NEET-PG 2015 - Physiology Practice Questions

Q: Intestinal absorption of calcium is mainly increased by?

Calcitriol. ***Calcitriol*** - **Calcitriol** (1,25-dihydroxyvitamin D3) is the hormonally active form of vitamin D, which is essential for increasing **calcium absorption** from the intestines. - It stimulates the synthesis of **calcium-binding proteins** in intestinal epithelial cells, facilitating active transport of calcium. *Parathormone* - **Parathormone (PTH)** primarily regulates calcium by increasing its reabsorption in the **kidneys** and stimulating its release from **bones**. - While it indirectly promotes calcitriol synthesis, its *direct* effect on intestinal calcium absorption is minimal compared to calcitriol. *Glucocorticoids* - **Glucocorticoids** generally have an *inhibitory* effect on calcium absorption in the intestine and can also increase renal excretion of calcium. - Prolonged use can lead to **osteoporosis** due to their negative impact on bone formation and calcium balance. *ACTH* - **ACTH (adrenocorticotropic hormone)** primarily stimulates the adrenal cortex to produce **cortisol** and other glucocorticoids. - It has **no direct role** in regulating calcium absorption from the intestines.

Q: Vitamin D absorption is decreased by ?

Fat malabsorption. ***Fat malabsorption*** - **Vitamin D** is a **fat-soluble vitamin**, meaning it requires dietary fat for proper absorption in the small intestine. - Conditions causing **fat malabsorption**, such as **cystic fibrosis**, **celiac disease**, or **pancreatic insufficiency**, significantly reduce the uptake of vitamin D. *Proteins* - **Proteins** do not directly decrease vitamin D absorption; in fact, some dietary proteins can enhance vitamin D binding and transport in the bloodstream. - Their primary role is in structural and enzymatic functions, not impeding fat-soluble vitamin uptake. *Acid* - **Gastric acid** is important for the absorption of some nutrients, but it generally does not directly hinder the absorption of **fat-soluble vitamins** like vitamin D. - Conditions like **achlorhydria** primarily affect the absorption of minerals and vitamin B12, rather than vitamin D. *Lactose* - **Lactose** is a sugar found in milk, and its malabsorption (lactose intolerance) primarily causes gastrointestinal symptoms like bloating and diarrhea. - It does not directly interfere with the absorption of **fat-soluble vitamins**; rather, it affects carbohydrate digestion.

Q: Small intestinal peristalsis is controlled by :

Myenteric plexus. ***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.

Q: Cholecystokinin is produced from:

Duodenal mucosa. ***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.

Q: Somatomedin-C deficiency causes?

Growth retardation. ***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.

Q: Inotropic effect of thyroid hormone is by ?

Enhancement of Catecholamines. ***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.

Q: What is the nature of the relationship between insulin and glucose concentration in the human body?

Sigmoidal. ***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.

Q: Which of the following statements about insulin-mediated transport of glucose is correct?

Seen in adipose tissue. ***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.

Q: What is the SI unit of luminous intensity?

Candela. ***Candela*** - The **candela (cd)** is the **SI base unit** used to measure **luminous intensity**. - **Luminous intensity** quantifies the power emitted by a light source in a particular direction per unit solid angle. *Lumen* - The **lumen (lm)** is the **SI derived unit** for **luminous flux**, which measures the total perceived power of light. - It describes the total amount of visible light emitted by a source in all directions, not its intensity in a specific direction. *Lux* - The **lux (lx)** is the **SI derived unit** for **illuminance**, which measures how much luminous flux is spread over a given area. - It indicates the perceived brightness of a surface, rather than the intensity of the light source itself. *Coulomb* - The **coulomb (C)** is the **SI derived unit** for **electric charge**. - It is completely unrelated to light or luminous intensity.

Q: What is the intensity in decibel of normal conversation in humans?

60dB. ***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 1

Intestinal absorption of calcium is mainly increased by?

Accepted Answer

Calcitriol

Answer

Parathormone

Answer

Glucocorticoids

Answer

ACTH

Question 2

Vitamin D absorption is decreased by ?

Accepted Answer

Fat malabsorption

Answer

Proteins

Answer

Acid

Answer

Lactose

Question 3

Small intestinal peristalsis is controlled by :

Accepted Answer

Myenteric plexus

Answer

Meissner's plexus

Answer

Vagus nerve

Answer

Parasympathetic system

Question 4

Cholecystokinin is produced from:

Accepted Answer

Duodenal mucosa

Answer

Hepatocyte

Answer

Gastric mucosa

Answer

Epithelial cells of distal common bile duct

Question 5

Somatomedin-C deficiency causes?

Accepted Answer

Growth retardation

Answer

Genetic dwarfism

Answer

Congenital hypothyroidism

Answer

Type 1 diabetes mellitus

Question 6

Inotropic effect of thyroid hormone is by ?

Accepted Answer

Enhancement of Catecholamines

Answer

Membrane receptors

Answer

cAMP

Answer

cGMP

Question 7

What is the nature of the relationship between insulin and glucose concentration in the human body?

Accepted Answer

Sigmoidal

Answer

Linear

Answer

Hyperbola

Answer

Bell Shaped

Question 8

Which of the following statements about insulin-mediated transport of glucose is correct?

Accepted Answer

Seen in adipose tissue

Answer

Via GLUT-2

Answer

Main mechanism in RBCs

Answer

Occurs primarily in the brain

Question 9

What is the SI unit of luminous intensity?

Accepted Answer

Candela

Answer

Lumen

Answer

Lux

Answer

Coulomb

Question 10

What is the intensity in decibel of normal conversation in humans?

Accepted Answer

60dB

Answer

30dB

Answer

90dB

Answer

150dB

NEET-PG 2015 — Physiology