GIT- Physiology

✅ *5-10 seconds*
This is the standard, expected frequency for normal bowel sounds, indicating regular and healthy peristaltic activity in the intestines.

Bowel sounds (or borborygmi) are the gurgling and rumbling noises produced by the movement of gas and fluid through the intestines during peristalsis. Auscultation of the abdomen is a key part of the physical exam to assess gastrointestinal motility.

Clinical Significance:

• Normal Motility: The sound of normal peristalsis is heard approximately every 5 to 10 seconds. This translates to about 5-12 sounds per minute. This frequency indicates a healthy, active digestive system.
• Hyperactive Sounds: Sounds occurring more frequently than every 5 seconds (e.g., 1-5 seconds) are considered hyperactive. This can indicate increased motility, often seen in early bowel obstruction, gastroenteritis, or diarrhea.
• Hypoactive Sounds: Sounds with intervals longer than 10 seconds (e.g., only 1-3 per minute) are hypoactive. This indicates reduced motility, which can be a normal finding after abdominal surgery but is also a concerning sign for paralytic ileus or peritonitis if accompanied by other symptoms like distension and pain.
• Absent Sounds: The complete absence of bowel sounds for a full 3-5 minutes of careful auscultation is an abnormal finding that requires urgent investigation, as it can signify a complete cessation of bowel activity.

The 5-10 second interval is the clinical gold standard for defining normal bowel activity.

Explanation of the Incorrect Options

❌ *1-5 seconds*
This frequency is too high and describes hyperactive bowel sounds. While sometimes normal in a hungry person, this pattern is often associated with conditions like diarrhea, early obstruction, or irritable bowel syndrome.

❌ *15-20 seconds*
This interval is too long and would be classified as hypoactive bowel sounds. This reduced frequency can be a sign of slowed intestinal motility.

❌ *10-20 seconds*
*This range is incorrect because its lower end (10 seconds) is at the very upper limit of normal, and its upper end (20 seconds) is clearly hypoactive. The standard definition for normal is more precise (5-10 sec).*

❌ *1-3 minutes*
*Hearing sounds only once every 1-3 minutes is a definitive sign of severely hypoactive or absent bowel sounds. This is a red flag for conditions like paralytic ileus and requires immediate medical attention.*

✅ Blood sugar level will increase.

• Protein breakdown supplies gluconeogenic substrates.

• Liver (and to a smaller extent kidney) converts them to glucose, raising fasting/illness-state blood glucose.

• Clinically, catabolic states (sepsis, severe dehydration/pre-renal azotemia, steroid excess) often show high BUN/urea with stress hyperglycemia.

Why the other options are wrong (with specifics):
❌ It will decrease up to a given point and then increase.

• A U-shaped (biphasic) relationship would require an early mechanism that lowers hepatic glucose output as urea rises and a later mechanism that raises it—no such physiology exists.

• In catabolism, the dominant, continuous effect is ↑ gluconeogenesis → monotonic tendency toward higher glucose, not down-then-up.

❌ Blood sugar level will decrease.

• Decreasing glucose would require net suppression of gluconeogenesis or marked enhancement of insulin action.

• Catabolic hormones do the opposite: they increase hepatic glucose production and induce insulin resistance in peripheral tissues.

• Edge case note: advanced kidney failure can sometimes predispose to hypoglycemia (reduced renal gluconeogenesis and impaired insulin clearance), but that is a multifactorial uremic state, not a direct effect of “high urea” per se—and it’s not the typical exam-tested relationship.

❌ There will be no effect.

• Urea itself isn’t a regulator of glycemia, but it is a strong marker of the underlying nitrogen/energy metabolism.

• When urea is high from proteolysis, the same process is feeding gluconeogenesis—so “no effect” ignores a well-linked metabolic coupling.

❌ It will increase up to a given point and then decrease.

• This would imply saturation or negative feedback whereby very high urea lowers glucose output.

• No physiological pathway uses urea to inhibit gluconeogenesis or enhance glucose disposal; no high-urea “ceiling effect” on blood glucose is described.

✅ Anaerobic respiration occurs
During strenuous exercise, oxygen supply to muscles becomes insufficient to meet the high energy demand. As a result, muscles rely more on anaerobic glycolysis, where glucose is converted to lactate for rapid ATP production, though much less efficient than aerobic respiration. This leads to lactic acidosis, contributing to muscle fatigue.

Incorrect Options

❌ Large amount of energy is produced by aerobic respiration
Aerobic respiration produces more ATP overall, but during strenuous exercise, oxygen delivery is limited, so the body switches largely to anaerobic metabolism.

❌ Heart rate drops
Heart rate actually increases during exercise to deliver more oxygen and nutrients to tissues.

❌ Frequency of Krebs cycle corresponds to breathing rate
The Krebs cycle runs according to substrate and oxygen availability, not directly in sync with breathing rate.

❌ Krebs cycle becomes faster
In strenuous exercise with low oxygen, the Krebs cycle actually slows down because NAD⁺ is less available (trapped as NADH when the ETC slows).

✅ Myosin heads have less ATPase activity
In smooth muscle, the cycling of myosin cross-bridges is slower than in skeletal muscle because the myosin heads possess lower ATPase activity. This means ATP hydrolysis occurs at a slower rate, leading to slower contraction and relaxation cycles. This property is advantageous, as smooth muscles (like those in blood vessels, GI tract, and airways) need to maintain sustained contractions (tonic activity) with low energy consumption.

Incorrect Options

❌ There are less actin molecules in smooth muscles
Smooth muscle actually has a higher actin-to-myosin ratio compared to skeletal muscle, so this is not the reason.

❌ There are more actin molecules in smooth muscles
True fact, but not the explanation for slower cycling—the limiting factor is ATPase activity of myosin heads.

❌ Myosin heads have more ATPase activity
This would make contraction faster, like in skeletal muscle, not slower.

❌ Myosin heads have no ATPase activity
Incorrect—ATPase activity is essential for cross-bridge cycling. Smooth muscle myosin has ATPase activity, but it is reduced compared to skeletal muscle.

✅ Secretin
Secretin, released from S cells of the duodenum in response to acidic chyme from the stomach, stimulates the secretion of bicarbonate-rich fluid from the pancreas and bile ducts. This bicarbonate neutralizes gastric acid, creating an optimal pH for pancreatic enzymes to function in the small intestine.

Incorrect Options

❌ Motilin
Increases gastrointestinal motility and initiates migrating motor complexes, but does not stimulate bicarbonate secretion.

❌ Cholecystokinin (CCK)
Secreted by I cells in response to fats and proteins. It stimulates gallbladder contraction and pancreatic enzyme secretion, but not bicarbonate secretion.

❌ Vasoactive intestinal peptide (VIP)
Relaxes smooth muscle and stimulates intestinal secretion of water and electrolytes, but bicarbonate secretion is specifically stimulated by secretin.

❌ Gastrin
Secreted by G cells of the stomach antrum; it stimulates acid secretion and gastric motility, not bicarbonate release.

✅ Antimicrobial
Lysozyme in saliva has an antimicrobial function. It breaks down the peptidoglycan layer of bacterial cell walls, especially in gram-positive bacteria, leading to cell lysis. This helps control oral microbial populations and contributes to innate immunity in the oral cavity.

Incorrect Options

❌ Lubrication
Lubrication of food for swallowing is mainly the role of mucins in saliva, not lysozyme.

❌ Resist digestion
Resistance to digestion is provided by epithelial barriers and mucosal factors, not lysozyme.

❌ Epithelial protection
While lysozyme indirectly protects epithelia by controlling microbes, direct epithelial protection comes mainly from mucins and IgA.

❌ Bicarbonate ion secretion
Bicarbonate in saliva buffers acids and maintains oral pH, but this is unrelated to lysozyme.

✅ Gastrin
Gastrin, secreted by G cells in the antrum of the stomach, promotes gastric motility and stomach emptying. It stimulates acid secretion, increases gastric contractions, and relaxes the pyloric sphincter, allowing chyme to move into the duodenum.

Incorrect Options

❌ Secretin
Secreted by S cells in the duodenum in response to acid. It slows gastric emptying to allow neutralization of acid and stimulates bicarbonate secretion from the pancreas.

❌ Ghrelin
Secreted mainly by the stomach, it stimulates appetite (“hunger hormone”) and growth hormone release, but it does not directly promote gastric emptying.

❌ Cholecystokinin (CCK)
Secreted by I cells of the duodenum in response to fats and proteins. It slows gastric emptying to allow more time for fat digestion.

❌ Intrinsic factor
Secreted by parietal cells, it is essential for vitamin B₁₂ absorption in the ileum, not for regulating stomach emptying.

✅ Leptin
Leptin is a hormone secreted by adipose tissue that signals satiety to the hypothalamus and also improves insulin sensitivity. It decreases appetite, enhances energy expenditure, and modulates glucose metabolism. In obesity, however, leptin resistance develops, so despite high leptin levels, appetite suppression and insulin sensitivity are impaired.

Incorrect Options

❌ Thyrotropin (TSH)
Secreted by the anterior pituitary to regulate thyroid function, not adipose tissue.

❌ Ghrelin
Secreted by the stomach, it stimulates appetite and increases food intake (“hunger hormone”), opposite to leptin’s effect.

❌ Cholecystokinin (CCK)
Secreted by I-cells of the duodenum in response to fats and proteins; it stimulates pancreatic enzyme secretion and gallbladder contraction, not insulin sensitivity.

❌ Glucagon
Secreted by pancreatic α-cells, it increases blood glucose by stimulating glycogenolysis and gluconeogenesis, opposing insulin’s effects.

• Trypsinogen, the inactive precursor of trypsin, is the most abundant protein in pancreatic juice.
• When released into the duodenum (the first part of the small intestine), trypsinogen is activated to trypsin by the enzyme enteropeptidase.
• Once activated, trypsin plays a central and crucial role by activating all the other major proteolytic enzymes, including chymotrypsin, carboxypolypeptidase, and others.

While the pancreas produces large amounts of amylase and lipase, trypsinogen is secreted in the highest concentration as it is the master activator of the other pancreatic proteases.

✅ 6.0 – 7.0
The normal pH of saliva is slightly acidic to neutral, ranging between 6.0 and 7.0. Saliva helps maintain oral health by buffering acids, beginning starch digestion (via salivary amylase), lubricating food, and providing antimicrobial action (via lysozyme and IgA).

Incorrect Options

❌ 7.0 – 8.0
This range is more alkaline than typical resting saliva.

❌ 7.1 – 7.9
Again, this is above the usual physiological pH of saliva, though temporary alkalinization can occur after stimulation.

❌ 8.0 – 9.0
Too alkaline for saliva; such a pH is not physiologically normal.

❌ 5.0 – 7.0
This range includes acidic values below normal. Persistent pH ≤5.5 increases risk of dental caries due to enamel demineralization.

✅ Starvation
During starvation (fasting), liver glycogen stores are progressively depleted because glycogenolysis is activated to maintain blood glucose. Initially, glycogen breakdown provides glucose, but within 24 hours of fasting, glycogen is nearly exhausted, and gluconeogenesis becomes the main source of glucose.

Incorrect Options

❌ High ATP concentration
High ATP inhibits glycolysis and promotes glycogen synthesis rather than glycogen breakdown. It does not directly cause glycogen depletion.

❌ Low adenosine monophosphate (AMP) concentration
Low AMP signals an energy-rich state, so glycogen breakdown is suppressed, not enhanced. Glycogen decreases when AMP is high (indicating energy demand), not low.

❌ Low glucagon levels
Low glucagon favors glycogen storage, not breakdown. Glycogen decreases when glucagon is high, such as in fasting.

❌ High insulin levels
High insulin promotes glycogen synthesis and storage in the liver. Glycogen decreases when insulin is low (e.g., starvation or diabetes).

✅ Oxygenation of blood
The liver does not oxygenate blood. Oxygenation occurs in the lungs via gas exchange in the alveoli. The liver instead receives oxygenated blood from the hepatic artery and nutrient-rich blood from the portal vein, then processes and detoxifies it before returning it to circulation.

Incorrect Options

❌ Detoxification of chemicals
A major function of the liver, which breaks down toxins, drugs, and metabolic byproducts.

❌ Bile production and secretion
The liver continuously produces bile, essential for emulsifying fats and excreting bilirubin and cholesterol.

❌ Storage of glycogen, vitamins, and minerals
The liver stores glycogen, fat-soluble vitamins (A, D, E, K), vitamin B12, and minerals like iron and copper.

❌ Metabolism of fats, proteins, and carbohydrates
The liver plays a central role in metabolism: gluconeogenesis, glycogenolysis, lipogenesis, β-oxidation, and urea cycle.

✅ Upward and anteriorly
During swallowing, the larynx moves upward and anteriorly. This movement has two main purposes:

1. It helps the epiglottis tilt backward, covering the laryngeal inlet and preventing food or liquid from entering the airway.

2. It pulls the laryngopharynx upward, helping to open the upper esophageal sphincter so the bolus can pass into the esophagus.

Incorrect Options

❌ Does not move
The larynx clearly does move during swallowing; immobility would risk aspiration.

❌ Upward and posteriorly
Posterior movement is not correct—the larynx moves forward (anteriorly) to assist in airway protection and esophageal opening.

❌ Downward and posteriorly
This would push the larynx toward the esophagus but does not occur in normal swallowing.

❌ Downward and anteriorly
The larynx does not move downward during swallowing; instead, it elevates.

The primary role of villi (in the small intestine) is absorption of nutrients by increasing the surface area. However, in the large intestine, true villi are absent; instead, it has numerous straight tubular glands (crypts of Lieberkühn). The large intestine mainly absorbs water, electrolytes, and some vitamins (like vitamin K from gut bacteria).

So, while the listed correct physiological function is absorption, the important note is that large intestine doesn’t have villi—absorption happens through its mucosa and crypts instead.

Incorrect Options

❌ Proprioception
This refers to body position sense, mediated by muscles, tendons, and joints—not intestinal villi.

❌ Breakdown of enzymes
Enzymatic breakdown happens in the small intestine with pancreatic enzymes, not via villi. Villi aid in absorption, not enzyme secretion.

❌ Exocytosis
Villi themselves do not perform exocytosis; this is a cellular mechanism, not a villus function.

❌ Phagocytosis
Phagocytosis is performed by immune cells (like macrophages), not villi.

The enteric nervous system (ENS), often called the “second brain,” is an intrinsic neural network within the gastrointestinal tract. It is composed of the myenteric (Auerbach’s) plexus and the submucosal (Meissner’s) plexus. Together, they regulate gut motility, local reflexes, and secretory functions, largely independent of the central nervous system (though modulated by sympathetic and parasympathetic input).

Incorrect Options

❌ Controls voluntary movements
Voluntary control involves skeletal muscles and the somatic nervous system, not the ENS. The ENS controls involuntary smooth muscle activity of the gut.

❌ Links GIT to heart
That is the role of the autonomic nervous system (especially via the vagus nerve), not the ENS directly.

❌ Controls gut bacteria
The ENS does not directly regulate microbiota. Gut bacteria are influenced more by diet, immunity, and chemical environment.

❌ Provides pain sensation
Pain sensation is carried by visceral afferent nerves, not the ENS itself. The ENS mainly coordinates motor and secretory activity, not sensory pain transmission.

• The pH scale measures how acidic or basic a substance is. A pH of 7.0 is neutral. A pH below 7.0 is acidic, and a pH above 7.0 is alkaline (basic).
• Saliva has a pH range of approximately 6.2 to 7.6, which is very close to neutral. Its function is to begin carbohydrate digestion and moisten food, and this neutral environment is ideal for the enzymes it contains.
• Gastric juice is highly acidic, with a pH of about 1.5 to 3.5, due to the presence of hydrochloric acid. This acidity is necessary to break down food and kill bacteria.
• Pancreatic juice is alkaline (basic), with a pH of about 8.0 to 8.3. Its high alkalinity is essential for neutralizing the acidic chyme that enters the small intestine from the stomach, creating an optimal environment for pancreatic enzymes to function.
• Bile is also alkaline, with a pH of 7.5 to 8.5. It helps in the digestion and absorption of fats.
• Urine is not a gastrointestinal secretion. While it is a bodily fluid, its pH can vary widely from 4.5 to 8.0 depending on diet and other factors, but it is not directly involved in the digestive process.

✅ HCl and intrinsic factor
Parietal cells of the gastric glands (fundus and body of the stomach) secrete hydrochloric acid (HCl), which lowers gastric pH to aid protein digestion and kill pathogens, and intrinsic factor, which is essential for the absorption of vitamin B₁₂ in the ileum. Loss of intrinsic factor leads to pernicious anemia.

Incorrect Options

❌ HCl and HCO₃⁻
Parietal cells do not secrete bicarbonate into the stomach lumen. Instead, bicarbonate is released by mucous cells and into the bloodstream as a byproduct of acid secretion (“alkaline tide”).

❌ Somatostatin and somatomedin
Somatostatin is secreted by D cells, not parietal cells. Somatomedin (IGF-1) is produced in the liver, not the stomach.

❌ Water and sodium
These are not the specialized secretions of parietal cells. Water and electrolytes may be present in gastric juice, but they mainly come from mucous cells and general fluid balance.

❌ Gastrin and secretin
Gastrin is secreted by G cells in the antrum, and secretin is secreted by S cells in the duodenum, not by parietal cells.

✅ 50 ml
The gallbladder normally has a storage capacity of about 50 mL of bile. It concentrates bile (by absorbing water and electrolytes) and then releases it into the duodenum in response to cholecystokinin (CCK), especially after a fatty meal.

Incorrect Options

❌ 7 ml
This is far too small for the gallbladder’s capacity; 7 mL is closer to the volume of a single teaspoon.

❌ 0 ml
Incorrect, as the gallbladder’s main function is storage of bile. Without this, its physiological role would be meaningless.

❌ 450 ml
This is much larger than the gallbladder’s actual storage. Such a volume would suggest severe pathological distension (e.g., mucocele or hydrops of the gallbladder).

❌ 600 ml
Similarly, this is far beyond normal physiological capacity and would indicate gross pathology, not a normal state.

Step 1: Normal physiology of swallowing

Swallowing occurs in three stages:

1. Oral stage (voluntary): bolus moved to pharynx.

2. Pharyngeal stage (involuntary):

   • Nasopharynx closed by soft palate

   • Larynx elevated, epiglottis covers glottis

   • Respiratory center inhibited (so we don’t aspirate) ✅

   • Pharyngoesophageal sphincter (upper esophageal sphincter) relaxes ✅

3. Esophageal stage (involuntary):

   • Peristaltic waves move bolus down

   • Gastroesophageal sphincter (LES) relaxes ✅ to allow entry into stomach

Step 2: Which is wrong?

• The gastroesophageal sphincter is not inhibited — it relaxes during swallowing.

• So, “Inhibit gastroesophageal sphincter” is the incorrect statement.

Step 3: Why the other options are correct

• Inhibits respiratory center ✅ → prevents breathing during swallowing.

• Relaxes pharyngoesophageal sphincter ✅ → allows bolus to enter esophagus.

• Relaxes gastroesophageal sphincter ✅ → allows bolus into stomach.

• None of these ❌ → wrong because one option is clearly incorrect.

Quick memory aid

👉 Swallowing = Stop breathing, open both gates (upper & lower esophageal sphincters).

Step 1: Normal saliva composition

• Saliva is mostly water, with electrolytes, enzymes (like amylase, lipase), and mucins.

• It plays a role in lubrication, digestion, and protection against bacteria.

Step 2: Salivary pH

• Normal resting saliva has a slightly acidic to neutral pH, typically 6.2 to 7.4.

• It can shift depending on stimulation and flow rate:

  • Lower flow → more acidic (closer to 6).

  • Higher flow → more alkaline (closer to 7.5).

Step 3: Why the other options are wrong

• 4–5 ❌ → Too acidic, this would damage enamel. Seen in gastric reflux, not normal saliva.

• 2–3 ❌ → Strongly acidic, like stomach acid. Definitely not saliva.

• 12–15 ❌ → Extremely alkaline, outside biological limits.

• 10–12 ❌ → Too alkaline, not compatible with oral physiology.

Quick clinical pearl

• Normal salivary pH helps maintain tooth enamel.

• Drop below 5.5 → demineralization and dental caries risk.

• Esophagus ❌ – Only transports food; no role in fat digestion.

• Stomach ❌ – Gastric lipase does a little fat breakdown, but minimal (~10–15%).

• Colon ❌ – No digestion; mainly water and electrolyte absorption.

• Small intestine ✅ – The primary site:

  • Pancreatic lipase hydrolyzes triglycerides → monoglycerides + free fatty acids.

  • Bile salts emulsify fat → form micelles → facilitate absorption.

  • Occurs mainly in the duodenum and jejunum.

• The most important physiological driver of elevated gastric acid secretion is hormonal regulation, especially gastrin.

• In gastric ulcer disease:

  • H. pylori infection reduces somatostatin → leads to unchecked gastrin secretion → ↑ parietal cell stimulation → excess HCl output.

  • Other hormones like histamine (from ECL cells) and acetylcholine (vagal stimulation) amplify the effect, but gastrin dysregulation is the key hormonal factor.

Why the others are less likely

• Dietary habits ❌ – Can aggravate symptoms but don’t directly cause persistently elevated gastric acid output.

• GERD ❌ – A consequence of acid reflux, not the cause of increased secretion.

• Medication use ❌ – NSAIDs cause ulcers, but via mucosal damage, not by directly raising gastric acid output.

• Stress ❌ – Can modestly increase acid, but not to the level of markedly elevated output described here.

• Hormonal changes ✅ – Most direct explanation: hypergastrinemia driving acid hypersecretion.

• Hepatic bile (freshly secreted from liver): watery, isotonic with plasma.

• Gallbladder bile: concentrated because the gallbladder mucosa actively absorbs water, sodium, chloride, and bicarbonate, while relatively retaining bile salts, bilirubin, cholesterol, and lecithin.

So compared with hepatic bile:

• Sodium ions → ↓ (absorbed actively).

• Bilirubin → ↑ concentration.

• Cholesterol → ↑ concentration.

• Lecithin → ↑ concentration.

• Bile salts → ↑ concentration.

This concentration process makes gallbladder bile thicker and more effective for fat digestion.

Why the others are wrong

• Bilirubin ❌ – More concentrated in gallbladder bile.

• Cholesterol ❌ – More concentrated, can predispose to gallstones.

• Lecithin ❌ – More concentrated in gallbladder bile.

• Bile salts ❌ – More concentrated.

• Sodium ions ✅ – Reduced, because actively absorbed during bile concentration.

The pancreas produces many proteolytic enzymes (trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidases). To avoid autodigestion, these enzymes are secreted in inactive zymogen form.

But the most critical safeguard is:

• Pancreatic acinar cells secrete a trypsin inhibitor (pancreatic secretory trypsin inhibitor, PSTI).

• This prevents premature activation of trypsinogen → trypsin inside the pancreas.

• If trypsin were to activate early, it would trigger a cascade activating all proteases, leading to acute pancreatitis.

Why the other options are wrong

• Storage of enzymes in zymogen granules in acinar cells ❌ – True mechanism, but not the enzyme preventing activation.

• Inflammatory blockage of pancreatic duct ❌ – That’s a complication, not a protective mechanism.

• Absence of enterokinase in the intestinal epithelium ❌ – Wrong, enterokinase is present in duodenal brush border and is needed to activate trypsinogen.

• Secretion of trypsin inhibitor by acinar cells ✅ – Correct protective mechanism.

• Decreased secretion of sodium bicarbonate in ducts ❌ – Leads to acidity and damage, not protection.

• During the fasting state, the GI tract shows a special motor pattern called the migrating motor complex (MMC).

• MMC = waves of strong, sequential contractions that start in the stomach, move through the small intestine, and fade in the ileum.

• This “housekeeping wave” clears residual food, mucus, and bacteria between meals.

• Motilin, secreted from the M cells of the small intestine, is the key hormone that initiates MMC.

Why the others are wrong

• Gastrin ❌ – Secreted in fed state, stimulates acid secretion and gastric motility, not MMC.

• VIP (Vasoactive Intestinal Peptide) ❌ – Relaxes smooth muscle, increases intestinal secretions, not MMC.

• Secretin ❌ – Stimulates bicarbonate secretion from pancreas in response to acid, not MMC.

• Somatostatin ❌ – Inhibitory hormone, suppresses GI activity, not initiator of MMC.

• Enterokinase (also called enteropeptidase) is a brush-border enzyme in the duodenum.

• Its job: convert trypsinogen → trypsin.

• Trypsin is the master protease that activates all other pancreatic proteases (chymotrypsinogen, proelastase, procarboxypeptidases).

• Without enterokinase → no trypsin → almost no activation of pancreatic proteases → severe impairment of protein digestion.

Why the others are wrong

• Ptyalin (salivary amylase) ❌ – Carbohydrate digestion, not protein.

• Enterokinase ✅ – Essential for protein digestion via trypsin activation.

• Pancreatic amylase ❌ – Starch digestion, not protein.

• Chymotrypsin ❌ – Important protease, but even if chymotrypsin is absent, trypsin and others can still partly digest proteins.

• Aminopeptidase ❌ – Helps in final brush-border digestion of peptides, but not as critical as enterokinase.

• The gastric mucosa produces several important substances:

  • HCO₃⁻ → protects mucosa from acid.

  • Pepsin → protein digestion, but other proteases in intestine can compensate.

  • Intrinsic factor → essential for vitamin B₁₂ absorption in the ileum.

  • Mucin → protects epithelium from acid/enzymes.

  • Somatostatin → inhibitory hormone, regulates acid secretion.

• If the gastric mucosa atrophies, loss of intrinsic factor has the most serious long-term consequence → leading to vitamin B₁₂ deficiency → pernicious anemia (megaloblastic anemia + neurological deficits due to demyelination).

• The other losses (pepsin, mucin, HCO₃⁻, somatostatin) are significant but can be partly compensated by pancreatic enzymes or other regulatory mechanisms.

Why the others are less severe

• HCO₃⁻ ❌ – Loss increases mucosal injury risk but not systemic long-term deficiency.

• Pepsin ❌ – Protein digestion can still occur via pancreatic proteases.

• Intrinsic factor ✅ – Essential, no alternative source; deficiency leads to irreversible B₁₂ malabsorption.

• Mucin ❌ – Loss predisposes to ulceration, but not systemic deficiency.

• Somatostatin ❌ – Loss causes excess acid secretion but not long-term deficiency effects like B₁₂ deficiency.

Saliva is unique among GI secretions:

• It is hypotonic because ductal cells reabsorb more Na⁺ and Cl⁻ than they secrete K⁺ and HCO₃⁻.

• It contains high HCO₃⁻ (important for neutralizing oral acids).

• Its secretion depends heavily on vagal parasympathetic stimulation, so it drops sharply after vagotomy.

• Pancreatic juice ❌

  • Rich in HCO₃⁻, but it is isotonic (not hypotonic).

  • Also regulated mainly by secretin, not vagus.

• Bile ❌

  • Isotonic, not hypotonic. HCO₃⁻ content is modest.

• Gastric juice ❌

  • Mainly HCl (parietal cells), not rich in HCO₃⁻, and hypertonic/isotonic depending on secretion.

• Succus entericus (intestinal juice) ❌

  • Isotonic with plasma, not hypotonic.

Since the recorded basic electrical rhythm is 8 per minute, this matches the slow wave frequency of the ileum.

• Stomach ❌ – Too slow (3/min).

• Duodenum ❌ – Too fast (12/min).

• Jejunum ❌ – Slightly faster (~10–11/min).

• Ileum ✅ – Matches the given rate (~8/min).

• Esophagus ❌ – No regular BER.

The defecation reflex has multiple coordinated phases:

• Filling phase → Rectum gradually fills with feces, wall distends.

• RAIR (Rectoanal inhibitory reflex) → Distension of the rectum causes reflex relaxation of the internal anal sphincter (involuntary, mediated by myenteric plexus). This allows stool to enter the anal canal and gives the conscious urge to defecate.

• Parasympathetic phase → Pelvic splanchnic nerves enhance rectal contraction and further internal sphincter relaxation.

• Inhibition phase → Voluntary relaxation of the external anal sphincter (somatic control via pudendal nerve).

• Efferent phase → Final motor output leading to coordinated defecation.

Thus, the first key step where internal sphincter relaxes and urge is felt = RAIR.

Why others are wrong

• Efferent phase ❌ – Refers to motor output, not initial sphincter relaxation.

• Filling phase ❌ – Rectum distends but internal sphincter hasn’t relaxed yet.

• Inhibition phase ❌ – Voluntary relaxation of external sphincter, comes later.

• Parasympathetic phase ❌ – Strengthens rectal contraction after RAIR, not the initial trigger.

• Pancreatic lipase is the primary enzyme for hydrolyzing dietary triglycerides into monoglycerides and free fatty acids.

• These products, along with bile salts, are essential for micelle formation, which allows lipids to be transported across the unstirred water layer to the intestinal epithelium.

If pancreatic lipase is severely deficient:

• Triglycerides cannot be properly broken down.

• Micelles cannot form efficiently, because their building blocks (monoglycerides and fatty acids) are missing.

• This leads to fat malabsorption and steatorrhea.

Why the other options are wrong

• Upregulation of gastric lipase activity ❌ – Gastric lipase does contribute a little, but it cannot compensate enough for pancreatic lipase deficiency.

• Enhanced synthesis of bile salts ❌ – Bile salt synthesis is a hepatic function, not regulated by pancreatic lipase deficiency.

• Reduced formation of micelles ✅ – Correct → micelles need lipase products.

• Decreased production of cholecystokinin ❌ – Fat in the duodenum actually increases CCK secretion, not decreases.

• Increased absorption of dietary triglycerides ❌ – Opposite happens → malabsorption.

• Zollinger–Ellison syndrome = gastrinoma (gastrin-secreting tumor, usually in pancreas or duodenum).

• Gastrin’s normal role:

  • Stimulates parietal cells directly → ↑ HCl secretion.

  • Stimulates chief cells → ↑ pepsinogen release.

  • Increases gastric mucosal growth.

• In Zollinger–Ellison:

  • Uncontrolled excess gastrin → massive hypersecretion of gastric acid (hyperchlorhydria).

  • This leads to peptic ulcers, diarrhea, and steatorrhea (due to inactivation of pancreatic lipase by low pH).

Now the other options:

• Decreased release of pepsinogen ❌ – Gastrin increases pepsinogen, not decreases.

• Enhanced secretion of somatostatin ❌ – Somatostatin inhibits gastrin, but here the tumor bypasses normal control.

• Hyperchlorhydria (Excessive HCl production) ✅ – Correct.

• Hypochlorhydria (Reduced HCl production) ❌ – Opposite of what happens.

• Reduced synthesis of intrinsic factor ❌ – Intrinsic factor secretion from parietal cells is preserved, often increased along with HCl.

• G cells in the pyloric antrum secrete gastrin, which stimulates parietal cells (HCl secretion) and gastric motility.

• Regulation of gastrin secretion:

  Stimulants (increase gastrin release):

  • Gastric distension → via local reflexes.

  • Vagal stimulation → via gastrin-releasing peptide (GRP).

  • Peptides and amino acids in food.

  • Alkaline pH (removes inhibitory effect of acid).

  Inhibitors (decrease gastrin release):

  • Increased acidity (low pH < 3) → negative feedback, directly inhibits G cells.

  • Somatostatin from D cells (triggered by acid).

• Therefore, increased acidity in the antrum is the main factor that inhibits gastrin secretion.

Why the other options are wrong

• Distension of stomach ❌ – Stimulates gastrin release via vagovagal reflex.

• Increased acidity ✅ – Inhibits gastrin (correct).

• Alkaline pH ❌ – Promotes gastrin secretion.

• Activation of vagal efferent ❌ – Stimulates gastrin via GRP.

• Epinephrine release ❌ – Not the primary regulator of G cell activity.

• Alpha-amylase (ptyalin) is the enzyme in saliva that begins starch digestion.

• All major salivary glands contribute, but in different proportions:

  • Parotid gland → purely serous secretion, richest source of alpha-amylase → secretes the highest concentration and maximum amount.

  • Submandibular gland → mixed serous and mucous, contributes a moderate amount of amylase.

  • Sublingual gland → mainly mucous, only small amounts of amylase.

  • Minor salivary glands (labial, buccal, palatine, lingual) → mostly mucous, negligible amylase.

So, the parotid gland is the main contributor of salivary amylase for starch digestion.

Why others are wrong

• Buccal glands ❌ – Minor glands, mucous secretion, little to no amylase.

• Submandibular glands ❌ – Mixed, some amylase but not as much as parotid.

• Parotid glands ✅ – Purely serous, secrete maximum amylase.

• Labial glands ❌ – Minor, mucous, negligible amylase.

• Sublingual glands ❌ – Mostly mucous, very little amylase.

Swallowing (deglutition) occurs in stages:

1. Voluntary (oral preparatory + oral propulsive stage) → Food is chewed, mixed with saliva, and pushed back by the tongue into the oropharynx. Respiration continues normally.

2. Pharyngeal stage → Involuntary reflex once the bolus reaches the pharynx.

   • The nasopharynx closes (soft palate elevates).

   • The larynx elevates and the epiglottis closes over the glottis.

   • The upper esophageal sphincter relaxes.

   • Respiration is temporarily inhibited to prevent aspiration → this is called the deglutition apnea.

3. Esophageal stage → Peristaltic waves propel the bolus down to the stomach; respiration resumes.

Why others are wrong

• Postprandial stage ❌ – No such standard stage in swallowing classification.

• Esophageal stage ❌ – Bolus moves by peristalsis, breathing is not inhibited.

• Voluntary stage ❌ – Mouth to oropharynx, still breathing normally.

• Oral propulsive stage ❌ – Tongue pushes bolus back, respiration continues.

• Gastric emptying is regulated by both mechanical factors (distension, pyloric tone) and chemical factors (nutrient composition of chyme).

• Among macronutrients:

  • Carbohydrates (starch, lactose) → empty the fastest.

  • Proteins / amino acids → slower than carbs, but faster than fats.

  • Fats (fatty acids) → empty the slowest.

• Why? Fatty acids in the duodenum trigger the release of cholecystokinin (CCK) and also stimulate the enterogastric reflex, both of which strongly inhibit gastric emptying to allow more time for digestion and absorption.

Why the others are not correct

• Starch ❌ – Carbohydrate, empties relatively fast.

• Lactose ❌ – Also a carbohydrate, similar to starch in terms of emptying speed.

• Amino acids ❌ – Slow down emptying, but not as much as fats.

• Proteins ❌ – Same as above, slower than carbs but faster than fats.

• The brush border of the small intestine contains disaccharidases that finish carbohydrate digestion.

• Key linkages:

  • Maltase → breaks α-1,4 glycosidic bonds in maltose.

  • Sucrase → breaks sucrose into glucose + fructose.

  • Lactase → breaks lactose into glucose + galactose.

  • Glucoamylase → acts on α-1,4 bonds of oligosaccharides (similar to maltase).

  • Isomaltase → the only enzyme that cleaves α-1,6 glycosidic linkages, the branch points in starch/glycogen.

So the brush border enzyme specifically responsible for breaking α-1,6 bonds is isomaltase.

• In the small intestine, different monosaccharides use different transporters:

  • Glucose & Galactose → absorbed via SGLT-1 (sodium-dependent active transport).

  • Fructose → absorbed via GLUT-5 (facilitated diffusion across the apical/brush border membrane).

  • Once inside the enterocyte, all three sugars exit into the blood via GLUT-2 on the basolateral membrane.

Now the other options:

• GLUT-2 ❌ – Important for moving all monosaccharides (glucose, galactose, fructose) from enterocyte → blood, not for apical fructose entry.

• GLUT-1 ❌ – Basal transporter in many tissues (RBCs, blood-brain barrier).

• GLUT-4 ❌ – Insulin-sensitive transporter in skeletal muscle and adipose tissue.

• GLUT-3 ❌ – High-affinity glucose transporter in neurons.

The swallowing center, located in the medulla oblongata, coordinates the complex reflex of swallowing. One of its most important actions is to temporarily inhibit the respiratory center to prevent inspiration while swallowing. This protective mechanism ensures that food or liquid does not enter the airway (aspiration prevention).

❌ Incorrect Options Explained:

• Stimulates salivary secretion
  → Wrong. Salivary secretion is controlled mainly by the salivatory nuclei (superior and inferior), under parasympathetic control—not the swallowing center.

• Contracts pharyngoesophageal sphincter
  → Wrong. The swallowing center actually causes relaxation of the upper esophageal sphincter (UES) at the right time to allow the food bolus to pass.

• Stimulates respiratory centre
  → Wrong. It does the opposite—it inhibits respiration during swallowing.

• None of these
  → Wrong. Because one of the listed options is correct: it inhibits the respiratory center.

• Urine is composed mostly of water, which acts as the solvent for metabolic waste products such as urea, creatinine, and electrolytes.

• Typically, urine is about 95% water and 5% solutes.

• This high water content allows the kidneys to maintain fluid and electrolyte balance in the body.

Incorrect Options:

• 99% ❌ – Overestimates water content; urine always contains solutes.

• 80% ❌ – Underestimates water content; would make urine unusually concentrated.

• 85% ❌ – Slightly low; normal urine is more dilute.

• 75% ❌ – Far below normal water content; not physiologically typical.

The lower esophageal sphincter (LES) plays a key role in preventing gastroesophageal reflux, but it is important to understand its nature:

1. Anatomical vs. Physiological sphincters:

   • Anatomical sphincters have a distinct, thickened ring of smooth muscle that is visibly different from surrounding tissue (e.g., pyloric sphincter, ileocecal valve).

   • Physiological sphincters function as sphincters due to muscle tone, pressure differences, and anatomical arrangements, but they lack a distinct thickened ring of muscle.

2. LES characteristics:

   • The LES is not a sharply demarcated structure — it is essentially a zone of increased smooth muscle tone at the distal esophagus.

   • Its closure is aided by the diaphragmatic crura, angle of His, and intra-abdominal pressure, making it mainly a physiological sphincter.

❌ Why the Other Options Are Wrong

• Anatomical and physiological: Incorrect, because the LES lacks a discrete anatomical thickening.

• Autonomous: The LES tone is influenced by neural and hormonal factors (vagus nerve, gastrin), so it is not completely autonomous.

• None of these: Wrong, because there is a correct category.

• Anatomical: Incorrect — it does not have a defined anatomical sphincter muscle.

Swallowing (deglutition) has three phases:

1. Voluntary (Oral) Phase –

   • The bolus is pushed by the tongue toward the pharynx.

   • This phase is under conscious control.

   • Respiration is not inhibited here.

2. Pharyngeal Phase (Involuntary) –

   • Triggered when the bolus enters the pharynx.

   • Respiration is reflexively inhibited to prevent aspiration into the airway.

   • The soft palate closes the nasopharynx, and the epiglottis covers the laryngeal inlet.

3. Esophageal Phase (Involuntary) –

   • The bolus moves down the esophagus via peristalsis.

   • Breathing resumes.

Why the other options are incorrect:

• Esophageal involuntary phase – No inhibition of breathing occurs here.

• Voluntary phase – Initiation of swallow but breathing continues.

• Pharyngeal voluntary phase – No such distinct phase exists; the pharyngeal phase is involuntary.

• Esophageal phase – Breathing resumes, not inhibited.

Bile salts are synthesized in the liver from cholesterol and secreted into bile to aid fat emulsification in the small intestine.

• Absorption site:

  • Terminal ileum is specialized for active reabsorption of bile salts via sodium-dependent bile salt transporters.

  • After absorption, bile salts are returned to the liver via the portal circulation → this is called the enterohepatic circulation.

• Clinical correlation:

  • Resection of the terminal ileum (e.g., in Crohn’s disease) → bile salt malabsorption, leading to steatorrhea and fat-soluble vitamin deficiencies.

Option breakdown:

• Terminal ileum – Correct: Main site for active bile salt absorption.

• Jejunum – Incorrect: Only minor passive absorption occurs.

• Proximal ileum – Incorrect: Less specialized for bile salt uptake than terminal ileum.

• Cecum – Incorrect: No significant bile salt absorption.

• Duodenum – Incorrect: Site of fat emulsification, not primary bile salt absorption.

Key point:
Terminal ileum is essential for recycling bile salts, which is crucial for efficient fat digestion and absorption.

Primary salivary secretion is the initial fluid produced by salivary glands. It is isotonic with plasma and contains water, electrolytes, and some proteins.

• Source:

  • Produced by the acini (both serous and mucous) of all salivary glands, including:

    • Parotid gland – mostly serous acini

    • Submandibular gland – mixed serous and mucous acini

    • Sublingual gland – mostly mucous acini

    • Minor salivary glands – mucous or mixed acini

• Modification:

  • Ducts modify the primary secretion by reabsorbing sodium and chloride and secreting potassium and bicarbonate, making the final saliva hypotonic.

Option breakdown:

• Acini of submandibular gland – Incorrect: Only one gland; all glands contribute.

• Ducts of all major salivary glands – Incorrect: Ducts modify, do not produce primary secretion.

• Parenchyma of all minor salivary glands – Incorrect: Minor glands contribute but are not the sole source.

• Acini of parotid gland – Incorrect: Only one gland; all acini contribute.

• Acini of all salivary glands – Correct: Primary saliva originates from acini throughout all glands.

Key point:
The acini of all salivary glands are responsible for producing the primary secretion, which is later modified by the ductal system to form final saliva.

The small intestine is the primary site of digestion and absorption:

• Duodenum: Receives bile and pancreatic enzymes → chemical digestion of fats, proteins, and carbohydrates.

• Jejunum: Major site of nutrient absorption (amino acids, sugars, vitamins).

• Ileum: Absorbs bile salts, vitamin B12, and remaining nutrients.

Clinical correlation:

• Fatty diarrhea (steatorrhea): Suggests malabsorption of fats, typically due to small intestinal dysfunction or pancreatic enzyme deficiency.

• Weakness and anemia: Could result from malabsorption of iron, folate, and fat-soluble vitamins (A, D, E, K) in the small intestine.

Option breakdown:

• Small intestine – Correct: Main site for digestion and absorption.

• Large intestine – Incorrect: Primarily absorbs water and electrolytes; minimal digestion.

• Oral cavity – Incorrect: Mechanical breakdown and salivary enzyme action, not primary absorption.

• Esophagus – Incorrect: Transports food; no digestion or absorption.

• Stomach – Incorrect: Initial protein digestion and acid secretion; limited absorption (some drugs, alcohol).

Key point:
Small intestine dysfunction is the most likely cause of malabsorption syndromes, leading to steatorrhea, nutrient deficiencies, and anemia

Secretin is a peptide hormone secreted by S-cells in the duodenal mucosa when acidic chyme enters the duodenum.

• Primary function:

  • Inhibits gastric acid secretion

  • Stimulates pancreatic bicarbonate secretion to neutralize acid

  • Protects the duodenum from acidic damage

Other hormones and neurotransmitters:

• Gastrin – Incorrect: Stimulates gastric acid secretion.

• Secretin – Correct: Directly inhibits gastric acid secretion and stimulates bicarbonate release.

• Histamine – Incorrect: Potent stimulator of gastric acid secretion via H2 receptors.

• Gastric inhibitory peptide – Incorrect: Mainly inhibits gastric motility, less potent on acid secretion than secretin.

• Acetylcholine – Incorrect: Parasympathetic neurotransmitter that stimulates gastric acid secretion.

Key point:
Secretin acts as a protective hormone, inhibiting gastric acid secretion and promoting bicarbonate release from the pancreas to maintain duodenal pH.

In skeletal and cardiac muscle, troponin binds calcium to regulate actin-myosin interaction. However, smooth muscle lacks troponin. Instead:

• Calmodulin serves as the calcium-binding protein in smooth muscle.

• When calcium enters the cell, it binds calmodulin, forming a Ca²⁺-calmodulin complex.

• This complex activates myosin light-chain kinase (MLCK), which phosphorylates myosin light chains, allowing myosin to interact with actin → smooth muscle contraction.

Option breakdown:

• Myoglobin – Incorrect: Oxygen-binding protein in muscle, unrelated to calcium regulation.

• Caveolae – Incorrect: Membrane invaginations in smooth muscle, involved in signaling but not calcium binding for contraction.

• Calmodulin – Correct: Replaces troponin, binds calcium, activates MLCK.

• Dense bodies – Incorrect: Analogous to Z-discs in smooth muscle, anchoring actin filaments; structural, not regulatory.

• None of these – Incorrect: Calmodulin is indeed the correct answer.

Key point:
In smooth muscle, calmodulin substitutes for troponin in calcium-mediated contraction regulation.

Cholecystokinin (CCK) is a peptide hormone secreted by I-cells in the duodenum and jejunum in response to fatty acids and amino acids in the chyme.

• Excitatory function:

  • Stimulates contraction of the gallbladder, releasing bile to aid fat digestion.

• Inhibitory function:

  • Inhibits gastric emptying, slowing the movement of food from the stomach into the duodenum, allowing adequate time for digestion of fats.

• CCK also stimulates pancreatic enzyme secretion.

Option breakdown:

• Gastrin – Incorrect: Stimulates gastric acid secretion; does not respond to fats.

• Gastric inhibitory peptide (GIP) – Incorrect: Primarily inhibits gastric acid secretion and stimulates insulin release; weaker effect on gallbladder.

• Secretin – Incorrect: Stimulates pancreatic bicarbonate secretion in response to acid, not fats.

• Motilin – Incorrect: Regulates migrating motor complexes during fasting, not postprandial fat digestion.

• Cholecystokinin – Correct: Stimulated by fats, contracts gallbladder (excitatory) and slows gastric emptying (inhibitory).

Key point:
CCK is unique because it has dual actions in the GI tract depending on the organ: stimulates bile release and inhibits gastric motility, optimizing digestion of a fatty meal.

Secretin was the first gastrointestinal hormone to be discovered (by Bayliss and Starling in 1902).

• Source: Secreted by S cells of the duodenal mucosa.

• Stimulus: Acidic chyme entering the duodenum.

• Action:

  • Stimulates pancreatic bicarbonate secretion

  • Inhibits gastric acid secretion

• It laid the foundation for the concept of hormones as chemical messengers in the GIT.

Option breakdown:

• Motilin – Incorrect: Discovered later; regulates migrating motor complexes.

• Gastric inhibitory peptide (GIP) – Incorrect: Inhibits gastric secretion, discovered after secretin.

• Cholecystokinin (CCK) – Incorrect: Stimulates gallbladder contraction and pancreatic enzyme secretion; discovered after secretin.

• Gastrin – Incorrect: Stimulates gastric acid secretion; discovered after secretin.

• Secretin – Correct: The first discovered gastrointestinal hormone, stimulates pancreatic bicarbonate secretion in response to duodenal acid.

Key point:
Secretin is historically important as the first identified GIT hormone, marking the beginning of the study of gastrointestinal endocrinology.

Gastrointestinal (GI) activity is primarily controlled by the autonomic nervous system:

• Parasympathetic stimulation:

  • Neurotransmitter: Acetylcholine (ACh)

  • Effect: Increases motility, secretion, and peristalsis → excites GI activity

• Sympathetic stimulation:

  • Neurotransmitters: Norepinephrine, epinephrine

  • Effect: Inhibits GI activity → relaxes smooth muscles, reduces secretions

Option breakdown:

• Atropine – Incorrect: Muscarinic antagonist; blocks ACh, inhibiting GI activity.

• Adrenergic agonists – Incorrect: Stimulate sympathetic receptors, inhibit GI motility.

• Norepinephrine – Incorrect: Sympathetic neurotransmitter → inhibits GI activity.

• Acetylcholine – Correct: Parasympathetic neurotransmitter → excites GI motility and secretion.

• Epinephrine – Incorrect: Sympathetic agonist → inhibits GI activity.

Key point:
Acetylcholine is the main excitatory neurotransmitter for the GI tract, promoting digestion and motility.

✅ Correct Answer: Secretin

Explanation:

Step 1: Function of secretin

• Secretin is a hormone secreted by S cells of the duodenum in response to acidic chyme entering from the stomach.

• Its main actions include:

  • Stimulating pancreatic bicarbonate secretion to neutralize acid

  • Inhibiting gastric acid (HCl) secretion from parietal cells

  • Slowing gastric emptying

Step 2: Clinical relevance

• Secretin ensures that the duodenum is not overwhelmed by acidic gastric contents.

• It is the basis for the secretin stimulation test for pancreatic function.

❌ Why the other options are incorrect:

Gastrin

• ❌ Stimulates gastric acid secretion, not inhibits it.

Histamine

• ❌ Stimulates parietal cells via H2 receptors to produce HCl.

Gastric inhibitory peptide (GIP)

• ❌ Mainly inhibits gastric motility, has mild inhibitory effect on acid but its main function is stimulating insulin release.

Acetylcholine

• ❌ Stimulates gastric acid secretion via vagal activation of parietal cells.

The ileocecal valve regulates the flow of chyme from the ileum into the cecum and prevents reflux of colonic contents into the small intestine.

Feedback control is mediated by distension or chemical irritation of the cecum, which triggers reflexes (through the enteric nervous system and autonomic pathways) that:

• Contract the ileocecal sphincter

• Inhibit peristalsis in the ileum

This mechanism prevents the backflow of bacteria and colonic contents into the sterile environment of the small intestine.

Other options:

• Jejunum – Incorrect: Plays no direct role in ileocecal valve regulation.

• Rectum – Incorrect: Involved in defecation reflexes, not ileocecal control.

• Transverse colon – Incorrect: Has no direct role in regulating the ileocecal valve.

• Ileum – Incorrect: The ileum delivers chyme but does not control the feedback mechanism; the reflex originates from the cecum.

The gallbladder functions mainly to store and concentrate bile between meals. This concentration is achieved by active absorption of sodium (Na⁺) and chloride (Cl⁻) from the bile into the gallbladder mucosa. The osmotic gradient created by this ion movement leads to passive absorption of water, making the bile more concentrated and ready for release during digestion.

Other options:

• Calcium, chloride, and bicarbonate – Incorrect: Calcium and bicarbonate are not primarily absorbed during bile concentration.

• Calcium, chloride, and sodium – Incorrect: Sodium and chloride are absorbed, but calcium is not significantly involved in this process.

• Bicarbonate, chloride, and potassium – Incorrect: These are not the main ions absorbed in the gallbladder for bile concentration.

• Calcium, bicarbonate, and sodium – Incorrect: Again, calcium and bicarbonate absorption are not key processes in concentrating bile.

Saliva normally has a pH range of 6 to 7, which is slightly acidic to neutral. This pH is maintained due to the presence of bicarbonate and phosphate buffers that help keep the oral cavity stable and protect teeth from demineralization. The pH can vary slightly depending on several factors, such as the rate of saliva secretion, hydration status, and stimulation (like chewing).

• 4-5 – Incorrect: This range is more acidic than normal saliva. Such low pH levels are typically associated with conditions like dry mouth (xerostomia) or after consumption of acidic foods and beverages but are not the normal baseline.

• 2-3 – Incorrect: This pH level is comparable to the stomach’s gastric acid. Such an environment is far too acidic for saliva and would severely damage oral tissues.

• 12-15 – Incorrect: This represents a highly alkaline environment, which is not physiologically compatible with the oral cavity or human body fluids.

• 10-12 – Incorrect: Similarly, this pH is too alkaline and would not be present in normal saliva under any conditions.

Correct Answer: GLUT2 ✅

• Fructose enters the enterocyte from the intestinal lumen via GLUT5 (facilitated diffusion).

• To leave the enterocyte and enter the bloodstream (basolateral membrane), fructose (along with glucose and galactose) uses GLUT2.

• So the exit transporter is GLUT2.

Why the Others Are Incorrect

• SGLT1 ❌ – Active Na⁺-dependent transporter for glucose and galactose into the cell, not fructose and not for exit.

• GLUT5 ❌ – Specific for fructose, but only mediates entry from lumen into enterocyte, not exit.

• GLUT4 ❌ – Insulin-sensitive transporter in muscle and adipose tissue; no role in intestines.

• SGLT3 ❌ – Glucose sensor, not a transporter involved in intestinal absorption.

Correct Answer: Bradykinin ✅

• Salivary glands contain kallikrein, an enzyme secreted by acinar cells.

• Kallikrein acts on kininogen in plasma to release bradykinin, a potent vasodilator.

• This vasodilation increases blood flow and nutrition to salivary glands during secretion.

Why the Others Are Incorrect

• Angiotensin ❌ – Typically a vasoconstrictor (esp. Angiotensin II), not activated by salivary kallikrein.

• Dopamine ❌ – A neurotransmitter that can cause vasodilation in some beds, but not linked to salivary enzyme activity.

• Kallikrein ❌ – This is the enzyme produced by salivary cells, not the vasodilator itself.

• Vasopressin ❌ – Causes vasoconstriction (via V1 receptors), the opposite effect.

Correct Answer: Blockage of pancreatic ducts by thick mucus ✅

• In cystic fibrosis, defective CFTR chloride channels cause thick, viscous secretions.

• In the pancreas, this mucus obstructs small ducts → prevents digestive enzymes from reaching the duodenum.

• The result: pancreatic insufficiency with maldigestion of fat, protein, and carbohydrates.

Why the Others Are Incorrect

• Deficiency of HCO₃⁻ ions ❌ – CFTR also affects bicarbonate secretion, but the main cause of insufficiency is duct obstruction, not bicarbonate loss alone.

• Genetic mutation affecting enzyme production ❌ – The mutation affects chloride transport, not direct enzyme synthesis. The pancreas can produce enzymes, but they don’t reach the gut.

• Inflammation of the pancreas ❌ – Seen in pancreatitis, not the hallmark of cystic fibrosis.

• Scarring of the pancreas ❌ – May occur later due to chronic damage, but the primary mechanism is duct blockage by thick mucus.

Correct Answer: Reduced formation of micelles ✅

• Pancreatic lipase is the key enzyme that hydrolyzes dietary triglycerides into free fatty acids and monoglycerides.

• These products are what combine with bile salts and phospholipids to form micelles.

• Without pancreatic lipase → triglycerides remain largely intact → insufficient fatty acid/monoglyceride release → micelle formation falls sharply, impairing fat absorption.

Why the Others Are Incorrect

• Decreased production of CCK ❌ – In fact, undigested fat stimulates more CCK release (to contract the gallbladder and increase pancreatic secretions).

• Enhanced synthesis of bile salts ❌ – Bile salt production occurs in the liver, independent of pancreatic lipase activity.

• Increased absorption of dietary triglycerides ❌ – The opposite occurs; absorption is reduced because intact triglycerides cannot be absorbed.

• Upregulation of gastric lipase activity ❌ – Gastric lipase contributes slightly, but it cannot compensate significantly for the loss of pancreatic lipase. There’s no major “upregulation” mechanism here.

Correct Answer: Bile salts and phospholipids ✅

• Bile salts (amphipathic molecules) arrange themselves around lipid droplets, breaking them into micelles.

• Phospholipids (esp. lecithin) join in, stabilizing the micelles.

• Together, they create a soluble structure that can transport fatty acids, monoglycerides, cholesterol, and fat-soluble vitamins to the intestinal mucosa for absorption.

Why the Others Are Incorrect

• Bile acids and bile salts ❌ – Bile acids are precursors; bile salts (their conjugated form) are the active emulsifiers. Simply saying both together is redundant and misses the phospholipid component.

• Cholesterol and bile pigments ❌ – These are excretory products in bile, not micelle-forming agents.

• Cholesterol and phospholipids ❌ – Cholesterol is carried inside micelles but does not form them.

• Fatty acids and phospholipids ❌ – Fatty acids are passengers inside micelles, not structural builders.

Correct Answer: Isomaltase ✅

• Isomaltase (also called α-dextrinase) is a brush border enzyme that specifically breaks α-1,6 glycosidic bonds in limit dextrins (branch points of starch and glycogen).

• This is the only intestinal enzyme that can handle those branch linkages.

Why the Others Are Incorrect

• Glucoamylase ❌ – Hydrolyzes α-1,4 linkages at the non-reducing ends of starch, maltose, and dextrins, but not α-1,6 bonds.

• Lactase ❌ – Breaks down lactose into glucose + galactose. No role in starch/glycogen digestion.

• Maltase ❌ – Hydrolyzes maltose (α-1,4 bonds) into glucose, not branch points.

• Sucrase ❌ – Splits sucrose into glucose + fructose (α-1,2 bond).

Correct Answer: Luminal digestion of starch ✅

• Pancreatic amylase is essential for breaking down dietary starch in the intestinal lumen into maltose, maltotriose, and α-limit dextrins.

• In pancreatic insufficiency, this enzyme is lacking → impaired luminal digestion of starch.

• Later steps (brush border enzymes, absorption) cannot proceed efficiently because the substrate is never properly prepared.

Why the Others Are Incorrect

• Absorption of monosaccharides ❌ – Once monosaccharides are present, absorption (via SGLT-1 for glucose/galactose, GLUT-5 for fructose) is intact; the problem here is generating monosaccharides.

• Activation of pancreatic enzymes ❌ – Refers to zymogen activation (trypsinogen → trypsin), relevant to protein digestion, not carbohydrates.

• Brush border digestion of disaccharides ❌ – Enzymes like lactase, sucrase, and maltase are mucosal, not pancreatic; they’re usually intact in pancreatic insufficiency.

• Digestion of alpha-limit dextrins ❌ – Done by isomaltase at the brush border; not impaired by lack of pancreatic enzymes.

Correct Answer: SGLT-1 ✅

• SGLT-1 (Sodium–Glucose Linked Transporter-1) is found in the small intestine brush border.

• It performs active, Na⁺-dependent uptake of glucose and galactose from the intestinal lumen.

• If defective → glucose absorption is impaired → delayed rise in blood sugar → postprandial hypoglycemia.

Why the Others Are Incorrect

• GLUT-1 ❌ – Facilitates basal glucose uptake into most cells (esp. brain, RBCs). Not involved in intestinal absorption.

• GLUT-4 ❌ – Found in muscle & adipose tissue; insulin-dependent uptake, not gut absorption.

• GLUT-5 ❌ – Fructose transporter in the intestine; does not carry glucose.

• SGLT-2 ❌ – Located in renal proximal tubule; reabsorbs glucose from urine, not from gut.

Correct Answer: Aminopeptidase ✅

• Aminopeptidases in the brush border of the small intestine perform the final step of protein digestion, breaking peptides into single amino acids for absorption.

• Without them, protein breakdown stops at small peptides, leading to malabsorption.

Why Others Are Incorrect

• Chymotrypsin ❌ – Pancreatic enzyme; cuts proteins into peptides, not amino acids.

• Elastase ❌ – Breaks elastin and peptide bonds; also leaves peptides.

• Pepsin ❌ – Works in the stomach; starts protein digestion, not final breakdown.

• Trypsin ❌ – Pancreatic enzyme; cleaves into smaller peptides and activates others, but doesn’t free amino acids.

🔎 Step 1: Background

The gastrointestinal (GI) tract exhibits different patterns of electrical and motor activity depending on whether the person is fed or fasting:

• Fed state:

  • Segmentation → mixes food and enhances absorption

  • Peristalsis → moves chyme along the gut

• Fasting state:

  • The stomach and small intestine are mostly empty, but the gut is not silent.

  • It exhibits a cyclical pattern of electrical and motor activity called the migratory motor complex (MMC).

  • MMC clears residual food, secretions, and bacteria from the stomach and small intestine.

✅ Correct Answer: Migratory motility complex

• MMC occurs every 90–120 minutes during fasting.

• It has three phases:

  1. Quiescent period (minimal contractions)

  2. Intermittent contractions

  3. Intense, regular contractions sweeping from the stomach to the ileum

❌ Why the Other Options Are Incorrect

• Segmentation → Occurs during the fed state to mix chyme and enhance absorption.

• Peristalsis → Continuous, but the strong peristaltic waves are primarily postprandial (after eating).

• Slow wave complex / Basic electrical rhythm → These are the electrical oscillations of the smooth muscle (pacemaker activity), but on their own they do not constitute a motor pattern that sweeps contents.

🔎 Step 1: Understanding Sugar Absorption

• Monosaccharides absorbed in the small intestine include glucose, galactose, and fructose.

• Their transport mechanisms differ:

  • Glucose and galactose: Active transport via SGLT1 (sodium-dependent)

  • Fructose: Facilitated diffusion via GLUT5

• Once inside the enterocyte, all three sugars can exit the basolateral membrane via GLUT2 into the blood.

✅ Correct Answer: GLUT5

• GLUT5 is a facilitated diffusion transporter specific for fructose, located on the apical membrane of enterocytes.

• Fructose uptake does not require sodium or active transport.

❌ Why the Other Options Are Incorrect

• GLUT4 → Insulin-dependent glucose transporter in muscle and adipose tissue, not intestinal epithelium.

• SGLT1 → Sodium-dependent transporter for glucose and galactose, not fructose.

• SGLT2 → Sodium-dependent glucose transporter in the renal proximal tubule, not intestine.

• GLUT2 → Basolateral transporter in enterocytes; transports glucose, galactose, and fructose out of the cell, not into the cell from the lumen.

🔎 Step 1: Role of Hepcidin

• Hepcidin is a peptide hormone produced by the liver.

• It is the key regulator of systemic iron homeostasis.

• Mechanism:

  • Hepcidin binds to ferroportin, the iron-export protein on enterocytes, macrophages, and hepatocytes.

  • This causes internalization and degradation of ferroportin, blocking iron release into the blood.

  • Result: Decreased dietary iron absorption and reduced iron mobilization from stores.

✅ Correct Answer: Iron

• By preventing iron absorption, hepcidin prevents iron overload in the blood.

• Hepcidin levels increase in inflammation, infection, and high iron stores.

❌ Why the Other Options Are Incorrect

• Vitamin B12 → Absorbed via intrinsic factor in the ileum; hepcidin has no role.

• Folate → Absorbed in the jejunum; not regulated by hepcidin.

• Magnesium → Absorbed passively in small intestine; not affected by hepcidin.

• Copper → Absorbed in the small intestine; regulated by other transporters, not hepcidin.

🔎 Step 1: Regulation of Gastric Acid Secretion

Parietal cells secrete HCl under stimulation from:

• Histamine (H2 receptors) → ↑ cAMP → ↑ H⁺ secretion

• Acetylcholine (M3 receptors) → ↑ intracellular Ca²⁺ → ↑ H⁺ secretion

• Gastrin (CCK-B receptors) → ↑ intracellular Ca²⁺ → ↑ H⁺ secretion

Inhibitors of acid secretion act either directly on parietal cells or indirectly via other pathways.

✅ Correct Answer: Prostaglandin E

• Prostaglandin E (PGE2) acts directly on parietal cells to inhibit adenylate cyclase, decreasing cAMP, which reduces H⁺ secretion.

• It also stimulates mucus and bicarbonate secretion, protecting the gastric mucosa.

❌ Why the Other Options Are Incorrect

• Histamine → Strong stimulant via H2 receptors; increases acid secretion.

• Acetylcholine → Stimulates parietal cells via M3 receptors; increases acid.

• Gastrin → Stimulates parietal cells directly and indirectly (via histamine release).

• Epinephrine → Mainly acts on blood vessels; has minimal direct effect on parietal cells for acid secretion.

🔎 Step 1: Understanding Gastric Acid Secretion

Gastric acid (HCl) secretion from parietal cells is controlled by three main stimulatory pathways:

1. Histamine (H2 receptors) → Activates adenylate cyclase → ↑ cAMP → stimulates H⁺/K⁺ ATPase

2. Acetylcholine (M3 muscarinic receptors) → Via vagus nerve → ↑ intracellular Ca²⁺ → stimulates H⁺/K⁺ ATPase

3. Gastrin (CCK-B receptors) → ↑ intracellular Ca²⁺ → stimulates H⁺/K⁺ ATPase

Importantly, maximal acid secretion occurs when all three pathways act together. Individually, each pathway produces less than the maximal response.

✅ Correct Answer: Cholinergic receptor stimulation

• Stimulation of cholinergic (M3) receptors mimics vagal stimulation, which:

  • Directly stimulates parietal cells

  • Indirectly stimulates G cells to release gastrin

  • Enhances histamine release from enterochromaffin-like cells

• This combined effect produces maximum gastric acid secretion.

❌ Why the Other Options Are Incorrect

• H2 receptor stimulation → Increases acid via cAMP, but alone produces less than maximal secretion.

• Neurogenic stimulation → General nerve activity is less specific; maximal effect requires targeted cholinergic pathways.

• Inhibition of acetylcholine release → Decreases acid secretion, not increase.

• Na/K ATPase pump stimulation → Parietal cells require H⁺/K⁺ ATPase for acid secretion; stimulating Na/K pump alone is insufficient for maximal HCl output.

🔎 Step 1: Recall the physiology of gastrin

• Source: G cells in the antrum of the stomach.

• Main actions: Stimulates gastric acid (HCl) secretion from parietal cells, and promotes gastric mucosal growth and motility.

• Regulation:

  • Stimulated by: products of protein digestion (especially peptides and amino acids), gastric distension, vagal stimulation (via GRP – gastrin-releasing peptide).

  • Inhibited by: low pH (acid), somatostatin, secretin, GIP, VIP.

✅ Correct Answer: Products of protein digestion

• Peptides and amino acids are the strongest natural stimuli for gastrin release because they signal the stomach that food (protein) has arrived and more acid is needed for digestion.

❌ Why the Other Options Are Incorrect

• Low pH of gastric juice → Inhibits gastrin release (negative feedback to prevent excessive acidity).

• Vasoactive intestinal peptide (VIP) → Inhibits gastric acid secretion; it promotes intestinal secretion instead.

• Somatostatin → Potent inhibitor of gastrin secretion.

• Gastric inhibitory peptide (GIP) → Inhibits gastric acid secretion; stimulates insulin release.

🔎 Step 1: General role of parasympathetic system

• The parasympathetic nervous system (PNS) is the “rest and digest” system.

• In the gastrointestinal tract, its stimulation (via vagus nerve and pelvic splanchnics) generally:

  • Increases motility (smooth muscle contraction, peristalsis).

  • Relaxes sphincters (to allow food passage).

  • Increases glandular secretion (saliva, gastric, pancreatic, intestinal).

✅ Correct Answer: Increase in motility and tone

• Parasympathetic stimulation enhances peristalsis and increases tone of the gut wall, promoting movement of food.

❌ Why the Other Options Are Incorrect

• Increase in absorption of nutrients → Absorption is not directly under parasympathetic control; it depends on digestive/transport processes.

• Inhibition of secretion from the stomach → Opposite is true; PNS stimulates gastric secretion (via vagus).

• Inhibition of intestinal secretions → Wrong, because PNS actually stimulates intestinal secretions.

• Contraction of sphincters → Parasympathetic stimulation causes sphincter relaxation, not contraction.

• Secretin is released from S cells of the duodenal mucosa in response to acidic chyme entering from the stomach.

• Its main action is to stimulate the pancreatic ductal cells to secrete bicarbonate-rich fluid.

• This neutralizes gastric acid, creating an optimal pH (~7–8) for pancreatic enzyme activity in the small intestine.

Why the Other Options Are Wrong ❌

Cholecystokinin (CCK)

• Released by I cells in duodenum/jejunum.

• Stimulates pancreatic enzyme secretion and gallbladder contraction, not bicarbonate secretion.

Trypsinogen

• Inactive zymogen secreted by pancreas, converted to trypsin in the duodenum.

• Involved in protein digestion, not bicarbonate release.

Gastric inhibitory peptide (GIP)

• Secreted by K cells.

• Stimulates insulin secretion in response to glucose and fat.

• No role in bicarbonate secretion.

Somatostatin

• Universal inhibitory hormone (secreted by D cells).

• Inhibits gastric acid, pancreatic secretions, and many hormones.

• Does not stimulate bicarbonate.

I cells

• Cholecystokinin (CCK) is secreted by I cells located in the mucosa of the duodenum and jejunum.

• Stimuli for release: presence of fatty acids, amino acids, and partially digested proteins in the small intestine.

• Functions of CCK:

  • Stimulates gallbladder contraction → bile release.

  • Stimulates pancreatic enzyme secretion.

  • Relaxes sphincter of Oddi.

  • Slows gastric emptying to allow digestion.

Why the Other Options Are Wrong ❌

Ito cells

• Stellate cells of the liver, store vitamin A and play a role in fibrosis.

• Not related to gut hormone secretion.

S cells

• Found in the duodenum.

• Secrete secretin, which stimulates pancreatic bicarbonate secretion.

K cells

• Found in the duodenum/jejunum.

• Secrete GIP (glucose-dependent insulinotropic peptide).

G cells

• Found in the gastric antrum.

• Secrete gastrin, which stimulates gastric acid secretion.

• In the gastrointestinal tract, the parasympathetic nervous system stimulates motility and secretion.

• The primary neurotransmitter here is acetylcholine (ACh), which acts on muscarinic receptors in smooth muscle and glands.

• Effects:

  • ↑ Peristalsis

  • ↑ Secretion of digestive enzymes and mucus

  • Relaxation of sphincters (indirectly via inhibitory neurons)

Thus, acetylcholine is the major neurotransmitter that stimulates GI activity.

Why the Other Options Are Wrong ❌

Epinephrine

• Sympathetic neurotransmitter.

• Inhibits GI motility and secretion (causes relaxation of gut smooth muscle).

Norepinephrine

• Another sympathetic neurotransmitter.

• Reduces gut activity by inhibiting peristalsis and constricting sphincters.

Glutamate

• Excitatory neurotransmitter in the CNS.

• Not a major player in peripheral GI motility regulation.

Dopamine

• In the GI tract, dopamine generally inhibits motility by reducing acetylcholine release from enteric neurons.

• Excess dopamine can cause constipation.