NEET-PG 2012 Practice Questions

Q: DNA microarrays allow detection of gene mutations through which process?

Hybridization. ***Hybridization*** - DNA microarrays detect mutations by **hybridizing labeled patient DNA** to **thousands of oligonucleotide probes** containing known DNA sequences immobilized on a solid surface. - A mismatch between the patient's DNA and the probe results in **reduced or absent hybridization**, indicating a **mutation or genetic variation**. - This principle allows **high-throughput screening** of multiple genes simultaneously. *Polymerase Chain Reaction* - PCR is used to **amplify specific DNA sequences exponentially**, creating millions of copies from minimal starting material. - While PCR may be used to **prepare DNA samples** before microarray analysis, it is **not the detection mechanism** on the chip itself. *Cloning* - Cloning involves creating **identical copies of DNA fragments, cells, or organisms** using vectors and host cells. - It's a method for **producing large quantities** of specific DNA sequences but **not a detection technique** for mutations on microarrays. *Southern Blotting* - Southern blotting detects specific DNA sequences through **gel electrophoresis, membrane transfer, and probe hybridization**. - While it also uses hybridization, it is a **low-throughput technique** analyzing one sample at a time, unlike the **high-throughput parallel analysis** of DNA microarrays.

Q: Protein glycosylation occurs in:

Endoplasmic reticulum (ER). ***ER*** - **N-linked glycosylation**, the most common type of protein glycosylation, initiates in the **endoplasmic reticulum (ER)**, where an oligosaccharide precursor is transferred to asparagine residues of newly synthesized proteins. - The ER environment facilitates protein folding and quality control, ensuring correctly folded glycoproteins are transported further. *Golgi bodies* - While **further modification and processing** of glycosylated proteins occur in the Golgi apparatus, the initial step of N-linked glycosylation begins in the ER. - The Golgi is responsible for trimming and adding different sugar residues to complete the **glycan chains** and for sorting the glycoproteins to their final destinations. *Mitochondria* - Mitochondria are primarily involved in **cellular respiration** and **ATP production**. - They do not play a significant role in protein glycosylation; most mitochondrial proteins are imported from the cytoplasm in an unglycosylated state. *Peroxisomes* - Peroxisomes are involved in various **metabolic processes**, including fatty acid oxidation and detoxification. - They are not known to be sites of protein glycosylation.

Q: Which molecule serves as the ultimate source of acetyl groups for fatty acid synthesis?

Acetyl CoA. ***Acetyl CoA*** - **Acetyl CoA** is the ultimate source of all acetyl groups used in fatty acid synthesis - It serves as the substrate for **acetyl CoA carboxylase**, which converts it to **malonyl CoA** - After transport from mitochondria via **citrate**, acetyl CoA is the precursor for all two-carbon units incorporated into fatty acids - One molecule of acetyl CoA also serves as the primer for fatty acid synthesis *Malonyl CoA* - **Malonyl CoA** is the direct two-carbon donor to the growing fatty acid chain - However, it is derived from **acetyl CoA** through carboxylation by **acetyl CoA carboxylase** - It is an intermediate, not the ultimate source of acetyl groups *Palmitate* - **Palmitate** is a 16-carbon saturated fatty acid that is the end product of de novo fatty acid synthesis - It is the product of fatty acid synthesis, not a donor of acetyl groups *Citrate* - **Citrate** transports acetyl groups from the **mitochondria** to the **cytosol** where fatty acid synthesis occurs - In the cytosol, **ATP citrate lyase** cleaves citrate back into **acetyl CoA** and oxaloacetate - Citrate is a transport vehicle, not the ultimate source of acetyl groups

Q: Indole ring is present in?

Tryptophan. ***Tryptophan*** - Tryptophan is an **aromatic amino acid** characterized by the presence of an **indole ring** in its side chain. - The indole ring consists of a **benzene ring fused to a pyrrole ring**, which is unique to tryptophan among the standard amino acids. *Tyrosine* - Tyrosine is an **aromatic amino acid** containing a **phenol group** (a benzene ring with a hydroxyl group), not an indole ring. - It is derived from phenylalanine and is a precursor for important molecules like **thyroid hormones** and **catecholamines**. *Phenylalanine* - Phenylalanine is an **aromatic amino acid** with a **benzyl group** (a benzene ring attached to a methylene group) in its side chain. - It lacks the distinct heterocyclic indole structure found in tryptophan. *Threonine* - Threonine is an **aliphatic amino acid** with a **hydroxyl group** on its side chain, classifying it as a **polar, uncharged amino acid**. - It does not contain any ring structures, especially not an indole ring.

Q: Major source of energy for brain in fasting/starvation?

Ketone bodies. ***Ketone bodies*** - During **prolonged fasting or starvation**, the body depletes its **glycogen stores** and begins to break down fatty acids. The liver converts these fatty acids into **ketone bodies**, such as **acetoacetate and beta-hydroxybutyrate**. - These **ketone bodies** can cross the **blood-brain barrier** and be used by the brain as an alternative energy source when glucose becomes scarce, preventing protein breakdown for gluconeogenesis. *Glucose* - While **glucose** is the primary and preferred energy source for the brain under normal physiological conditions, its availability significantly decreases during **prolonged fasting or starvation**. - The brain requires a continuous supply of glucose, but in states of severe caloric restriction, the body must conserve glucose for other critical functions and adapt by using alternative fuels. *Glycogen* - **Glycogen** is a stored form of glucose found predominantly in the **liver and muscles**. - The brain itself has minimal **glycogen stores**, which are rapidly depleted during fasting, and thus cannot be a major long-term energy source. *Fatty acids* - **Fatty acids** are a major energy source for many tissues in the body, especially during fasting, but they **cannot directly cross the blood-brain barrier** in significant amounts to fuel the brain. - Instead, **fatty acids** are metabolized into **ketone bodies** in the liver, which then serve as the brain's alternative fuel.

Q: Enzyme deficient in Type I Hyperlipidemia?

Lipoprotein lipase. ***Lipoprotein lipase*** - **Type I hyperlipidemia**, also known as **familial hyperchylomicronemia**, is characterized by a deficiency in **lipoprotein lipase (LPL)**. - LPL is crucial for hydrolyzing triglycerides in **chylomicrons** and **VLDLs** into fatty acids and glycerol, allowing their uptake by tissues. *HMG CoA reductase* - This enzyme is involved in the **rate-limiting step of cholesterol synthesis** in the liver. - While it plays a role in lipid metabolism, its deficiency is not characteristic of **Type I hyperlipidemia**. *Peroxidase* - **Peroxidase** is an enzyme involved in various oxidative reactions, including the breakdown of **hydrogen peroxide**. - It is not directly involved in the metabolism of **chylomicrons** or **triglycerides**, and its deficiency is unrelated to hyperlipidemia. *Cholesterol acyl transferase* - This enzyme, often referring to **lecithin-cholesterol acyltransferase (LCAT)** or **acyl-CoA:cholesterol acyltransferase (ACAT)**, is involved in **cholesterol esterification**. - While important for cholesterol transport and storage, its deficiency is not the primary cause of **Type I hyperlipidemia**, which is marked by severe **chylomicronemia**.

Q: Which of the following is an amino sugar formed from fructose-6-phosphate?

Glucosamine-6-phosphate. ***Glucosamine-6-phosphate*** - This amino sugar is directly synthesized from **fructose-6-phosphate** via a transamidation reaction, where an amino group replaces a hydroxyl group. - It is a key intermediate in the biosynthesis of other **amino sugars** and **glycosaminoglycans**. *N-acetylglucosamine-6-phosphate* - This is formed from **glucosamine-6-phosphate** by the addition of an **acetyl group**, making it a subsequent product, not the initial amino sugar from fructose-6-phosphate. - The N-acetylation step is crucial for its role in cellular signaling and structural components. *Galactosamine-6-phosphate* - While an amino sugar, **galactosamine-6-phosphate** is derived from UDP-N-acetylglucosamine, not directly from fructose-6-phosphate. - Its formation involves an **epimerization** step of an existing N-acetylglucosamine structure. *UDP-N-acetylglucosamine* - This is an **activated form** of N-acetylglucosamine, formed by the addition of UTP to N-acetylglucosamine-1-phosphate. - It serves as a precursor for the synthesis of complex **carbohydrates** and glycoproteins, far downstream from fructose-6-phosphate.

Q: Li–Fraumeni syndrome is associated with mutations in which of the following genes?

Gene TP53. ***Gene TP53*** - Li-Fraumeni syndrome is a rare, inherited cancer susceptibility syndrome associated with germline mutations in the **TP53 tumor suppressor gene**. - The **TP53 gene** encodes the p53 protein, which plays a critical role in cell cycle arrest, DNA repair, and initiation of apoptosis in response to cellular stress, thus preventing tumor formation. *Gene P21* - The **p21 gene** (CDKN1A) is a cyclin-dependent kinase inhibitor that acts downstream of p53, mediating p53-induced cell cycle arrest. - While p21 is involved in the p53 pathway, mutations in p21 itself are not the primary cause of Li-Fraumeni syndrome. *Gene RB1* - The **RB1 gene** encodes the retinoblastoma protein, a tumor suppressor involved in cell cycle regulation, particularly in controlling passage from G1 to S phase. - Mutations in **RB1** are primarily associated with hereditary retinoblastoma and osteosarcoma, not Li-Fraumeni syndrome. *Gene BRCA1* - The **BRCA1 gene** is a tumor suppressor gene involved in DNA repair, especially homologous recombination. - Germline mutations in **BRCA1** are strongly associated with hereditary breast and ovarian cancer syndrome, not Li-Fraumeni syndrome.

Q: What occurs during the stage of Grey hepatization?

Accumulation of fibrin. ***Accumulation of fibrin*** - Grey hepatization is characterized by the **presence of fibrinous exudate** in the alveoli, indicating significant lung pathology, usually in cases of pneumonia [1,2]. - This stage follows red hepatization and reflects the **progression of inflammation** within the lung tissue [1,2]. *RBC's fill the alveoli* - This occurs during the **red hepatization** stage, where RBCs invade alveoli, not grey hepatization [1,2]. - **Grey hepatization** is marked by **fibrinous deposits** instead of erythrocytes [1,2]. *Organisms fill the alveoli* - While organisms, such as bacteria, can be present, they are more characteristic of the **initial infection phase** rather than grey hepatization [1]. - This stage reflects more on the **inflammatory response** than the presence of pathogens. *WBC's fill the alveoli* - The infiltration of **WBCs (like neutrophils)** represents an earlier inflammatory process, usually preceding grey hepatization [1,2]. - In grey hepatization, the focus is on the **accumulation of fibrin**, not directly on WBC infiltration [1,2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 711-712. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318.

Question 1

DNA microarrays allow detection of gene mutations through which process?

Accepted Answer

Hybridization

Answer

Polymerase Chain Reaction

Answer

Cloning

Answer

Southern Blotting

Question 2

Protein glycosylation occurs in:

Accepted Answer

Endoplasmic reticulum (ER)

Answer

Peroxisomes

Answer

Mitochondria

Answer

Golgi bodies

Question 3

Which molecule serves as the ultimate source of acetyl groups for fatty acid synthesis?

Accepted Answer

Acetyl CoA

Answer

Malonyl CoA

Answer

Palmitate

Answer

Citrate

Question 4

Indole ring is present in?

Accepted Answer

Tryptophan

Answer

Tyrosine

Answer

Phenylalanine

Answer

Threonine

Question 5

Major source of energy for brain in fasting/starvation?

Accepted Answer

Ketone bodies

Answer

Glucose

Answer

Glycogen

Answer

Fatty acids

Question 6

Enzyme deficient in Type I Hyperlipidemia?

Accepted Answer

Lipoprotein lipase

Answer

HMG CoA reductase

Answer

Peroxidase

Answer

Cholesterol acyl transferase

Question 7

Which of the following best describes the difference between glucokinase and hexokinase?

Accepted Answer

Glucokinase has higher Km for glucose compared to hexokinase.

Answer

Glucokinase is not inhibited by glucose-6-phosphate unlike hexokinase.

Answer

Glucokinase has a low affinity for glucose.

Answer

Glucokinase activity increases with glucose concentration while hexokinase remains saturated.

Question 8

Which of the following is an amino sugar formed from fructose-6-phosphate?

Accepted Answer

Glucosamine-6-phosphate

Answer

N-acetylglucosamine-6-phosphate

Answer

Galactosamine-6-phosphate

Answer

UDP-N-acetylglucosamine

Question 9

Li–Fraumeni syndrome is associated with mutations in which of the following genes?

Accepted Answer

Gene TP53

Answer

Gene RB1

Answer

Gene BRCA1

Answer

Gene P21

Question 10

What occurs during the stage of Grey hepatization?

Accepted Answer

Accumulation of fibrin

Answer

Red blood cells fill the alveoli

Answer

White blood cells fill the alveoli

Answer

Bacteria fill the alveoli

NEET-PG 2012

Biochemistry

Pathology