High-yield Pharmacology concepts on medication for gastric hyperacidity, ulcers, diarrhea and constipation.
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Pharmacotherapy is aimed at
Associated with Neutralizing Acid
H. Pylori infection
Suppressing Acid production
Peptic Ulcers
Accelerating gastric emptying
Dyspepsia
H. Pylori treatment
Some causes:
Copyright F Khan 2021
, Gastric Acid Physiology
HCL ACID:
HCl is produced by the parietal cells of the stomach. To begin with, water
(H2O) and carbon dioxide (CO2) combine within the parietal cell cytoplasm to
produce carbonic acid (H2CO3). Carbonic acid dissociates into a hydrogen ion
(H+) and a bicarbonate ion (HCO3–).
The hydrogen ion that is formed is transported into the stomach lumen via the
H+– K+ ATPase ion pump. This pump uses ATP as an energy source to
exchange potassium ions into the parietal cells of the stomach with H+ ions.
The bicarbonate ion is transported out of the cell into the blood via a
transporter protein called anion exchanger which transports the bicarbonate
ion out the cell in exchange for a chloride ion (Cl–). This chloride ion is then
transported into the stomach lumen via a chloride channel.
This results in both hydrogen and chloride ions being present within the
stomach lumen. Their opposing charges leads to them associating with each
other to form hydrochloric acid (HCl).
Mucous cells in Gastric Mucosa:
Secretes Bicarbonate rich fluid to protect lining
Copyright F Khan 2021
, Drugs for the managements of excess GIT acidity
Copyright F Khan 2021
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