Gastric Secretions Flashcards
how is B12 absorbed?
B12 Absorption:
- attached to dietary protein (thats how its absorbed !)
- in stomach, HCl and pepsin cause B12 to dissociate from dietary protein
- then B12 associates with haptocorrin
- then dissociates from haptocorrin & binds with stomach intrinsic factor
- absorbed in terminal ileum & into blood
- attaches to transcobalamin
B12 must be complexed with what to be absorbed in terminal ileum?
B12 is transported in the portal circulation and transferred to what?
- stomach intrinsic factor :)
- B12 is transported in the portal circulation and transferred to transcobalamin II
name the 5 types of gastric epithelial cells xox
where do u find each one?
surface mucous cell - at the surface
mucus neck cell - at the neck
parietal cell - midway down
ECL cell - further down lol
chief cell - near the bottom of the crpyt
gastric epithelial cells:
- **parietal cell:
a) function? - what do they produce?
b) location?**
c) which organelle are they full of?
gastric epithelial cell:
functions:
- produce intrinsic factor
- *- secrete HCl**
location:
- base of gastric pits
organelle:
- full of mitochondria bc producing HCl requires ATP
gastric epithelial cells
- parietal cells produce HCl. But HCl is actually quite toxic. how does the body cell overcome this issue of not causing self harm via the HCl? (2)
1. HCl is only produced when food is in the stomach = get unstimualted and stimulated parietal cells:
a) unstimulated parietal cells have H+ ATPase Pumps in the cytosol
b) stimulated parietal cells have H+ ATPase Pumps on apical surface
2. surface mucus cells secrete mucus
- without mucus = would directly interact with cells
- mucus works as:
a) physical barrier; gel layer
b) chemical barrier; bicarbonate
explain the MoA of how HCl is produced xo
HCl production:
H+:
in the interstitial space:
- bicarbonate (HCO3) can react with H+ to form H2CO3 (carbonic acid)
- carbonic acid reacts via enzyme carbonic anhydrase and turn into H20 and CO2
- H2O and CO2 can then enter parietal cell
in the parietal cell:
- bicarbonate reforms = useful bc its an important buffer!
- H+ ion is left. pumped via proton pump on apical membrane of parietal cell into lumen
Chlorine:
- when bicarbonate pumped out out of parietal cell into interstitial space, Cl- pumped in.
- when in parietal cell, Cl- then pumped into lumen via CFTR channel :)
= HCl formed
(probs just important to know that uses bicarbonate, CFTR & proton pump is key)
gastric acid secretion:
in the process of HCl production, as we release more acid and subsequently we make more of what?
in the process of HCl production, as we release more acid, we make more bicarbonate due to it being an important buffer
what can mucus production be disrupted by? (4)
mucus production can be disrupted by stress / chemicals / alchohol / nsaids
stomach acid is stimulated by which nerve? - explain innervation for it to be released (from which 2 cells?)
which hormone is the booster in the stomach that causes the release of more stomach acid?
- vagus nerve stimulates, via the enteric nervous system, release of Ach, which stimulates production of stomach acid.
- Ach binds on M3 receptor on parietal cell (produces HCl) & enterchromaffin-like cell (ECL) (produces histamine, which actiavtes the H2 receptors on the parietal cells to make HCl) = produce stomach acid
booster = gastrin (hormone)
which cells produce gastrin?
when do cells produce gastrin?
where are they?
why is gastrin produced?
produced by: G cells!! g 4 gastrin xox
located @ atrium of stomach -> bc at the bottom of the stomach. if they sense that there are big proteins - stimulate the formation of more acid.
BUT HOW COMMUNICATE to the other cells?
- gastrin produced and excreted into blood. = therefore a hormone ! (endocrine activity)
- goes to ECL and parietal cells
what is zollinger-ellison syndrome? (ZES)
- Ectopic hormone secretion (innappropriate hormone secretion) of gastrin into the blood
- leads to severe gastroesophogeal peptic ulcer disease (high levels of acid overcomes the mucous layer !)
- usually present in duodenum
explain mehcanism of how we stop producing stomach acid?
which cells do this?
where located?
what type of cell signalling is involved in this?
-
cell type: D cell: produces somatostatin
- cell location: stomach antrum - somatostatin binds to patietal cell’s somatostatin receptor
- puts break onthe system.
- cell signalling:
a) this in a paracrine cell signalling (bc all close together)
AND
b) endocrine (in blood)
* what are the three ways can stimulate pumping H+ into lumen of stomach? *
* what are the two ways can inhibit stomach pumping H+ into lumen of stomach?
can stimulate pumping H+ into lumen of stomach:
- Ach binding to M3 receptor
- Histamine binding to H2 receptor
- Gastrin binding to CCK2 receptor
all in the parietal cells
can inhibit stomach pumping H+ into lumen of stomach
- somatostatin binding to somatostatin receptor
- *- prostoglandin** binding to prostoglandin receptor
what are the important anatomical features which prevent reflux? (4)
- LOS seals off stomach
- angle at which oes enters stomach: angle of His
- prescence of terminal portion of oes. inside the abdominal cavity: more pressure below than above.
- contraction of diaphragm: pinch-cock
what is defintiion of GERD?
what can be caused by (5) what is not caused by?
what do drugs target to stop symptos of GERD?
- GERD: retrograde flow of gastric contents into oesophagus that causes troublesome symptoms
- (10-20% of pop have it)
caused by
a) increased frequency of transient LOS relaxations (TLOSR)
b) weakend lower oes. sphincter
c) hiatal hernia
d) hypersensitvity of oes. pain sensing nerves
e) by bile and non bile acid components of gastric juice
not caused by
overproduction of HCl !!!!
drugs: proton pump inhibitors
what are 3 medical options for GORD?
why do u have to be careful if taking NSAIDS with GORD / GERD? (2)
1. inhibited by PPI
2. block the H2 receptor: (cant target others bc the receptors are so common)
3. neutralised by antacids: form a protective raft over acid pocket
/
- *- NSAIDs:** block the prostoglandins from binding to prostaglandin receptors on the parietal cells = means that body’s natural inhibitor is blocked :(.
- will cause less mucous and bicarbonate secretion :(
what are surgical options for GORD?
-
fundiplication:
- tightens and reinforces the LOS.
- upper part of stomach is wrapped around the outside of the LO to strengthen the S.
not often used !!
how does Helicobacter pylori cause a peptic ulcer? (4)
- H. pylori produces urea in stomach.
- urea turns into NH3: as a result: 1. raises acid. 2. degels the mucin (lose mucous layer)
- builds up
- eventually mucin layer removed and mucosal damage is caused by the pepsin and H+ of HCl :(
* MESS NOTES *
describe the differences of pH within the stomach and why they occur
cell surface = pH 7: HCO3- layer neutralises stomach acid = chemical barrier
then
mucous layer: physical barrier
then
stomach acid = pH 2
