NEET-PG 2017 Practice Questions

Q: Name the product marked as X in the image shown below:

Indolequinone. ***Indolequinone*** - The image depicts the **melanin biosynthesis pathway** starting from **tyrosine**. - Tyrosine is converted to **L-DOPA** by tyrosinase, which is then oxidized to **dopaquinone** (also called DOPA-quinone). - Dopaquinone undergoes intramolecular cyclization to form **leucodopachrome**, which is subsequently oxidized to **dopachrome**. - Dopachrome is then converted through a series of steps to **5,6-dihydroxyindole**, which is finally oxidized to **indole-5,6-quinone** (indolequinone). - **Indolequinone** is a key intermediate that polymerizes to form **melanin**, the pigment responsible for coloration in skin, hair, and eyes. - Based on the pathway shown, X represents indolequinone, an oxidized indole derivative in melanin synthesis. *Tetrabenazine* - **Tetrabenazine** is a pharmaceutical drug that inhibits **vesicular monoamine transporter 2 (VMAT2)**. - It is used therapeutically to treat hyperkinetic movement disorders such as **Huntington's disease** and tardive dyskinesia. - It is not a natural metabolic intermediate in the tyrosine-to-melanin biosynthetic pathway. *Homovanillic acid* - **Homovanillic acid (HVA)** is a major end metabolite of **dopamine** in the catecholamine degradation pathway. - It is formed by the sequential actions of **monoamine oxidase (MAO)** and **catechol-O-methyltransferase (COMT)** on dopamine. - This represents a completely different branch of tyrosine metabolism (catecholamine pathway), not the melanin synthesis pathway. *Kynurenine* - **Kynurenine** is an intermediate metabolite in the **kynurenine pathway**, which is the major route of **tryptophan** degradation. - The kynurenine pathway leads to the formation of NAD+ and various neuroactive metabolites. - This pathway is completely separate from tyrosine metabolism and is unrelated to the melanin synthesis pathway shown in the image.

Q: All are correct about the amino acid marked as X, EXCEPT:

Ketogenic. ***Correct Answer: Ketogenic*** ✓ - Histidine is **purely glucogenic**, NOT ketogenic - Its carbon skeleton is converted to α-ketoglutarate (a TCA cycle intermediate), which can be used for gluconeogenesis - It does NOT produce acetyl-CoA or acetoacetate (ketone body precursors) - **This statement is FALSE, making it the correct answer for this EXCEPT question** *Incorrect: Maximum buffering action* - This statement is TRUE (so not the answer) - Histidine contains an **imidazole ring** with pKa ~6.0, close to physiological pH - Provides crucial **buffering capacity** in blood and tissues - Most effective amino acid buffer at physiological pH *Incorrect: Contributes to one carbon pool* - This statement is TRUE (so not the answer) - Histidine breakdown produces **Formimino glutamic acid (FIGLU)** - FIGLU donates its formimino group to **Tetrahydrofolate (THF)** - Contributes to the **one-carbon pool** essential for biosynthetic pathways *Incorrect: Excess amount leads to mental retardation* - This statement is TRUE (so not the answer) - **Histidinemia** results from histidase enzyme deficiency - Elevated histidine levels can be associated with **developmental delays and speech defects** in some cases - Though many affected individuals remain asymptomatic

Q: Name the plot dealing with kinetics of enzyme inhibition?

Dixon plot. ***Dixon plot*** - The **Dixon plot** is specifically used to determine the type of enzyme inhibition and to calculate the **inhibition constant (Ki)**. - It plots the reciprocal reaction velocity (1/V) against the **inhibitor concentration ([I])** at different substrate concentrations. *Donnan-Gibbs equation plot* - The **Donnan-Gibbs equation** describes the distribution of charged particles across a semi-permeable membrane at equilibrium. - It is irrelevant to enzyme kinetics or inhibition. *Lineweaver-Burk plot* - While the Lineweaver-Burk plot is used in enzyme kinetics to determine **Km** and **Vmax** and analyze inhibition, it plots **1/V against 1/[S]**. - The image provided, showing 1/V against [I], is characteristic of a Dixon plot, not a Lineweaver-Burk plot which plots 1/V against 1/[S]. *Hanes-Woolf plot* - The **Hanes-Woolf plot** is another linearization of the Michaelis-Menten equation, plotting **[S]/V against [S]**. - Like the Lineweaver-Burk plot, it is used for analyzing general enzyme kinetics but not specifically for determining Ki from varying inhibitor concentrations in the manner shown.

Q: Which enzyme marked as $X$ is missing in synthesis of vitamin $D_{3}$ ?

17-alpha-hydroxylase. ***17-alpha-hydroxylase*** - The diagram illustrates the synthesis of **vitamin D3**, which involves hydroxylation steps at positions C-25 in the liver and C-1 in the kidneys. These are catalyzed by **25-hydroxylase** and **1-alpha-hydroxylase**, respectively. - **17-alpha-hydroxylase** is involved in the synthesis of steroid hormones (like cortisol, androgens, and estrogens) from cholesterol, not in the synthesis or metabolism of vitamin D3; therefore, its absence would not be relevant to vitamin D synthesis. *3-beta-hydroxylase* - **3-beta-hydroxysteroid dehydrogenase** is crucial for the synthesis of all steroid hormones, converting delta-5-3-hydroxysteroids to delta-4-3-ketosteroids. - Its presence is essential for **steroidogenesis**, but it does not play a direct role in the specific hydroxylation steps for vitamin D activation. *21-hydroxylase* - **21-hydroxylase** is an enzyme involved in the synthesis of steroid hormones such as cortisol and aldosterone from progesterone and 17-hydroxyprogesterone. - Deficiency of this enzyme leads to **congenital adrenal hyperplasia**, a condition unrelated to vitamin D metabolism. *24-hydroxylase* - **24-hydroxylase** is responsible for the inactivation of vitamin D metabolites by adding a hydroxyl group at position C-24, leading to degradation. - This enzyme is part of the **catabolic pathway** to regulate vitamin D levels, rather than being a missing enzyme in the primary synthesis of active vitamin D.

Q: The following reaction occurs in which part of kidney?

Proximal convoluted tubule. **Proximal convoluted tubule** - The image shows the conversion of 25-hydroxycholecalciferol to **1,25 (OH)₂-D₃**, also known as calcitriol, via the enzyme **1α-hydroxylase**. - This critical hydroxylation reaction, occurring primarily in the **proximal convoluted tubule** cells of the kidney, produces the biologically active form of vitamin D. *Distal convoluted tubule* - The distal convoluted tubule is primarily involved in **fine-tuning** water and electrolyte reabsorption, influenced by hormones like aldosterone and antidiuretic hormone. - It does not contain the necessary enzymes, specifically **1α-hydroxylase**, for the final activation step of vitamin D. *Loop of Henle* - The loop of Henle's main function is to create a **medullary osmotic gradient** through countercurrent multiplication, crucial for concentrating urine. - It plays no significant role in the **hydroxylation of vitamin D** precursors. *Collecting duct* - The collecting duct is responsible for final adjustments to urine volume and concentration, largely under the influence of **antidiuretic hormone**. - It lacks the **enzymatic machinery** (1α-hydroxylase) required for the activation of vitamin D.

Q: Name the antigen marked as X determining blood group A.

N-Acetyl-Galactosamine. ***N-Acetyl-Galactosamine*** - Blood group A antigens are formed by the addition of **N-acetylgalactosamine** to the H antigen precursor molecule on the surface of red blood cells. - This sugar modification is catalyzed by the **A transferase enzyme**, which is specific for N-acetylgalactosamine. *N-Acetyl-Glucosamine* - While N-acetylglucosamine is a component of many glycans, it is not the terminal sugar that defines the **blood group A antigen**. - **N-acetylglucosamine** is a key building block for the H antigen and other blood group precursors, but not the specific modifying sugar for A. *Dermatan sulphate* - **Dermatan sulfate** is a **glycosaminoglycan** primarily found in connective tissues, skin, and blood vessels. - It plays a role in wound healing and coagulation, but is not involved in **ABO blood group determination**. *Keratan sulfate* - **Keratan sulfate** is another **glycosaminoglycan** found in cartilage, cornea, and bone. - It contributes to tissue hydration and structural integrity, but it is not part of the **ABO blood group antigens**.

Q: Which of the following will occur on efferent arteriolar constriction?

Increased GFR. ***Increased GFR*** - **Efferent arteriolar constriction** increases resistance to blood flow out of the glomerulus, causing blood to 'back up' and increase the **glomerular hydrostatic pressure (PGC)** - Higher **glomerular hydrostatic pressure** leads to increased net filtration pressure, which directly results in **increased glomerular filtration rate (GFR)** - This is the **primary and most clinically significant effect** of efferent arteriolar constriction - The increased PGC helps maintain GFR even when renal blood flow decreases slightly *Decreased GFR* - This is incorrect because **efferent arteriolar constriction** increases glomerular hydrostatic pressure, thereby **increasing GFR**, not decreasing it - Only severe efferent constriction that critically reduces renal plasma flow would eventually decrease GFR - The immediate and primary effect is always an increase in GFR *Increase flow in vasa recta* - This is incorrect; **efferent arteriolar constriction** actually **decreases** flow to the vasa recta - The constriction reduces blood flow exiting the glomerulus, which means less blood reaches the downstream peritubular capillaries and vasa recta - This decreased perfusion of the vasa recta can enhance urine concentration by reducing washout of the medullary concentration gradient *Decreased flow in vasa recta* - While this is physiologically true (efferent constriction does reduce peritubular and vasa recta blood flow), it is **not the primary or most significant effect** being tested - In the context of efferent arteriolar constriction, the **increased GFR** is the dominant and most clinically relevant consequence - The question asks "which will occur" expecting the primary hemodynamic effect on glomerular function - Decreased vasa recta flow is a secondary consequence, whereas increased GFR is the direct and immediate result

Q: The A wave in His bundle electrogram shows presence of:

Atrial depolarization. ***Atrial depolarization*** - The **A wave** in a His bundle electrogram represents the electrical activity corresponding to **atrial depolarization**. This is the first electrical event recorded prior to ventricular activation. - It signifies the activation of the atria, preceding the impulse transmission through the AV node and His bundle. *Atrial repolarization* - **Atrial repolarization** is generally not clearly visible as a distinct wave in a His bundle electrogram, as its electrical signal is usually small and often obscured by the much larger QRS complex from ventricular depolarization. - The T-wave on a surface ECG corresponds to ventricular repolarization, and there isn't a directly analogous, easily identifiable wave for atrial repolarization in standard His bundle recordings. *AV node activation* - **AV node activation** itself is a slow electrical process that does not generate a distinct, sharply defined wave in the His bundle electrogram. - The time taken for conduction through the AV node is represented by the **AH interval**, which is the duration between the A wave (atrial activation) and the H wave (His bundle activation). *Atrial depolarization to AV node activation* - This option describes a **duration or interval**, specifically the **AH interval**, which reflects the time from the beginning of atrial activation (A wave) to the beginning of His bundle activation (H wave) and primarily represents AV nodal conduction. - The A wave itself signifies a specific electrical event (**atrial depolarization**), not the entire period from atrial depolarization up to AV node activation.

Q: Which of the following is correct about the pressure volume loop of left ventricle?

Aortic valve opens at 2. ***Aortic valve opens at 2*** - Point 2 marks the moment when **left ventricular pressure exceeds aortic pressure**, causing the aortic valve to open. - This is the transition point between **isovolumetric contraction** (1→2) and **ventricular ejection** (2→3). - From point 2 onwards, blood is actively ejected from the left ventricle into the aorta during **systole**. *1 to 2 indicates isovolumetric relaxation* - The phase from point 1 to point 2 shows an increase in **pressure at constant volume**, which represents **isovolumetric contraction**, not relaxation. - During **isovolumetric contraction**, both the mitral and aortic valves are closed, and the ventricle contracts without changing volume, building up pressure. - **Isovolumetric relaxation** occurs from point 3 to point 4, where pressure drops at constant volume after the aortic valve closes. *2 to 3 indicates ventricular diastole* - The period from point 2 to point 3 represents **ventricular ejection**, which is part of **ventricular systole**, not diastole. - During this phase, the aortic valve is open, and blood is being ejected from the left ventricle into the aorta while ventricular volume decreases. - **Ventricular diastole** includes isovolumetric relaxation (3→4) and ventricular filling (4→1). *Pulmonic valve opens at 3* - Point 3 represents the **closure of the aortic valve** at the end of ventricular ejection, not its opening. - The **pulmonic valve** is part of the right ventricular circuit, not the left ventricle; it opens during right ventricular ejection into the pulmonary artery. - This question specifically addresses the **left ventricular** pressure-volume loop.

Question 1

What is incorrect about the shown basement membrane?

Accepted Answer

Only molecules which are larger than 50,000 Daltons can traverse the filtration barrier

Answer

Part of filtration barrier

Answer

Stained with PAS

Answer

It has Lamina Densa and Lamina Rara

Question 2

Name the product marked as X in the image shown below:

Accepted Answer

Indolequinone

Answer

Tetrabenazine

Answer

Homovanillic acid

Answer

Kynurenine

Question 3

All are correct about the amino acid marked as X, EXCEPT:

Accepted Answer

Ketogenic

Answer

Maximum buffering action

Answer

Contributes to one carbon pool

Answer

Excess amount leads to mental retardation

Question 4

Name the plot dealing with kinetics of enzyme inhibition?

Accepted Answer

Dixon plot

Answer

Donnan-Gibbs equation plot

Answer

Lineweaver-Burk plot

Answer

Hanes-Woolf plot

Question 5

Which enzyme marked as $X$ is missing in synthesis of vitamin $D_{3}$ ?

Accepted Answer

17-alpha-hydroxylase

Answer

3-beta-hydroxylase

Answer

21-hydroxylase

Answer

24-hydroxylase

Question 6

The following reaction occurs in which part of kidney?

Accepted Answer

Proximal convoluted tubule

Answer

Distal convoluted tubule

Answer

Loop of Henle

Answer

Collecting duct

Question 7

Name the antigen marked as X determining blood group A.

Accepted Answer

N-Acetyl-Galactosamine

Answer

N-Acetyl-Glucosamine

Answer

Dermatan sulphate

Answer

Keratan sulfate

Question 8

Which of the following will occur on efferent arteriolar constriction?

Accepted Answer

Increased GFR

Answer

Decreased GFR

Answer

Increase flow in vasa recta

Answer

Decreased flow in vasa recta

Question 9

The A wave in His bundle electrogram shows presence of:

Accepted Answer

Atrial depolarization

Answer

Atrial repolarization

Answer

AV node activation

Answer

Atrial depolarization to AV node activation

Question 10

Which of the following is correct about the pressure volume loop of left ventricle?

Accepted Answer

Aortic valve opens at 2

Answer

1 to 2 indicates isovolumetric relaxation

Answer

2 to 3 indicates ventricular diastole

Answer

Pulmonic valve opens at 3

NEET-PG 2017

Anatomy

Biochemistry

Physiology