Biochemistry
6 questionsPhosphofructokinase-1 occupies a key position in regulating glycolysis and is also subjected to feedback control. Which among the following are the allosteric activators of phosphofructokinase-1?
Which of the following statements about gluconeogenesis is correct?
Which of the following tissues relies EXCLUSIVELY on anaerobic glycolysis for ATP production?
The energy for glycogenesis is provided by -
Inhibition of glycolysis by increased supply of O2 is called ?
Ketone bodies are not used by?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 401: Phosphofructokinase-1 occupies a key position in regulating glycolysis and is also subjected to feedback control. Which among the following are the allosteric activators of phosphofructokinase-1?
- A. 2,3-Bisphosphoglycerate (2,3-BPG)
- B. Fructose 2,6-bisphosphate (Correct Answer)
- C. Glucokinase
- D. Phosphoenolpyruvate (PEP)
Explanation: ***Fructose 2,6-bisphosphate*** - **Fructose 2,6-bisphosphate** is a potent **allosteric activator** of **phosphofructokinase-1 (PFK-1)**, increasing its affinity for fructose 6-phosphate and overcoming ATP inhibition. - Its synthesis is regulated by **insulin** (stimulating) and **glucagon** (inhibiting), linking glucose availability to glycolytic flux. *2,3-Bisphosphoglycerate (2,3-BPG)* - **2,3-BPG** is an important regulator of **hemoglobin oxygen affinity** in red blood cells. - It is not an allosteric activator of **PFK-1**; its primary role is in oxygen delivery. *Glucokinase* - **Glucokinase** is an **enzyme** in glycolysis, specifically catalyzing the phosphorylation of glucose to glucose 6-phosphate in the liver and pancreatic beta cells. - It is not an allosteric activator of **PFK-1** but rather an upstream enzyme in the pathway. *Phosphoenolpyruvate (PEP)* - **PEP** is an intermediate in glycolysis, formed from 2-phosphoglycerate and converted to pyruvate by pyruvate kinase. - It acts as an **allosteric inhibitor** of phosphofructokinase-1, signaling high energy status and slowing down glycolysis.
Question 402: Which of the following statements about gluconeogenesis is correct?
- A. Occurs mainly in the liver (Correct Answer)
- B. It uses exactly the same enzymes as glycolysis in reverse
- C. It only occurs during fed state when insulin levels are high
- D. Fatty acids are the primary substrate for gluconeogenesis
Explanation: ***Occurs mainly in the liver*** - The **liver** is the primary site for **gluconeogenesis**, responsible for maintaining blood glucose levels during fasting. - The kidneys also contribute, especially during prolonged fasting, but to a lesser extent. *It uses exactly the same enzymes as glycolysis in reverse* - While gluconeogenesis shares some enzymes with glycolysis, there are **three irreversible steps in glycolysis** that require different enzymes in gluconeogenesis to bypass them. - Key bypass enzymes include **pyruvate carboxylase**, **phosphoenolpyruvate carboxykinase (PEPCK)**, **fructose-1,6-bisphosphatase**, and **glucose-6-phosphatase**. *It only occurs during fed state when insulin levels are high* - **Gluconeogenesis is activated during fasting or starvation** when blood glucose levels are low, and it is largely **inhibited by high insulin levels**. - Its purpose is to produce new glucose to prevent hypoglycemia, not to store excess glucose. *Fatty acids are the primary substrate for gluconeogenesis* - **Fatty acids cannot be directly converted to glucose** in significant amounts in humans because they are broken down into acetyl-CoA, which cannot be used for net glucose synthesis. - Primary substrates include **lactate**, **amino acids** (from protein breakdown), and **glycerol** (from triglyceride breakdown).
Question 403: Which of the following tissues relies EXCLUSIVELY on anaerobic glycolysis for ATP production?
- A. Skeletal muscle during exercise (anaerobic)
- B. Liver hepatocytes (primarily aerobic)
- C. Cardiac muscle (primarily aerobic)
- D. Mature RBCs (exclusively anaerobic) (Correct Answer)
Explanation: ***Mature RBCs (exclusively anaerobic)*** - **Mature red blood cells** lack mitochondria, making them incapable of **oxidative phosphorylation** and thus relying entirely on **anaerobic glycolysis** for ATP. - This pathway produces **2 net ATP** molecules per glucose molecule, which is sufficient for their metabolic needs like maintaining ion gradients. *Skeletal muscle during exercise (anaerobic)* - While skeletal muscle can perform **anaerobic glycolysis** during intense exercise when oxygen supply is limited, it is not an exclusive reliance. - Skeletal muscle also utilizes **aerobic respiration** and **creatine phosphate** for ATP production depending on activity level and oxygen availability. *Cardiac muscle (primarily aerobic)* - **Cardiac muscle** has a very high metabolic demand and is rich in **mitochondria**, relying almost exclusively on **aerobic respiration** for ATP production. - It uses fatty acids, glucose, and lactate as fuel sources, producing a large amount of ATP efficiently with oxygen. *Liver hepatocytes (primarily aerobic)* - **Liver hepatocytes** are highly metabolically active and primarily rely on **aerobic respiration** for ATP production, performing diverse functions such as gluconeogenesis, glycogenolysis, and detoxification. - Although the liver can perform some anaerobic glycolysis under hypoxic conditions, it is not its exclusive or primary mode of ATP synthesis.
Question 404: The energy for glycogenesis is provided by -
- A. GTP
- B. GDP
- C. UTP (Correct Answer)
- D. AMP
Explanation: ***UTP*** - **Uridine triphosphate (UTP)** is essential for **glycogenesis** as it activates glucose by forming **UDP-glucose** from glucose-1-phosphate. - The reaction (Glucose-1-P + UTP → UDP-glucose + PPi) creates a **high-energy intermediate** that drives glycogen synthesis. - The subsequent hydrolysis of pyrophosphate (PPi) makes this activation step **irreversible**, and the energy stored in UDP-glucose is used for **glycosidic bond formation** when glucose is added to the growing glycogen chain. *GTP* - **Guanosine triphosphate (GTP)** is primarily involved in **protein synthesis**, G-protein signaling, and the citric acid cycle. - It is not used for glucose activation in glycogenesis; that role is specific to **UTP**. *GDP* - **Guanosine diphosphate (GDP)** is a product of GTP hydrolysis and functions in regulatory processes. - It does not serve as an energy donor for glycogen synthesis. *AMP* - **Adenosine monophosphate (AMP)** is a low-energy signal molecule that indicates cellular energy depletion. - High AMP levels **inhibit glycogenesis** and activate glycogenolysis through allosteric regulation of key enzymes. - It does not provide energy for anabolic pathways like glycogen synthesis.
Question 405: Inhibition of glycolysis by increased supply of O2 is called ?
- A. Pasteur effect (Correct Answer)
- B. Crabtree phenomenon
- C. Lewis phenomenon
- D. None of the options
Explanation: ***Pasteur effect*** - The **Pasteur effect** describes the phenomenon where the rate of **glycolysis** is inhibited when **oxygen** is available (aerobic conditions). - This inhibition occurs because **oxidative phosphorylation** is more efficient at generating ATP, leading to reduced reliance on glycolysis for energy production. *Crabtree phenomenon* - The **Crabtree phenomenon** is the opposite of the Pasteur effect, where high concentrations of **glucose** inhibit oxygen consumption in the presence of oxygen. - This is primarily observed in some **cancer cells** and yeast, leading to increased glycolysis even under aerobic conditions. *Lewis phenomenon* - The **Lewis phenomenon** (also known as the hunting reaction) refers to the cyclical vasodilation and constriction of peripheral blood vessels in response to **cold exposure**. - It's a physiological response to protect tissues from **frostbite** and is not related to glycolysis or oxygen supply. *None of the options* - This option is incorrect as the phenomenon described, inhibition of glycolysis by increased O2, is a well-established biochemical process known as the **Pasteur effect**.
Question 406: Ketone bodies are not used by?
- A. Brain
- B. Muscle
- C. RBC (Correct Answer)
- D. Renal cortex
Explanation: ***RBC*** - Red blood cells **lack mitochondria**, which are essential organelles for the **oxidation of ketone bodies** (acetoacetate and β-hydroxybutyrate) for energy production. - Their primary energy source is **anaerobic glycolysis** of glucose. *Muscle* - **Skeletal and cardiac muscles** readily utilize **ketone bodies** as an alternative fuel source, especially during prolonged fasting or starvation. - This helps to conserve glucose for other tissues, particularly the brain. *Brain* - The brain can adapt to use **ketone bodies** for energy when glucose supply is limited, such as during prolonged fasting or in cases of uncontrolled diabetes. - This process is crucial for brain function when glucose levels are low. *Renal cortex* - The **renal cortex** is capable of utilizing **ketone bodies** for energy, particularly during starvation. - The kidney is also involved in the **synthesis of glucose** (gluconeogenesis) and the excretion of ketone bodies.
Pathology
3 questionsMALT lymphoma is positive for which of the following markers?
In which condition are Michaelis Gutmann bodies typically seen?
In glomerulus subendothelial deposits are seen in?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 401: MALT lymphoma is positive for which of the following markers?
- A. CD20 (Correct Answer)
- B. CD19
- C. CD43
- D. CD5
Explanation: ***CD20*** - MALT lymphoma is a type of **B-cell non-Hodgkin lymphoma**, and CD20 is a **pan B-cell marker consistently expressed** in MALT lymphomas. - CD20 positivity is **crucial for diagnosis** and is the **primary therapeutic target** for anti-CD20 monoclonal antibody therapy (Rituximab). - In diagnostic practice, **CD20 is the most important B-cell marker** for identifying MALT lymphoma and guiding treatment decisions. *CD19* - CD19 is also a **pan B-cell marker** and is **typically positive in MALT lymphoma** along with CD20. - However, in the context of this question, **CD20 is the preferred answer** because it is the **standard diagnostic marker emphasized in clinical practice** and the **primary therapeutic target**. - Both markers are positive, but CD20 has greater **clinical and therapeutic significance** in MALT lymphoma management. *CD43* - CD43 is primarily a **T-cell and myeloid marker**, but can show **aberrant expression in 40-50% of MALT lymphomas**. - While it may be positive in some cases, it is **not a defining B-cell lineage marker** and is not used as a primary diagnostic criterion for MALT lymphoma. - Its variable expression makes it **less reliable** than consistent B-cell markers like CD20. *CD5* - CD5 is typically associated with **T-cells** and certain B-cell lymphomas, particularly **chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL)** and **mantle cell lymphoma**. - **MALT lymphoma is characteristically CD5-negative**, which is an important feature for **differentiating it from CD5+ B-cell lymphomas**.
Question 402: In which condition are Michaelis Gutmann bodies typically seen?
- A. Xanthogranulomatous
- B. Pyelonephritis
- C. Malakoplakia (Correct Answer)
- D. Nail patella syndrome
Explanation: ***Malakoplakia*** - **Michaelis-Gutmann bodies** are pathognomonic histological features of malakoplakia, representing calcified concretions containing **iron and calcium** within macrophages. - These are formed around **partially digested bacteria** within defective macrophages, appearing as basophilic inclusions with a "target-like" or "owl's eye" appearance. - Malakoplakia is a chronic granulomatous inflammatory condition most commonly affecting the **urinary tract** (bladder, kidney), but can occur in other organs. *Xanthogranulomatous* - This condition is characterized by an infiltrate of **lipid-laden macrophages** (xanthoma cells, foam cells) and occasional giant cells, but **not** Michaelis-Gutmann bodies. - It most commonly affects the kidney (**xanthogranulomatous pyelonephritis**) and is a destructive inflammatory process with a mass-like appearance. *Pyelonephritis* - Refers to **inflammation of the kidney and renal pelvis**, usually due to bacterial infection (commonly E. coli). - Histologically, it is characterized by acute or chronic inflammatory cells, neutrophil infiltration, and potential abscess formation, **without** Michaelis-Gutmann bodies. *Nail patella syndrome* - This is a **genetic disorder** (autosomal dominant) affecting primarily the **nails, bones** (absent/hypoplastic patella, elbow dysplasia), and sometimes the kidneys (glomerular disease). - It is associated with developmental abnormalities and has **no association** with Michaelis-Gutmann bodies or malakoplakia.
Question 403: In glomerulus subendothelial deposits are seen in?
- A. Goodpasture syndrome (linear IgG deposits in the basement membrane)
- B. MPGN type I (subendothelial deposits) (Correct Answer)
- C. MPGN type II (intramembranous deposits)
- D. IgA nephropathy (mesangial IgA deposits)
Explanation: ***MPGN type I*** - **Subendothelial deposits** are a hallmark of MPGN type I, often associated with **immune complex deposition** [1]. - This condition can present with **hematuria**, **proteinuria**, and can be triggered by infections or autoimmune diseases [1]. *Good pasture syndrome* - Primarily involves **anti-GBM antibodies** leading to **glomerulonephritis** and pulmonary hemorrhage, not subendothelial deposits. - Typically, it presents with **crescent formation** in the glomeruli rather than deposits. *MPGN type II* - Characterized by **dense deposit disease**, it features **intramembranous** rather than subendothelial deposits [1]. - It is often associated with **C3 nephritic factor** and does not show classic subendothelial pathology. *IgA nephropathy* - Characterized by **IgA deposits** primarily in the **mesangium**, not subendothelially. - It presents with **hematuria** and recurrent episodes of **macrohematuria**, especially after infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 925-927.
Pharmacology
1 questionsWhich of the following substances is not classified as a carcinogen for bladder cancer?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 401: Which of the following substances is not classified as a carcinogen for bladder cancer?
- A. Acrolein
- B. Phenacetin
- C. Benzidine
- D. Isopropyl alcohol (Correct Answer)
Explanation: ***Isopropyl alcohol*** - Research does not link **isopropyl alcohol** to an increased risk of bladder cancer, making it a non-carcinogenic substance in this context. - It is commonly used as a solvent and antiseptic, but has not shown **urogenic carcinogenicity** in studies. *Phenacetin* - **Phenacetin** is an analgesic that has been associated with an increased risk of bladder cancer, particularly due to its metabolite, which can be nephrotoxic. - Its use has significantly declined due to its carcinogenic effects on the urinary system. *Benzidine* - **Benzidine** is a well-known bladder carcinogen, primarily linked to the dye industry, where exposure has led to increased rates of bladder cancer [1]. - This substance has been implicated in **urothelial carcinoma** due to its mutagenic properties. *Acrolein* - **Acrolein** is a toxic compound that can cause bladder irritation and has been studied for its potential carcinogenic effects related to bladder cancer. - It is released during the combustion of materials and is known to contribute to **chemical injury** in the bladder. **References:** [1] 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. 217-218.