Biochemistry
2 questionsWhat is the approximate half-life of albumin in the human body?
What is the half-life of Prealbumin?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 381: What is the approximate half-life of albumin in the human body?
- A. 30 days
- B. 20 days (Correct Answer)
- C. 3 days
- D. 7 days
Explanation: ***20 days*** - The **half-life of albumin** in the human body is approximately **20 days**, reflecting the time it takes for half of the circulating albumin to be catabolized or excreted. - This relatively long half-life means that changes in albumin levels, such as those due to malnutrition or liver disease, may take several weeks to become evident. *3 days* - A half-life of 3 days is too short for albumin, which is a major, long-lasting plasma protein. - Proteins with such a short half-life typically include more rapidly turnover proteins or small peptides. *7 days* - A half-life of 7 days is also too short for albumin, which plays a critical role in maintaining plasma oncotic pressure and transporting various substances. - While some proteins have a 7-day half-life, albumin's is considerably longer. *30 days* - A half-life of 30 days is longer than the typical half-life of albumin. - While some proteins may have half-lives in this range, 20 days is the more commonly accepted value for albumin.
Question 382: What is the half-life of Prealbumin?
- A. 2 days (Correct Answer)
- B. 10 days
- C. 20 days
- D. 40 days
Explanation: ***2 days*** - Prealbumin, also known as transthyretin, has a **short half-life** of approximately 2-3 days, making it a sensitive indicator of recent changes in **nutritional status**. - Its rapid turnover allows for prompt reflection of improvement or deterioration in protein synthesis. *10 days* - A half-life of 10 days would make prealbumin less responsive to acute changes in nutrition compared to its actual turnover rate. - This duration is longer than the typical half-life of proteins used to monitor **short-term nutritional status**. *20 days* - A 20-day half-life would indicate a protein with a much slower turnover, unsuitable for monitoring **acute nutritional interventions**. - Proteins with such long half-lives, like **albumin**, reflect more chronic states rather than rapid changes. *40 days* - A half-life of 40 days is characteristic of proteins like **albumin**, which are influenced by longer-term nutritional and inflammatory processes. - Such a long half-life would not be useful for assessing immediate responses to **nutritional support** or acute disease states.
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 381: 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.
Physiology
7 questionsWhat does spermiogenesis refer to?
Which of the following does not stimulate growth hormone (GH) release?
During starvation, which hormone level increases?
What is the blood supply of the liver in ml/min/100g?
Mechanism of action of cholecystokinin?
Which hormone acts on JAK-STAT kinase receptor?
Normal range of serum osmolality is (mOsm/Kg)?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 381: What does spermiogenesis refer to?
- A. Formation of spermatozoa from spermatogonia
- B. Formation of spermatozoa from spermatids (Correct Answer)
- C. Formation of spermatids from spermatocytes
- D. Formation of secondary spermatocytes from primary spermatocytes
Explanation: ***Formation of spermatozoa from spermatids*** - **Spermiogenesis** is the final stage of spermatogenesis, involving the remarkable transformation of a round **spermatid** into a motile, mature **spermatozoon**. - This process includes crucial morphological changes such as the formation of the **acrosome**, condensation of the nucleus, development of the flagellum, and shedding of excess cytoplasm. *Formation of spermatozoa from spermatogonia* - This describes the entire process of **spermatogenesis**, which begins with **spermatogonia** and encompasses multiple stages including mitosis, meiosis, and spermiogenesis. - While it's the ultimate outcome, it doesn't specifically define the detailed transformation from spermatid to sperm. *Formation of spermatids from spermatocytes* - This stage refers to **meiosis II**, where **secondary spermatocytes** undergo division to produce **spermatids**. - Spermatids are precursors to spermatozoa and still require significant morphological changes to become mature sperm. *Formation of secondary spermatocytes from primary spermatocytes* - This describes **meiosis I**, where a **primary spermatocyte** divides to form two **secondary spermatocytes**. - This step reduces the chromosome number by half but doesn't involve the final morphological changes seen in spermiogenesis.
Question 382: Which of the following does not stimulate growth hormone (GH) release?
- A. Exercise
- B. Free fatty acids (Correct Answer)
- C. Fasting
- D. Stress
Explanation: ***Free fatty acids*** - High levels of **free fatty acids** in the bloodstream inhibit growth hormone (GH) secretion. - This occurs through a **negative feedback loop** at the level of the hypothalamus and pituitary gland. *Fasting* - **Fasting** (especially prolonged) is a potent stimulus for GH release, helping to mobilize fat stores and maintain **glucose homeostasis**. - During fasting, ghrelin levels increase, which further promotes GH secretion. *Exercise* - **Physical exercise** is a well-known physiological stimulus for GH release, contributing to muscle growth and repair. - The intensity and duration of exercise can influence the magnitude of GH secretion. *Stress* - Various forms of **stress**, including physical (e.g., trauma, surgery) and psychological stress, stimulate GH release. - This response is mediated in part by the **sympathetic nervous system** and increased cortisol levels.
Question 383: During starvation, which hormone level increases?
- A. Leptin
- B. MSH
- C. Insulin
- D. Ghrelin (Correct Answer)
Explanation: ***Ghrelin*** - **Ghrelin** is often referred to as the "hunger hormone" because its levels typically rise during fasting or periods of starvation. - It stimulates **appetite** and signals the brain to increase food intake, playing a crucial role in energy balance. *Leptin* - **Leptin** is a hormone produced by **adipose tissue** that signals satiety and helps regulate long-term energy balance. - During starvation, **leptin levels typically decrease** as fat stores are depleted, which further increases appetite and reduces energy expenditure. *MSH* - **Melanocyte-stimulating hormone (MSH)** is involved in skin pigmentation and appetite regulation, but its levels do not primarily increase in response to starvation. - While MSH can influence appetite, it is often seen to decrease appetite when present in higher concentrations, which is counterintuitive during starvation. *Insulin* - **Insulin** is a hormone produced by the **pancreas** that helps regulate blood glucose levels by promoting glucose uptake into cells. - During starvation, blood glucose levels decrease, leading to a **reduction in insulin secretion** to preserve glucose for vital organs like the brain.
Question 384: What is the blood supply of the liver in ml/min/100g?
- A. 1500-2000 ml/min/100g
- B. 1000-1500 ml/min/100g
- C. 50-60 ml/min/100g (Correct Answer)
- D. 250-300 ml/min/100g
Explanation: ***50-60 ml/min/100g*** - The liver receives a substantial blood supply, but when expressed per 100 grams of tissue, the value is around **50-60 mL/min/100g**. This demonstrates the organ's high metabolic demand. - This value represents the total blood flow from both the **hepatic artery** and the **portal vein** per unit weight of liver tissue. *1500-2000 ml/min/100g* - This value is extremely high and does not accurately represent the **blood flow per 100g of liver tissue**. Such a high flow rate would imply an unrealistic perfusion. - While the total blood flow to the liver is large, it's not at this magnitude when normalized to tissue weight. *1000-1500 ml/min/100g* - This range is closer to the **total blood flow to the entire liver** (1000-1800 ml/min), not the blood flow per 100 grams of tissue. - It's crucial to differentiate between total organ flow and flow density (per 100g). *250-300 ml/min/100g* - This value is significantly higher than the actual blood supply per 100g of liver tissue, suggesting an overestimation of the **perfusion density**. - While the liver is highly perfused, this rate is not physiologically accurate when normalized to the tissue weight.
Question 385: Mechanism of action of cholecystokinin?
- A. Activation of adenylyl cyclase
- B. Opening of ion channels
- C. Through IP3- DAG system (Correct Answer)
- D. Transcription factors
Explanation: ***Through IP3- DAG system*** - Cholecystokinin (CCK) primarily acts via **Gq protein-coupled receptors**, leading to the activation of **phospholipase C**. - This activation results in the hydrolysis of **PIP2 into IP3 and DAG**, which then mediate intracellular signaling cascades, causing actions like gallbladder contraction and pancreatic enzyme secretion. *Activation of adenylyl cyclase* - This mechanism is typically associated with **Gs protein-coupled receptors**, leading to increased levels of **cyclic AMP (cAMP)**. - Hormones like **glucagon** and **epinephrine** often utilize this pathway, which is distinct from CCK's primary signaling. *Opening of ion channels* - While ion channels are crucial for many cellular processes, CCK's direct mechanism of action typically involves **intracellular second messengers** rather than direct gating of ion channels. - Neurotransmitters like **acetylcholine** can directly open ion channels, but this is not the main signaling pathway for CCK. *Transcription factors* - Transcription factors regulate **gene expression** by binding to DNA, which is a slower, more long-term cellular response. - While CCK can eventually influence gene expression, its direct and immediate effects (e.g., gallbladder contraction) are mediated by **rapid second messenger systems**, not primary transcription factor modulation.
Question 386: Which hormone acts on JAK-STAT kinase receptor?
- A. TSH
- B. Thyroxine
- C. GH (Correct Answer)
- D. FSH
Explanation: ***GH*** - **Growth Hormone (GH)** binds to a **cytokine receptor** that lacks intrinsic tyrosine kinase activity and instead signals through associated **JAK-STAT kinases**. - This binding leads to **JAK phosphorylation**, which then phosphorylates and activates **STAT proteins**, regulating gene expression. *TSH* - **Thyroid-stimulating hormone (TSH)** acts on a **G protein-coupled receptor** to stimulate thyroid hormone production and release. - Its signaling pathway primarily involves the activation of **adenylyl cyclase** and increases in **cAMP**, not the JAK-STAT pathway. *Thyroxine* - **Thyroxine (T4)** is a **thyroid hormone** that primarily acts by binding to **intracellular nuclear receptors**, which then regulate gene transcription. - It directly influences gene expression, rather than signaling through cell surface receptors and kinase pathways like JAK-STAT. *FSH* - **Follicle-stimulating hormone (FSH)**, like TSH, signals through a **G protein-coupled receptor** on target cells in the gonads. - This activation primarily leads to an increase in **intracellular cAMP levels** to mediate its effects on gamete production and hormone synthesis.
Question 387: Normal range of serum osmolality is (mOsm/Kg)?
- A. 280 - 300 (Correct Answer)
- B. 250 - 270
- C. 300 - 320
- D. 210 - 230
Explanation: ***280 - 300*** - The normal range for **serum osmolality** is generally considered to be 280-300 mOsm/Kg. - This range reflects the appropriate balance of solutes (like sodium, glucose, and urea) in the blood, which is crucial for **fluid homeostasis**. *250 - 270* - A serum osmolality in this range would indicate **hypoosmolality**, suggesting a relative excess of water or a deficit of solutes in the blood. - This could be seen in conditions like **syndrome of inappropriate antidiuretic hormone (SIADH)** or primary polydipsia. *300 - 320* - This range suggests **hyperosmolality**, meaning there's a relative deficit of water or an excess of solutes. - Conditions such as **dehydration**, uncontrolled diabetes mellitus, or severe hypernatremia can lead to values in this range. *210 - 230* - Such a significantly low osmolality would represent severe **hypoosmolality**, usually associated with extreme overhydration or profound solute depletion. - This deviation is critically abnormal and would indicate severe electrolyte imbalance, potentially leading to **cerebral edema**.