Pharmacology for Dentistry

264 Section 7/ Drugs Acting on GIT

It has poor CNS entry but in elderly
and in patients with impaired renal
functions, CNS symptoms may occur. It
displaces dihydrotestosterone from
cytoplasmic receptors (antiandrogenic
action) and inhibits estradiol degrada-
tion by liver. High doses given for
longer periods produce gynaecomastia,
decreased libido and impotence. It
inhibits cytochrome P450 catalyzed
hydroxylation of estradiol in men, also
slowing metabolism of many drugs and
concurrent administration of cimetidine
will prolong the half life of many drugs
(warfarin, phenytoin, theophylline,
phenobarbital, benzodiazepines,
propranolol, nifedipine, digitoxin,
quinidine, mexiletine, tricyclic antide-
pressants).

RANITIDINE

5 to 8 times more potent than cimetidine.
Produces higher suppression of gastric acid
and action lasts longer than cimetidine. No
clinically significant drug interaction and
side effects are seen.

FAMOTIDINE

On a weight basis 20 times more
potent than cimetidine and 7.5 times more
potent than ranitidine in inhibiting basal
and pentagastrin stimulated gastric acid
secretion. It is a competitive-noncompeti-
tive inhibitor of H 2 receptors. It has a long-
er duration of action. Oral bioavailability
is 40-50% and is excreted unchanged (70%)
in urine. Incidence of adverse effects is
low.

It is more useful in ZE syndrome and
prophylaxis of aspiration pneumonia.

ROXATIDINE

Roxatidine inhibit H 2 induced gastric

secretion with a potency greater than

cimetidine and in the same range as

ranitidine. Its acetate salt is more than 95%

absorbed after oral administration and

rapidly converted to roxatidine by esterases

in small intestine and liver. Plasma t½ is 6

hours. Peak plasma levels occur about 8

hours after dosing. Effects of the drug persist

for about 12 hours.

It has use in prophylaxis of acid

aspiration syndrome after induction of

anaesthesia. In a dose of 150 mg HS as

premedication affords reliable protection

against the consequences of acid aspiration

until 11 AM the next day and decreases the

danger of aspiration by reducing the high

volumes of gastric juice.

PROTON PUMP INHIBITOR

OMEPRAZOLE

Omeprazole is gastric proton pump

inhibitor which reduces gastric acid

secretion. It inhibits the enzyme

H+K+ATPase in the parietal cells of gastric

mucosa. It effectively inhibits both basal and

stimulated acid secretion irrespective of the

stimulus. It has quick onset of action and

effective control of gastric acid secretion is

achieved with once daily dosing. It has no

effect on pepsin, intrinsic factor, juice

volume and gastric motility. Proton pump

inhibitors do not exhibit anticholinergic or

H 2 receptor antagonistic properties.

Omeprazole distributes widely and is

rapidly eliminated from plasma by

metabolism in liver. The antisecretory effect