GIT - Lecture 7 Flashcards
Where is mucin secreted in the GIT?
everywhere
What secretes mucin?
surface epithelial cells
Why is there an increase in production of mucin at the level of the stomach?
because we have an tubular glands in the cardiac and pyloric regions that fill with mucin producing cells
Which part of the stomach are mucous neck cells present?
fundus and corpus
What is the pH of the mucous gel below the mucous layer?
2
What is the pH of the mucous gel above the mucous layer
around 7
Why does the mucous layer have some degree of protection?
because surface epithelial cells also release bicarbonate-rich fluid in addition to mucin
Where do the bicarbonate ions get adsorbed?
into the mucous gel layer
What is the mucous gel layer also known as?
muci-bicarb layer
What happens when H+ enter the muci-bicarb layer?
they combine with the bicarbonate to produce water and CO2
What prevents a change in the pH below the mucosal layer?
the muci-bicarb layer
What is the main thing that protects the gastric mucosa?
gastric mucosal barrier (GMB)
Where is the gastric mucosal barrier (GMB) found?
apical surfaces and tight junctions
What are the 3 things that protect gastric mucosa?
- muci-bicarb layer
- gastric mucosal barrier
- rapid cell turnover
What happens during rapid cell turnover?
re-epitheliazation
People with a normal ___ output can have a ___ barrier, which causes ulceration of the gastric mucosa.
normal, weak
Which 2 drugs can weaken the barrier and cause ulcers?
aspirin and NSAIDS
Which bacteria weakens the barrier and causes ulcers?
helicobacter pylori
Where does helicobacter pylori go to release its toxin?
between the mucous and the top of the surface epithelial cells
People with a ___ barrier can have an ___ HCl output, which causes ulceration of the gastric mucosa.
normal, excessive
What is produced when there is excessive HCl output?
gastrin-producing tumors
Regulation of gastric secretions happen via which 2 systems?
nervous and hormonal
What division and nerve contributes to the nervous regulation of gastric secretions?
sympathetic and vagus nerve
What are the 3 phases of gastric secretion?
- cephalic
- gastric
- intestinal
What are the 2 parts of the cephalic phase of gastric secretion?
psychic and gustatory
What is the neural regulation of secretion?
ENS neurons synapse on the smooth muscle of the GIT and then synapse on the secretory cell
The ENS sends excitatory input (ACh) onto which 3 secretory cells to increase their secretion?
- parietal
- peptic
- mucous
The cephalic phase is ___-mediated.
vagally
Activating secretory cells to produce secretions also causes…
vasodilation
What does sympathetic system do to secretion? What else does it cause?
inhibits secretion, causes vasoconstriction
What activates sensory neurons that leads to ACh secretion on secretory cells
distention and vago-vagal inputs
What do proteins produce when they get broken down into the stomach?
secretagogues
What are secretagogues?
amino acids or partially digested proteins?
What do secretagogues act on?
Gastrin-Releasing Cells (G-cells)
What do secretagogues lead to the release of when they act on G-cells?
gastrin
When secretagogues cause gastrin to be released from G-cells, what increases?
the parietal cell release of HCl
Gastrin released by endocrine cells in the antrum (G-cells) in response:
- secretagogues
- local enteric reflexes
- vagally-mediated reflexes
Which phase does vagally-mediated release of gastrin happen?
cephalic phase
How is gastrin regulated?
it is self-regulated
Where do secretagogues get excreted?
atrum
What happens to secretagogues when HCl released by parietal cells increases?
it increases since it converts pepsinogen to pepsin
What kind of feedback is the gastrin regulation?
positive
What is gastrin release inhibited by? (2)
low pH in the stomach and somatostatin
What do inhibitions contribute to the negative feedback on gastrin secretion?
low pH and somatostatin
What are the 2 physiological roles of gastrin?
- stimulates HCl secretion
- stimulates production of more parietal cells
What kind of effect does gastrin have on parietal cells?
trophic effect
When is somatostatin released?
at low pH in the stomach
What does somatostatin inhibit?
the release of gastrin from G-cells and HCl secretion from parietal cells
What is present in large quantities in the gastric mucosa?
histamine
What does histamine elicit?
large volumes of gastric juice with lots of HCl
What is the common mediator hypothesis?
Gastrin and ACh cause Histamine release. Histamine is the
FINAL local COMMON
CHEMOSTIMULATOR of the parietal cell.
Parietal cells have receptors for what 3 things on their surface?
- ACh
- gastrin
- histamine
What receptor is found on the parietal cell that binds histamine?
H2 receptor
What happens when one receptor binds to the parietal cell?
it sensitizes it from the stimulation of the other two
What kind of effect is between the 3 different stimulators of the parietal cell?
cooperative effect
Which substance is normally the one that activates the parietal cell since it is always present in the mucosa?
histamine
What is the permissive hypothesis?
histamine is constantly released in the gastric mucosa and presented to the Parietal Cells as a tonic background, sensitizing them to other stimuli
What happens to acid secretion in response to ACh and gastrin when the release of histamine is blocked or when there is an H2-receptor antagonist present?
it is inhibited
When are H2 receptor blockers used?
during ulcer disease
H2-receptor blockers are used to decrease ___ secretion.
HCl
In addition to H2-receptor blockers, what other blocker is used to decrease HCl secretion?
H+/K+ ATPase blockers
What is the feedback during intestinal phase of secretion?
inhibitory
When is there a small burst of excitation during the intestinal phase?
when the secretagogues come in and activate cells in the duodenum
What factors produce a negative feedback on secretion at the level of the stomach?
- distension
- pH<3.5
- osmolarity
- chemical composition
Both motor and secretory activities of the stomach reflect a balance between what 2 influences on the muscular and glandular cells in the gastric wall?
excitatory and inhibitory
Optimal secretory activity is the result of an interplay between which 2 mechanisms?
neural and hormonal
Gastric secretion at any moment in time reflects a balances between what 2 influences?
stimulatory and inhibitory influences
What are the pre-intestinal changes before digestion?
- meal reduced to semi-liquid consistency
- acidified, osmotic pressure is unchanged
- limited digestion
What are the pre-intestinal changes to some polysaccharides, some proteins and lipids?
-> Disaccharides
-> Polypeptides
-> Di-, monoglycerides, fatty acids
What are the 4 upper intestine functions?
- chyme neutralization
- osmotic equilibration
- digestion continues
- absorption begins
By the time the chyme leaves the small intestine, it will be ___.
isotonic
What are the accessory organs that secrete substances into the small intestine?
- liver
- gallbladder
- pancreas
How do the accessory organs send their excretions to the duodenum?
through the sphincter of Oddi into the ampulla of Vater
What is the swelling of the duodenum called?
ampulla of Vater
Which ducts merge to drain into the sphincter of Oddi?
right and left hepatic ducts
cystic duct
common bile duct
pancreatic dut
Where are all the pancreatic enzymes produced?
the head of the pancreas
What is the volume of pancreatic juice in the body?
0.5-1.5L/day
What kind of solution is pancreatic juice?
isotonic (300 mOsm)
What are the 4 main electrolytes of pancreatic juice?
Na+, K+, Cl-, HCO3-
What is the main electrolyte of pancreatic juice?
HCO3-
What is the pH of pancreatic juice?
7.2-8.2
Pancreas produces the largest quantities and the most powerful digestive ___.
enzymes
How many g% of enzymes present in the pancreatic juice?
3 g %
What are the 3 enzymes found in pancreatic juice?
amylases, proteases, lipases
For absorption, disaccharides must be converted to ___.
monosaccharides
All the proteases released at the level of the pancreas are in what kind of form?
inactive form
Where do inactive pancreative proteases become active?
when they get cleaves in the small intestine
What enzyme is produced in the small intestine to convert the inactive trypsinogen into trypsin?
enterokinase
Why are enzymes inactive when they are released by the pancreas?
because they are very strong so they might damage the pancreas if they are released active
What does trypsin convert chymotrypsinogen into?
chymotrypsin
What does trypsin convert proelastase into?
elastase
What does trypsin convert procarboxypeptidase into?
carboxypeptidase
What is secreted by the pancreas to inactivate trypsin?
trypsin inhibitor
