Digestion In Stomach – Motility & Gastric Emptying

DIGESTION IN STOMACH – MOTILITY & GASTRIC EMPTYING

Q. 1

During a fast, a brief phase of intense sequential contractions begins in the stomach and gradually migrates to the ileum. Release of which of the following intestinal hormones is most likely responsible for this observed effect?

 A

Cholecystokinin

 B

Gastrin

 C

Gastrin-releasing peptide

 D

Motilin

Q. 1

During a fast, a brief phase of intense sequential contractions begins in the stomach and gradually migrates to the ileum. Release of which of the following intestinal hormones is most likely responsible for this observed effect?

 A

Cholecystokinin

 B

Gastrin

 C

Gastrin-releasing peptide

 D

Motilin

Ans. D

Explanation:

Motilin is a hormone released by the small intestine during the fasting state. Its waxing and waning blood levels correlate with the initiation and ending of migrating motor complexes (MMC). Furthermore, injection of motilin has been shown to evoke MMC activity. The MMC typically begins in the stomach, and over a 90-120 minute period, migrates to the ileum, where it dies out. As one complex dies out in the ileum, another complex begins in the stomach provided the fasting state continues. Eating a meal interrupts the MMC activity.

Cholecystokinin is released during the intestinal phase of the digestive period (not during a fast). Its secretion is evoked by the presence of fat and protein digestion products in the duodenum. It induces contraction of the gallbladder and relaxation of the sphincter of Oddi.

Gastrin is released from G cells in the antrum, mostly during the gastric phase of the digestive period

(not during a fast). It tends to increase stomach motility, although the rate of emptying is decreased because gastrin also causes the pyloric sphincter to contract. It also may contribute to the increase in ileal and colonic motility as part of the gastroileal and gastrocolic reflexes, respectively.

Gastrin-releasing peptide mediates the neural release of gastrin. Antral enteric neurons that are activated by vagal efferents or by local reflexes release gastrin-releasing peptide, which stimulates the G cells to secrete gastrin.

Ref: Barrett K.E., Barman S.M., Boitano S., Brooks H.L. (2012). Chapter 25. Overview of Gastrointestinal Function & Regulation. In K.E. Barrett, S.M. Barman, S. Boitano, H.L. Brooks (Eds), Ganong’s Review of Medical Physiology, 24e.


Q. 2

Major regulator of interdigestive myoelectric complexes

 A

VIP

 B

GIP

 C

Motilin

 D

Neurotensin

Q. 2

Major regulator of interdigestive myoelectric complexes

 A

VIP

 B

GIP

 C

Motilin

 D

Neurotensin

Ans. C

Explanation:

C i.e. Motilin

Glucagon derivative GLP- 1 (7-36) amide (most potent) > gastric inhibitory peptide (GIP) also known as glucose –dependent insulinotropic polypeptide >> gastrin, CCK, secretin and glucagon stimulates insulin secretionQ. But only GLP-1 (7-36) amide & GIP stimulate insulin secretion when adminstered in dose that produce blood levels comparable to those produced by oral glucose.

–  Motolin is secreted by entero chromaffin cells & M0 cells in stomach, small intestine and colon during fasting. It is released

cyclically (so 1 ed levels) at intervals of 90- 100 minutes in a fasted person which stimulates waves of gastrointestinal motality called myoelectric interdigestive cmplexes (MIC). Erythromycin binds to motolin receptors so its derivatives may be of value in treating decreased intestinal motality.

– Neurotensin is produced by neurons & cells of ileum. Its release is stimulated by fatty acid and it increases ileal blood flow and inhibits gastro intestinal motality.

– GIP is produced by K cells in mucosa of duodenum & jejunum. Its secretion is stimulated by glucose & fatQ in duodenum. It is named so because in large doses it inhibits gastric secretion & motality. However in small dose (that are seen after meal) it does not have significant gastric inhibitory activity.


Q. 3

Which of the following is TRUE regarding gastric emptying:

 A

Decreased by CCK.

 B

Decreased by gastrin

 C

Increased by secretin

 D

Decreased by insulin.

Q. 3

Which of the following is TRUE regarding gastric emptying:

 A

Decreased by CCK.

 B

Decreased by gastrin

 C

Increased by secretin

 D

Decreased by insulin.

Ans. A

Explanation:

A i.e. Decreased by CCK


Q. 4

Stimulation for gastric emptying :

 A

Secretin

 B

CCK

 C

Gastrin

 D

All

Q. 4

Stimulation for gastric emptying :

 A

Secretin

 B

CCK

 C

Gastrin

 D

All

Ans. C

Explanation:

C i.e. Gastrin


Q. 5

Emptying of stomach is facilitated by:

September 2012

 A

Secretin

 B

CCK-PZ

 C

GIP

 D

Gastrin

Q. 5

Emptying of stomach is facilitated by:

September 2012

 A

Secretin

 B

CCK-PZ

 C

GIP

 D

Gastrin

Ans. D

Explanation:

Ans. D i.e. Gastrin

Gastrin

  • It is a peptide hormone that stimulates secretion of gastric acid (HC1) by the parietal cells of the stomach and aids in gastric motility.
  • It is released by G cells in the antrum of the stomach (the portion of the stomach adjacent the pyloric valve), duodenum, and the pancreas.
  • Its release is stimulated by peptides in the lumen of the stomach.

Q. 6

Migrating motor complex is due to which GI hormone ‑

 A

Gastrin

 B

Motilin

 C

CCK

 D

VIP

Q. 6

Migrating motor complex is due to which GI hormone ‑

 A

Gastrin

 B

Motilin

 C

CCK

 D

VIP

Ans. B

Explanation:

Ans. is ‘b’ i.e., Motilin

Migratory motor complex (MMC)

The gastric antrum shows bursts of propulsive (peristalitic) muscular activity every 90 minutes. The activity is conducted along the entire length of the small intestine, from stomach to distal ileum, at a rate of about 5 cm per minute. As soon as the activity reaches the terminal ileum, a new wave begins in the stomach. The purpose of MMC is to clear the stomach and small intestine of luminal contents in preparation for the next meal. The MMCs are initiated by motilin.


Q. 7

Gastric emptying is delayed by ‑

 A

Distension of stomach

 B

Gastrin

 C

Acid in duodenum

 D

Vagal stimulation

Q. 7

Gastric emptying is delayed by ‑

 A

Distension of stomach

 B

Gastrin

 C

Acid in duodenum

 D

Vagal stimulation

Ans. C

Explanation:

Ans. is ‘c’ i.e., Acid in duodenum

Gastric emptying

The rate at which the stomach empties into the duodenum depends on the quantity and the type of food ingested. Distension of stomach triggers long (vagally mediated) and short (intrinsic neural plexus mediated) reflexes leading to strong peristaltic waves and increased gastric emptying. The local hormone gastrin also increases the rate of gastric emptying .

Certain signals from the duodenum have a more important regulatory control over the gastric emptying. Distension of the duodenum; Hyperosmolarity in the duodenum (hyperosmolar chyme) ; and presence of acid, fatsand products of protein digestion in duodenum decrease gastric emptying by : –

i)  Hormonal mechanism :- Release of several intestinal hormones like secretin, cholecystokinin, VIP, GIP inhibit gastrin emptying, but also gastric acid secretion.

ii) Enterogastric reflex : – Inhibit gastric emptying through the intrinsic enteric neural plexus.

The rate at which the stomach empties into the duodenum depends on the type of food ingested. Food rich in carbohydrate leaves the stomach in a few hours. Protein rich food leaves more slowly, and emptying is slowest after a meal containing fat.



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