Biochemistry
1 questionsWhat is the half-life of Prealbumin?
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 161: 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.
Physiology
9 questionsWhich of the following statements about thyroid hormone receptors is correct?
After injecting testosterone in a hypoandrogenic male, which of the following occurs ?
Which of the following does not stimulate growth hormone (GH) release?
What is the effect of moderate exercise on cerebral blood flow?
What is the role of gap junctions in cardiac muscle function?
What is the blood supply of the liver in ml/min/100g?
Plasma volume is measured by ?
Mechanism of action of cholecystokinin?
LH surge is associated with?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 161: Which of the following statements about thyroid hormone receptors is correct?
- A. They directly bind to thyrotropin-releasing hormone (TRH)
- B. They directly bind to thyroid-stimulating hormone (TSH)
- C. They cause nuclear transcription after binding with T4
- D. They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3. (Correct Answer)
Explanation: ***They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3.*** - **Thyroid hormone receptors** are indeed **intracellular** and act as **ligand-activated transcription factors**, regulating gene expression. - While both **T3** and **T4** can bind, **T3 (triiodothyronine)** is the more potent and active form, binding with much higher affinity to the receptors to exert its primary metabolic effects. *They directly bind to thyrotropin-releasing hormone (TRH)* - **TRH (thyrotropin-releasing hormone)** is produced by the hypothalamus and acts on the **pituitary gland** to stimulate TSH release, not directly on thyroid hormone receptors. - Thyroid hormone receptors bind to thyroid hormones (**T3 and T4**), not to the hypothalamic releasing hormones like TRH. *They directly bind to thyroid-stimulating hormone (TSH)* - **TSH (thyroid-stimulating hormone)** is produced by the pituitary gland and primarily acts on receptors located on the **thyroid gland cells** to stimulate thyroid hormone synthesis and release. - Thyroid hormone receptors are distinct from TSH receptors and bind to the hormones themselves (**T3/T4**), not the stimulating hormone TSH. *Causes nuclear transcription after binding with T4* - While **T4 (thyroxine)** can bind to thyroid hormone receptors, it is primarily a **prohormone**. - T4 is largely converted to the more active **T3** within target cells, and **T3** is the main mediator of nuclear transcription through these receptors.
Question 162: After injecting testosterone in a hypoandrogenic male, which of the following occurs ?
- A. Decreased LH secretion
- B. Decreased FSH secretion (Correct Answer)
- C. Increased spermatogenesis
- D. None of the options
Explanation: ***Decreased FSH secretion*** - Exogenous testosterone administration leads to **negative feedback** on the hypothalamic-pituitary-gonadal axis, suppressing **GnRH** release, which in turn decreases both **LH** and **FSH** secretion. - FSH suppression is particularly clinically significant because it results in **inhibition of spermatogenesis**, which is a key consideration when using testosterone replacement therapy. - The decrease in FSH, combined with reduced **intratesticular testosterone** (due to LH suppression), impairs Sertoli cell function and sperm production. *Decreased LH secretion* - **This also occurs** with exogenous testosterone administration due to negative feedback on the hypothalamus and pituitary. - Testosterone primarily suppresses **LH** through direct negative feedback at the hypothalamic-pituitary level. - However, in the context of this question focusing on the consequences in a hypoandrogenic male receiving testosterone, the **FSH suppression** and its impact on spermatogenesis is the more clinically emphasized outcome. - **Note:** Both LH and FSH decrease; this question likely emphasizes FSH due to its role in fertility concerns with testosterone therapy. *Increased spermatogenesis* - This is **incorrect**. Exogenous testosterone actually **suppresses spermatogenesis** through multiple mechanisms: - Decreased **FSH** (essential for Sertoli cell function) - Decreased **intratesticular testosterone** concentration (despite high systemic levels) - The high local testosterone concentration within the seminiferous tubules (30-100x serum levels) cannot be achieved by systemic testosterone alone. *None of the options* - This is incorrect because exogenous testosterone administration clearly causes **suppression of gonadotropins** (both LH and FSH) through well-established negative feedback mechanisms.
Question 163: 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 164: What is the effect of moderate exercise on cerebral blood flow?
- A. Decreases
- B. Initially decreases then increases
- C. Increases (Correct Answer)
- D. Does not change
Explanation: ***Increases*** - Moderate exercise leads to an **increase in systemic arterial pressure** and an increase in **cardiac output**, which often results in a moderate increase in cerebral blood flow. - This increase is also attributed to **vasodilation of cerebral arteries** in response to metabolic demands and changes in blood gas levels during exercise. *Decreases* - A decrease in cerebral blood flow is generally associated with conditions leading to **hypoperfusion** or **severe vasoconstriction**, which are not typical effects of moderate exercise. - While extreme exercise could potentially cause some transient vasoconstriction, moderate exercise typically has the opposite effect due to compensatory mechanisms. *Initially decreases then increases* - There is generally no physiological mechanism by which moderate exercise would cause an initial decrease in cerebral blood flow followed by an increase. - Cerebral autoregulation usually maintains a stable blood flow, and the overall trend with moderate exercise is an increase. *Does not change* - While **cerebral autoregulation** aims to keep cerebral blood flow stable over a range of blood pressures, moderate exercise often pushes parameters (like CO2 levels and systemic pressure) enough to cause a measurable, albeit modest, **increase in blood flow**. - The brain's metabolic demand also increases during exercise, necessitating an increased blood supply.
Question 165: What is the role of gap junctions in cardiac muscle function?
- A. Are not found in cardiac muscles
- B. Are not found in smooth muscles
- C. Have no significant role in cardiac muscle function
- D. Facilitate impulse transmission between cardiac myocytes (Correct Answer)
Explanation: ***Facilitate impulse transmission between cardiac myocytes*** - **Gap junctions** are specialized channels between adjacent cells that allow for direct communication and rapid movement of **ions** and small molecules. - In cardiac muscle, they form an essential part of **intercalated discs**, enabling the heart to function as a **syncytium** by allowing electrical impulses to spread quickly from one myocyte to another. *Are not found in cardiac muscles* - This statement is incorrect; **gap junctions** are a defining feature of **cardiac muscle** and are crucial for its coordinated contraction. - They are located within the **intercalated discs** that connect individual cardiac muscle cells. *Are not found in smooth muscles* - This statement is incorrect; **gap junctions** are indeed found in **smooth muscle**, particularly in single-unit smooth muscle, where they contribute to synchronized contractions, such as in the **gastrointestinal tract**. - They allow for the rapid propagation of electrical signals, leading to coordinated muscle activity. *Have no significant role in cardiac muscle function* - This statement is incorrect; **gap junctions** play a critically significant role in cardiac muscle function by ensuring the **rapid and synchronized spread of electrical impulses**. - Without functional gap junctions, the heart would not be able to contract efficiently or effectively as a pump.
Question 166: 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 167: Plasma volume is measured by ?
- A. Inulin
- B. Evans blue (Correct Answer)
- C. D2O
- D. Mannitol
Explanation: ***Evans blue*** - **Evans blue** is a dye that binds to plasma proteins and **does not readily cross capillary membranes**, making it an effective tracer for measuring plasma volume. - After intravenous injection, its concentration can be measured to calculate the dilution space, which corresponds to the **plasma volume**. *Inulin* - **Inulin** is a polysaccharide primarily used to measure the **glomerular filtration rate (GFR)** because it is freely filtered by the glomeruli and neither reabsorbed nor secreted by the renal tubules. - It distributes into the **extracellular fluid compartment** and is not confined to the plasma, making it unsuitable for plasma volume measurement. *Mannitol* - **Mannitol** is an osmotic diuretic that distributes in the **extracellular fluid (ECF)**, it is generally used for its osmotic effects to reduce edema or intracranial pressure. - Due to its distribution beyond the plasma compartment, it is not used directly to measure **plasma volume**. *D20* - **D2O (deuterium oxide)**, or heavy water, is used to measure **total body water (TBW)** as it distributes throughout all fluid compartments of the body. - It does not selectively remain within the plasma compartment, making it unsuitable for measuring **plasma volume** alone.
Question 168: 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 169: LH surge is associated with?
- A. Increased estrogen & decreased progesterone (Correct Answer)
- B. Increased estrogen & increased progesterone
- C. Decreased estrogen & increased progesterone
- D. Decreased estrogen & decreased progesterone
Explanation: ***Increased estrogen & decreased progesterone*** - The **LH surge** is triggered by a significant rise in **estrogen** levels from the dominant follicle, indicating ovarian readiness. - At the time of the LH surge, **progesterone** levels remain low; they only begin to rise significantly after ovulation, when the corpus luteum forms. *Increased estrogen & increased progesterone* - While **estrogen** levels are high, **progesterone** only significantly increases *after* ovulation, as the corpus luteum develops. - High estrogen *and* high progesterone together are typically seen in the **luteal phase**, not at the peak of the LH surge. *Decreased estrogen & increased progesterone* - A decrease in **estrogen** would suppress LH, not trigger a surge. - Increased **progesterone** would also inhibit LH release via negative feedback in the follicular phase if it were to occur pre-ovulation. *Decreased estrogen & decreased progesterone* - Both **decreased estrogen** and **decreased progesterone** would lead to low FSH/LH levels and would not promote an LH surge or ovulation. - This hormonal profile is more characteristic of the very early follicular phase or menopause.