GI VII Flashcards
(35 cards)
What is the most significant site for digestion and absorption of nutrients in the GI system?
Describe.
small intestine
Intense motility and secretions in the lumen and a large surface area of mucosal cells are the basis for digestion/absorption of nutrients.
Increased gallbladder contraction.
Relaxation of the sphincter of Oddi.
Secretion of pancreatic and biliary juices.
Regulation of gastric emptying (control of pylorus).
Inhibition of gastric secretion.
Describe gastric emptying into the duodenum. How does glucose differ from protein?
After a meal about bow much food does the stomach contain?
What is the rate of emptying gastric contents to the duodenum?
How do liquids/solids differ? Isotonic/hypotonic/hypertonic?
What size must particles be to enter the duodenum?
Slide 4
After a meal, the stomach contains about 1.5L of material (solid, liquid, secretions).
Emptying of the gastric contents to the duodenum is slow – takes ~3hours.
Liquids empty more rapidly, but solids empty after a log phase.
Isotonic contents empty more rapidly than either hypotonic or hypertonic contents.
Solids must be reduced to particles of
Gastric emptying happens after…
4 factors
An increase in tone (intraluminal pressure) in the proximal portion of stomach
Increased strength of antral contractions
Opening of the pylorus so the contents can move
Simultaneous inhibition of duodenal segmental contractions.
What happens to gastric emptying as the meal enters duodenum?
Describe the nature of the chyme and the neural response as it enters the duodenum.
What serves to decrease the strength of antral contractions? What else results in they pylorus and proximal gastric motility?
What is the net result?
What happens as chyme moves further down small intestine?
As meal enters the duodenum, it initiates feedback inhibition of gastric emptying.
This involves both neural and hormonal pathways based on the nature of chyme.
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.
The net result is an inhibition (slowing) of gastric emptying.
As chyme moves further down the small intestine, the feedback inhibition is reduced- gastric emptying starts again.
What are the two major factors that contribute to inhibition or slowing of gastric emptying?
The presence of fat in the duodenum
The presence of H+ (low pH) in the duodenum.
What mediates the effect of fat?
The effect of fat is mediated by Cholecystokinin (CCK) – secreted when fatty acids are present in the duodenum.
What is the effect of CCK?
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+?
What do H+ receptors in duodenal mucosa detect?
What is the effect?
The effect of H+ is mediated via reflexes in the enteric nervous system.
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-.
This neutralization is critical for pancreatic enzymes to function properly.
Describe the exocrine pancreas’ contributions toward digestion process.
What are the components of the pancreatic secretion? Describe each.
It secretes about 1L of fluid per day into the lumen of duodenum (10 times its weight).
Pancreatic secretion has two components:
An aqueous component, high in HCO3-
An enzymatic component.
The HCO3- - containing aqueous component neutralizes the H+ delivered to the duodenum from incoming chyme.
The enzymatic component is enriched with enzymes that digests carbohydrates, proteins and lipids into absorbable molecules.
Draw/describe the anatomy of the gall bladder and the ducts.
Slide 11.
Describe the structure of pancreatic exocrine glands:
endocrine pancreas
exocrine pancreas
Endocrine pancreas – islets of Langerhans (2% of pancreatic volume): insulin, glucagon, somatostatin (inhibitor of G stomach cells), pancreatic polypeptide;
Exocrine pancreas – (90% of pancreatic volume) - Secretion of enzymatic and aqueous components.
Describe how the exocrine is organized. What does it consist of? Describe each component.
Slide 16.
The exocrine pancreas is organized very similar to the salivary glands – consists of ducts and acini.
The acinus – is the blind end of a branching ductular system – lined by acinar cells.
The acinar cells secrete the enzymatic component.
The ducts are lined with ductal epithelial cells, which extend into a region of centroacinar cells in the acinus.
The centroacinar and ductal cells secrete the aqueous component
Draw a model of the pancreatic secretions (ducts/acinus) Which are stimulated by CCK or secretin?
Slide 17.
What regulates pH?
Describe the role of secretin. When is it released? What does it stimulate?
How does release stop?
Flow chart slide 18
The ducts are the effector arms of a pH regulatory system.
When luminal pH is below ~4.5, the S cells (in the small intestinal epithelium) are triggered to release Secretin.
Secretin then stimulates secretion of bicarbonate – results in increase of pH in the intestinal lumen.
This then produces negative feedback to stop secretin release.
What is the second messenger of secretin? What is the downstream effect? Describe.
What is the net result?
Slide 19
Secretin increases cAMP in duct cells.
This opens the CFTR Cl- channels and an outflow of Cl- into the duct lumen.
This drives the antiporter that exchanges chloride ions for bicarbonate.
H+ is transported into blood by Na+ -H+ exchanger (NHE-1).
Net result
Secretion of HCO3- in the lumen
Absorption of H+, acidification of pancreatic venous blood
What are the two courses for bicarb?
Two sources for bicarbonate:
Some taken across basolateral membrane via symporter NBC-1 (Na-bicarbonate cotransporter type 1).
Some generated intracellularly by carbonic anhydrase.
What is Cystic fibrosis? Explain why pancreatic function is defective in this disease.
A genetic disease that affects function of various epithelial organs – lung, intestine, biliary system and pancreas.
In cystic fibrosis, CFTR (cystic fibrosis transmembrane conductance regulator) is mutated (inactive).
As a result, the bicarbonate secretory process is defective – CFTR not functional.
This results in a decrease in pancreatic ductal secretion, high concentration and precipitation of the acinar enzymes in the duct - ultimately destroying gland.
This explains why pancreatic function is defective in this disease.
Describe control of pancreatic acinar secretion by CCK.
What type of cell releases CCK?
What stimulates these cells?
Draw.
Slide 21
CCK release from I cells (in the small intestinal epithelium) is triggered by:
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.
What are the two ways by which CCK stimulates pancreatic acinar secretion?
Draw a diagram.
Slide 22
As an endocrine factor and binds to acinar cell CCK1 receptor.
It also 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.
By what mechanism do CCK, Ach, and GRP act?
What does stimulation of acinar cells lead to?
What is the effect?
Slide 23
CCK, ACh and GRP acts via mobilizing intracellular Ca++ .
The secretory products here are already pre-synthesized and stored in granules (zymogen granules).
Stimulation of acinar cells leads to phosphorylation of various regulatory and structural proteins.
This moves the granules closer to the apical membrane, where they fuse with plasma membrane.
Granular contents are released into the lumen (exocytosis) – and subsequently washed by ductal secretions.
Summarize the main pathways for stimulation of pancreatic secretions in cephalic phase, gastric phase, and intestinal phase.
Slide 26
Describe bile. What is it? Where is it synthesized and secreted?
Where is it stored?
What does in help digest/absorb?
What factor stimulates contraction of gallbladder and relaxation of sphincter of Oddi.
Another important digestive juice that is mixed with chyme in the small intestinal lumen is bile.
Bile is synthesized and secreted by hepatocytes into the bile canaliculi that drain into the bile ducts.
It is stored and concentrated in the Gallbladder.
Bile helps in the digestion and absorption of lipids.
CCK stimulates the contraction of Gallbladder and relaxation of Sphincter of Oddi.
Describe the major constituents of bile.
Describe the structure. What do they form and why?
Major constituents of bile:
Bile acids – 65%
Phospholipids (mainly lecithins = PC) – 20%
Proteins – 5%
Cholesterol – 4%
Bile pigments (bilirubin for example) – 0.3%
Electrolytes (similar and isotonic to plasma) – 5-6%
Bile acids are detergents and form micelles.
These micelles shield the hydrophobic products of lipid digestion from the aqueous environment of lumen.
What is enterohepatic circulation?
Can conjugated bile acids cross intestinal epithelial lining?
When are conjugated bile acids reabsorbed? How?
Flow chart slide 29
Majority of bile acid pool is recycled from the intestine back to the liver – via enterohepatic circulation.
Conjugated bile acids are unable to passively cross the intestinal epithelial lining.
When chyme reaches the terminal ileum and lipid absorption is completed, conjugated bile acids are reabsorbed by a symporter known as apical Na+ -dependent bile acid transporter (asbt).
A minor fraction of bile acids enters the colon –become deconjugated and is reabsorbed passively.
