NEET-PG 2019 - Biochemistry Practice Questions

Q: In patients with Retinitis pigmentosa, which of the following substances is known to have decreased levels?

Docosahexaenoic acid (DHA). ***Docosahexaenoic acid (DHA)*** - **Docosahexaenoic acid (DHA)** is a crucial **omega-3 fatty acid** abundantly found in the **photoreceptor cell membranes**, particularly in the retina. - Reduced levels of DHA are frequently observed in patients with **retinitis pigmentosa**, suggesting its role in disease pathogenesis and retinal health. *Arachidonic acid* - **Arachidonic acid** is an **omega-6 fatty acid** and a precursor to many signaling molecules, but its levels are **not typically decreased** in retinitis pigmentosa. - It plays a **pro-inflammatory role** and is involved in various physiological processes, distinct from the primary metabolic defects in retinitis pigmentosa. *Linoleic acid* - **Linoleic acid** is an essential **omega-6 fatty acid** and a precursor to arachidonic acid, but its deficiencies are not characteristic of retinitis pigmentosa. - It is crucial for **skin barrier function** and overall health, but its metabolic pathways are distinct from those primarily affected in retinal degenerations. *Thromboxane* - **Thromboxane** is a **lipid mediator** primarily involved in **platelet aggregation** and vasoconstriction. - It is not directly associated with the metabolic pathways or structural integrity of the retina, and its levels are not typically altered in retinitis pigmentosa.

Q: In case of LPL deficiency, which of the following will increase after a fat rich diet?

Chylomicron. ***Chylomicron*** - **LPL (lipoprotein lipase)** is crucial for the breakdown of **chylomicrons** and VLDL. A deficiency leads to an accumulation of undigested chylomicrons in the bloodstream after a fat-rich meal. - **Chylomicrons** transport dietary triglycerides from the intestines to tissues. Without LPL, these triglycerides remain packaged in chylomicrons. *LDL* - **LDL (low-density lipoprotein)** levels are not directly increased by a short-term fat-rich diet in the context of LPL deficiency. LDL primarily carries cholesterol and is formed from VLDL remnants, a process that is also impaired by LPL deficiency indirectly. - While chronic LPL deficiency can affect overall lipid metabolism, the immediate post-meal increase is not in LDL but in triglyceride-rich lipoproteins. *HDL* - **HDL (high-density lipoprotein)** is involved in reverse cholesterol transport and is generally not directly increased after a fat-rich diet, especially in LPL deficiency. - In fact, severe hypertriglyceridemia, often seen in LPL deficiency, can sometimes lead to lower HDL levels due to altered lipid exchange. *Lipoprotein (a)* - **Lipoprotein (a)**, or Lp(a), is a genetically determined lipoprotein similar to LDL but with an added apolipoprotein (a) and its levels are not acutely affected by dietary fat intake or LPL deficiency. - Lp(a) levels are determined primarily by genetic factors and do not participate in the post-prandial handling of dietary fats.

Q: True regarding mitochondrial DNA is:

Inherited from mother. ***Inherited from mother*** - **Mitochondrial DNA (mtDNA)** is exclusively inherited from the mother because the sperm's mitochondria are typically destroyed after fertilization or do not enter the oocyte. - This **maternal inheritance pattern** makes mtDNA useful for tracing lineage and studying human population movements. *Linear double stranded* - **Mitochondrial DNA** is typically **circular**, not linear, and double-stranded, similar to a plasmid in bacteria. - **Linear DNA** is characteristic of nuclear chromosomes in eukaryotes. *All respiratory proteins are synthesized within mitochondria itself* - While mitochondria contain their own ribosomes and synthesize some proteins, the majority of **respiratory chain proteins** are encoded by **nuclear DNA** and imported into the mitochondria. - The **mitochondrial genome** encodes only a small fraction of the proteins necessary for mitochondrial function, primarily components of the electron transport chain. *Low mutation rate* - **Mitochondrial DNA** has a **higher mutation rate** compared to nuclear DNA due to a less robust DNA repair system and exposure to reactive oxygen species generated during oxidative phosphorylation. - The high mutation rate can contribute to mitochondrial diseases and can also be used in evolutionary studies.

Q: Retinitis pigmentosa is associated with deficiency of:

DHA. ***DHA*** - **Docosahexaenoic acid (DHA)** is the major polyunsaturated fatty acid in the **retinal photoreceptor outer segments** and is crucial for their function. - Deficiency in DHA has been linked to several retinal degeneration disorders, including **retinitis pigmentosa**, suggesting its importance in maintaining retinal health. *Timnodonic acid* - This is an older term for **eicosapentaenoic acid (EPA)**, which is an omega-3 fatty acid. - While EPA is beneficial for overall health, it is **not the primary fatty acid** associated with the direct structural and functional health of retinal photoreceptors as DHA is. *Eicosa pentaenoic acid* - **Eicosapentaenoic acid (EPA)** is an omega-3 fatty acid found in fish oil, known for its anti-inflammatory properties. - While important for general health, EPA is **not as abundant or critical for retinal structure and function** as DHA. *Arachidonic acid* - **Arachidonic acid (AA)** is an omega-6 fatty acid found in cell membranes and is a precursor to pro-inflammatory mediators. - While present in the retina, AA is generally **not associated with a protective or causative role in retinitis pigmentosa** in the same way DHA is.

Q: Amino acid required for conversion of norepinephrine to epinephrine:-

Methionine. ***Methionine*** - **Norepinephrine** is converted to **epinephrine** by the enzyme **phenylethanolamine N-methyltransferase (PNMT)**. - This enzyme uses **S-adenosylmethionine (SAM)** as a **methyl donor**, which is derived from methionine. *Lysine* - **Lysine** is an essential amino acid primarily involved in **protein synthesis**, **calcium absorption**, and the production of **carnitine**. - It does not directly participate in the methylation reaction converting norepinephrine to epinephrine. *Tryptophan* - **Tryptophan** is a precursor for **serotonin** and **niacin** synthesis. - It is not involved in the catecholamine synthesis pathway from norepinephrine to epinephrine. *Phenylalanine* - **Phenylalanine** is the initial amino acid in the **catecholamine synthesis pathway**, being converted to **tyrosine**, then to DOPA, dopamine, and norepinephrine. - While it's crucial for the synthesis *up to* norepinephrine, it is not directly involved in the *conversion of norepinephrine to epinephrine*.

Q: Type-I hyperlipoproteinemia is caused by deficiency of:-

Lipoprotein lipase. ***Lipoprotein lipase*** - **Type I hyperlipoproteinemia**, also known as **familial lipoprotein lipase deficiency**, is caused by a genetic defect leading to **deficiency or defect in lipoprotein lipase (LPL)** or its cofactor **apolipoprotein C-II**. - LPL is crucial for the **hydrolysis of triglycerides** in chylomicrons and VLDL at the capillary endothelium. - This enzymatic deficiency leads to **massive accumulation of chylomicrons** and severe hypertriglyceridemia (often >1000 mg/dL). - Clinical features include **eruptive xanthomas, lipemia retinalis, hepatosplenomegaly**, and **recurrent pancreatitis**. *Elevated triglycerides in plasma* - This is indeed the **most prominent laboratory finding** in Type I hyperlipoproteinemia, with triglyceride levels often exceeding 1000-2000 mg/dL. - However, this is the **consequence/manifestation** of the LPL deficiency, not the underlying cause. - The question asks what causes Type I hyperlipoproteinemia, which is the enzyme deficiency itself. *Elevated LDL* - Type I hyperlipoproteinemia typically has **normal or even reduced LDL levels**. - **Elevated LDL** is characteristic of **Type IIa hyperlipoproteinemia (familial hypercholesterolemia)**, which involves defects in LDL receptor or ApoB-100. - Type I primarily affects **chylomicron metabolism**, not LDL. *Elevated cholesterol* - Cholesterol levels are typically **normal or only mildly elevated** in Type I hyperlipoproteinemia. - The triglyceride elevation is disproportionately massive compared to any cholesterol elevation. - Significant isolated cholesterol elevation points to Type IIa or IIb dyslipidemias.

Q: Mark the false statement regarding mitochondrial DNA:

Does not show heteroplasmy. ***Does not show heteroplasmy*** - This statement is false because **mitochondrial DNA (mtDNA)** commonly exhibits **heteroplasmy**, meaning the presence of more than one type of mitochondrial genome within a cell or individual. - **Heteroplasmy** arises due to the presence of both normal and mutated mtDNA, which can be passed down from the mother. *AGA and AGG are stop codons in mitochondrial DNA* - This statement is true; in the **universal genetic code**, AGA and AGG code for **arginine**, but in **human mitochondrial DNA**, they serve as **stop codons**. - This is an example of the **differences** in genetic code interpretation between the nuclear genome and the mitochondrial genome. *Kearns-Sayre Syndrome is a large deletion in mitochondrial DNA* - This statement is true; **Kearns-Sayre Syndrome** is a well-known mitochondrial disorder caused by a **large single deletion** in the mitochondrial DNA. - This deletion often leads to chronic progressive **external ophthalmoplegia**, **retinal pigmentary degeneration**, and **cardiac conduction defects**. *1% of cellular DNA, 13 proteins of respiratory chain* - This statement is true; **mitochondrial DNA constitutes** approximately **1% of the total cellular DNA** by mass. - It codes for **13 essential proteins** that are part of the **electron transport chain** (respiratory chain) complexes in the mitochondrion, along with ribosomal RNAs (rRNAs) and transfer RNAs (tRNAs).

Q: In type I diabetes, which of the following is the MOST characteristic metabolic change that distinguishes it from type II diabetes:-

Increased lipolysis. ***Increased lipolysis*** - In **type 1 diabetes** (T1D), there is an **absolute deficiency of insulin**, which is a potent **anti-lipolytic hormone**. [1] - This lack of insulin leads to unopposed **lipolysis**, resulting in increased free fatty acid (FFA) release, which can be metabolized into **ketone bodies** and contribute to **diabetic ketoacidosis (DKA)**. [2] *Increased protein catabolism* - While protein catabolism is increased in uncontrolled T1D due to the lack of insulin and increased counter-regulatory hormones, it is not the *most characteristic* metabolic change that clearly distinguishes it from type 2 diabetes (T2D), especially in early stages of T2D where some insulin may still be present. [1] - **Protein breakdown** produces amino acids for gluconeogenesis, contributing to hyperglycemia, but **lipolysis leading to ketosis** is more specific to severe insulin deficiency. [3] *Decreased glucose uptake* - **Decreased glucose uptake** by peripheral tissues (especially muscle and adipose tissue) is a characteristic feature of both T1D and T2D. [1] - In T1D, it's due to insulin deficiency, while in T2D, it's primarily caused by **insulin resistance**, making it less specific to distinguish T1D. *Increased hepatic glucose output* - **Increased hepatic glucose output** is a significant contributor to hyperglycemia in both T1D and T2D. [1] - In T1D, it's due to the lack of insulin's suppressive effect on the liver, whereas in T2D, it's due to **hepatic insulin resistance** and increased gluconeogenesis.

Q: Which amino acid is involved in the synthesis of creatinine, NO, and urea?

Arginine. ***Arginine*** - **Arginine** is a precursor for **Nitric Oxide (NO)** synthesis via **nitric oxide synthase**. - It is also a substrate for **creatinine** synthesis (along with glycine and methionine) and plays a key role in the **urea cycle**. *Glycine* - **Glycine** is a precursor for **creatinine** synthesis, but not directly involved in NO or urea production as the primary amino acid. - It is also a component of glutathione and purine synthesis. *Aspartate* - **Aspartate** is a key intermediate in the **urea cycle**, contributing one nitrogen atom to urea. - It is not directly a precursor for NO or creatinine. *Citrulline* - **Citrulline** is an intermediate in the **urea cycle** and is converted to arginine. - It is not directly involved in the synthesis of creatinine or as the primary precursor for NO.

Question 1

Which of the following statements regarding mitochondrial DNA is FALSE?

Accepted Answer

All respiratory proteins are synthesized within the mitochondria

Answer

Double stranded

Answer

Inherited from mother

Answer

High mutation rate

Question 2

In patients with Retinitis pigmentosa, which of the following substances is known to have decreased levels?

Accepted Answer

Docosahexaenoic acid (DHA)

Answer

Thromboxane

Answer

Arachidonic acid

Answer

Linoleic acid

Question 3

In case of LPL deficiency, which of the following will increase after a fat rich diet?

Accepted Answer

Chylomicron

Answer

LDL

Answer

HDL

Answer

Lipoprotein (a)

Question 4

True regarding mitochondrial DNA is:

Accepted Answer

Inherited from mother

Answer

Linear double stranded

Answer

All respiratory proteins are synthesized within mitochondria itself

Answer

Low mutation rate

Question 5

Retinitis pigmentosa is associated with deficiency of:

Accepted Answer

DHA

Answer

Timnodonic acid

Answer

Eicosa pentaenoic acid

Answer

Arachidonic acid

Question 6

Amino acid required for conversion of norepinephrine to epinephrine:-

Accepted Answer

Methionine

Answer

Lysine

Answer

Tryptophan

Answer

Phenylalanine

Question 7

Type-I hyperlipoproteinemia is caused by deficiency of:-

Accepted Answer

Lipoprotein lipase

Answer

Elevated triglycerides in plasma

Answer

Elevated LDL

Answer

Elevated cholesterol

Question 8

Mark the false statement regarding mitochondrial DNA:

Accepted Answer

Does not show heteroplasmy

Answer

AGA and AGG are stop codons in mitochondrial DNA

Answer

Kearns-Sayre Syndrome is a large deletion in mitochondrial DNA

Answer

1% of cellular DNA, 13 proteins of respiratory chain

Question 9

In type I diabetes, which of the following is the MOST characteristic metabolic change that distinguishes it from type II diabetes:-

Accepted Answer

Increased lipolysis

Answer

Increased protein catabolism

Answer

Decreased glucose uptake

Answer

Increased hepatic glucose output

Question 10

Which amino acid is involved in the synthesis of creatinine, NO, and urea?

Accepted Answer

Arginine

Answer

Glycine

Answer

Aspartate

Answer

Citrulline

NEET-PG 2019 — Biochemistry