Gastric Secretion Flashcards
Fundus function
Storage
Body of stomach function
Storage, mucus, HCl, Pepsinogen, Intrinsic factor
Antrum function
mixing/grinding, gastrin
HCl function in stomach
marinating
What is pepsinogen the inactive form of
pepsin - a proteolytic enzyme
why is pepsin stored in its inactive form
so as to not erode the stomach
chyme definition
mixed food as it leaves the antrum
gastrin definition
hormone released in antrum from G-cells and secreted into the circulation - acts on cells of body
what is the cellular composition of a gastric gland
Gastric Pit -
1.surface mucous cells
Gastric Gland -
- mucous neck cells
- parietal cells
- chief cells
Mucous neck cells secrete
mucus
parietal cells secrete
HCl, intrinsic factor
chief cells secrete
pepsinogens
Why are the junctions between cells very tight
to stop stomach acid entering
How is HCl made in the stomach
THIS IS A VERY LONG ANSWER
- CO2 into cell – combines with water – makes carbonic acid – made faster by carbonic anhydrase – H2CO3 doesn’t last long – immediately dissociates to form H ions and bicarbonate
- H ions pumped out (need ATP) – works similar to NaK pump – one H out, one K in
HCO3 – pumped out on exchange protein – HCO3 out, – HCO3 out causes temporary alkalisation - Cl in (through cell and out the other side-joins with the other H and water to make the HCl in the stomach)
when is the only time HCl is produced in the stomach
when eating
What three molecules control acid production
- Gastrin
- Histamine
- Acetylcholine
What controls the switch off mechanism for acid production
prostaglandins
how does gastrin work
Binds to its receptor – g-protein coupled receptor – causes a rise in Ca – acts through protein kinase C to increase turn around of K/H proton pump
how does histamine work
stomach has a unique histamine receptor – H2 receptor – coupled with Gs
how does acetylcholine work
neurotransmitter – acts on muscarinic cholinergic receptros (M3) – g protein coupled – rise in Ca – rise in turn around of H/K
How do prostaglandins inhibit acid production
Gi – inhibitor protein – coupled with that prevents reaction taking place – take away stimulus – turn pump off
what three mechanisms is gastric acid section controlled by
- Neurocrine - (vagus/local reflexes)
- Endocrine (gastrin)
- Paracrine (histamine)
What are the two phases of acid secretion
- cephalic - anticipation of food
2. gastric - food reaching stomach
What is the only essential (non-compensated) function of the stomach
the production of intrinsic factor
where is intrinsic factor produced
parietal cells
intrinsic factor function
vitamin B12 absorption - intrinsic factor/B12 complex is absorbed from the ileum
what does a defect in the production of intrinsic factor cause
pernicious anaemia (failure of erythrocyte maturation)
what is the role of gastric mucus
CYTOPROTECTIVE role
- protects mucosal surface from mechanical injury
- neutral pH (HCO3) - protects against gastric acid corrosion and pepsin digestion
How does the gastric mucus protect against corrosion
High bicarbonate content – protects – makes pH around 7 at cell surface
Acid buffered and neutralised by bicarbonate as it enters mucus layer
what is interesting about when acid is neutralised in the stomach
only neutralised on the way IN to the stomach - not on the way out
Describe the processes that occur during the cephalic stage of acid production
- anticipation of food stimulates vagus nerve = release of ACh
- vagus nerve stimulation casues stimulation of G-cells = release of Gastrin
- With both Gastrin and ACh present ECL cells are stimulated = release of histamine
- With ACh, gastrin and histamine all present -Parietal cells are activated
Describe the processes that occur during the gastric phase of acid production
- arrival of food in stomach takes over for stimulating vagus nerve = release of ACh
- Peptides present in lumen take over for stimulation of G-cells = release of gastrin
- With both Gastrin and ACh present ECL cells continue to be stimulated = release of histamine
- With ACh, gastrin and histamine all present -Parietal cells are activated
what are the two indicators that stop acid production
- acid in the duodenum
2. fat in the duodenum
how does acid in the duodenum stop acid production
- stimulates enterogastric (splanchnic) reflex
- stimulates secretin release
- both of these processes lead to a decease in gastrin secretion which causes a decease in the stimulation of parietal cells
how does fat in the duodenum stop acid production
- causes release of GIP
2. leads to a decrease in gastrin secretion which leads to a decrease in HCl secretion from parietal cells
what are enterogastrones
hormones released from gland cells in duodenal mucosa - act collectively to prevent further acid build up
name the three enterogastrones
- secretin
- cholecystokinin (CCK)
- GIP (Gastro-inhibitory peptide)
when are enterogastrones released
in response to acid or hypertonic solutions (mainly secretin) and fatty acids or monoglycerides (mainly GIP) in the duodenum
what are the two strategies by which enterogastrones work
- inhibit gastric acid secretion
2. reduce gastric emptying (inhibit motility/contract pyloric sphincter)
what is the name of the inactive form of an enzyme precursor (eg pepsinogen)
zymogen
where is pepsinogen secreted
chief cells
what determines secretion of pepsinogen
low pH (<3) - causes secretion of pepsinogen which is then converted to pepsin
what kind of feedback mechanism does pepsin production use
positive feedback - i.e. presence of pepsin makes more pepsin
how is the pepsin reaction stopped
by raising the pH - inactivated at neutral pH
