Biochemistry
5 questionsMost abundant source of fuel in starvation -
Most important carbohydrate store for maintaining blood glucose homeostasis -
Which of the following is an example of an antiapoptotic gene?
Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
Enzyme deficient in Hers disease -
NEET-PG 2015 - Biochemistry NEET-PG Practice Questions and MCQs
Question 361: Most abundant source of fuel in starvation -
- A. Liver glycogen
- B. Muscle glycogen
- C. Adipose tissue (Correct Answer)
- D. Blood glucose
Explanation: ***Adipose tissue*** - **Adipose tissue** stores **triglycerides**, which are hydrolyzed into fatty acids and glycerol to serve as the body's primary energy source during prolonged starvation. - The energy reserve in adipose tissue is significantly larger than glycogen stores, providing **sustained fuel** for days or weeks. *Liver glycogen* - **Liver glycogen** is a readily available source of glucose but is rapidly depleted within **12-24 hours** during starvation. - Its primary role is to maintain **blood glucose levels** for glucose-dependent tissues like the brain. *Muscle glycogen* - **Muscle glycogen** is used primarily for **muscle contraction** and cannot be directly released into the bloodstream to maintain blood glucose levels. - While it's a significant energy reserve for working muscles, it does not contribute to systemic fuel needs during starvation. *Blood glucose* - **Blood glucose** is the immediate circulating fuel, but it is tightly regulated and its levels decrease during starvation as glycogen stores are depleted. - It is not an abundant stored source of fuel but rather a transport form of energy.
Question 362: Most important carbohydrate store for maintaining blood glucose homeostasis -
- A. Blood glucose
- B. Glycogen in adipose tissue
- C. Hepatic glycogen (Correct Answer)
- D. None of the options
Explanation: ***Hepatic glycogen*** - The liver contains **100-120g of glycogen**, which is the most crucial carbohydrate store for **maintaining blood glucose homeostasis**. - **Hepatic glycogen** can be mobilized and released as glucose into the bloodstream to supply all body tissues, especially during fasting. - Although muscle glycogen is quantitatively larger (~400-500g), it cannot contribute to blood glucose as muscle lacks glucose-6-phosphatase. - The liver's unique ability to release free glucose makes hepatic glycogen the **most metabolically important** carbohydrate store. *Blood glucose* - **Blood glucose** (~5g total in circulation) represents carbohydrates available for immediate energy, not a storage form. - This is far too small to be considered a major carbohydrate reserve. *Glycogen in adipose tissue* - **Adipose tissue** primarily stores **fat (triglycerides)**, with negligible glycogen content. - Adipose tissue plays virtually no role in carbohydrate storage. *None of the options* - This is incorrect because **hepatic glycogen** is indeed the most important carbohydrate store for glucose homeostasis.
Question 363: Which of the following is an example of an antiapoptotic gene?
- A. FLIP (Correct Answer)
- B. P53
- C. BAX
- D. BIM
Explanation: ***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.
Question 364: Which of the following statements about the enzymes involved in the conversion of glucose to glucose-6-phosphate in glycolysis is true?
- A. Glucokinase is induced by insulin. (Correct Answer)
- B. Hexokinase is specific for glucose.
- C. Glucokinase is inhibited by glucose-6-phosphate.
- D. Hexokinase has a high Km for glucose.
Explanation: ***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.
Question 365: Enzyme deficient in Hers disease -
- A. Muscle phosphorylase
- B. Liver phosphorylase (Correct Answer)
- C. Acid maltase
- D. Debranching enzyme
Explanation: ***Liver phosphorylase*** - Hers disease, also known as Glycogen Storage Disease Type VI, is specifically caused by a deficiency of **liver phosphorylase**. - This enzyme is crucial for the breakdown of **glycogen in the liver**, leading to an inability to release glucose into the bloodstream during fasting. *Muscle phosphorylase* - Deficiency of **muscle phosphorylase** (myophosphorylase) causes **McArdle disease** (Glycogen Storage Disease Type V), which primarily affects muscle energy. - Patients typically present with exercise intolerance, muscle pain, and cramps, not the hepatic symptoms seen in Hers disease. *Acid maltase* - Deficiency of **acid maltase** (also known as alpha-glucosidase) is responsible for **Pompe disease** (Glycogen Storage Disease Type II), a lysosomal storage disorder. - This enzyme deficiency leads to glycogen accumulation in lysosomes in various tissues, including muscle, liver, and heart, causing muscle weakness and cardiomyopathy. *Debranching enzyme* - A deficiency in the **debranching enzyme** (amylo-1,6-glucosidase) causes **Cori disease** or **Forbes disease** (Glycogen Storage Disease Type III). - This results in the accumulation of abnormally structured glycogen with short outer branches in the liver, muscle, and heart.
Pathology
3 questionsDuring cell death, myelin figures are derived from which of the following?
Which of the following is not an apoptotic gene?
Caseating necrosis most commonly occurs in
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 361: During cell death, myelin figures are derived from which of the following?
- A. Cell membrane (lipid bilayer) (Correct Answer)
- B. Cytoplasmic components
- C. Mitochondrial structures
- D. Nuclear membrane
Explanation: ***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 362: Which of the following is not an apoptotic gene?
- A. Mcl-1
- B. Bax
- C. P53
- D. n-myc (oncogene) (Correct Answer)
Explanation: ***n-myc*** - **n-myc** is primarily known for its role in **cell proliferation and differentiation**, not specifically associated with apoptosis [2]. - It is an **oncogene** that can contribute to tumorigenesis, but does not directly regulate apoptotic pathways [3]. *P53* - **P53** is a well-known **tumor suppressor gene** that plays a crucial role in inducing apoptosis in response to DNA damage [1]. - Activation of P53 leads to the transcription of genes that promote cell death, thus it is definitely an apoptotic gene [1]. *Bax* - **Bax** is a pro-apoptotic member of the **Bcl-2 family**, promoting apoptosis by facilitating mitochondrial outer membrane permeabilization [4,5]. - It plays a direct role in the apoptotic pathway, making it an important apoptotic gene [5]. *Mcl-1* - **Mcl-1** is an anti-apoptotic member of the **Bcl-2 family**, which helps prevent apoptosis by inhibiting pro-apoptotic factors [2,3]. - Its function is to **promote cell survival**, not apoptosis, but it is still classified as part of the apoptotic regulatory network [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 303-304. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [4] 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. 65-67. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 80-81.
Question 363: Caseating necrosis most commonly occurs in
- A. Brain
- B. Liver
- C. Kidney
- D. Lung (Correct Answer)
Explanation: ***lung*** - **Caseating necrosis** is classically associated with **tuberculosis**, which primarily affects the lungs [1]. - It is characterized by the presence of **granulomatous inflammation**, often leading to the formation of cavities in pulmonary tissue. *Brain* - While certain infections can lead to necrosis in the brain, they typically do not present as **caseating necrosis**, which is specific to certain conditions like tuberculosis. - The brain may show **liquefactive necrosis** or other types of necrosis, rather than **caseation**. *liver* - The liver usually shows **macrovesicular steatosis** or **apoptosis** in conditions like hepatitis, not caseating necrosis. - **Granulomatous hepatitis** can occur, but it does not typically result in **caseating** type necrosis associated with lung pathology. *kidney* - The kidneys can experience necrosis from various causes, but caseating necrosis is not typical; they are more often involved in **focal segmental glomerulosclerosis** or **acute tubular necrosis**. - Chronic kidney conditions may involve granulomas, but they usually are not characterized by **caseation** similar to that seen in pulmonary tissue. **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, p. 55.
Physiology
2 questionsWhich of the following receptors is stimulated by sustained pressure?
The major role of 2,3-bisphosphoglycerate in RBCs is -
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 361: Which of the following receptors is stimulated by sustained pressure?
- A. Ruffini's end organ (Correct Answer)
- B. Merkel's disc
- C. Hair cells
- D. Meissner Corpuscles
Explanation: ***Ruffini's end organ*** - These are **slowly adapting mechanoreceptors** located deep in the dermis and subcutaneous tissue. - They are responsible for detecting **sustained pressure**, stretch, and position sense. *Merkel's disc* - These are **slowly adapting mechanoreceptors** found in the basal epidermis. - They are crucial for sensing **light touch** and **two-point discrimination**. *Hair cells* - These are **mechanoreceptors** primarily found in the inner ear, responsible for hearing and balance. - They are not involved in the perception of somatosensory stimuli like pressure on the skin. *Meissner Corpuscles* - These are **rapidly adapting mechanoreceptors** located in the dermal papillae, close to the skin surface. - They are primarily involved in detecting **light touch** and **discriminative touch**, especially changes in texture.
Question 362: The major role of 2,3-bisphosphoglycerate in RBCs is -
- A. Acid-base balance
- B. Reversal of glycolysis
- C. Release of oxygen (Correct Answer)
- D. Binding of oxygen
Explanation: ***Release of oxygen*** - **2,3-bisphosphoglycerate (2,3-BPG)** binds allosterically to **deoxyhemoglobin**, stabilizing its T (tense) state. - This binding reduces hemoglobin's affinity for oxygen, promoting the **release of oxygen** to tissues. *Acid-base balance* - While red blood cells play a role in **acid-base balance** through the bicarbonate buffer system, 2,3-BPG's primary role is not buffering. - The **chloride shift** and **carbonic anhydrase** are more directly involved in RBC acid-base regulation. *Reversal of glycolysis* - 2,3-BPG is an intermediate of the **Rapoport-Luebering shunt**, a side pathway of glycolysis. - It does not reverse glycolysis but rather is produced during glycolysis to serve a specific function in oxygen transport. *Binding of oxygen* - 2,3-BPG **decreases** hemoglobin's affinity for oxygen, thus promoting its *release* from hemoglobin, not its binding. - Oxygen binding to hemoglobin occurs primarily at the **heme iron** without 2,3-BPG.