Maximum density of muscle spindle is found in?
During the sympathetic fight-or-flight response, what is the primary cardiovascular effect of epinephrine and norepinephrine on skeletal muscle vasculature?
EPSP is due to?
Small intestinal peristalsis is controlled by :
Cholecystokinin is produced from:
Somatomedin-C deficiency causes?
Inotropic effect of thyroid hormone is by ?
What is the nature of the relationship between insulin and glucose concentration in the human body?
Which of the following statements about insulin-mediated transport of glucose is correct?
Which of the following is not a component of a mature sperm cell?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 41: Maximum density of muscle spindle is found in?
- A. Calf muscle
- B. Lumbricals (Correct Answer)
- C. Triceps
- D. Quadriceps muscle
Explanation: ***Lumbricals*** - **Lumbricals** are small, intricate muscles in the hand, responsible for fine motor control and precise movements like grasping and manipulating objects. - The high density of **muscle spindles** in lumbricals allows for extremely accurate feedback on muscle length and tension, crucial for **proprioception** and delicate tasks. *Calf muscle* - **Calf muscles** (gastrocnemius and soleus) are large muscles primarily involved in powerful movements like walking and running. - While they do contain muscle spindles for proprioception, their density is lower compared to muscles involved in fine motor control. *Quadriceps muscle* - The **quadriceps femoris** is a large muscle group in the thigh responsible for knee extension and powerful leg movements. - They contain muscle spindles to monitor muscle stretch, but not with the extreme density seen in muscles with fine motor functions. *Triceps* - The **triceps brachii** is a large muscle on the back of the upper arm, primarily responsible for elbow extension. - It has a moderate density of muscle spindles, sufficient for coordinating arm movements but not as high as muscles designed for precision.
Question 42: During the sympathetic fight-or-flight response, what is the primary cardiovascular effect of epinephrine and norepinephrine on skeletal muscle vasculature?
- A. Increased blood flow to muscles (Correct Answer)
- B. Increased blood flow to the skin
- C. Bronchoconstriction
- D. Decreased heart rate
Explanation: ***Increased blood flow to muscles*** - **Epinephrine** and **norepinephrine** cause **vasodilation** in skeletal muscle arterioles, shunting blood toward tissues critical for immediate physical action. - This response ensures that muscles have adequate **oxygen** and **nutrients** to support intense activity, enabling a quick escape or confrontation. *Increased blood flow to the skin* - During fight-or-flight, the body prioritizes essential organs, causing **vasoconstriction** in the skin to redirect blood flow away from non-essential areas. - This redirection helps to conserve blood and reduce potential blood loss from surface injuries. *Bronchoconstriction* - **Epinephrine** and **norepinephrine** actually cause **bronchodilation**, leading to the relaxation of airway smooth muscles. - This effect increases the diameter of the airways, allowing more air to enter and exit the lungs, thereby enhancing **oxygen intake** and carbon dioxide expulsion. *Decreased heart rate* - The primary effect of **epinephrine** and **norepinephrine** is to **increase heart rate** and myocardial contractility. - This cardiac acceleration enhances **cardiac output**, ensuring rapid and efficient delivery of oxygenated blood throughout the body to meet the demands of stress.
Question 43: EPSP is due to?
- A. Sodium ion influx (Correct Answer)
- B. Potassium ion influx
- C. Sodium ion efflux
- D. Calcium ion influx
Explanation: ***Sodium ion influx*** - An **Excitatory Postsynaptic Potential (EPSP)** is caused primarily by the binding of an **excitatory neurotransmitter** to its receptor, leading to the opening of **ligand-gated ion channels** permeable to sodium (Na+) ions. - The **influx of positively charged sodium ions** into the postsynaptic neuron causes a **depolarization** of the membrane potential, making it more likely to reach the threshold for an action potential. *Potassium ion influx* - **Potassium (K+) influx** is not the primary mechanism for generating an EPSP; instead, **potassium efflux** (movement out of the cell) is typically involved in **repolarization** after an action potential or in generating **Inhibitory Postsynaptic Potentials (IPSPs)**. - The movement of K+ into the cell would make the membrane potential more negative, leading to **hyperpolarization** or preventing depolarization. *Sodium ion efflux* - **Sodium (Na+) efflux** is mediated by the **Na+/K+ pump** and is crucial for maintaining the resting membrane potential, but it does **not directly cause an EPSP**. - Pumping Na+ out of the cell would **hyperpolarize** the cell or oppose depolarization, making an action potential less likely. *Calcium ion influx* - While **calcium (Ca2+) influx** is vital for many neuronal processes, including **neurotransmitter release** from the presynaptic terminal, it is **not the primary ionic basis** for generating an EPSP in the postsynaptic neuron itself. - Significant Ca2+ influx can occur during an **action potential** or lead to intracellular signaling, but it's not the main depolarizing current responsible for an EPSP.
Question 44: Small intestinal peristalsis is controlled by :
- A. Meissner's plexus
- B. Vagus nerve
- C. Parasympathetic system
- D. Myenteric plexus (Correct Answer)
Explanation: ***Myenteric plexus*** - The **myenteric (Auerbach's) plexus** is located between the longitudinal and circular muscle layers of the muscularis propria and is primarily responsible for **controlling gastrointestinal motility**, including peristalsis. - Its neurons coordinate the contractions and relaxations of these muscle layers to propel contents through the alimentary canal. *Meissners plexus* - The **Meissner's (submucosal) plexus** is located in the submucosa and mainly controls **glandular secretion**, local blood flow, and absorption, rather than muscle motility. - While it subtly influences motility through local reflexes, it is not the primary controller of peristalsis. *Vagus nerve* - The **vagus nerve (cranial nerve X)** provides parasympathetic innervation to the small intestine, modulating activity but not directly initiating or solely controlling peristalsis. - It influences the activity of the enteric nervous system (including the myenteric plexus) but does not itself generate the complex, coordinated patterns of muscle contraction. *Parasympathetic system* - The **parasympathetic nervous system**, through nerves like the vagus, generally **stimulates gastrointestinal motility**, but it acts by modulating the intrinsic enteric nervous system. - The local control and generation of specific peristaltic movements are primarily mediated by the enteric nervous system, especially the myenteric plexus.
Question 45: Cholecystokinin is produced from:
- A. Hepatocyte
- B. Gastric mucosa
- C. Duodenal mucosa (Correct Answer)
- D. Epithelial cells of distal common bile duct
Explanation: ***Duodenal mucosa*** - **Cholecystokinin (CCK)** is primarily secreted by **I cells**, which are specialized enteroendocrine cells located in the **mucosa of the duodenum** and jejunum. - The release of CCK is stimulated by the presence of **fatty acids** and **amino acids** in the small intestine. *Hepatocyte* - **Hepatocytes** are the main functional cells of the liver, responsible for bile production, metabolism, and detoxification. - They **do not produce regulatory hormones** like cholecystokinin. *Gastric mucosa* - The **gastric mucosa** primarily produces **gastrin**, hydrochloric acid, and pepsinogen, which are involved in gastric digestion. - It does **not secrete cholecystokinin**, which is involved in stimulating gallbladder contraction and pancreatic enzyme release. *Epithelial cells of distal common bile duct* - The **epithelial cells of the common bile duct** are involved in bile transport and modification, but **not in hormone production**. - Their primary role is to line the duct and contribute to the composition of bile.
Question 46: Somatomedin-C deficiency causes?
- A. Growth retardation (Correct Answer)
- B. Genetic dwarfism
- C. Congenital hypothyroidism
- D. Type 1 diabetes mellitus
Explanation: ***Growth retardation*** - **Somatomedin-C** (also known as **Insulin-like Growth Factor 1 or IGF-1**) is a crucial mediator of **growth hormone's** effects on growth. - A deficiency in Somatomedin-C, therefore, directly leads to **impaired growth** and **stature**, manifesting as **growth retardation**. *Genetic dwarfism* - This term generally refers to dwarfism caused by various **genetic conditions** (e.g., achondroplasia), which may or may not involve the **growth hormone/IGF-1 axis**. - While Somatomedin-C deficiency can be genetic, "genetic dwarfism" is a broader term and not the most precise answer for the direct consequence. *Congenital hypothyroidism* - This condition results from **deficient thyroid hormone production** from birth. - It leads to neurological impairment and **growth failure**, but it is due to **thyroid hormone deficiency**, not Somatomedin-C deficiency. *Type 1 diabetes mellitus* - This is an **autoimmune disease** characterized by the **destruction of pancreatic beta cells**, leading to **insulin deficiency**. - It is entirely unrelated to **Somatomedin-C** or the growth hormone axis.
Question 47: Inotropic effect of thyroid hormone is by ?
- A. Membrane receptors
- B. cAMP
- C. cGMP
- D. Enhancement of Catecholamines (Correct Answer)
Explanation: ***Enhancement of Catecholamines*** - Thyroid hormones **potentiate the effects of catecholamines** (like adrenaline and noradrenaline) on the heart, leading to increased heart rate and contractility, which is an **inotropic effect**. - This occurs by increasing the number and sensitivity of **beta-adrenergic receptors** on cardiac muscle cells. *Membrane receptors* - While thyroid hormones do have some rapid, non-genomic effects that may involve **membrane receptors**, their primary and well-established inotropic effect is mediated indirectly through catecholamine sensitivity. - The classic action of thyroid hormones is via intracellular receptors that modulate gene expression, not direct membrane receptor signaling for inotropic effects. *cAMP* - **cAMP** is a common second messenger for many hormones, particularly those acting via G protein-coupled receptors. - While catecholamines themselves act through cAMP to exert their cardiac effects, thyroid hormones *enhance the action* of catecholamines rather than directly using cAMP as their primary inotropic mechanism. *cGMP* - **cGMP** is a second messenger often associated with nitric oxide signaling and vasodilation, contributing to cGMP-dependent protein kinases. - It is not the primary mediator for the *positive inotropic effect* of thyroid hormones on the heart.
Question 48: What is the nature of the relationship between insulin and glucose concentration in the human body?
- A. Linear
- B. Hyperbola
- C. Sigmoidal (Correct Answer)
- D. Bell Shaped
Explanation: ***Sigmoidal*** - The relationship between insulin and glucose concentration is best described as **sigmoidal**, characterized by a slow initial rise in insulin secretion at low glucose levels, followed by a steep increase at physiological glucose concentrations, and then a plateau at very high glucose levels. - This shape reflects the **beta cell's sensitivity to glucose**, where a minimal threshold of glucose is required to trigger insulin release, and then a maximal release capacity is reached. *Linear* - A **linear relationship** would imply that for every unit increase in glucose, there is a constant, proportional increase in insulin secretion, which is not physiologically accurate. - While insulin secretion does increase with glucose, the rate of increase varies significantly across different glucose concentrations. *Hyperbola* - A **hyperbolic relationship** typically suggests a rapid initial response that then gradually plateaus, often seen in enzyme kinetics. - While there is a plateau in insulin secretion at high glucose levels, the initial phase is not as rapid or proportionally inverse as a hyperbolic function would suggest. *Bell Shaped* - A **bell-shaped curve** describes a relationship where there is an optimal point, and deviations in either direction lead to a decrease in the response (e.g., enzyme activity vs. pH). - This is not characteristic of insulin secretion, as insulin levels generally continue to rise or plateau at higher glucose concentrations and do not decrease beyond an optimal point.
Question 49: Which of the following statements about insulin-mediated transport of glucose is correct?
- A. Via GLUT-2
- B. Main mechanism in RBCs
- C. Seen in adipose tissue (Correct Answer)
- D. Occurs primarily in the brain
Explanation: ***Seen in adipose tissue*** - **Adipose tissue** and **skeletal muscle** are the primary sites where glucose uptake from the bloodstream is significantly enhanced by insulin. - Insulin stimulates the translocation of **GLUT4 transporters** to the cell membrane in these tissues, increasing glucose entry. *Occurs primarily in the brain* - Glucose uptake into the **brain** is largely **insulin-independent**, primarily mediated by **GLUT1** and **GLUT3 transporters**. - The brain requires a constant supply of glucose and does not rely on insulin to facilitate its entry. *Via GLUT-2* - **GLUT2** is a **low-affinity, high-capacity** glucose transporter primarily found in the **liver**, **pancreatic beta cells**, kidneys, and small intestine. - It allows for rapid equilibration of glucose across membranes but is not directly involved in the **insulin-mediated uptake** seen in peripheral tissues. *Main mechanism in RBCs* - **Red blood cells (RBCs)** primarily use **GLUT1** for glucose transport, which is an **insulin-independent** process. - RBCs do not contain mitochondria and rely on glycolysis for energy, so they require a continuous, insulin-independent supply of glucose.
Question 50: Which of the following is not a component of a mature sperm cell?
- A. Lysosome
- B. Golgi apparatus
- C. Mitochondria
- D. Endoplasmic reticulum (Correct Answer)
Explanation: ***Endoplasmic reticulum*** - The **endoplasmic reticulum** is prominent in spermatogonia and spermatocytes but largely absent in **mature sperm** as organelles are shed during spermiogenesis to reduce cell volume. - Its primary functions of protein synthesis and lipid metabolism are not required in a terminally differentiated, motile cell like a mature sperm. *Golgi apparatus* - The **Golgi apparatus** reorganizes during spermiogenesis to form the **acrosome**, which is a crucial structure for fertilization. - While the distinct Golgi stacks are not present, its modified derivative, the acrosome, is an essential component. *Mitochondria* - **Mitochondria** are abundant in the midpiece of the sperm tail, arranged in a spiral sheath. - They are vital for generating the **ATP** required for the flagellum's motility, enabling the sperm to swim. *Lysosome* - Although typical lysosomes are not found, the **acrosome** of the sperm is considered a modified lysosome. - The acrosome contains **hydrolytic enzymes** similar to lysosomes, which are critical for penetrating the egg's outer layers during fertilization.