PHARM GIT Clinical Cases - Week 4

Question 1

Explain basal & receptor-mediated secretion of HCl from gastric parietal cells.

Answer 1

CO2 diffuses from ECF/CO2 present in cell already is used in the reaction: CO2 + H2O  H2CO3 -> rapidly dissociated into H+ & HCO3- -> bicarbonate ions are exchanged for Cl- ions in veins draining into the stomach -> HCO3- enter veins draining into the stomach (forming alkaline tide).
H+ ions need to be actively pumped out of parietal cells via H/K ATPase pumps & Cl- ions leave via chloride channels.
Anion exchange is located on basolateral side of the parietal cell – which is close to the location of the blood vessels.

Question 2

3 x regulatory molecules that stimulate parietal HCl secretion (state where they act, what they are secreted by):

Answer 2

• ACh (from PSNS via vagus nerve) – act on M receptors on gut or ECL cells.
• Gastrin (from G cell) – binds to cholecystokinin B receptors in the gut. Also activates gastrin receptors on enterochrommaggin-like (ECL) cells, which causes histamine release from the ECL cell.
• Histamine (from ECL cells) – acts on H2 receptors in the gut.

Question 3

3 x classifications of drugs that increase GIT motility w purgation

Answer 3

Bulk, osmotic, stimulant.

Question 4

First line treatment for H. pylori induced ulcers

Answer 4

Triple therapy - clarithromycin, amoxicillin, PPI

Question 5

Second line treatment for H. pylori induced ulcers & when to initiate.

Answer 5

Quadruple therapy - bismuth, PPI, metronidazole, tetracycline. Initiate 7-14 days post triple therapy if no improvement observed.

Question 6

Where do PPIs accumulate?

Answer 6

Canaliculi of parietal cell.