NEET-PG 2015 Practice Questions

Q: Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?

Glucokinase is induced by insulin.. ***Glucokinase is induced by insulin.*** - **Insulin** promotes glucose uptake and utilization in the liver and pancreatic beta cells, where glucokinase is primarily expressed. - Induction of **glucokinase** by insulin ensures that glucose is efficiently phosphorylated and trapped within hepatocytes when blood glucose levels are high. - This is a key mechanism for postprandial glucose homeostasis. *Incorrect: Hexokinase is specific for glucose.* - **Hexokinase** is NOT specific for glucose; it can phosphorylate various hexoses including **fructose**, **mannose**, and **galactose**. - Its broad substrate specificity distinguishes it from glucokinase, which has greater specificity for glucose. *Incorrect: Glucokinase is inhibited by glucose-6-phosphate.* - Unlike **hexokinase**, which is subject to product inhibition by glucose-6-phosphate, **glucokinase is NOT inhibited** by its product. - This lack of feedback inhibition allows glucokinase to continue phosphorylating glucose even when glucose-6-phosphate levels are elevated, which is appropriate for its role as a glucose sensor in liver and pancreatic beta cells. *Incorrect: Hexokinase has a high Km for glucose.* - **Hexokinase** has a **low Km** (~0.1 mM) for glucose, meaning it has high affinity and is saturated at normal blood glucose levels. - In contrast, **glucokinase** has a high Km (~10 mM), allowing it to respond proportionally to changes in blood glucose concentration.

Q: Pyruvate dehydrogenase requires all cofactors except:

Pyridoxin (Vitamin B6). ***Pyridoxin (Vitamin B6)*** - **Pyridoxin** (vitamin B6) is a coenzyme for many enzymes involved in **amino acid metabolism**, but it is **not directly required** by the pyruvate dehydrogenase complex. - The pyruvate dehydrogenase complex uses **thiamine pyrophosphate**, **lipoic acid**, **FAD**, **NAD+**, and **Coenzyme A** as cofactors. *Thiamin* - **Thiamin pyrophosphate** (TPP), derived from thiamin (vitamin B1), is a crucial coenzyme for the **E1 subunit** of the pyruvate dehydrogenase complex. - It participates in the **decarboxylation** of pyruvate, releasing CO2. *Riboflavin* - **FAD** (flavin adenine dinucleotide), derived from riboflavin (vitamin B2), is a coenzyme for the **E3 subunit** (dihydrolipoyl dehydrogenase) of the pyruvate dehydrogenase complex. - It is involved in the **regeneration of oxidized lipoamide**. *Niacin* - **NAD+** (nicotinamide adenine dinucleotide), derived from niacin (vitamin B3), is a coenzyme for the **E3 subunit** of the pyruvate dehydrogenase complex. - It acts as an **electron acceptor** during the reoxidation of FADH2.

Q: Which of the following is not a substrate for gluconeogenesis?

Leucine. ***Leucine*** - **Leucine** is an exclusively **ketogenic amino acid**, meaning its breakdown products can only be converted into **ketone bodies** or fatty acids, not glucose. - It does not have a carbon skeleton that can be directly converted into **pyruvate** or **oxaloacetate**, which are key intermediates in gluconeogenesis. *Lactate* - **Lactate** is a major substrate for gluconeogenesis, particularly during exercise or fasting. - It is converted to **pyruvate** by **lactate dehydrogenase**, and pyruvate can then enter the gluconeogenic pathway. *Propionate* - **Propionate** is a fatty acid with an odd number of carbon atoms, primarily derived from the catabolism of odd-chain fatty acids or from bacterial fermentation in the colon. - It can be converted into **succinyl CoA**, an intermediate of the citric acid cycle, which can then be used for gluconeogenesis. *Glycerol* - **Glycerol**, released during the breakdown of triglycerides, is an important substrate for gluconeogenesis. - It is phosphorylated to **glycerol-3-phosphate**, which is then oxidized to **dihydroxyacetone phosphate (DHAP)**, an intermediate in glycolysis and gluconeogenesis.

Q: The characteristic color of adipocere is:

Grayish white. ***Grayish white*** - Adipocere, also known as **grave wax**, is a waxy substance formed during the decomposition of a body in specific environmental conditions. - Its characteristic appearance is that of a **grayish-white, greasy, or crumbly** material, resulting from the hydrolysis and hydrogenation of body fats. *Black* - A **black discoloration** in a decomposing body is typically associated with **putrefaction** and the formation of **sulfmethemoglobin**, not adipocere formation. - This indicates a different stage and process of decomposition, usually in the presence of oxygen and bacterial activity. *Brown* - **Brown discoloration** can be seen in various stages of decomposition due to the breakdown of blood pigments, but it is not the characteristic color of **adipocere**. - Adipocere's formation involves the transformation of fat into fatty acids, giving it a distinct pale color. *Red* - **Red discoloration** is generally associated with fresh blood or **carbon monoxide poisoning (cherry-red lividity)** in a deceased body. - It is not a feature of adipocere formation, which involves chemical changes to body fat over a longer period.

Q: Which of the following statements is true about cadaveric spasm?

Occurs immediately at the moment of death.. ***Occurs immediately at the moment of death.*** - **Cadaveric spasm** is a rare form of muscle stiffening that occurs **instantly** at the moment of death, without the flaccid stage seen in rigor mortis. - This is the **primary defining characteristic** that distinguishes cadaveric spasm from all other postmortem changes. - It is typically associated with deaths involving **intense emotional stress**, fear, or extreme physical exertion just before death. *May develop several hours after death.* - This statement describes **rigor mortis**, which is the stiffening of muscles that typically begins 2-6 hours after death. - Cadaveric spasm is distinct from rigor mortis due to its **immediate onset**. *Develops only in certain muscle groups.* - While this statement has some validity (cadaveric spasm is typically **localized** to specific muscle groups like hands or limbs that were under extreme tension), it is not the **best answer**. - The key distinguishing feature of cadaveric spasm is its **immediate onset at death**, not merely its localized distribution. - Many postmortem changes can be localized; what makes cadaveric spasm unique is its instantaneous occurrence. *Can affect any muscle in the body.* - This is too broad and inaccurate. Cadaveric spasm is characteristically **localized or regional**, not generalized. - It typically involves muscles that were under **extreme voluntary contraction** at the moment of death (e.g., clutching a weapon, grasping an object). - Unlike rigor mortis, which eventually affects all muscles, cadaveric spasm remains confined to specific muscle groups.

Q: Best temperature for putrefaction is -

10-45 °C. ***10-45 °C*** - This temperature range is optimal for the **bacterial and enzymatic activity** required for putrefaction, as most decomposition bacteria thrive in mesophilic conditions. - Temperatures within this range accelerate the breakdown of complex organic matter into simpler compounds, leading to the characteristic changes of **decomposition**. *0-10 °C* - Temperatures below 10°C significantly **slow down bacterial metabolism** and enzymatic activity, thereby retarding the process of putrefaction. - At temperatures near 0°C, decomposition is almost entirely halted due to **cold preservation** effects. *45-100 °C* - Temperatures above 45°C can begin to **denature enzymes** and kill many of the bacteria responsible for putrefaction, especially as temperatures approach the upper end of this range. - While some thermophilic bacteria exist, the overall rate of decomposition for a cadaver typically **decreases at very high temperatures** due to sterilization effects or protein coagulation. *100-150 °C* - At these very high temperatures, most **bacteria would be destroyed**, and enzymatic activity would be completely inhibited due to extensive protein denaturation. - Such temperatures are more likely to cause **cremation or desiccation** rather than putrefaction.

Q: Which of the following is an example of an antiapoptotic gene?

FLIP. ***FLIP*** - **FLIP** is an **antiapoptotic gene** that inhibits the activation of caspase-8, thereby blocking the extrinsic apoptotic pathway. - It acts as an **FLICE-inhibitory protein**, preventing the formation of the death-inducing signaling complex (DISC) or its downstream activation. *P53* - **P53** is a **tumor suppressor gene** that promotes apoptosis in response to DNA damage or cellular stress. - It is a **pro-apoptotic gene**, orchestrating cell cycle arrest and apoptosis to prevent the propagation of damaged cells. *BAX* - **BAX** is a **pro-apoptotic gene** belonging to the Bcl-2 family, which promotes the release of cytochrome c from mitochondria. - This release initiates the **intrinsic apoptotic pathway**, leading to caspase activation and cell death. *BIM* - **BIM** is a **pro-apoptotic gene** of the Bcl-2 family, acting as a sensitizer for apoptosis by binding to and inhibiting anti-apoptotic Bcl-2 family proteins. - Its activation leads to the **neutralization of survival factors**, thereby promoting mitochondrial outer membrane permeabilization and apoptosis.

Q: What is the definition of lipofuscin?

Wear and tear pigment. ***Wear and tear pigment*** - Lipofuscin is known as **wear and tear pigment** that accumulates in cells over time, especially in aging cells [1]. - It is a byproduct of **cellular lipid peroxidation** and protein degradation, indicative of oxidative stress [1]. *Form of calcification* - Not to be confused with calcification, lipofuscin is a **pigment** and not related to calcium deposition [1]. - Calcification usually occurs in response to tissue injury or necrosis, which differs fundamentally from lipofuscin accumulation. *Fat deposits* - Lipofuscin is made up of **an insoluble complex** and is not classified simply as fat or fat deposits [1]. - It is the result of the **degradation of cellular components**, rather than the accumulation of unutilized fats [1]. *Blood pigment* - Lipofuscin is not derived from **hemoglobin** or any blood components, distinguishing it from true blood pigments like **bilirubin**. - It is associated with **cellular aging** rather than with any specific blood function or metabolism [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 75-77.

Q: During cell death, myelin figures are derived from which of the following?

Cell membrane (lipid bilayer). ***Cell membrane (lipid bilayer)*** - **Myelin figures** are whorled phospholipid masses formed during cell injury and death from the breakdown of **cellular membranes**, particularly the plasma membrane and **endoplasmic reticulum**. - These structures represent damaged membrane lipids (phospholipids) that undergo structural rearrangement into concentric lamellar (layered) configurations resembling myelin. - The term "cell membrane" encompasses both the plasma membrane and lipid-rich intracellular membranes, making this the most accurate answer among the options provided. - They are a characteristic morphologic feature of **irreversible cell injury** and can be seen with electron microscopy. *Cytoplasmic components* - While cytoplasmic proteins and organelles do degrade during cell death, they do not form the organized **phospholipid structures** characteristic of myelin figures. - Cytoplasmic breakdown produces different morphologic changes such as cytoplasmic eosinophilia and loss of ribosomes. *Mitochondrial structures* - Mitochondria have their own membranes that are damaged during cell death (leading to release of cytochrome c and other apoptotic factors). - However, mitochondrial membranes are not the primary source of **myelin figures**, which predominantly arise from ER and plasma membranes. *Nuclear membrane* - The nuclear envelope does fragment during cell death, contributing to nuclear changes like **karyopyknosis, karyorrhexis, and karyolysis**. - While technically a membrane structure, the nuclear envelope is not the primary source of myelin figures, which are mainly derived from the more abundant plasma and ER membranes.

Question 1

Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?

Accepted Answer

Glucokinase is induced by insulin.

Answer

Hexokinase is specific for glucose.

Answer

Glucokinase is inhibited by glucose-6-phosphate.

Answer

Hexokinase has a high Km for glucose.

Question 2

Pyruvate dehydrogenase requires all cofactors except:

Accepted Answer

Pyridoxin (Vitamin B6)

Answer

Thiamin

Answer

Riboflavin

Answer

Niacin

Question 3

Which of the following is not a substrate for gluconeogenesis?

Accepted Answer

Leucine

Answer

Lactate

Answer

Propionate

Answer

Glycerol

Question 4

The characteristic color of adipocere is:

Accepted Answer

Grayish white

Answer

Black

Answer

Brown

Answer

Red

Question 5

Which of the following statements is true about cadaveric spasm?

Accepted Answer

Occurs immediately at the moment of death.

Answer

May develop several hours after death.

Answer

Develops only in certain muscle groups.

Answer

Can affect any muscle in the body.

Question 6

Best temperature for putrefaction is -

Accepted Answer

10-45 °C

Answer

0-10 °C

Answer

45-100 °C

Answer

100-150 °C

Question 7

Which of the following is an example of an antiapoptotic gene?

Accepted Answer

FLIP

Answer

P53

Answer

BAX

Answer

BIM

Question 8

What is the definition of lipofuscin?

Accepted Answer

Wear and tear pigment

Answer

Fat deposits

Answer

Blood pigment

Answer

Form of calcification

Question 9

During cell death, myelin figures are derived from which of the following?

Accepted Answer

Cell membrane (lipid bilayer)

Answer

Cytoplasmic components

Answer

Mitochondrial structures

Answer

Nuclear membrane

Question 10

Which molecule is primarily responsible for nuclear fragmentation during apoptosis?

Accepted Answer

Caspases

Answer

Apaf - 1

Answer

Oxygen free radicals

Answer

Endonuclease G

NEET-PG 2015

Biochemistry

Forensic Medicine

Pathology