PPIs and Ant-acids
These drugs act to reduce gastric acid production or build a protective barrier against the acid.
Inhibiting Gastric Acid secretion
Proton-Pump Inhibitors (PPI) – Omeprezole, lansoprazole, pantoprazole
These drugs inhibit the parietal cell H+/K+-ATPase proton pumps.
Improvements can take several days and their bioavailability is significantly decreased by food, so it is important to take them 1 hour before a meal.
Side effects
– Hyponatraemia, hypomagnesaemia and osteoporosis (increased risk of fractures)
– They can predispose to C. difficile infections
H2 antagonists – Ranitidine, famotidine, cimetidine
These drugs block the histamine H2 receptor on parietal cells, which leads to a marked decrease in acid secretion.
They work much faster than PPIs and are used if the PPI is not tolerated/as add-on therapy.
Their use in clinical practice has declined since the advent of the PPIs.
Side effects
– Headache, GI disturbances
– Cimetidine is androgen receptor antagonist and can cause gynaecomastia and reduced libido in males
Stomach Protection
Prostaglandins – Misoprostol
This is an analogue of prostaglandin E which stimulates mucus production.
It also increases HCO3 secretion which helps form a protective barrier against acid.
It is often used with NSAIDs in combination therapy to protect against ulcers.
Arthrotec = Diclofenac (NSAID) + Misoprostol (prostaglandin)
Antacids – Sodium Bicarbonate, Calcium carbonate
These are weak bases that neutralise gastric acid and relieve ulcer pain.
They have largely been replaced by specific drugs but are used as over-the-counter remedies for dyspepsia.
Side effects
– Sodium bicarbonate increases fluid retention, so used with caution in heart failure
– They also alter bioavailability of other drugs (tetracycline, quinolones, and bisphosphonates) as they change gastric pH, so separate the dose by at least 2 hours
Sucralfate
This is a carbohydrate complexed with aluminium.
It has dual protective actions as it forms an acid buffer through reaction with HCl.
It also forms complexes with proteins on ulcer surfaces to prevent ulcerated areas from more damage as well as stimulating prostaglandin production.
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