CHOLECYSTOKININ (CCK)

CHOLECYSTOKININ (CCK)

Q. 1 Cholecystokinin is produced from:

 A Hepatocyte

 B

Gastric mucosa

 C

Duodenal mucosa

 D

Epithelial cells of distal common bile duct

Q. 1

Cholecystokinin is produced from:

 A

Hepatocyte

 B

Gastric mucosa

 C

Duodenal mucosa

 D

Epithelial cells of distal common bile duct

Ans. C

Explanation:

The major factor controlling the contraction of the gallbladder is the  hormone cholecystokinin (CCK), which is released from the duodenal mucosa (I cells) in response to the ingestion of fats and amino acids.

Reference:

Harrisons Principles of Internal Medicine, 18th Edition, Page 2616

 


Q. 2

Release of which of the following peptides leads to an increase in the secretion of pancreatic enzymes into the small intestine?

 A

Cholecystokinin

 B

Gastrin

 C

Motilin

 D

Secretin

Ans. A

Explanation:

Ans. A. Cholecystokinin 

  • The release of cholecystokinin is stimulated by the presence of peptides, amino acids, or fatty acids in the small intestine. Cholecystokinin acts on the pancreas to stimulate the secretion of pancreatic enzymes that aid in the digestion of these compounds.
  • Gastrin secretion is stimulated by the presence of peptides or amino acids in the lumen of the stomach, and produces an increase in gastric H+ secretion.
  • Motilin is a hormone that regulates the migrating myoelectric complex, a series of contractions that occur during fasting, clearing the stomach and small intestine of any residual food.
  • Secretin secretion is stimulated by the presence of H+ and fatty acids in the duodenum, and causes an increase in pancreatic and biliary HCO3; release and a decrease in gastric H+ release.

Q. 3 All of the following statements are true for ‘Intestinal Motility’ except:

 A

Does not depend on Gastric motility

 B

Increased by Distension

 C

Increased by Acetylcholine

 D

Increased by cholecystokinin

Ans. A

Explanation:

A i.e. Does not depend on gastric motality

Intestinal motality is dependent of gastric motality; as explained below

– Peristalitic activity of small intestine is greatly increased by distension of stomach wall (gastro enteric reflex) and duodenal wall.

– Chyme is sometimes blocked at ileocecal valve for several hours, until the person eats another meal, which initiates gastro-ileal reflex. This intensifies perstalsis in ileum and forces the remaining chyme through ileo-cecal valve into cecum (large intestine)

– Gastro- colic & duodeno- colic autonomic reflexes result from distension of stomach and duodenum. These facilitate appearance of propulsive mass movements after meals, in large intestineQ.

– Entero- gastric reflex inhibits stomach secretions and motality (by inhibiting pyloric pump propulsive contractions & increasing tone of pyloric sphincter) based on the signals from small intestine and colon.

– Reflexes from colon inhibit emptying of ileal content into the colon via colono-ileal reflex.


Q. 4 Which of the following is true about gastric emptying:

 A Decreased by cholecystokinin

 B

Deceased by gastrin

 C

Increased by secretin

 D

Increased by GIP

Ans. A

Explanation:

A i.e. Decreased by cholecystokinin


Q. 5

Actions of cholecystokinin include which one of the following?

 A

Contraction of gall bladder

 B

Secretion of pancreatic juice rich in enzymes

 C

Increases the secretion of enterokinase

 D

All

Ans. D

Explanation:

FUNCTIONS:

  • Stimulates pancreatic acinar cell enzymes secretion.
  • Causes contraction of gall bladder.
  • Relaxation of sphincter of oddi.
  • Secretion of enzyme-rich pancreatic juice.
  • Potentiates action of secretin on pancreas.
  • Inhibits gastric emptying
  • Increases motility of small intestine & colon.
  • Increases enterokinase secretion
  • Produces satiety

Q. 6

Effect of cholecystokinin on GIT ‑

 A

Increases gastric acid secretion

 B

Increases small intestinal peristlasis

 C

Increases gastric motility

 D

Relaxes gall bladder

Ans. B

Explanation:

Ans. is ‘b’ i.e., Increases small intestinal peristalsis



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