learning outcome
describe acid created and regulated Describe the consequences poor control gastric acid
how
gut is of of
·
·
the mechanisms that control acid production
.
Drug development of : · outline
· Histamine receptor blockers · describe how acid reducers work
· Muscarinic receptor blockers · describe how anti-acids work
·
proton pump inhibitor · describe how hellobacter pylori is a
leading culprit in
·
gastrin receptor blockers ulcer development
how does antacids (phosphate/carbonate salts) work
Why is acid
something to worry about ?
acid aids digestion by
gastric :
·
creating the optimal pH for pepsin and gastric lipase
·
stimulating pancreatic biocarbonate secretion
get GORD
&
The principal clinical indications for reducing acid secretion are peptic ulceration (both duodenal and gastric
·
gastro oesophageal reflux disease or GORD
·
oesophageal stricture due to acidic inflammation
I food doesn't come in
Zollinger-Ellison syndrome
Ca rare
hypersecretory gastrin producing tumor)
dysplasia
&
change in the epithelial to that stop the sphincter
form They become metastatic and begins grow and can
get non-cancerous tumors can
·
.
acid to enter
From closing allowing causing acid reflux
, The parietal cell-acid factories
early target for acid secretion
From blood
>
-
cenzyme
ku7 1
. carbonic acid
-
dissociate
hydrogen I Y
potassium bicarbonate
in
pump (FTR exchange
For C1-
At comes out
The parietal cell DYNAMIC acid factories
Vesicle fusion ISNARE prese
- proton pump
-parietal X protonpumps are
· HKA stored in vesicles
· stimulation causesreside fusion to membrane
what makes the proton pump spread out -> stimulation of acid production
Acetylcholine from parasympathetic nerves
Y vagus
gastrin from G cells
Histamine from enterochromaffin cells (ECL)
inhibition of acid production
acid in the antrum stimulates somatostatin release from D cells
describe acid created and regulated Describe the consequences poor control gastric acid
how
gut is of of
·
·
the mechanisms that control acid production
.
Drug development of : · outline
· Histamine receptor blockers · describe how acid reducers work
· Muscarinic receptor blockers · describe how anti-acids work
·
proton pump inhibitor · describe how hellobacter pylori is a
leading culprit in
·
gastrin receptor blockers ulcer development
how does antacids (phosphate/carbonate salts) work
Why is acid
something to worry about ?
acid aids digestion by
gastric :
·
creating the optimal pH for pepsin and gastric lipase
·
stimulating pancreatic biocarbonate secretion
get GORD
&
The principal clinical indications for reducing acid secretion are peptic ulceration (both duodenal and gastric
·
gastro oesophageal reflux disease or GORD
·
oesophageal stricture due to acidic inflammation
I food doesn't come in
Zollinger-Ellison syndrome
Ca rare
hypersecretory gastrin producing tumor)
dysplasia
&
change in the epithelial to that stop the sphincter
form They become metastatic and begins grow and can
get non-cancerous tumors can
·
.
acid to enter
From closing allowing causing acid reflux
, The parietal cell-acid factories
early target for acid secretion
From blood
>
-
cenzyme
ku7 1
. carbonic acid
-
dissociate
hydrogen I Y
potassium bicarbonate
in
pump (FTR exchange
For C1-
At comes out
The parietal cell DYNAMIC acid factories
Vesicle fusion ISNARE prese
- proton pump
-parietal X protonpumps are
· HKA stored in vesicles
· stimulation causesreside fusion to membrane
what makes the proton pump spread out -> stimulation of acid production
Acetylcholine from parasympathetic nerves
Y vagus
gastrin from G cells
Histamine from enterochromaffin cells (ECL)
inhibition of acid production
acid in the antrum stimulates somatostatin release from D cells
