adequate. Nearly all duodenal ulcers and most gastric
ulcers that are not associated with NSAIDs are associated
withH. pylori, which should be eradicated (see above).
Most regimens include an H 2 -receptor antagonist or a
proton-pump inhibitor. It is essential to exclude carcinoma
endoscopically, as H 2 -blockers can improve symptoms
caused by malignant ulcers. Without gastric acid, the
functions of which include providing a barrier to
infection, patients on H 2 -antagonists and proton-pump
inhibitors are predisposed to infection by enteric
pathogens and the rate of bacterial diarrhoea is increased.
2.Oesophagitis may be treated with H 2 -antagonists, but
proton-pump inhibitors are more effective.
3.In cases of acute upper gastrointestinal haemorrhage and
stress ulceration, the use of H 2 -blockers is rational,
although their efficacy has not been proven.
4.Replacement of pancreatic enzymes in steatorrhoea due to
pancreatic insufficiency is often unsatisfactory due to
destruction of the enzymes by acid and pepsin in the
stomach. H 2 -blockers improve the effectiveness of these
enzymes in such cases.
5.In anaesthesia, H 2 -receptor blockers can be given before
emergency surgery to prevent aspiration of acid gastric
contents, particularly in obstetric practice (Mendelson’s
syndrome).
6.The usual oral dose of cimetidineis 400 mg bd or 800 mg
nocte, while for ranitidineit is 150 mg bd or 300 mg nocte
to treat benign peptic ulceration.
CIMETIDINE
Cimetidineis well absorbed (70–80%) orally and is subject to
a small hepatic first-pass effect. Intramuscular and intra-
venous injections produce equivalent blood levels. Diarrhoea,
rashes, dizziness, fatigue, constipation and muscular pain
(usually mild and transient) have all been reported. Mental
confusion can occur in the elderly. Cimetidinetransiently
increases serum prolactin levels, but the significance of this
effect is unknown. Decreased libido and impotence have occa-
sionally been reported during cimetidinetreatment. Chronic
cimetidine administration can cause gynaecomastia, which is
reversible and appears with a frequency of 0.1–0.2%. Rapid
intravenous injection of cimetidinehas rarely been associated
with bradycardia, tachycardia, asystole or hypotension. There
have been rare reports of interstitial nephritis, urticaria and
angioedema.Drug interactions- Absorption of ketoconazole(which requires a low pH)
anditraconazoleis reduced by cimetidine.
2.Metabolism of several drugs is reduced by cimetidinedue
to inhibition of cytochrome P450, resulting in raised
plasma drug concentrations. Interactions of potential
clinical importance include those with warfarin,
theophylline,phenytoin,carbamazepine,pethidineand
other opioid analgesics, tricyclic antidepressants,
lidocaine(cimetidine-induced reduction of hepatic blood
flow is also a factor in this interaction), terfenadine,
amiodarone, flecainide, quinidineandfluorouracil.
3.Cimetidineinhibits the renal excretion of metforminand
procainamide, resulting in increased plasma
concentrations of these drugs.
RANITIDINE
Ranitidineis well absorbed after oral administration, but its
bioavailability is only 50%, suggesting that there is appre-
ciable first-pass metabolism. Absorption is not affected by food.250 ALIMENTARY SYSTEM ANDLIVER
Table 34.2:AntacidsAntacid Features Adverse effects
Sodium bicarbonate Rapid action Produces carbon dioxide, causing
belching and distension; excess can
cause metabolic alkalosis; best avoided
in renal and cardiovascular disease
Calcium carbonate High acid–neutralizing capacity Acid rebound; excess may cause
hypercalcaemia and constipation
Magnesium salts (e.g. Poor solubility, weak antacids; Diarrhoea
dihydroxide, carbonate, the trisilicates inactivate pepsin;
trisilicate) increase lower oesophageal sphincter
tone, and may be of use in reflux
Aluminium hydroxide Forms an insoluble colloid in Constipation; absorption of dietary
the presence of acid, and lines phosphate may lead to calcium
the gastric mucosa to provide a depletion and negative calcium balance
physical and chemical barrier;
weak antacid, slow onset
of action, inactivates pepsin