Anatomy
1 questionsWhat is incorrect about the shown basement membrane?
NEET-PG 2017 - Anatomy NEET-PG Practice Questions and MCQs
Question 321: What is incorrect about the shown basement membrane?
- A. Part of filtration barrier
- B. Only molecules which are larger than 50,000 Daltons can traverse the filtration barrier (Correct Answer)
- C. Stained with PAS
- D. It has Lamina Densa and Lamina Rara
Explanation: ***Only molecules which are larger than 50,000 Daltons can traverse the filtration barrier*** - This statement is **incorrect**. The **glomerular filtration barrier** is highly selective and allows molecules **smaller than 70,000 Daltons** to pass through, not larger ones. - The filtration barrier primarily restricts molecules **larger than 70 kDa** and maintains selectivity based on size and charge, preventing passage of most plasma proteins like **albumin**. *Part of filtration barrier* - The **glomerular basement membrane (GBM)** is indeed a crucial component of the **renal filtration barrier**, situated between the fenestrated endothelium and the podocytes. - It plays a vital role in selectively filtering plasma, preventing the passage of large molecules and negatively charged proteins into Bowman's capsule. - This is a **correct statement**. *Stained with PAS* - The **glomerular basement membrane** is rich in **glycoproteins** and **proteoglycans**, which are carbohydrates that stain intensely with **Periodic Acid-Schiff (PAS)** stain. - This staining property helps in visualizing the basement membrane in histological sections and diagnosing certain kidney diseases. - This is a **correct statement**. *It has Lamina Densa and Lamina Rara* - The **glomerular basement membrane** has a trilaminar structure consisting of **lamina rara externa**, **lamina densa** (central dense layer), and **lamina rara interna**. - The **lamina densa** provides structural support and size-based filtration, while the **lamina rara** layers contain proteoglycans that contribute to charge selectivity. - This is a **correct statement**.
Biochemistry
6 questionsA patient reports a change in colour of urine on air exposure. All are true about the condition shown below except:
All are correct about the amino acid marked as X, EXCEPT:
Name the plot dealing with kinetics of enzyme inhibition?
Which enzyme marked as $X$ is missing in synthesis of vitamin $D_{3}$ ?
The following reaction occurs in which part of kidney?
Name the antigen marked as X determining blood group A.
NEET-PG 2017 - Biochemistry NEET-PG Practice Questions and MCQs
Question 321: A patient reports a change in colour of urine on air exposure. All are true about the condition shown below except:
- A. Blackening of urine is accelerated on exposure to sunlight
- B. Alkaptone bodies are deposited in intervertebral disc
- C. Urine Benedict's test is negative (Correct Answer)
- D. The condition is caused by deficiency of homogentisate 1,2-dioxygenase
Explanation: ***Urine Benedict's test is negative*** - This is FALSE - Benedict's test is actually **POSITIVE** in alkaptonuria because **homogentisic acid** is a reducing agent. - Homogentisic acid readily **reduces Benedict's reagent**, giving a positive test result in alkaptonuria patients. *Blackening of urine is accelerated on exposure to sunlight* - This is TRUE - **UV light** and sunlight accelerate the **oxidation of homogentisic acid** in urine. - The characteristic **dark discoloration** occurs more rapidly when exposed to light and air. *Alkaptone bodies are deposited in intervertebral disc* - This is TRUE - **Homogentisic acid (alkaptone bodies)** polymerizes to form **ochronotic pigment** deposits. - These deposits accumulate in **cartilage** including intervertebral discs, causing degenerative changes and spondylosis. *The condition is caused by deficiency of homogentisate 1,2-dioxygenase* - This is TRUE - Alkaptonuria is caused by deficiency of **homogentisate 1,2-dioxygenase** enzyme in the **tyrosine metabolic pathway**. - This enzyme deficiency leads to accumulation of **homogentisic acid** in blood and urine, causing the characteristic symptoms.
Question 322: All are correct about the amino acid marked as X, EXCEPT:
- A. Maximum buffering action
- B. Ketogenic (Correct Answer)
- C. Contributes to one carbon pool
- D. Excess amount leads to mental retardation
Explanation: ***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
Question 323: Name the plot dealing with kinetics of enzyme inhibition?
- A. Donnan-Gibbs equation plot
- B. Lineweaver-Burk plot
- C. Dixon plot (Correct Answer)
- D. Hanes-Woolf plot
Explanation: ***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.
Question 324: Which enzyme marked as $X$ is missing in synthesis of vitamin $D_{3}$ ?
- A. 3-beta-hydroxylase
- B. 17-alpha-hydroxylase (Correct Answer)
- C. 21-hydroxylase
- D. 24-hydroxylase
Explanation: ***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.
Question 325: The following reaction occurs in which part of kidney?
- A. Proximal convoluted tubule (Correct Answer)
- B. Distal convoluted tubule
- C. Loop of Henle
- D. Collecting duct
Explanation: **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.
Question 326: Name the antigen marked as X determining blood group A.
- A. N-Acetyl-Glucosamine
- B. Dermatan sulphate
- C. Keratan sulfate
- D. N-Acetyl-Galactosamine (Correct Answer)
Explanation: ***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**.
Physiology
3 questionsName the product marked as X in the image shown below:
Which of the following will occur on efferent arteriolar constriction?
The A wave in His bundle electrogram shows presence of:
NEET-PG 2017 - Physiology NEET-PG Practice Questions and MCQs
Question 321: Name the product marked as X in the image shown below:
- A. Indolequinone (Correct Answer)
- B. Tetrabenazine
- C. Homovanillic acid
- D. Kynurenine
Explanation: ***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.
Question 322: Which of the following will occur on efferent arteriolar constriction?
- A. Increased GFR (Correct Answer)
- B. Decreased GFR
- C. Increase flow in vasa recta
- D. Decreased flow in vasa recta
Explanation: ***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
Question 323: The A wave in His bundle electrogram shows presence of:
- A. Atrial depolarization (Correct Answer)
- B. Atrial repolarization
- C. AV node activation
- D. Atrial depolarization to AV node activation
Explanation: ***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.