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71 Cards in this Set

  • Front
  • Back
Inactive at pH < 4 but because there can be little mixing in
the orad stomach, α-amylase can be active on up to 75% of ingested starch.
Salivary α−amylase is identical to the pancreatic enzyme.
a-Amylase
hydrolyzes triglycerides. Lingual lipase has an acidic pH
optimum and is active in the stomach.
lingial lipase
protective functions
Saliva dilutes noxious or toxic substances. Salivation prior to
vomiting, neutralizes gastric juices. The bacteriocidal components of saliva are
lysozyme, secretory IgA, and lactoferrin.
Salivary secretions
1. A large volume of saliva is
produced relative to the weight of
salivary glands.
2. The K+ concentration is higher than
plasma.
3. The HCO3 concentration is higher
than plasma.
4. The osmolarity of saliva is lower
than plasma.
5. Saliva contains special organic
material.
Salivary secretins
Na and CL- LEAVE the duct
As secretory rate increases, the saliva
approaches but never never reaches osmotic equilibrium, more sodium is left in etc.
sodium and chloride leaves duct via
Na/K and Na/H, CL/HCO3 on apical membrane

Cl and Na are pumped out of the basolateral via blah

see pg. 44
salivary secretion is

removal of paras give gland atrophy
Completely under autonomic control.
- GI peptides have no role.
- Parasympathetics and sympathetics both stimulate secretion.
- Parasympathetic is the stronger stimulus.
- Parasympathetic stimulation is also required for gland growth.
parasymp efects on salivary include
1. Activation of ion transport pathways.
2. Contraction of myoepithelial cells in acini and intercalated ducts.
3. Vasodilation.
4. Increased oxygen and glucose utilization - metabolic vasodilation.
5. Release of kallikrein leads to vasodilation via bradykinin production.
Gastric juice has
1. Hydrochloric acid (HCl) from parietal cells.
2. Pepsinogen from Chief cells.
3. Mucins from surface epithelial cells.
4. Intrinsic factor from parietal cells.
Intrinsic
factor is the only indispensable secretory product of the stomach.
All ingested protein can be digested and absorbed in the small
intestine without acid or pepsin from the stomach.
stomach has two secretory parts
Proximal 80% is the acid secreting
oxyntic gland mucosa and distal 20%
(antrum) is the pyloric gland mucosa
with lots of endocrine G cells (gastrin
secreting cells).
Pyloric Glands
1. mucous cells.
2. G cells - gastrin secretion.
3. stem cells in neck region.
Oxyntic glands (pictured at left)
contain:
parietal or oxyntic cells - acid
producers
2. Chief or peptic cells – pepsinogen
3. mucous neck cells - proliferative;
migrate up to become surface
epithelia or down to become oxyntic or
chief cells.
Parietal cells secrete acid in amounts
up to 150-160 mEq/L (pH = 0.8) Parietal
cells also secrete intrinsic factor.
yep,
resting vs. active parietl cells
The resting cell has
intracellular canaliculi (IC), which open
on the apical membrane of the cell and
many tubulovesicular structures (TV) in
the cytoplasm. When the cell is
activated the TVs fuse with the cell
membrane so that the area of cell
membrane in contact with gastric lumen
is greatly amplified.
secretory canaliculous and tubulovesicle membranes
contain the H/K ATPase, K,
and Cl channels that mediate acid secretion. When they are exposed to the gastric
lumen there is an explosive increase in acid secretion.
When the parietal cell is stimulated
When the parietal cell is stimulated, H-K
pumps (fueled by ATP hydrolysis) extrude H+ into the lumen of the gastric gland in
exchange for K+.
How does Cl- get out
Cl- exits
through channels in the luminal membrane, completing the net process of HCl
secretion.
How does the parietal cell get H+
The H+ needed by the H-K pump is provided by the entry of CO2 and H2O,
which are converted to H+ and HCO3
- by carbonic anhydrase
HC03 needs to get out how???
The HCO3
- exits across
the basolateral membrane via the Cl-HCO3 exchanger
It is important to know that gastric juice
At all rates of secretion, gastric
juice is isotonic to plasma. However,
ionic composition varies with secretion
rate.
However, ionic composistion of gastric juice will change at varying secretion rates
At basal rates, secretion is mainly
NaCl with some H+ and K+.As rate
increases, Na content decreases and H+
increases. .
At all rates
HCL is secreted against an electrochemical gradient
HCL concentration and rate
at basal rate H+ = 10-20 mEq/L, pH = 2
at peak rate H+ = 130-150 mEq/L pH < 1
Gastric secretions come from two different places
1. Nonparietal cells (surface epithelia) produce a constant, low volume of a NaCl and
KHCO3-rich fluid.
2. Parietal cells secrete an HCl- and KCl-rich fluid. The rate of secretion is
regulated
Protection from acidity
There is a million-fold H+ concentration gradient from the lumen of the stomach to
the blood. However, there is very little back flux of acid or other electrolytes into the
blood due to the gastric mucosal barrier. This barrier can be compromised by bile acids,
aspirin, alcohol, and other drugs. Some prostaglandins promote mucin and HCO3
secretion, which protect this barrier.
Gastric epithelial cells will protect the stomach
by secreting a mucous layer high in HC03
Stimulators of acid secretion
The antral hormone gastrin
2. The neurotransmitter acetylcholine (ACh)
3. The paracrine histamine
Gastrin and ACh are released in response to a meal. Gastrin is the most potent.
It is 1500X more potent than histamine.
gastrin and secretion also have INDIRECT action
by stimulating histamine secretion from an enterchrommafin like cell that causes H+ secretion up regulation in the parietal cell
WHen applied alone, gastrin, histamine, and acetycholine have small effects but when applied togethor
they have a much higher output than the sum of their individual contributions....potentiation ....the difference is that they all use differnt signaling cascade mechanisms. even though gastrin and acetylcholine both use Gq and a PLC mechanism that activates PKC
In the CORPUS of the stomach the vagus nerve also stimulates D cells and ECL cells
ECL stimulation causes histamine release, D cell stimulation inhibits somatostain releas that would inhibt histamine release.
IN the ANTRUM of the stomach the vagus stimulates both G cells and D cells
Vagus stimulates the G via GRP (gastrin releasing peptide) which releases gastrin.
G cell stimulates gastric acid secretion bytwo mechansims after vagus stimulation
stimulating the pariatel cell directly and indirectly via the ECL cell which causes histamine release,
D cell stimulation by vagus in the antrum again
inhibits somatostain release which would inhibt gastrin release and acid secretion from the parietal gland
Lumenal H+
directly stimulates D cells to release somatostatin
in contrast, products of degradtion, proteins and aa
cause g cells to makes gastrin , which makes more gastric acid by parietal stimulation and is thus positive feedback
3 modes of acid secretion
next
cephalic phase is .30 of acid secretion
and is stimulated by mechano and chemo receptors of the mouth
Gastric phase
elicited by food in the stomach but can be blocked if the stomach is already acidic...<2....so vagal response is blocked to distention. AAs work on parietal cells here, BUT CERTAINLY not on G cells.
chyme in the duodenum intially stimulates and later inhibts acid production
when duodenal chyme pH is above 3, then acid secretion is stimulated, if below 3 then inhibited.
duodenum has g cells
that can be stimulated to reease gastrin and by distention and amino acids.
INtestinal phse is 5%
of acid secretion. Gastric was 50. and cephalic was 30%
SO the intestinal phase of 5% is regulated by
aa and peptides, duodenal gastrin, and intestinal peptide enter-oxyntin
acid, fat digestion products, and hypertonicity in the duodenum
all inhibt GASTRIC ACID release
acid in duodenum causes the RELEASE of SECRETIN which acts to
inibt the release of gastrin from G cells and stop the effects of Gastrin
Fatty acids cause release of CCK and GIP.
GIP inhibits gastrin release and parietal cells directly.
Somatostain inhibits

prostaglandins have similar effects
gastrin release in
the antrum, histamine release in the
corpus, and antagonizes histamine
stimulation of the parietal cell.
higher the volume of food
the higher the pH, but also the higher the rate of acid secretion. Acid secretion food volume and pH fall togethor
Pepsinogen secretion is increased by
-Cholinergic fibers - Vagal stimulation during cephalic and gastric
-Gastrin
-Acid in contact with gastric mucosa (Local cholinergic reflex)
Stimulators of pepsinogen secretion that inhibit acid secretion are:
Secretin in response to duodenal acid
CCK in response to duodenal fatty acids
Cyclic AMP and calcium are second messengers for pepsinogen secretion.
yep
Acid is necessary for activation of pepsinogen to pepsin. Conversion begins slowly
pH 5 and is instantaneous at a pH of 2 or less.
yep
Intrinsic Factor - The only indispensable secretory product of the stomach.
Intrinsic factor is a large glycoprotein secreted by parietal cells. It complexes with
vitamin B12 and protects it from proteolysis in the small intestine. In the ileum, intrinsic
factor promotes vitamin B12 absorption
Salivary glands
1. High volume (for the size of salivary glands).
2. High in K+ and HCO3.
3. Low in Na+ and Cl-.
4. Always hypotonic to plasma.
5. Contains α-amylase and lingual lipase.
In the antral region of the stomach is the pyloric gland mucosa, which contains:
The G cells that produce the GI hormone gastrin.
Mucous cells that produce mucus important for the gastric mucosal barrier.
omeprazole (Prilosec),
stops the H/K ATPASE that functions in the parietal cell to make H+ and CL- work
Histamine from gastric mast cells
stimulates gastric acid secretion
Histamine
potentiates the stimulating effects of gastrin and acetylcholine. This the basis for the
effectiveness of antihistamines in the treatment of gastric acid hypersecretion.
yep
Acetylcholine (ACH) potentiates the effects of histamine and gastrin. Atropine blocks
ACH stimulation.
yep
Gastric acid secretion is inhibited by low intragastric pH. This is due to
somatostatin release, which can inhibit both the G cell and the parietal cell.
yep
There is a reciprocal relationship between H+ and Na+ in gastric juice; as
flow rate increases H+ rises and Na+ declines. This reflects the relative contribution of
parietal cell and surface mucosa cell secretion to the total composition of gastric juice.
yep
Cephalic - (30%) Primarily mediated by vagal stimulation (ACH and gastrinreleasing
peptide).
ach inhibts somatostatin and stmulates gastrin release
How is pepsin secreted
Secretion of pepsinogen is stimulated
most strongly by acetylcholine and by low intragastric pH. The latter is most likely
mediated by the enteric nervous system (a local ENS reflex).
ZOLLINGER-ELLISION SYNDROME
caused by a pancreatic tumor that is
hypersecretory for gastrin. Results in duodenal ulcers from high gastric acid production
and increased gastric emptying, diarrhea (gastrin stimulates colonic fluid secretion),
steatorrhea (fat in stool) due to inactivation of pancreatic lipases and titration of bile
acids, and gastroesophageal reflux disease (GERD).
Gastric acid secretion is inhibited by low intragastric pH. This is due to
somatostatin release, which can inhibit both the G cell and the parietal cell.
yep
There is a reciprocal relationship between H+ and Na+ in gastric juice; as
flow rate increases H+ rises and Na+ declines. This reflects the relative contribution of
parietal cell and surface mucosa cell secretion to the total composition of gastric juice.
yep
Cephalic - (30%) Primarily mediated by vagal stimulation (ACH and gastrinreleasing
peptide).
ach inhibts somatostatin and stmulates gastrin release
How is pepsin secreted
Secretion of pepsinogen is stimulated
most strongly by acetylcholine and by low intragastric pH. The latter is most likely
mediated by the enteric nervous system (a local ENS reflex).
ZOLLINGER-ELLISION SYNDROME
caused by a pancreatic tumor that is
hypersecretory for gastrin. Results in duodenal ulcers from high gastric acid production
and increased gastric emptying, diarrhea (gastrin stimulates colonic fluid secretion),
steatorrhea (fat in stool) due to inactivation of pancreatic lipases and titration of bile
acids, and gastroesophageal reflux disease (GERD).
Many patients hospitalized in the intensive care unit (ICU) receive prophylactic
antiulcer treatment (e.g. histamine-2 receptor antagonist, such as cimetidine) that either
neutralize existing acid or block its secretion and thereby raise gastric pH
The higher the gastric pH, the greater
the risk of pneumonia.