NEET-PG 2012 Practice Questions

Q: Which of the following is NOT an anterior relation of the right kidney?

4th part of duodenum. ***4th part of duodenum*** - The **4th part of the duodenum** is located to the **left of the vertebral column** and is related to the **left kidney**, not the right kidney. - This segment passes superiorly along the left side of the aorta to become continuous with the jejunum at the duodenojejunal flexure. *Liver* - The **right kidney's superior part** is in direct contact with the **right lobe of the liver**, often separated only by the peritoneum [1]. - This is a significant anterior relation, explaining why liver enlargement can sometimes displace the right kidney. *Hepatic flexure* - The **hepatic flexure** (right colic flexure) of the colon lies immediately inferior to the liver and anterior to the **lower part of the right kidney**. - This anatomical relationship means that the right kidney can be affected by diseases of the colon in this region. *2nd part of duodenum* - The **descending (2nd) part of the duodenum** lies anterior to the **hilum and medial part of the right kidney** [1]. - Its retroperitoneal position places it in close proximity to the renal structures, making it a key anterior relation.

Q: Glucose is converted to glucuronate by which process?

Oxidation of the terminal alcohol group. ***Oxidation of the terminal alcohol group*** - **Glucuronate** is formed by the **oxidation of the C-6 carbon** (the terminal primary alcohol group) of glucose. - This process is crucial for the detoxification of various substances in the body, as glucuronate is a key component in **glucuronidation reactions**. *Oxidation of aldehyde group* - Oxidation of the **aldehyde group (C-1)** of glucose typically forms **gluconic acid**, not glucuronate. - Gluconate is derived from the oxidation of the first carbon, while glucuronate is derived from the oxidation of the last carbon. *Oxidation of both* - If both the aldehyde group (C-1) and the terminal alcohol group (C-6) of glucose were oxidized, it would result in the formation of **glucaric acid** (saccharic acid), not glucuronate. - Glucaric acid has two carboxyl groups, one at each end of the molecule. *None of the options* - This option is incorrect because the specific biochemical pathway for glucuronate formation involves the oxidation of the terminal alcohol group. - The conversion of glucose to glucuronate is a well-established metabolic process.

Q: Km value is defined as:

Substrate concentration at Vmax/2. ***Substrate concentration at Vmax/2*** - The **Michaelis constant (Km)** is defined as the **substrate concentration** at which the reaction velocity is **half of the maximum velocity (Vmax/2)**. - It reflects the **affinity of an enzyme for its substrate**; a lower Km indicates higher affinity. *Substrate concentration at which reaction rate is maximum* - The **maximum reaction rate (Vmax)** is achieved when the enzyme is **saturated with substrate**, meaning all active sites are occupied. - Km specifically refers to the substrate concentration needed to reach **half of this maximum rate**, not the maximum rate itself. *Substrate concentration at Vmax* - At **Vmax**, the enzyme is fully saturated with substrate, and the reaction rate cannot increase further by adding more substrate. - The **Km value** is a measure related to the **efficiency of substrate binding** at conditions below saturation, specifically at half Vmax. *Substrate concentration at which enzyme activity is optimal* - **Optimal enzyme activity** is generally influenced by factors such as **pH and temperature**, which affect the enzyme's structure and catalytic efficiency. - Km is specifically related to the **substrate concentration** required to achieve a specific reaction rate, not the overall optimal environmental conditions for the enzyme.

Q: Which of the following is monoenoic acid ?

Oleic acid. ***Oleic acid*** - **Oleic acid** is a **monounsaturated fatty acid** (MUFA), meaning it has **one double bond** in its hydrocarbon chain. - Its presence in many natural fats and oils makes it a significant component of the human diet. *Arachidonic acid* - **Arachidonic acid** is a **polyunsaturated fatty acid** (PUFA) containing **four double bonds**. - It is a precursor for **eicosanoids**, including prostaglandins and leukotrienes, involved in inflammation and other physiological processes. *Linoleic acid* - **Linoleic acid** is an **essential omega-6 polyunsaturated fatty acid** with **two double bonds**. - It is crucial for human health and serves as a precursor for other fatty acids like arachidonic acid. *Linolenic acid* - **Linolenic acid** refers to two essential fatty acids: **alpha-linolenic acid (ALA)**, an omega-3 fatty acid with **three double bonds**, and **gamma-linolenic acid (GLA)**, an omega-6 fatty acid also with three double bonds. - Both are **polyunsaturated fatty acids** with multiple double bonds.

Q: What is the primary function of reverse transcription?

Synthesis of DNA from an RNA template. ***Synthesis of DNA from an RNA template*** - **Reverse transcription** is catalyzed by the enzyme **reverse transcriptase**, which uses an **RNA template** to synthesize a complementary DNA (cDNA) strand. - This process is fundamental in the life cycle of **retroviruses** like HIV, allowing them to integrate their genetic material into the host genome. *Synthesis of RNA from a DNA template* - This process is known as **transcription**, where genetic information is copied from **DNA to RNA**, not the reverse. - It is a key step in gene expression, leading to the production of various types of RNA molecules. *Synthesis of DNA from a DNA template* - This describes **DNA replication**, the process by which DNA makes copies of itself, ensuring genetic continuity during cell division. - It involves enzymes like **DNA polymerase** and creates two identical DNA molecules from one original DNA molecule. *Synthesis of RNA from an RNA template* - This process is known as **RNA replication** and is characteristic of certain **RNA viruses** (e.g., influenza virus), where RNA serves as both the template and the genetic material. - It involves an enzyme called **RNA-dependent RNA polymerase**.

Q: Which enzyme catalyzes the rate limiting step in the TCA cycle?

α-ketoglutarate dehydrogenase. **α-ketoglutarate dehydrogenase** - The **α-ketoglutarate dehydrogenase complex** catalyzes the oxidative decarboxylation of α-ketoglutarate to succinyl-CoA, producing NADH and CO2. - This step is a **major control point** in the TCA cycle and is highly regulated by: - **Product inhibition**: Succinyl-CoA and NADH - **Calcium ions**: Activate the enzyme - Along with isocitrate dehydrogenase and citrate synthase, it represents one of the three key regulatory enzymes of the TCA cycle. *Fumarase* - **Fumarase** catalyzes the reversible hydration of fumarate to L-malate. - This enzyme is **not a regulatory step** in the TCA cycle; its activity is typically high and not a control point for the overall flux of the cycle. *Aconitase* - **Aconitase** catalyzes the reversible isomerization of citrate to isocitrate, via the intermediate cis-aconitate. - While important for the cycle's progression, aconitase activity is **not considered a rate-limiting step** for the overall regulation of the TCA cycle. *Thiokinase* - The term **thiokinase** (or succinyl-CoA synthetase) catalyzes the reversible conversion of succinyl-CoA to succinate, coupled with GTP/ATP production. - This enzyme is responsible for **substrate-level phosphorylation** in the TCA cycle but does not represent a primary regulatory or rate-limiting step.

Q: Which enzyme is deficient in Isovaleric acidemia?

Isovaleryl CoA dehydrogenase. ***Isovaleryl CoA dehydrogenase*** - **Isovaleric acidemia** is an **autosomal recessive** metabolic disorder caused by a deficiency in the enzyme **isovaleryl-CoA dehydrogenase** - This enzyme is crucial for the metabolism of **leucine**, a branched-chain amino acid, leading to the accumulation of toxic byproducts like **isovaleryl-CoA** and **isovaleric acid** - Characteristic **sweaty feet odor** due to isovaleric acid accumulation *Phenylalanine hydroxylase* - A deficiency in **phenylalanine hydroxylase** is responsible for **phenylketonuria (PKU)**, a different metabolic disorder involving the metabolism of **phenylalanine** - This enzyme converts **phenylalanine to tyrosine**, and its deficiency leads to the accumulation of phenylalanine and its metabolites, causing neurological damage if untreated *Arginase* - A deficiency in **arginase** causes **argininemia (hyperargininemia)**, which is a disorder of the **urea cycle** - This enzyme converts **arginine into urea and ornithine**, and its deficiency leads to the buildup of arginine and ammonia in the blood, causing neurological symptoms and developmental delay *Methylmalonyl CoA mutase* - A deficiency in **methylmalonyl CoA mutase** causes **methylmalonic acidemia**, another organic acidemia distinct from isovaleric acidemia - This disorder involves **propionate metabolism** and can present with metabolic acidosis, but affects a different metabolic pathway than leucine catabolism

Q: Neonatal tyrosinemia is due to deficiency of which enzyme?

Hydroxyphenyl pyruvate hydroxylase. ***Hydroxyphenyl pyruvate hydroxylase*** - **Neonatal (transient) tyrosinemia** is caused by delayed maturation or deficiency of **hydroxyphenylpyruvate hydroxylase** (also called 4-hydroxyphenylpyruvate dioxygenase or HPPD). - This enzyme converts 4-hydroxyphenylpyruvate to homogentisic acid in tyrosine catabolism. - Common in **premature infants** and newborns, leading to elevated tyrosine levels in blood. - The condition is **benign and self-limiting**, usually resolving with **vitamin C supplementation** or as the enzyme matures. - Note: Severe hereditary deficiency of this enzyme causes **tyrosinemia type III**, a distinct and rare disorder. *Fumarylacetoacetate hydroxylase* - Deficiency of **fumarylacetoacetate hydroxylase (FAH)** causes **tyrosinemia type I** (hepatorenal tyrosinemia), NOT neonatal tyrosinemia. - This is a severe hereditary disorder with liver failure, renal tubular dysfunction, and accumulation of toxic metabolites like succinylacetone. - Distinct from the benign transient neonatal form. *Tyrosine transaminase* - Deficiency of **tyrosine transaminase** (tyrosine aminotransferase) causes **tyrosinemia type II** (Richner-Hanhart syndrome). - Presents with corneal ulcers, palmoplantar hyperkeratosis, and sometimes intellectual disability. *Tyrosinase* - Deficiency of **tyrosinase** causes **albinism**, characterized by lack of melanin pigment in skin, hair, and eyes. - Not involved in tyrosine catabolism but in melanin synthesis.

Q: The cofactor vitamin B12 is required for the following conversion:

Methyl malonyl CoA to succinyl CoA. ***Methyl malonyl CoA to succinyl CoA*** - **Vitamin B12**, in its active form **adenosylcobalamin**, is a crucial cofactor for the enzyme **methylmalonyl-CoA mutase**, which catalyzes the isomerization of **methylmalonyl-CoA to succinyl-CoA**. - This conversion is vital for the metabolism of **odd-chain fatty acids** and certain **amino acids**, allowing their entry into the **Krebs cycle**. *Dopamine to Norepinephrine* - This conversion is catalyzed by **dopamine beta-hydroxylase**, which requires **vitamin C** (ascorbate) and **copper** as cofactors, not vitamin B12. - It is a key step in the synthesis of **catecholamines** within the nervous system. *Propionyl CoA to methyl malonyl CoA* - This conversion is catalyzed by **propionyl-CoA carboxylase** and requires **biotin** as a cofactor, not vitamin B12. - This reaction is the first step in the metabolic pathway that leads to succinyl-CoA from odd-chain fatty acids. *Homocysteine to cysteine* - This conversion occurs via the **transsulfuration pathway** and requires **vitamin B6** (pyridoxal phosphate) as a cofactor, not vitamin B12. - The enzymes involved are **cystathionine β-synthase** and **cystathionine γ-lyase**, both B6-dependent. - Vitamin B12 is involved in the **remethylation** of homocysteine to methionine (not in transsulfuration to cysteine).

Q: Which type of fatty acids should be included in the diet to manage chyluria?

Medium-chain fatty acids. ***Medium-chain fatty acids*** - **Medium-chain fatty acids (MCFAs)** are absorbed directly into the **portal circulation** without being re-esterified to triglycerides or incorporated into chylomicrons [1]. This helps bypass the compromised lymphatic system. - In **chyluria**, the lymphatic system's integrity is disrupted, leading to leakage of **chyle** (lymphatic fluid rich in chylomicrons) into the urinary tract. MCFAs provide a source of fat that does not rely on the lymphatic pathway for transport [1]. *Short-chain fatty acids* - **Short-chain fatty acids (SCFAs)** are primarily produced by bacterial fermentation in the colon and are absorbed directly into the portal circulation. - While they do not rely on the lymphatic system, their dietary contribution as a significant energy source is limited, and they are not the primary fat source for patients with chyluria. *Long-chain fatty acids* - **Long-chain fatty acids (LCFAs)** are absorbed with the help of bile salts, re-esterified into triglycerides, and packaged into **chylomicrons** within the intestinal cells [2]. - These chylomicrons then enter the **lymphatic system** and eventually the bloodstream, which is precisely the pathway that is compromised in chyluria, making them unsuitable [2]. *Omega-3 fatty acids* - **Omega-3 fatty acids** are a type of **long-chain polyunsaturated fatty acid** that also follow the chylomicron-lymphatic pathway for absorption [3]. - While beneficial for other health aspects, they are not suitable for managing chyluria due to their reliance on the **lymphatic system** for transport, which is dysfunctional in this condition.

Question 1

Which of the following is NOT an anterior relation of the right kidney?

Accepted Answer

4th part of duodenum

Answer

Hepatic flexure

Answer

Liver

Answer

2nd part of duodenum

Question 2

Glucose is converted to glucuronate by which process?

Accepted Answer

Oxidation of the terminal alcohol group

Answer

Oxidation of aldehyde group

Answer

Oxidation of both

Answer

None of the options

Question 3

Km value is defined as:

Accepted Answer

Substrate concentration at Vmax/2

Answer

Substrate concentration at which reaction rate is maximum

Answer

Substrate concentration at Vmax

Answer

Substrate concentration at which enzyme activity is optimal

Question 4

Which of the following is monoenoic acid ?

Accepted Answer

Oleic acid

Answer

Linoleic acid

Answer

Linolenic acid

Answer

Arachidonic acid

Question 5

What is the primary function of reverse transcription?

Accepted Answer

Synthesis of DNA from an RNA template

Answer

Synthesis of RNA from a DNA template

Answer

Synthesis of DNA from a DNA template

Answer

Synthesis of RNA from an RNA template

Question 6

Which enzyme catalyzes the rate limiting step in the TCA cycle?

Accepted Answer

α-ketoglutarate dehydrogenase

Answer

Fumarase

Answer

Aconitase

Answer

Thiokinase

Question 7

Which enzyme is deficient in Isovaleric acidemia?

Accepted Answer

Isovaleryl CoA dehydrogenase

Answer

Phenylalanine hydroxylase

Answer

Arginase

Answer

Methylmalonyl CoA mutase

Question 8

Neonatal tyrosinemia is due to deficiency of which enzyme?

Accepted Answer

Hydroxyphenyl pyruvate hydroxylase

Answer

Tyrosine transaminase

Answer

Fumarylacetoacetate hydroxylase

Answer

Tyrosinase

Question 9

The cofactor vitamin B12 is required for the following conversion:

Accepted Answer

Methyl malonyl CoA to succinyl CoA

Answer

Dopamine to Norepinephrine

Answer

Propionyl CoA to methyl malonyl CoA

Answer

Homocysteine to cysteine

Question 10

Which type of fatty acids should be included in the diet to manage chyluria?

Accepted Answer

Medium-chain fatty acids

Answer

Short-chain fatty acids

Answer

Long-chain fatty acids

Answer

Omega-3 fatty acids

NEET-PG 2012

Anatomy

Biochemistry

Internal Medicine