NEET-PG 2022 — Biochemistry
9 Previous Year Questions with Answers & Explanations
Which of the following statements is true regarding the telomerase theory of aging?
Which of the following helps in the transport of fatty acids across the inner mitochondrial membrane?
An adolescent male patient presents to you with exercise intolerance. He gives a history of developing cramps on exertion. Which of the following enzyme deficiencies could be the cause?
A young patient started to take a weight loss medication that acts by inhibiting fat absorption from food. After a few weeks, she developed easy bruising and increased menstrual bleeding. Deficiency of which of the following vitamins is responsible for her condition?
What is the term for a single mutation in a nucleotide base pair that results in a termination codon?
The electron transport chain is a series of redox reactions that result in ATP synthesis. Which of the following is a cytochrome complex IV inhibitor?
Cancer cells preferentially utilize glycolysis for energy production even in the presence of adequate oxygen. What is this phenomenon called?
A patient with hemolytic anemia has a defect in the enzyme glucose-6-phosphate dehydrogenase. Which of the following pathways is directly affected by this defect?
A patient is diagnosed with scurvy. This condition is due to a deficiency in which vitamin?
NEET-PG 2022 - Biochemistry NEET-PG Practice Questions and MCQs
Question 1: Which of the following statements is true regarding the telomerase theory of aging?
- A. Decreased telomere length is associated with aging (Correct Answer)
- B. Abnormal telomerase activation is associated with cancer
- C. Telomere stability directly maintains chromosomal integrity
- D. Increased telomere length is associated with prolonged cellular lifespan
Explanation: ***Decreased telomere length is associated with aging*** - Telomeres are protective DNA-protein caps at chromosome ends that **shorten with each cell division** - Progressive telomere shortening triggers **cellular senescence** (Hayflick limit) and apoptosis - This mechanism directly contributes to aging and **age-related diseases** - The telomere theory of aging (Olovnikov hypothesis) states that telomere attrition is a primary driver of biological aging *Abnormal telomerase activation is associated with cancer* - **Telomerase is reactivated in ~85-90% of cancers**, enabling unlimited replicative potential - Normal adult somatic cells have low/absent telomerase activity - While telomerase can extend cellular lifespan, its aberrant activation leads to malignancy, not healthy aging *Telomere stability directly maintains chromosomal integrity* - Telomeres prevent chromosome degradation, end-to-end fusions, and DNA damage responses - This is a **protective function**, not the basis of the telomere theory of aging - The aging theory focuses on **consequences of telomere shortening**, not stability maintenance *Increased telomere length is associated with prolonged cellular lifespan* - Longer telomeres do correlate with younger biological age and extended replicative capacity - However, this describes the **inverse relationship** rather than the core aging theory - The telomere theory specifically explains aging through **progressive shortening**, not length extension
Question 2: Which of the following helps in the transport of fatty acids across the inner mitochondrial membrane?
- A. Acyl carrier protein
- B. Carnitine (Correct Answer)
- C. Lecithin-cholesterol acyltransferase
- D. Carnitine and albumin
Explanation: ***Carnitine*** - **Carnitine** plays a crucial role in transporting long-chain fatty acids from the **cytosol** into the **mitochondrial matrix** for beta-oxidation. - It acts as a shuttling molecule, forming **acylcarnitine** which can cross the inner mitochondrial membrane via the **carnitine-acylcarnitine translocase**. *Acyl carrier protein* - **Acyl carrier protein (ACP)** is primarily involved in **fatty acid synthesis** in the cytoplasm, not in the transport of fatty acids into mitochondria for degradation. - It carries acyl groups during the elongation reactions of fatty acid synthesis. *Lecithin-cholesterol acyltransferase* - **Lecithin-cholesterol acyltransferase (LCAT)** is an enzyme found in plasma that catalyzes the formation of **cholesterol esters**, which are then transported by lipoproteins. - It is involved in **cholesterol metabolism** and reverse cholesterol transport, not in the mitochondrial transport of fatty acids. *Carnitine and albumin* - While **carnitine** is essential for mitochondrial fatty acid transport, **albumin** transports fatty acids in the blood plasma, from adipose tissue to other tissues. - Albumin does not transport fatty acids across the inner mitochondrial membrane; its role is extra-mitochondrial and related to systemic transport.
Question 3: An adolescent male patient presents to you with exercise intolerance. He gives a history of developing cramps on exertion. Which of the following enzyme deficiencies could be the cause?
- A. Myophosphorylase (Correct Answer)
- B. Hexokinase
- C. Glucose-6-phosphatase
- D. Hepatic glycogen phosphorylase
Explanation: ***Myophosphorylase*** - A deficiency in **myophosphorylase** (McArdle's disease, Glycogen Storage Disease Type V) impairs muscle glycogen breakdown, leading to **exercise intolerance** and **muscle cramps** due to insufficient ATP production during exertion. - Patients often experience a "second wind" phenomenon where symptoms improve after resting, as free fatty acids become an alternative fuel source. *Hexokinase* - A deficiency in **hexokinase** would affect the first step of glycolysis, impacting glucose phosphorylation in all tissues, not specifically causing exercise-induced muscle cramps. - This deficiency is rare and typically presents with **hemolytic anemia** due to impaired erythrocyte metabolism. *Glucose-6-phosphatase* - A deficiency in **glucose-6-phosphatase** (Von Gierke's disease, Glycogen Storage Disease Type Ia) primarily affects the liver and kidneys, leading to **fasting hypoglycemia**, lactic acidosis, and hepatomegaly, not exercise intolerance. - Muscle glycogen metabolism is unaffected in this condition. *Hepatic glycogen phosphorylase* - A deficiency in **hepatic glycogen phosphorylase** (Hers' disease, Glycogen Storage Disease Type VI) mainly causes **hepatomegaly** and **mild hypoglycemia** because the liver cannot effectively mobilize its glycogen stores. - **Muscle glycogen metabolism** remains normal, so exercise intolerance and cramps are not characteristic symptoms.
Question 4: A young patient started to take a weight loss medication that acts by inhibiting fat absorption from food. After a few weeks, she developed easy bruising and increased menstrual bleeding. Deficiency of which of the following vitamins is responsible for her condition?
- A. Vitamin E
- B. Vitamin K (Correct Answer)
- C. Vitamin B6
- D. Vitamin D
Explanation: ***Vitamin K*** - The patient is taking a **weight-loss medication** that **inhibits fat absorption**, leading to a deficiency in **fat-soluble vitamins**, including vitamin K. - **Vitamin K** is crucial for the synthesis of **coagulation factors** (II, VII, IX, X), and its deficiency leads to impaired clotting, manifesting as **easy bruising** and **increased menstrual bleeding**. *Vitamin E* - While vitamin E is a fat-soluble vitamin, its deficiency typically causes **neurological dysfunction** and **hemolytic anemia**, not bleeding diathesis. - Although malabsorption of vitamin E can occur with fat malabsorption, it does not directly explain the bleeding symptoms observed. *Vitamin B6* - Vitamin B6 is a **water-soluble vitamin**, so its absorption would not be directly affected by a medication inhibiting fat absorption. - Its deficiency can cause **neuropathy**, **dermatitis**, and **anemia**, but not increased bleeding. *Vitamin D* - Vitamin D is a **fat-soluble vitamin** whose deficiency is associated with **bone disorders** like **osteomalacia** and **rickets**, not bleeding. - While its absorption would be impacted by the medication, its deficiency would not cause easy bruising or increased menstrual bleeding.
Question 5: What is the term for a single mutation in a nucleotide base pair that results in a termination codon?
- A. Missense mutation
- B. Nonsense mutation (Correct Answer)
- C. Termination mutation
- D. Silent mutation
Explanation: ***Nonsense mutation*** - A **nonsense mutation** occurs when a single nucleotide base pair change leads to the formation of a **premature stop codon**, which results in a truncated and often non-functional protein. - The term "nonsense" refers to the fact that the new codon signals an early termination of protein synthesis. *Missense mutation* - A **missense mutation** involves a single nucleotide change that results in a codon coding for a **different amino acid**, potentially altering protein function but not necessarily terminating it. - This type of mutation can have varying effects on protein function, from benign to severe, depending on the amino acid substitution. *Termination mutation* - While a nonsense mutation does result in **premature termination**, "termination mutation" is not the standard or most precise scientific term used to describe this specific type of genetic alteration. - The more accurate and widely accepted terminology is **nonsense mutation** for a change leading to a stop codon. *Silent mutation* - A **silent mutation** is a type of point mutation that changes a single nucleotide, but does not change the amino acid sequence of the protein due to the **degeneracy of the genetic code**. - These mutations have **no observable effect** on the organism's phenotype as the protein produced remains unchanged.
Question 6: The electron transport chain is a series of redox reactions that result in ATP synthesis. Which of the following is a cytochrome complex IV inhibitor?
- A. Cyanide (Correct Answer)
- B. Carbon dioxide
- C. Oligomycin
- D. Ouabain
Explanation: ***Cyanide*** - **Cyanide** is a potent inhibitor of **cytochrome c oxidase (Complex IV)** in the electron transport chain, binding to the ferric iron (Fe3+) in the heme group of the enzyme. - This binding prevents the transfer of electrons to **oxygen**, thereby halting cellular respiration and ATP production. *Carbon dioxide* - **Carbon dioxide** is a metabolic waste product and a component of the **bicarbonate buffer system**, but it does not directly inhibit cytochrome complex IV. - While high levels can affect physiological pH and enzyme function, its primary role is not as an electron transport chain inhibitor. *Oligomycin* - **Oligomycin** inhibits **ATP synthase (Complex V)** by binding to its Fo subunit, which blocks the flow of protons through the ATP synthase channel. - This prevents the synthesis of ATP but does not directly affect the electron transfer steps of cytochrome complex IV. *Ouabain* - **Ouabain** is a cardiac glycoside that inhibits the **Na+/K+-ATPase pump** in the cell membrane. - It does not have any direct inhibitory effect on the components of the electron transport chain, including cytochrome complex IV.
Question 7: Cancer cells preferentially utilize glycolysis for energy production even in the presence of adequate oxygen. What is this phenomenon called?
- A. Warburg effect (Correct Answer)
- B. Hypoxic adaptation
- C. Anoxic survival
- D. Oxygen-independent metabolism
Explanation: ***Warburg*** - The **Warburg effect** describes how cancer cells preferentially use glycolysis for energy production even in the presence of oxygen, allowing them to thrive in **hypoxic conditions** [1]. - This metabolic adaptation supports **cell proliferation** and survival in tumor microenvironments where oxygen is limited [1][3]. - Cancer cells upregulate glucose uptake and express specific metabolic enzymes like the M2 isoform of pyruvate kinase that facilitate this altered metabolism [2][4]. *Wanton* - This term typically refers to recklessness or extravagance and is not used in the context of cancer metabolism or hypoxia. - There are no associations with **cancer cell adaptation** under adverse environmental conditions. *Wormian* - **Wormian bones** are extra bone pieces within sutures of the skull, unrelated to cancer cell metabolism or survival mechanisms. - This term does not connect to **hypoxia** or metabolic adaptations in cancer biology. *Wolf* - "Wolf" has no recognized connection to cancer cell biology, particularly regarding metabolic adaptations under **hypoxic stress**. - It does not imply any concept associated with how cancer cells cope with adverse conditions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 307-308. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 308-310. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 290-291. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 26-27.
Question 8: A patient with hemolytic anemia has a defect in the enzyme glucose-6-phosphate dehydrogenase. Which of the following pathways is directly affected by this defect?
- A. Glycolysis
- B. Pentose phosphate pathway (Correct Answer)
- C. TCA cycle
- D. Urea cycle
Explanation: ***Pentose phosphate pathway*** - **Glucose-6-phosphate dehydrogenase (G6PD)** is the **rate-limiting enzyme** in the **pentose phosphate pathway (PPP)**, initiating the oxidative phase. - Deficiency in G6PD impairs the production of **NADPH**, which is crucial for reducing **oxidative stress** in red blood cells. *Glycolysis* - This pathway metabolizes glucose to pyruvate for **ATP production** and does not directly involve G6PD. - While G6P is an intermediate in both pathways, its conversion in glycolysis is catalyzed by phosphoglucose isomerase, not G6PD. *TCA cycle* - The **tricarboxylic acid (TCA) cycle** is a central metabolic pathway for energy production occurring in the **mitochondria**. - It involves the oxidation of acetyl-CoA and does not directly utilize G6PD. *Urea cycle* - The **urea cycle** is responsible for detoxifying ammonia by converting it into urea, primarily occurring in the **liver**. - This pathway is unrelated to glucose metabolism or G6PD activity.
Question 9: A patient is diagnosed with scurvy. This condition is due to a deficiency in which vitamin?
- A. Vitamin A
- B. Vitamin C (Correct Answer)
- C. Vitamin D
- D. Vitamin E
Explanation: ***Vitamin C*** - **Scurvy** is directly caused by a prolonged and severe deficiency of **Vitamin C (ascorbic acid)**. - Vitamin C is essential for **collagen synthesis**, and its deficiency leads to impaired wound healing, fragile blood vessels, and gum disease, which are hallmarks of scurvy. *Vitamin A* - Deficiency in Vitamin A primarily causes **vision problems**, such as night blindness, and can lead to xerophthalmia, but not scurvy. - It plays a crucial role in **immune function** and cell growth, distinguishing its role from collagen synthesis. *Vitamin D* - A deficiency in Vitamin D is associated with **rickets** in children and **osteomalacia** in adults, conditions primarily affecting bone mineralization. - It is vital for **calcium and phosphate absorption**, which is unrelated to the collagen defects seen in scurvy. *Vitamin E* - Deficiency in Vitamin E is rare and can lead to **neurological symptoms** like ataxia and peripheral neuropathy. - It acts as a **powerful antioxidant**, protecting cells from oxidative damage, which is a different metabolic pathway than Vitamin C's role in collagen.