secretions in the stomach Flashcards
functions of the stomach
- stores food - compliant
- kills bacteria - acid
- liquefies food
- mixes chyme with gastric secretions
- kneading of food particles to <1mm
- regulates chyme release into duodenum
- produces intrinsic factor
- very little digestion (proteins) and absorption (alcohol, aspirin) takes place in the stomach
what is HCl production is stimulated by
gastrin
ACh
histamine
what is ACh
acetylcholine
acid/hcl stimulartion full explanation
- HCl production is stimulated by
-gastrin
-ACh = acetylcholine
-histamine
- stimulate parietal cells to secrete HCl
- increase in H+/K+ATPases and Cl- channels on parietal cells
- energetically expensive process (ATP) - 1532Cals/litre secreted - so have lots of mitochondria in the cells to produce ATP
when the parietal cells are stimulated what is released
desrcibe a resting parietal cell
unstimulated
lots of mitochondria - uses lots of energy
lots of tubulovesicles - H+/K+ ATPase or proton pumps - increase SA when acid needs to be secreted
resting parietal cell is ….
unstimulated
secreting parietal cell is …..
stimulated
secreting/stimulated parietal cell explanation
histamine, gastrin and ACh signal tubulovesicles to come together to produce canaliculi = increase cell surface area ready for acid secretion and insert proton pumps on the surface
how are stimulatory singals delivered to the pariental cell to induce HCl secretion
- histamine released from neighbouring gastric ECL cell
- gastrin released from stomach G-cells into blood
- comes back to stomach and stimulates parietal cell
- ACh released from neurones of vagus nerve
acid stimulation - what does the receptor have to be for binding
complimentary shape
what are the 3 phases of acid secretion
cephalic
gastric
intestinal
describe the cephalic phase
entirely neural phase
thought, sight, smell or approach of food leads to ACh release
from vagus
chewing/swallowing can do this too
describe the gastric phase
once food is in the stomach - distend it
detected by mechanoreceptors
leads to ACh release
roducts of protein digestion (peptides/AA’s) in stomach = detected by chemoreceptors - lead to gastrin release
describe the intestinal phase
primarily acid inhibitory phase
once food enters duodenum
HCl secretion needs to be stopped
presence of HCl in duodenum leads to somatostatin, secretin + CCK
all 3 = inhibit acid secretion from parietal cell
secretin stimulates HCO3- release from pancreas = neutralises acid entering duodenum
CCK = stimulated by lipids entering duodenum
can stimulate digestive enzyme + bile release from pancreas + gallbladder
peptic ulcer treatments
H2 - receptor antagonists
-block action f histamine receptor
-cimetidine, ranitidine
PROTON PUMP INHIBITORS
-block ATP driven H+/K+ exchange
-more effective than H2-R antagonists
-omeprazole, lansoprazole
the stomach can cope with large acid environment but what can’t
oesophagus and small intestine
what does reflux do to teeth
corrodes them
what dies acid attacking teeth lead to
high sensitivity rate
lots of caries
lose vertical dimension - become shorter
helicobacter pylori
- bacterium strongly associated with PUD
- linked with gastric cancer
- rate of re-infection after antibiotics is high
- route of transmission unclear - oral-oral?
- may survive on dental plaque
- dentists may be at greater risk of infection
- dentists may aid transmission
how does the alkaline tide happen
lots of HCO3- from parietal cells into blood after meals
disturbs plasma buffer system
mops up circulating H+ = increase plasma pH
detects temporary rise in pH - alkaline tide
what mops up the H+ in the alkaline tide
HCO3-
what is HCO3-
bicarbonate
what stimulates acid secretion
Ach
gastrin
histamine
Ach
neurocrine
Vagus
gastrin
endocrine
gastrin G-cells
paracrine
gastric ECL-cells
somatostatin
paracrine
gastric D-cells
secretin
endocrine
duodenal S-cells
CCK (cholecystokinin)
endocrine
duodenal I-cells
somatostatin -> pancreas
HCO3- release
CCK -> pancreas
enzyme release
CCK -> gallbladder
bile release
what substance do G cells secrete
gastrin
-stimulates acid
what substance do D cells secrete
somatostatin
-inhibits acid
what substance do chief cells secrete
pepsin - ogen
gastric lipase
what substance do enterochromaffin-like cells secrete
histamine
-stimulates acid
what substance do mucous neck cells secrete
mucus (protects lining)
bicarconate
what substance do parietal cells secrete
gastric acid - HCl
intrinsic factors (Ca++ absorption)
what does gastrin stimulate
acid
what does mucus do
protects lining
what does histamine stimulate
acid
what does somatostatin do
inhibits acid
what is the secreting cell for mucus/HCO3-
goblet cells - surface and mucous neck cells
what is the secreting cell for acid
parietal cells
what is the secreting cell for pepsinogen
chief (zymogen)
what is the secreting cell for histamine
enterochromaffin-like
what is the secreting cell for gastrin
G cells
what is the secreting cell for somatostatin
D cells
what is the secreting cell for intrinsic factor
parietal
function of mucus/HCO3- /goblet cells
neutralises acid at the lining of stomach = prevents damage to the stomach wall
function of acid / parietal cells
mechanical digestion- denatures proteins
converts pepsinogen into pepsin = denatures + digests proteins (15%) - chemical digestion
converts poorly absorbed ferric iron (Fe3+) ion into absorbable ferrous iron (Fe2+) - iron deficiency anaemia without acid
function of pepsinogen / chief cells
start protein digestion in the stomach
function of histamine/enterochromaffin-like
stimulate acid secretion from parietal cells
function of gastrin/G cells
stimulate acid + secretion from parietal cells
stimulates ECL cells to release histamine
function somatostatin/D cells
inhibit acid secretion from parietal cells
function of intrinsic factor/parietal cells
add absorption of vitamin B12 from ileum- vit.B12 essential for RBC maturation - pernicious anaemia without intrinsic factor
