NEET-PG 2024 Practice Questions

Q: Which transporter helps in the improvement of insulin resistance in type 2 diabetes mellitus (DM2) with regular exercise and physical activities?

GLUT 4. ***GLUT 4*** - **GLUT 4** is the **insulin-sensitive glucose transporter** predominantly found in **skeletal muscle** and **adipose tissue**. Regular exercise and physical activity increase the expression and translocation of GLUT 4 to the cell membrane, enhancing glucose uptake independent of insulin, thereby improving **insulin sensitivity** and reducing insulin resistance in DM2. - Exercise also stimulates **AMPK (AMP-activated protein kinase)**, which promotes GLUT 4 translocation to the cell surface, facilitating glucose uptake and utilization in active muscles. *GLUT 1* - **GLUT 1** is a basal glucose transporter found in nearly all cells, responsible for **basal glucose uptake** to meet basic metabolic needs, especially in **red blood cells** and the **blood-brain barrier**. - Its activity is largely **insulin-independent** and does not significantly contribute to the exercise-induced improvement in insulin sensitivity in skeletal muscle. *GLUT 2* - **GLUT 2** is primarily found in the **liver, pancreatic beta cells, kidneys, and small intestine**. It has a **low affinity** but **high capacity** for glucose transport, serving as a glucose sensor in beta cells and allowing efficient glucose uptake/release in the liver. - It plays a role in glucose homeostasis but is **not directly involved in the exercise-mediated improvement of insulin resistance** in peripheral tissues like muscle. *GLUT 3* - **GLUT 3** is a **high-affinity glucose transporter** primarily expressed in **neurons** and the **placenta**. It is crucial for providing a constant supply of glucose to the brain, even at low glucose concentrations. - Like GLUT 1 and GLUT 2, its activity is largely **insulin-independent** and does not play a significant role in improving insulin resistance through exercise in DM2.

Q: A 5-year-old girl was washing her doll with shampoo containing rotenone. Her mother noticed her in an unconscious state. Which enzyme is inhibited by the above chemical?

NADH dehydrogenase. ***NADH dehydrogenase*** - **Rotenone** is a potent **inhibitor of mitochondrial complex I (NADH dehydrogenase)**, preventing the transfer of electrons from NADH to ubiquinone. - This inhibition disrupts the **electron transport chain**, leading to a halt in ATP synthesis and cellular energy failure, causing symptoms like unconsciousness. *Succinate dehydrogenase* - **Succinate dehydrogenase** (Complex II) is involved in both the **Krebs cycle and electron transport chain**, but is not directly inhibited by rotenone. - Only severe compromise of the electron transport chain can cause a secondary effect, but not direct enzyme inhibition. *Cytochrome C* - **Cytochrome C** is a mobile electron carrier in the electron transport chain, but it is not directly inhibited by rotenone. - **Cytochrome C** transfers electrons from complex III to complex IV. *Cytochrome oxidase* - **Cytochrome oxidase** (Complex IV) is responsible for the final transfer of electrons to oxygen, which is not inhibited by rotenone. - Inhibitors like **cyanide and carbon monoxide** specifically target **cytochrome oxidase**. *Cytochrome b-c1 complex* - **Cytochrome b-c1 complex** (Complex III) catalyzes electron transfer from ubiquinol to cytochrome C, but is not inhibited by rotenone. - This complex is specifically inhibited by **antimycin A**, not rotenone.

Q: A patient with high triglycerides (TG) esterified with long-chain fatty acids (LCFA) presents with fatigue, and a biopsy of the muscle shows fat vacuoles. What is the most likely diagnosis?

Carnitine deficiency. ***Carnitine deficiency*** - **Carnitine** is essential for transporting **long-chain fatty acids (LCFAs)** into the mitochondria for beta-oxidation. - A deficiency leads to the accumulation of **LCFAs** as **triglycerides** in the cytoplasm, resulting in **fat vacuoles** in muscle and systemic fatigue due to impaired energy production. *Fatty acid synthase defect* - **Fatty acid synthase** is involved in the *de novo* synthesis of fatty acids, not their catabolism or transport. - A defect would impair fatty acid production, not lead to the accumulation of **triglycerides** from exogenous sources. *Lipoprotein lipase (LPL) defect* - **LPL** is crucial for cleaving **triglycerides** in circulating chylomicrons and VLDL, allowing fatty acids to be taken up by tissues. - A defect causes severe hypertriglyceridemia, but the primary issue in the muscle with fat vacuoles points towards a problem with intracellular fatty acid utilization rather than plasma triglyceride clearance. *LDL defect* - **LDL** is primarily responsible for transporting cholesterol to peripheral tissues. - Defects in **LDL** metabolism typically lead to hypercholesterolemia, not the accumulation of **triglycerides** or muscle fat vacuoles as described. *Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency* - **MCAD** deficiency is a fatty acid oxidation disorder affecting **medium-chain fatty acids** (C6-C12), not the **long-chain fatty acids** specifically mentioned in the stem. - It typically presents with hypoketotic hypoglycemia during fasting, often in infancy or childhood, rather than the characteristic muscle fat vacuole accumulation pattern seen with **carnitine deficiency**.

Q: A patient presents with xanthomas on the Achilles tendon. What is the most likely diagnosis?

Familial hypercholesterolemia. ***Familial hypercholesterolemia*** - **Xanthomas** on the **Achilles tendon** are a classic clinical sign of familial hypercholesterolemia, along with significantly elevated **LDL-C levels**. - This condition is an **autosomal dominant** genetic disorder characterized by defects in the **LDL receptor** pathway, leading to impaired clearance of LDL from the blood. - **Tendon xanthomas** (especially Achilles and extensor tendons) are pathognomonic for this condition. *Tangier's disease* - Characterized by very low or absent **HDL-C (high-density lipoprotein cholesterol)** levels, leading to **cholesterol ester accumulation** in various tissues. - While it can cause lipid deposition, its hallmark is **enlarged, orange tonsils** and peripheral neuropathy, not typically Achilles tendon xanthomas. *Familial hyperchylomicronemia* - This disorder primarily involves elevated **chylomicrons** and **triglycerides**, presenting with **eruptive xanthomas** (small, red-yellow papules) but not typically tendon xanthomas. - It is often associated with **pancreatitis** and **lipemia retinalis**. *Familial dysbetalipoproteinemia* - Characterized by elevated levels of **cholesterol** and **triglycerides** due to accumulation of remnant lipoproteins (IDL). - While it can cause **xanthomas**, these are typically **palmar xanthomas** (xanthoma striata palmaris) and **tuberoeruptive xanthomas**, less commonly Achilles tendon xanthomas. *Familial combined hyperlipidemia* - Most common familial lipid disorder, characterized by elevated **LDL-C** and/or **triglycerides** with variable phenotype. - While it causes premature coronary artery disease, it typically does **not** cause tendon xanthomas, which distinguishes it from familial hypercholesterolemia. - Xanthomas, if present, are usually **xanthelasma** (around eyelids) rather than tendon xanthomas.

Q: What is the source of Vitamin B1 (Thiamine)?

C. ***C*** - Element C appears to be a **grain-based flatbread**, which is a rich source of **thiamine (Vitamin B1)**. Whole grains, fortified cereals, and legumes are primary dietary sources of this essential vitamin. - **Thiamine** plays a crucial role in **carbohydrate metabolism** and nerve function. *A* - Element A appears to be **rice**, which is a **grain**. However, the question asks for the best source, and while rice can contain thiamine, the other option is a stronger candidate. - White rice, in particular, is often **enriched with thiamine** but naturally contains less than whole grains. *B* - Element B contains what appears to be **vegetables and salad**. While vegetables contain some thiamine, they are not typically considered the richest sources. - **Fruits and vegetables** are more commonly known for vitamins like C and A, and various minerals. *D* - Element D appears to be a **curry or stew**, likely containing lentils or other legumes. While some curries can contain thiamine, based on the image's clarity, it is not the most distinctly represented rich source compared to C. - The thiamine content in stews or curries can vary greatly depending on the **specific ingredients** used. *E* - Element E appears to be another food item in the image. While it may contain some nutrients, it is not the primary source of thiamine (Vitamin B1) among the options shown. - The **grain-based flatbread (C)** remains the richest and most reliable source of thiamine in this selection.

Q: A patient has multiple tendon xanthomas. Serum cholesterol ( $398 \mathrm{mg} / \mathrm{dL}$ ) and LDL ( 220 $\mathrm{mg} / \mathrm{dL}$ ) were found to be elevated. What is the most likely defect?

LDL receptor defect. ***LDL receptor defect*** - **Tendon xanthomas** are a classic sign of **familial hypercholesterolemia**, which is most commonly caused by a genetic defect in the **LDL receptor**. - **Elevated LDL cholesterol** levels are a hallmark of this condition, as dysfunctional LDL receptors lead to impaired clearance of LDL particles from the blood. *Lipoprotein lipase deficiency* - This condition primarily causes severe **hypertriglyceridemia** and can lead to **eruptive xanthomas**, but not typically tendon xanthomas. - While cholesterol levels might be elevated, the defining feature would be very high triglyceride levels, often exceeding 1000 mg/dL. *Apo E defect* - A defect in **ApoE** (specifically the **ApoE2/E2 genotype**) is associated with **familial dysbetalipoproteinemia** (Type III hyperlipoproteinemia). - This condition causes elevated remnants of chylomicrons and VLDL, leading to **palmar xanthomas**, but less commonly tendon xanthomas, and often presents with high triglyceride levels in addition to cholesterol. *Apo B-100 defect* - **Familial defective apoB-100** can present similarly to familial hypercholesterolemia with elevated LDL cholesterol. - However, this is much **rarer** than LDL receptor defects (affecting ~1:700 vs 1:250-500 for LDL receptor mutations). - The clinical presentation and lipid profile overlap significantly, but LDL receptor defects remain the most common cause of this clinical picture. *LCAT deficiency* - **Lecithin-cholesterol acyltransferase (LCAT)** deficiency leads to an accumulation of **unesterified cholesterol** in plasma and tissues. - This typically presents with **corneal opacities**, **hemolytic anemia**, and proteinuria, rather than predominantly tendon xanthomas and isolated severe LDL elevation.

Q: A patient presents with an X-ray showing cardiomegaly, along with symptoms of hypotonia, macroglossia, hepatomegaly, and floppy baby syndrome. The X ray of the infant is shown below. What is the most likely diagnosis?

Pompe's disease. ***Pompe's disease*** - Pompe's disease (Type II glycogen storage disease) is characterized by a deficiency of **alpha-glucosidase**, leading to **glycogen accumulation** in lysosomes. - This accumulation results in **cardiomegaly**, **hypotonia** ("floppy baby"), **hepatomegaly**, and **macroglossia**, which perfectly match the clinical presentation. *Ebstein anomaly* - This is a congenital heart defect involving the **tricuspid valve**, leading to its displacement into the right ventricle. - While it causes cardiomegaly, it does not typically present with the systemic features like **hypotonia, macroglossia, or hepatomegaly** described. *Transposition of great arteries* - This is a complex congenital heart defect where the **aorta and pulmonary artery are switched**, resulting in two separate circulatory systems. - It causes severe cyanosis and cardiomegaly but does not explain the widespread glycogen storage symptoms such as **hypotonia** or **hepatomegaly**. *Von Gierke's disease* - **Von Gierke's disease** (Type I glycogen storage disease) is caused by a deficiency of **glucose-6-phosphatase**. - It primarily affects the **liver and kidneys**, causing severe hypoglycemia, hepatomegaly, and **nephromegaly**, but typically not significant cardiomegaly or profound hypotonia. *Congenital hypothyroidism* - Can present with **macroglossia, hypotonia, and hepatomegaly** similar to Pompe's disease. - However, the **massive cardiomegaly** seen on X-ray is not typical of hypothyroidism, and other features like prolonged jaundice, constipation, and umbilical hernia would be more prominent.

Q: Phenobarbitone exerts its therapeutic effect primarily through which mechanism?

Enhancement of GABA-A receptor function. ***Enhancement of GABA-A receptor function*** - **Phenobarbitone** (phenobarbital) is a barbiturate that acts primarily by **enhancing GABA-A receptor activity** - It binds to a distinct **barbiturate binding site** on the GABA-A receptor complex - This binding **prolongs the duration of chloride channel opening** in response to GABA - Results in increased **chloride ion influx**, neuronal **hyperpolarization**, and **decreased neuronal excitability** - This mechanism underlies its **anticonvulsant** and **sedative-hypnotic** properties *NMDA receptor antagonism* - While some anticonvulsants work through NMDA receptor antagonism (e.g., ketamine, felbamate), this is **not the primary mechanism** of phenobarbitone *Voltage-gated sodium channel blockade* - Sodium channel blockade is the mechanism of action for drugs like **phenytoin, carbamazepine**, and **lamotrigine** - Phenobarbitone does not significantly block sodium channels at therapeutic concentrations *Voltage-gated calcium channel blockade* - Calcium channel blockers like **ethosuximide** (T-type) and **gabapentin** (α2δ subunit) work through this mechanism - This is not the primary mechanism for phenobarbitone *Potassium channel opening* - Potassium channel openers like **retigabine** increase potassium conductance - Phenobarbitone does not primarily work through this mechanism

Q: Which of the following are toxic metabolites associated with methanol poisoning?

Formic acid + Lactic acid. ***Formic acid + Lactic acid*** - **Methanol** is metabolized in the body into **formaldehyde** and then to **formic acid**, which is primarily responsible for its toxicity. - While not a direct derivative, **lactic acid** levels often rise significantly in severe methanol poisoning due to **hypoxia** and **metabolic acidosis** caused by formic acid-induced mitochondrial dysfunction. *Formic acid + Oxalic acid* - **Formic acid** is indeed a toxic metabolite of methanol, but **oxalic acid** is not. - **Oxalic acid** is a toxic metabolite of **ethylene glycol** poisoning, not methanol. *Glycolic acid + Oxalic acid* - Neither **glycolic acid** nor **oxalic acid** are toxic metabolites of methanol. - Both **glycolic acid** and **oxalic acid** are associated with **ethylene glycol** poisoning. *Oxalic acid + Lactic acid* - **Oxalic acid** is not a derivative of methanol poisoning. - While **lactic acid** can be elevated in methanol poisoning, its combination with oxalic acid is incorrect for methanol metabolites. *Hippuric acid + Formic acid* - **Formic acid** is correct, but **hippuric acid** is not a metabolite of methanol. - **Hippuric acid** is a metabolite of **toluene** and is used as a urinary marker for toluene exposure.

Question 1

Which transporter helps in the improvement of insulin resistance in type 2 diabetes mellitus (DM2) with regular exercise and physical activities?

Accepted Answer

GLUT 4

Answer

GLUT 1

Answer

GLUT 2

Answer

GLUT 3

Question 2

A 5-year-old girl was washing her doll with shampoo containing rotenone. Her mother noticed her in an unconscious state. Which enzyme is inhibited by the above chemical?

Accepted Answer

NADH dehydrogenase

Answer

Succinate dehydrogenase

Answer

Cytochrome C

Answer

Cytochrome oxidase

Answer

Cytochrome b-c1 complex

Question 3

A patient with high triglycerides (TG) esterified with long-chain fatty acids (LCFA) presents with fatigue, and a biopsy of the muscle shows fat vacuoles. What is the most likely diagnosis?

Accepted Answer

Carnitine deficiency

Answer

Fatty acid synthase defect

Answer

Lipoprotein lipase (LPL) defect

Answer

LDL defect

Answer

Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency

Question 4

A patient presents with xanthomas on the Achilles tendon. What is the most likely diagnosis?

Accepted Answer

Familial hypercholesterolemia

Answer

Tangier's disease

Answer

Familial hyperchylomicronemia

Answer

Familial dysbetalipoproteinemia

Answer

Familial combined hyperlipidemia

Question 5

What is the source of Vitamin B1 (Thiamine)?

Accepted Answer

C

Answer

A

Answer

B

Answer

D

Answer

E

Question 6

A patient has multiple tendon xanthomas. Serum cholesterol ( $398 \mathrm{mg} / \mathrm{dL}$ ) and LDL ( 220 $\mathrm{mg} / \mathrm{dL}$ ) were found to be elevated. What is the most likely defect?

Accepted Answer

LDL receptor defect

Answer

Lipoprotein lipase deficiency

Answer

Apo E defect

Answer

LCAT deficiency

Answer

Apo B-100 defect

Question 7

A patient came to the emergency room with severe abdominal pain. The serum triglyceride level was $1500 \mathrm{mg} / \mathrm{dL}$. What is the most likely defect?

Accepted Answer

Apo C-II

Answer

Apo B-48

Answer

Apo B-100

Answer

LDL receptor

Answer

Lipoprotein lipase

Question 8

A patient presents with an X-ray showing cardiomegaly, along with symptoms of hypotonia, macroglossia, hepatomegaly, and floppy baby syndrome. The X ray of the infant is shown below. What is the most likely diagnosis?

Accepted Answer

Pompe's disease

Answer

Ebstein anomaly

Answer

Transposition of great arteries

Answer

Von Gierke's disease

Answer

Congenital hypothyroidism

Question 9

Phenobarbitone exerts its therapeutic effect primarily through which mechanism?

Accepted Answer

Enhancement of GABA-A receptor function

Answer

Voltage-gated sodium channel blockade

Answer

Voltage-gated calcium channel blockade

Answer

Potassium channel opening

Answer

NMDA receptor antagonism

Question 10

Which of the following are toxic metabolites associated with methanol poisoning?

Accepted Answer

Formic acid + Lactic acid

Answer

Formic acid + Oxalic acid

Answer

Glycolic acid + Oxalic acid

Answer

Oxalic acid + Lactic acid

Answer

Hippuric acid + Formic acid

NEET-PG 2024

Biochemistry

Pediatrics

Pharmacology