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Flashcards in Intestinal Phase of a Meal Deck (48)
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What is the most significant site for digestion and absorption?

Small intestine


What is the basis for the small intestine's absorption and digestion?

Intense motility and secretions in the lumen and a large surface area of mucosal cells are the basis for digestion/absorption of nutrients.


What type of contents empty from the stomach most rapidly?

Liquids empty more rapidly and isotonic contents empty more rapidly than either hypotonic or hypertonic contents.


What needs to happen in the proximal stomach prior to gastric emptying?

An increase in tone (intraluminal pressure)


What needs to happen in the distal stomach prior to gastric emptying?

Increased strength of antral contractions
Opening of the pylorus so the contents can move


What needs to happen in the duodenum prior to gastric emptying?

Simultaneous inhibition of duodenal segmental contractions


What happens as the meal enters the duodenum?

As meal enters the duodenum, it initiates feedback inhibition of gastric emptying via the neural and hormonal pathways.


How does the vagus nerve respond to contents entering the duodenum?

Vagal afferents respond to nutrients (H+ and hyperosmotic content) of chyme as it enters duodenum. Reflex activation of vagal efferent outflow decrease the strength of antral contractions, contracts the pylorus, and decreases proximal gastric motility.

Overall gastric emptying is slowed as a result


What are the two major factors contribute to inhibition or slowing of gastric emptying?

o The presence of fat in the duodenum
o The presence of H+ (low pH) in the duodenum


What is the effect of fat in the duodenum mediated by?

The effect of fat is mediated by Cholecystokinin (CCK) – secreted when fatty acids are present in the duodenum.


How does CCK slow gastric emptying?

-> CCK slows gastric emptying – pylorus contraction, to ensure that there is adequate time for fat to be digested and absorbed.
-> CCK also regulates gallbladder contraction, relaxation of sphincter of Oddi and pancreatic secretion.


What mediates the effect of H+ in the duodenum?

Reflexes in the enteric nervous system


How does the enteric nervous system reflex respond to H+ in the duodenum?

H+ receptors in the duodenal mucosa detect low pH of chyme and relay this to gastric smooth muscle via interneurons in the myenteric plexus. This reflex ensures that gastric contents are delivered slowly to the duodenum, so ample time is available for neutralization of acid by pancreatic HCO3-.


What are the two components of pancreatic exocrine secretion?

o An aqueous component, high in HCO3-
o An enzymatic component


What is the function of HCO3- in the pancreatic secretion?

Neutralizes the H+ delivered to the duodenum from incoming chyme.


What is the function of the enzymatic component in the pancreatic secretion?

The enzymatic component is enriched with enzymes that digest carbohydrates, proteins and lipids into absorbable molecules.


What is the importance of pancreatic neutralization of the chyme in the duodenum?

Pancreatic enzymes are not active at acidic pH. Also, this neutralization reduces the possibility of intestinal mucosal damage by incoming gastric acid and pepsin.


How much of the pancreas is the exocrine pancreas?



How is the exocrine pancreas organized?

Similar to the salivary glands with acinar and ductal cells


What do the acinar cells of the pancreas secrete?

The enzymatic component


What do the ductal cells of the pancreas secrete?

The aqueous component


What happens with a decreased pH in the duodenum?

The S cells in the intestine secrete secretin


What is the effect of secretin release by the S cells?

Stimulates secretion of HCO3- which will increase the pH and this triggers feedback to inhibit secretin release


How does secretin control ductal cell secretion?

Secretin increases cAMP in duct cells which opens the CFTR Cl- channels and causes an outflow of Cl- into the duct lumen. The Cl- in the lumen drives the antiporter that exchanges chloride ions for bicarbonate with absorption of Cl- and release of HCO3- into the lumen.


What is the problem in cystic fibrosis?

In cystic fibrosis, CFTR (cystic fibrosis transmembrane conductance regulator) is mutated (inactive). This will prevent Cl- pumping and will prevent HCO3- pumping as a result. This will lead to destruction of the acinar gland and loss of pancreatic function.


What triggers CCK release from I cells?

 Direct interaction of fatty acids or amino acids or both with I cells themselves.
 Binding of fatty acids or amino acids or both to sensor paracrine cells that release CCK-RP (CCK- releasing factor or peptide).
 By the release of monitor peptide by pancreatic acinar cells.


How does CCK stimulate acinar secretion under the endocrine system?

-As an endocrine factor it binds to acinar cell CCK1 receptor.


How does CCK stimulate acinar secretion under neural control?

It stimulates neural reflexes that impinge on the pancreas – activates vagovagal reflex that leads to the release of ACh, GRP and VIP by pancreatic enteric neurons.


What do secretin and VIP act on?



What doe ACh and GRP act on?


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