pharmacology Flashcards
What do mucus cells secrete?
mucus and bicarbonate
what do parietal cells secrete?
hydrochloric acid
what do enterochromaffin cells secrete?
histamine
what do G cells secrete?
gastrin
What do D cells secrete?
somatostatin
What do chief cells secrete?
pepsinogen
Role of chloride bicarbonate exchanger?
It transports bicarbonate out of the cell and into the blood and chlorine out of the blood and into the cell.
Role of chloride potassium symport?
transports potassium and chloride out of the cell into the lumen
What is the role of H+/K+ ATPase (proton pump) ?
transports H+ out of the cell and into the lumen and it transports potassium from the lumen into the cell
What is the role of carbonic anhydrase?
Its the enzyme that plays a role in the rection of CO2 + H2O= H2CO3-
When is histamine released?
enterochromaffin like cells secrete histamine in response to stimulation by acetylcholine
What receptors does histamine bind to?
H2 receptors
What does the binding of histamine to H2 receptors trigger?
activation of adenylyl cyclase
What does activation of adenylyl cyclase trigger?
an increase in cAMP
What does an increase in cAMP trigger?
an increase in the number of proton pumps, increasing gastric acid secretion from parietal cells
What is ACh released by?
parasympathetic cholinergic neurons
What does ACh bind to?
muscarinic (M3) ACh receptors on parietal cells
What happens when ACh binds to the M3 ACh receptors on the parietal cells?
Phospholipase C (PLC) is activated
What does phospholipase C do?
It increases intracellular Ca2+ levels
What does an increase of intracellular Ca2+ lead to?
a number of signalling pathways which leads to an increase in proton pumps and so an increase in the gastric acid secretion (hydrochloric acid) by the parietal cells
What does gastrin bind to?
CCK2 receptors on parietal cells
What does the binding of gastrin to CCK2 receptor cells trigger?
activation of phospholipase C
Where are enterochromaffin, D and G cells located?
the gastric glands
What does somatostatin bind to?
SST2R receptors
What does binding of somatostatin to SST2R receptors in parietal cells trigger?
inhibition of adenylyl cyclase
What does decrease in adenyly cyclase lead to?
decrease in cAMP, decrease in proton pumps and decrease in gastric acid secretion
What does binding of somatostatin to SST2R receptors on enterochromaffin cells lead to ?
reduce histamine release
what does reduced histamine release cause?
decrease in activated adenylyl cyclase, so decrease cAMP and decrease in number of proton pumps and so causing a decrease in the gastric acid secreted by parietal cells
What are examples of antiacids?
Gaviscon and peptac
How to antiacids work?
they reduce the symprotms of excessive gastric acid by buffering HCl, this is done by them binding to the excess hydrogen greating H2CO3 which then becomes CO2 and H2O
Describe what effect do NSAIDS have on gastric secretion?
NSAIDS inhibit COX-1 decreasing production of prostaglandins, triggering histamine to be produced from the enterochromaffin cells which promotes HCl secretion from the parietal cells
What medication can be given to prevent NSAID induced peptic ulcer?
Misoprostol
What is misoprostol similar to?
Prostaglandin E1
What are the side effects of misoprostol?
abdominal pain, diarrhoea, may induce labour
What are examples of proton pump inhibitors?
Lansoprazole, omeprazole, pantoprazole
What effect do PPIs have?
irreversibly inhibit H+/K+ ATPase pump, leading to reduction of HCl secretion
When are PPIs used?
for benign gastric ulceration, NSAID gastric ulceration, gastro- oesophageal reflux disease and Zollinger-Ellison syndrome
What are the side effects of PPIs?
they reduce the pH in stomach, reducing defecne against infection via the GI tract
What are examples of histamine antagonists?
ranitidine, cimetidine, famotidine, and nizatidine
What do histamine antagonists do?
Block the H2 receptors, eventually leading to decrease in HCl
When are histamine antagonsits used?
benign gastric ulceration and NSAID gastric ulceration
