digestion - lecture 7 Flashcards
name and describe what each cell type in gastric glands in fundus and corpus secrete
parietal = intrinsic factor and hcl
chief cells = pepsinogen
mucous neck cell = mucin
surface epi cell = bicarb mucus
does mucin protect git mucosa from acid damage
huge layer of mucous
what is gmb
gastric mucosal barrier
apical surfaces and tjs = impermeable to hydrogen ions
what is muci bicarb layer
bicarb secreted and mucin
absorbed into mucous layers
h+ neutralized = bc bicarb also added to layer
protects acidic ph from getting to cells = like surface epi cells
describe gastric mucosa protection
muci bicarb layer
gmb
rapid cell turnover = reepithelization ~ 1 mil new cells = stomach and si
how do ulcers form
normal hcl output but weak barrie = aspirin and nsaids and helicobacter pylori contribute to weak barrier
or
normal barrier but excessive hcl output = gastrin producing tumours
describe neural regulation of secretion - cephalic phase
ens
excitatory
acts on secretory cells = hcl, mucin, pepsin
when stretch vagal inputs (cephalic)
vagally mediated
also vasodilation = parasym
symp = inhibits secretion and vasoconstricts
describe neural regulation of secretion - gastric phase
distension - stretch receptors
reinforced by vagal vagal reflex
affected by secretagogues
gastrin goes to heart and increase hcl output from parietal cells
what are secretagogues
aas or partially digested proteins which act on gastrin releasing cells = g cells = leads to release of gastrin
what is gastrin
peptide hormone
released by endocrine cells in antrum - g cells
what is gastrin released in response to
secretagogues - products of protein digestion
local enteric reflexed = distension in antrum
vagally mediated reflexes = vagovagal
what also happens during cephalic phase
vagally mediated release of gastrin also released during cephalic phase
want to be prepared before meal arrives
describe gastrin release
self regulating
secretagogues (products of protein breakdown) = act on g cell and inhibit acid release from parietal - somatostatin - neg = g cell stops gastrin = goes to heart = parietal cells (give hcl which activates pepsinogen to pepsin optimal ph)
when ph <2 = g cells sense when stop gastrin
so then ph rise = neg feedback loop
what does low ph do
Low pH causes the release of Somatostatin which inhibits the G-cell and the Parietal Cell
describe physiological roles of gastrin
stimulates hcl secretion
trophic effect = growth, stimulates production of more parietal cells = increase number
what does gastrin stimulate
hcl secretion from parietal cell
when is gastrin released
Precedes and accompanies meal
occurs as part of cephalic phase
describe pos feedback of gastric secretion
release stimulated by stretch in stomach and presence of secretagogues in stomach
describe neg feedback of gastric secretion
release inhibited by low ph in stomach and by somatostatin
describe somatostatin
release occurs in presence of low ph in stomach
inhibits gastrin release from g cells
inhibits hcl secretion from parietal cells
What Role does Histamine Play in HCl Secretion?
lots of histamine present in gastric mucosa
histamine administration elicits large vols of gastric juice with lots of hcl
what is common mediator hypothesis
gastrin and ach cause histamine release
histamine is final local common chemostimulator of parietal cell
WRONGGGGGGGG
describe Regulation of Parietal Cell HCl Secretion
PARIETAL cells have receptors for all 3 on surface = ach, gastrin and histamine
describe receptor interaction hypothesis
separate receptors
interaction among 3 receptors
blockade or stimulation of one receptor, changes properties of one or both of the other 2 receptors
cooperative effect = histamine sensitive to ach and gastrin
describe permissive hypothesis
histamine constantly released in gastric mucosa and presented to parietal cells as a tonic background = sensitize them to other stimuli
blocking tonic background release of histamine or using h2 receptor antagonists inhibits acid secretion in response to ach and gastrin
describe intestinal phase
secretagogues to heart –> enterooxyntin –> gastrin —> acts on parietal cell and secretes hcl
also inhibits gastric secretion
neg feedback on secretions = secretin, cck, gip, vip, neurotensin
describe motor and secretory activities of stomach
at any moment in time reflect balance between excite and inhibitory influences on muscular and glandular cells in gastric wall
describe optimal secretory activity
result of interplay between neural and hormonal mechanisms
gastric secretions at any moment in time reflects balance between excite and inhibit
describe pre intestinal changes
meal reduced to semi liquid consistency = chyme
acidified, osmotic pressure unchanged
limited digestion
describe pre intestinal changes - enzymes
some polysacc –some salivary amylase pytalin (inactivated in acidic ph of stomach)–> disacc
some proteins –gastric pepsin–> polypep
lipid –> di and monoglycerides, fatty acids - active at stomach only
describe upper intesine functions
chyme neutralization = alkaline secretions
osmotic equilibration = will be isotonic by time reaches colon = want nutrients to flow back to systems
Digestion continues
absorption begins
name accessory organs which secrete stuff into si
liver
gallbladder
pancrease
all into duo via common pathway = ampulla of water (sphincter of oddi)
describe liver and biliary system
right and left hepatic ducts
cystic duct
common bile duct
ampulla of water
pancreatic duct w/ sphincter of oddi
describe pancreas
endo and exocrine components
describe pancreatic juice - composition
0.5-1.5l/day
isotonic
main electrolytes = sodium, potassium, chloride, BICARB
ph = 7.2-8.2
describe pancreatic juice - enzymes
pancreas produces largest and most powerful digestive enzymes
enzymes = 3% protein, only breast milk has more proteins than this
= amylases, proteases, lipases
what is important for absorption
dissac must be converted to monosacc
right now = amylase converts poly to disacc
describe pancreatic proteases - trypsin
proenzyme – enteropeptidase - enterokinase –> enzyme
trypsinogen –> trypsin by enterokinase in SMALL INTESTINE
describe pancreatic proteases
chymotrypsinogen –> chymotrypsin
proelastase –> elastase
procarboxypeptidase –> carboxypeptidase
all BY TRYPSIN ENZYME
trypsin inhibitor = also secreted by pancreas = to prevent activation in pancreas
where is gastrin released
by g cells in stomach and duo
what does proton pump inhibitor do
blocks 90-95% of release of acid from parietal cells
what happens if block h2 receptor
ulcer diseases treatment = bc blocks 70% of acid release from parietal
used to decrease hcl secretion
also h+/k+ atpase blockers
