[Physiology] Gastric Secretion Flashcards
what is the role of the fundas
smooth muscle / thin and stretchy (storage little mixing little chemical material)
what is the role of the stomach body
Storage
secrete Mucus
produce HCl
pepsin stored in its inactive precursor Pepsinogen
Intrinsic factor
contrains cells that produce intrinsic factor (vitamin B12)
what is the role of the stomach antrum
musculature more powerful more mixing everything till lliquid
secretes GI hormone gastrin from G cells travels all over body and acts on the cells in the body just a few cm away
what is found on the surface of gastric glands
mucous secreting cells
what is the gastric pit
opening of the gastric gland
what are the three main cell types in gastric glands
mucous neck cell, parietal cell and chief cell
mucous neck cells
mucous producing
mainly immature surface mucous cells waiting to replace some of the cells that slide off
cheif cells
recruit inactive precursors to pepsin (pesinogen) - contain it as an inactive form prior to release
parietal cells
slightly odd shape - responsible for secretion of HCl and intrinsic factor
CO2 role in stomach lumen
waste product of respiration - goes across membrane into lumen of parietal cell and combines with water to form semi stable compound known as carbonic acid
what does CO2 combining with water to form carbonic acid require
catalyst (carbonic anhydrase)
what is the difficulty with carbonic acid
very unstable immediately dissociates to give H and a bicarbonate ion
what happens to the hydrogen ion that is produced
gets pumped out out apical membrane on hydrogen potassium ATPase
- uses atp proton pump, needs careful regulation
what happens to the bicarbonate ion that is produced
transported across basolateral membrane in exchange for chloride ion into blood
increases blood ph above 7.4
what is the increase in blood ph following meals known as
post prandial alkalanisatin
what occurs due to the entry and exit of chlorine and H
allows water to join stomach lumen causing it to become very acidic PH<2
what does gastrin produced from g cells and gastric antrum bind to
CCKB receptors
when gastrin binds to cckb calcium then acts on protein kinase c and increases actvity of hydrogen potassium atpase
increasing level of hydrogen being pumped onto lumen - lowering the ph
what does histamine act on
unique receptor in the stomach H2
H2 receptor is coupled up to an enzyme adenylate cyclase by the stimulatory G protein GS
what is the H2 receptor coupled up to
enzyme adenylate cyclase by the stimulatory G protein GS
what happens when histamine binds to Gs receptor
activates adenyate cyclase and that converts adenosine triphosphate ATP into cyclic AMP
what does cyclic AMP act on once stimulated by histamine
its own protein kinase A which also activates hydrogen potassium ATPase increasing its activity and producing more H into the lumen
what do prostaglandins act on
receptor E3 which is coupled up to adenocyclase by Gi the inhibitory protein
prevents production of camp
what does acetylcholine act on
vagus nerve innervates cells and releases acetylcholine which acts on a cholinergic receptor (muscarinic M3)
like a gastrin receptor causes a rise in intracellular calcium following acetylcholine binding to that M3 receptor
activate protein kinase 3
activating hydrogen potassium ATPase
what are the three mechanisms gastric acid secretion is controlled by
Neurocrine (vagus/local reflexes)
Endocrine (gastrin)
Paracrine (histamine)
what stimulates the vagus nerve
sight, smell and taste of food
what does stimulation of the vagus nerve stimulate
ACh (acetylcholine) and G cells (Gastrin) to parietal cells
what does gastrin and ACh stimulate
ECL cells which produce histamine to parietal cells
what does distention / physical presence of food cause
vagal/enteric reflexes releasing ACh to parietal cells
what do peptides in lumen stimulate
g cells which produce gastrin to parietal cells
gastrin/ACh
ECL cells releasing histamine
cephalic phase
stopping eating (reduces vagal activity)
gastric phase
reduces PH and increases HCl
reduces gastrin
intestinal phase
acid in duodenum
- enterogastric (splanchnic reflex)
- secretin release
what does the enterogastric (splanchnic reflex) and secretin release cause
reduced gastrin secretion and reduced gastrin stimn of parietal cells
what does fat/CHO in duodenum cause
GIP release
GIP release cause
Gastrin secrn
Parietal HCl secrn
Enterogastrones
Hormones released from gland cells in duodenal mucosa - secretin, cholecystokinin (CCK), GIP
when are enterogastrones released
in response to acid, hypertonic solutions, fatty acids or monoglycerides in duodenum
how do entergastrones act
Act collectively to prevent further acid build up in duodenum
what are the two strategies by which enterogastrones act
inhibit gastric acid secretion
reduce gastric emptying (inhibit motility/contract pyloric sphincter)
pepsinogen secretion
Pepsinogen (zymogen = inactive prcursor) secreted by Chief cells
Low pH (<3) → Pepsinogen → Pepsin
what does zymogen storage do
prevents cellular digestion
when are pepsins inactivated
neutral pH
Mechanisms for pepsin control of pepsin secretion parallel HCl secretion
where is gastric mucous produced from
produced by surface epithelial cells and mucus neck cells
what role does gastric mucous play
Protects mucosal surface from mechanical injury
Neutral pH (HCO3) → Protects against gastric acid corrosion and pepsin digestion due to high bicarbonate content
what is intrinsic factor
Only essential (non-compensated) function of stomach
Produced by parietal cells
Required for vitamin B12 absorption
what happens to intrinsix factor/B12 complex
Intrinsic factor/B12 complex absorbed from ileum
taken up to liver where it gets stored - three years worth in liver
what defect with intrinsic factor/B12
Pernicious Anaemia (failure of erythrocyte maturation)
