly adapting mechanoreceptors**, such as **Merkel cells** and **Ruffini endings**, are responsible for sustained pressure and touch. - They continue to fire as long as the stimulus is present, making them less suited for detecting transient vibratory stimuli. *Non-adapting* - The human body does not typically have **truly non-adapting** sensory receptors; most receptors show some form of adaptation to continuous stimuli. - This term is not standard in the classification of mechanoreceptors based on their adaptation rates. *None of the above* - This option is incorrect because rapidly adapting receptors are indeed responsible for detecting vibrations.

Q: Inhibition of heart by vagus is mediated by which receptors?

M2. ***M2*** - The **vagus nerve** primarily mediates its inhibitory effects on the heart through **muscarinic M2 receptors**. - Activation of M2 receptors by **acetylcholine** (released from the vagus nerve) decreases heart rate and contractility. *M1* - **M1 receptors** are primarily found in neuronal tissue and glands, playing a role in **gastric acid secretion** and cognitive functions. - They are not the primary muscarinic subclass responsible for vagal inhibition of the heart. *NN* - **NN receptors** are **nicotinic receptors** found on postganglionic neurons in autonomic ganglia. - They are involved in **ganglionic transmission** and are not directly responsible for efferent vagal effects on the heart. *NM* - **NM receptors** are **nicotinic receptors** found at the **neuromuscular junction** of skeletal muscles. - Their activation leads to **skeletal muscle contraction**, and they have no role in regulating heart function.

Q: Which of the following statements is true regarding smooth muscle contraction?

Phosphorylation of myosin is essential for contraction.. **Phosphorylation of myosin is essential for contraction.** - In **smooth muscle**, the **myosin light chain (MLC)** must be phosphorylated by **myosin light chain kinase (MLCK)** to enable interaction with actin and initiate contraction. - This phosphorylation causes a conformational change in the **myosin head**, increasing its ATPase activity and allowing cross-bridge cycling. *Calmodulin plays no role in smooth muscle contraction.* - **Calmodulin (CaM)** is crucial for smooth muscle contraction, as it binds **calcium ions (Ca²⁺)** forming a Ca²⁺-CaM complex. - This complex then activates **myosin light chain kinase (MLCK)**, which phosphorylates myosin, triggering contraction. *None of the options.* - This statement is incorrect because one of the provided options, "Phosphorylation of myosin is essential for contraction," is indeed true. *Troponin plays a significant role in smooth muscle contraction.* - Unlike **striated muscle (skeletal and cardiac)**, **smooth muscle** does not contain **troponin**. - Regulation of smooth muscle contraction is primarily **calcium-calmodulin-dependent**, with roles for **MLCK** and **MLCP**, rather than troponin.

Question 1

B cells are located in which region of lymph nodes?

Accepted Answer

Cortical follicles

Answer

Paracortical region

Answer

Subcapsular region

Answer

Medullary sinuses

Question 2

Chymotrypsinogen is activated into chymotrypsin by:

Accepted Answer

Trypsin

Answer

Pepsin

Answer

Renin

Answer

HCl

Question 3

Which protein is defective in dilated cardiomyopathy?

Accepted Answer

Dystrophin

Answer

Tropomyosin

Answer

Myosin

Answer

Troponin

Question 4

Which of the following does not predispose to leukemia?

Accepted Answer

Alcohol

Answer

Smoking

Answer

Chemical exposure

Answer

Genetic disorder

Question 5

Which sympathomimetic drug is primarily known to increase heart rate?

Accepted Answer

Isoprenaline

Answer

Phenylephrine

Answer

Noradrenaline

Answer

Adrenaline

Question 6

What is the primary process involved in Wallerian degeneration?

Accepted Answer

Nerve degeneration

Answer

Muscle degeneration

Answer

Nerve regeneration

Answer

Muscle regeneration

Question 7

Mechanism of secretion of ammonia in distal tubule is?

Accepted Answer

Passive diffusion

Answer

Primary active transport

Answer

Symport

Answer

Antiport

Question 8

Vibrations are detected by which types of receptors?

Accepted Answer

Rapidly adapting

Answer

Slowly adapting

Answer

Non-adapting

Answer

None of the above

Question 9

Inhibition of heart by vagus is mediated by which receptors?

Accepted Answer

M2

Answer

M1

Answer

NN

Answer

NM

Question 10

Which of the following statements is true regarding smooth muscle contraction?

Accepted Answer

Phosphorylation of myosin is essential for contraction.

Answer

None of the options.

Answer

Calmodulin plays no role in smooth muscle contraction.

Answer

Troponin plays a significant role in smooth muscle contraction.

NEET-PG 2015

Anatomy

Biochemistry

Pathology

Pharmacology

Physiology