The major role of 2,3-bisphosphoglycerate in RBCs is -
'Flare' in Triple response is mediated by :
Which of the following is a potassium Channelopathy?
Fastest receptor mediated action is through?
Which of the following is an action of muscarinic cholinergic receptors?
What is the PRIMARY mechanism by which the Na+-Ca2+ exchanger functions in cardiac muscle cells?
Rebound increase in gastric acid secretion after stopping proton pump inhibitor therapy is due to?
Lower esophageal sphincter pressure is increased by all of the following substances, EXCEPT:
What is the intensity in decibel of normal conversation in humans?
What is the caloric requirement for an adult male engaged in heavy physical work?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 91: 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.
Question 92: 'Flare' in Triple response is mediated by :
- A. Axon reflex (Correct Answer)
- B. Arteriolar dilation
- C. Histamine release
- D. Local hormones
Explanation: ***Axon reflex*** - The "flare" component of the triple response is caused by an **axon reflex**, where sensory nerve endings release **vasoactive neuropeptides** such as substance P and calcitonin gene-related peptide (CGRP). - These neuropeptides cause **vasodilation** in the surrounding area, leading to the characteristic red, irregularly shaped halo around the wheal. *Arteriolar dilation* - While arteriolar dilation is a component of the triple response and contributes to the **redness (flush)** and **flare**, it is not the direct mediator of the flare itself. - The initial arteriolar dilation is primarily due to **histamine** acting directly on the vessels, whereas the flare is a broader, neurally mediated spread of vasodilation. *Histamine release* - **Histamine** release from mast cells is the primary mediator of the initial **redness (flush)** and the formation of the **wheal** (swelling due to capillary permeability). - While histamine plays a role in the overall response, it does not directly mediate the "flare" component, which involves neuronal signaling via the axon reflex. *Local hormones* - While various **local mediators** (which could be broadly considered "local hormones" in a sense) are involved in inflammatory responses, the specific term "local hormones" is too general and does not precisely describe the mechanism of the flare. - The axon reflex, involving specific **neuropeptides**, is the precise mechanism for the flare, not a general category of local hormones.
Question 93: Which of the following is a potassium Channelopathy?
- A. Hyperkalemic periodic paralysis
- B. Long QT-syndrome
- C. Episodic ataxia I (Correct Answer)
- D. Hypokalemic periodic paralysis
Explanation: ***Episodic ataxia I*** - This condition is caused by mutations in the **KCNA1 gene**, which encodes the **Kv1.1 voltage-gated potassium channel**. - It represents a **classic neuromuscular potassium channelopathy** with episodes of **ataxia**, **dysarthria**, and myokymia. - This is a pure potassium channelopathy affecting the nervous system. *Hyperkalemic periodic paralysis* - This condition is caused by mutations in the **SCN4A gene**, which encodes a **sodium channel** subunit in skeletal muscle. - Despite the name suggesting potassium involvement, it is a **sodium channelopathy**, not a potassium channelopathy. - Episodes are triggered by elevated serum potassium levels. *Long QT syndrome* - Several subtypes (LQT1, LQT2, LQT5) are indeed caused by mutations in **potassium channel genes** (KCNQ1, KCNH2, KCNE1). - However, Long QT syndrome is a **heterogeneous group** that also includes sodium (LQT3) and calcium channelopathies. - It is classified as a **cardiac channelopathy** affecting ventricular repolarization. - In the context of this question, **Episodic ataxia I** is the most specific example of a pure potassium channelopathy. *Hypokalemic periodic paralysis* - This condition is most commonly caused by mutations in the **CACNA1S gene** (encoding a **calcium channel**) or **SCN4A gene** (encoding a **sodium channel**). - It is not a potassium channelopathy despite the hypokalemia that triggers episodes.
Question 94: Fastest receptor mediated action is through?
- A. Intrinsic ion channels (Correct Answer)
- B. Intracellular receptors
- C. Cell surface receptors
- D. Receptor tyrosine kinases
Explanation: ***Intrinsic ion channels*** - Receptors that are also **ion channels** (ligand-gated ion channels) allow direct and rapid ion flow across the membrane upon ligand binding, leading to immediate changes in membrane potential. - This direct mechanism bypasses complex intracellular signaling cascades, resulting in the **fastest cellular response** compared to other receptor types. *Cell surface receptors* - This is a broad category that includes **G protein-coupled receptors** and **receptor tyrosine kinases**, which typically involve more complex and slower signaling pathways. - While located on the cell surface, not all receptors in this category mediate action as quickly as intrinsic ion channels. *Receptor tyrosine kinases* - These receptors initiate signaling by **phosphorylating tyrosine residues** on target proteins, triggering a cascade of intracellular events that take time to manifest. - Their action involves **multiple phosphorylation steps** and protein interactions, making their response slower compared to direct ion channels. *Intracellular receptors* - These receptors, such as **steroid hormone receptors**, are located in the cytoplasm or nucleus and require their ligands to diffuse across the cell membrane. - The activated receptor then typically translocates to the nucleus to regulate gene transcription, a process that is much **slower** due to gene expression and protein synthesis.
Question 95: Which of the following is an action of muscarinic cholinergic receptors?
- A. Skeletal muscle contraction
- B. Acid secretion in stomach
- C. Decreased heart rate (Correct Answer)
- D. Salivation and lacrimation
Explanation: ***Decreased heart rate*** - Activation of **muscarinic cholinergic receptors (M2 receptors)** in the heart leads to a decrease in heart rate and conduction velocity. - This effect is mediated by the **vagus nerve (parasympathetic nervous system)**, which releases acetylcholine to act on these receptors. - This is the **most characteristic and clinically significant cardiovascular effect** of muscarinic receptor activation, making it the expected answer. *Skeletal muscle contraction* - **Skeletal muscle contraction** is mediated by **nicotinic acetylcholine receptors (nAChRs)** at the **neuromuscular junction**, NOT muscarinic receptors. - Nicotinic receptors are **ligand-gated ion channels** that cause direct depolarization and muscle contraction when activated. - This is the only option that is **NOT a muscarinic receptor action**. *Acid secretion in stomach* - **Gastric acid secretion** IS mediated by **M3 muscarinic receptors** on parietal cells. - Acetylcholine from the vagus nerve directly stimulates parietal cells and also stimulates histamine release from enterochromaffin-like cells. - While this is a valid muscarinic action, in the context of distinguishing muscarinic effects, **cardiac effects** (decreased heart rate) are more emphasized as the classic teaching point. *Salivation and lacrimation* - **Salivation and lacrimation** ARE mediated by **M3 muscarinic receptors** in exocrine glands. - These are classic parasympathetic/muscarinic effects taught in physiology. - However, when distinguishing key muscarinic actions, **M2 receptor-mediated cardiac effects** are typically highlighted as the primary cardiovascular manifestation, while M3 effects on glands are secondary teaching points.
Question 96: What is the PRIMARY mechanism by which the Na+-Ca2+ exchanger functions in cardiac muscle cells?
- A. Na+-Ca2+ exchanger requires ATP directly
- B. Na+-Ca2+ exchanger acts to remove Ca2+ from heart muscle cells (Correct Answer)
- C. The Na+-Ca2+ exchanger operates in reverse mode during normal cardiac contraction
- D. The Na+-Ca2+ exchanger primarily moves Ca2+ into cardiac muscle cells during systole
Explanation: ***Na+-Ca2+ exchanger acts to remove Ca2+ from heart muscle cells.*** - The primary function of the **Na+-Ca2+ exchanger (NCX)** in cardiac muscle is to **extrude calcium from the cell** into the extracellular space. - It uses the electrochemical gradient of **sodium (Na+)** which flows into the cell, to power the removal of **calcium (Ca2+)** from the cell, contributing to muscle relaxation during diastole. *The Na+-Ca2+ exchanger operates in reverse mode during normal cardiac contraction* - While it can theoretically operate in reverse, its **primary physiological role** during normal cardiac contraction is forward mode (Ca2+ extrusion). - Reverse mode operation (Ca2+ influx) is typically seen under specific conditions, such as **pathological states** or severely altered intracellular Na+ concentrations. *Na+-Ca2+ exchanger requires ATP directly* - The **Na+-Ca2+ exchanger** is a **secondary active transporter** and does not directly use ATP. - Its energy comes from the **electrochemical gradient of Na+**, which is maintained by the **Na+/K+-ATPase** (primary active transport, which *does* use ATP). *The Na+-Ca2+ exchanger primarily moves Ca2+ into cardiac muscle cells during systole.* - Moving **Ca2+ into the cell** during systole would primarily be the role of **L-type calcium channels** on the sarcolemma. - The NCX's main role is to **reduce intracellular Ca2+** after contraction, facilitating relaxation during diastole.
Question 97: Rebound increase in gastric acid secretion after stopping proton pump inhibitor therapy is due to?
- A. Parietal cell hyperplasia
- B. Increased histamine release
- C. Hypergastrinemia (Correct Answer)
- D. Hypersensitivity of Ach receptors
Explanation: ***Hypergastrinemia*** - Proton pump inhibitors (PPIs) create a state of **hypochlorhydria** (reduced stomach acid), which in turn stimulates the **G cells** in the stomach to produce more **gastrin**. - This elevated gastrin level leads to a compensatory increase in the number and activity of **parietal cells**, causing a rebound hypersecretion of acid when PPI therapy is discontinued. *Parietal cell hyperplasia* - While parietal cell hyperplasia can occur, it is a consequence of chronic **hypergastrinemia**, not the primary driver of rebound acid secretion. - The direct effect of increased gastrin stimulating existing parietal cells is more immediate and significant for the rebound phenomenon. *Increased histamine release* - Elevated histamine release from **enterochromaffin-like (ECL) cells** is a downstream effect of hypergastrinemia, as gastrin stimulates ECL cells. - While increased histamine contributes to acid secretion, the root cause for its increase in this context is the **hypergastrinemia** induced by PPIs. *Hypersensitivity of Ach receptors* - **Acetylcholine (Ach) receptors** on parietal cells are involved in direct neural stimulation of acid secretion. - There is no evidence that stopping PPIs causes an increased sensitivity of these receptors, or that this is the primary mechanism of rebound acid secretion.
Question 98: Lower esophageal sphincter pressure is increased by all of the following substances, EXCEPT:
- A. Motilin
- B. Gastrin
- C. Substance P
- D. Secretin (Correct Answer)
Explanation: ***Secretin*** - **Secretin** is a gastrointestinal hormone that *decreases* lower esophageal sphincter (LES) pressure - This hormone is released from S cells in the duodenum in response to acidic chyme - Its primary role is to stimulate the pancreas to release **bicarbonate-rich fluid** to neutralize acidic chyme entering the duodenum - By decreasing LES pressure, it facilitates the passage of gastric contents into the duodenum during digestion *Gastrin* - **Gastrin** is a hormone that *increases* lower esophageal sphincter (LES) pressure - This helps prevent gastroesophageal reflux when the stomach is distended - It also stimulates the secretion of **gastric acid** by parietal cells in the stomach - Released from G cells in the gastric antrum in response to protein ingestion *Motilin* - **Motilin** is a peptide hormone that *increases* lower esophageal sphincter (LES) pressure - It initiates the **migrating motor complex (MMC)** during the interdigestive period - Stimulates gastric and intestinal motility - Released from M cells in the duodenum and jejunum *Substance P* - **Substance P** is a neuropeptide that *increases* lower esophageal sphincter (LES) pressure - Functions as both a neurotransmitter and neuromodulator in the enteric nervous system - Plays a role in **smooth muscle contraction** and gastrointestinal motility - Also involved in pain transmission and inflammatory responses
Question 99: What is the intensity in decibel of normal conversation in humans?
- A. 30dB
- B. 60dB (Correct Answer)
- C. 90dB
- D. 150dB
Explanation: ***60dB*** - The sound intensity of **normal human conversation** is typically around **60 decibels (dB)**. - This level is considered **moderate** and is comfortably audible without causing discomfort or hearing damage. *30dB* - A sound intensity of **30dB** is characteristic of a **quiet whisper** or a **soft rustle of leaves**. - This level is much **quieter** than a normal conversation and would require closer proximity to be clearly heard. *90dB* - **90dB** represents a significantly **louder sound**, comparable to that of a **lawnmower** or a **heavy truck** passing by. - Prolonged exposure to sounds at this intensity can start to cause **hearing damage**. *150dB* - **150dB** is an **extremely loud** and potentially **painful** sound level, similar to a **jet engine at takeoff** or a **firecracker** exploding nearby. - Exposure to sounds this intense can cause **immediate and permanent hearing loss**.
Question 100: What is the caloric requirement for an adult male engaged in heavy physical work?
- A. 3500 kcal/d (Correct Answer)
- B. 2000 kcal/d
- C. 2500 kcal/d
- D. 3000 kcal/d
Explanation: ***3500 kcal/d*** - Adult males engaged in **heavy physical work** have significantly higher energy demands due to increased **metabolic expenditure**. - This level of caloric intake is necessary to support physical activity, maintain muscle mass, and prevent weight loss in individuals with demanding occupations. *2000 kcal/d* - This caloric intake is typically recommended for adult females who are **sedentary** or for adult males engaging in light activity, which is insufficient for heavy physical work. - It would likely lead to a **caloric deficit** and weight loss for an individual performing heavy labor. *2500 kcal/d* - This level of intake is more appropriate for moderately active adult males, but it would often be **insufficient** for those performing heavy physical work. - Individuals engaged in heavy labor require additional energy to fuel their intense activities to maintain **energy balance**. *3000 kcal/d* - While a higher intake, 3000 kcal/d might still be **borderline** or insufficient for an adult male engaged in very heavy or sustained physical work. - This value might be appropriate for moderately heavy work, but heavy work often necessitates an even higher **caloric intake** to meet energy demands.