Intestinal absorption of calcium is mainly increased by?
Vitamin D absorption is decreased by ?
Small intestinal peristalsis is controlled by :
Cholecystokinin is produced from:
Somatomedin-C deficiency causes?
Inotropic effect of thyroid hormone is by ?
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:
Miracle fruit is used to change the taste from?
What is the most common mechanism responsible for causing arrhythmias in the heart?
NEET-PG 2015 - Physiology NEET-PG Practice Questions and MCQs
Question 91: Intestinal absorption of calcium is mainly increased by?
- A. Calcitriol (Correct Answer)
- B. Parathormone
- C. Glucocorticoids
- D. ACTH
Explanation: ***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.
Question 92: Vitamin D absorption is decreased by ?
- A. Proteins
- B. Acid
- C. Lactose
- D. Fat malabsorption (Correct Answer)
Explanation: ***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.
Question 93: 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 94: 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 95: 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 96: 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 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: Miracle fruit is used to change the taste from?
- A. Sour to Bitter
- B. Sour to Sweet (Correct Answer)
- C. Bitter to Sweet
- D. Salty to Sweet
Explanation: ***Sour to Sweet*** - The **miracle fruit** (Synsepalum dulcificum) contains a glycoprotein called **miraculin**. - Miraculin binds to taste receptors on the tongue and modifies their perception, making **sour foods taste sweet**. *Sour to Bitter* - The primary effect of miracle fruit is to convert **sour tastes into sweet tastes**, not bitter ones. - No known natural compound consistently changes sour perception to bitter. *Bitter to Sweet* - While miraculin makes sour foods sweet, it does not typically convert **bitter tastes into sweet sensations**. - Bitter taste perception involves different receptor pathways that are not significantly altered by miraculin. *Salty to Sweet* - Miracle fruit primarily targets **sour taste receptors**. - It does not have a significant effect on altering the perception of **salty tastes to sweet**.
Question 100: What is the most common mechanism responsible for causing arrhythmias in the heart?
- A. Re-entry (Correct Answer)
- B. Early after depolarization
- C. Late after depolarization
- D. Automaticity
Explanation: ***Re-entry*** - **Re-entry** is the most common mechanism for arrhythmias and involves a re-excitation of cardiac tissue due to a circulating electrical impulse. - This requires at least two pathways with differing conduction velocities and refractory periods, creating a path for the impulse to re-excite an area after its normal refractory period has ended. *Early after depolarization* - **Early afterdepolarizations (EADs)** occur during phase 2 or 3 of the action potential when repolarization is incomplete, often due to prolonged action potential duration. - They are typically associated with conditions like **long QT syndrome** and can trigger polymorphic ventricular tachycardia, but are less common than re-entry. *Late after depolarization* - **Late afterdepolarizations (DADs)** occur during phase 4 of the action potential, after repolarization is complete, due to excessive intracellular calcium. - They are often seen in conditions like **digoxin toxicity** or **catecholaminergic polymorphic ventricular tachycardia**, but are not the most prevalent mechanism. *Automaticity* - **Abnormal automaticity** refers to pacemaker activity arising in non-pacemaker cells or an acceleration of normal pacemaker activity. - While it can cause arrhythmias such as accelerated idioventricular rhythm, re-entry is far more frequently implicated in the etiology of clinical arrhythmias.