ANTI-HISTAMINE &

PPI
H1-RECEPTOR ANTAGONISTS
Both neutral H1 antagonists and inverse
H1 agonists reduce or block the actions
of histamine by reversible competitive
binding to the H1 receptor.
Oral antihistamines are the drugs of
choice in controlling the symptoms of
allergic rhinitis and urticaria because
histamine is the principal mediator
released by mast cells.
AntiHistamine is well absorbed orally, max
serum level in 1-2 hrs
Old first-generation agents have wide
tissue distribution including CNS
Newer 2nd generation are not (non-
sedative)
Duration of older members: 4-6 hrs, 2nd
generation drugs have a long duration of
≥24 hrs
1st generation antihistamines are of poor
H1 receptor selectivity. They block other
receptors leading to adverse effects:
Cholinergic R blockade: dry mouth, &
urinary retention
-adrenergic R blockade, by promethazine,
leading to hypotension, tachycardia &
dizziness
Serotonin R blockade leading to increased
appetite
H2-RECEPTOR ANTAGONISTS
Gastric acid secretion is stimulated by
acetylcholine, histamine, and gastrin. The
receptor-mediated binding of acetylcholine,
histamine, or gastrin results in the
activation of protein kinases, which in turn
stimulates the H+/K+-adenosine
triphosphatase (ATPase) proton pump to
secrete hydrogen ions in exchange for K+
into the lumen of the stomach
The histamine H2-receptor antagonists act
selectively on H2 receptors in the stomach.
They are competitive antagonists of
histamine and are fully reversible.
All these agents are rapidly absorbed from the
intestine; peak concentrations in plasma are
attained within 1 or 2 hours.
Ranitidine and famotidine undergo first pass
hepatic metabolism resulting in a bioavailability
of approximately 50%.
Nizatidine has little first pass metabolism and a
bioavailability of 90%.
The serum half-lives of ranitidine and
famotidine are 2 to 3 hours, while that of
nizatidine is somewhat shorter about 1.3 hours;
however duration of action depends on the dose
given.
H2 antagonists are cleared by a combination of
a) hepatic metabolism b) glomerular filtration
and c) renal tubular secretion. Dose reduction is
required in patients with moderate to severe
renal  and possibly severe hepatic)
insufficiency.
PROTON PUMP INHIBITOR
Gastric acid secretion is stimulated by
acetylcholine, histamine, and gastrin. The
receptor-mediated binding of
acetylcholine, histamine, or gastrin results
in the activation of protein kinases, which
in turn stimulates the H+/K+-adenosine
triphosphatase (ATPase) proton pump to
secrete hydrogen ions in exchange for K+
into the lumen of the stomach
Proton pump inhibitor suppresses stomach
acid secretion by specific inhibition of the
H+/K+-ATPase system found at the
secretory surface of gastric parietal cells
PPI are Pro-drugs - require acidic
environment for activation.
Ideally should be given about 30 min before
meals so that the peak serum is equal with
the maximal activity of proton pump
secretion.
Rapidly absorbed in the small bowel
Provides a prolonged (up to 24 - 48hrs)
suppression of acid secretion, despite the
much shorter plasma half-lives (0.5 - 2 hrs)
of the parent compounds
In standard doses, PPIs inhibit 90–98% of
24-hour acid secretion
Highly protein bound, and extensively
metabolized by hepatic
RELATION WITH CASE
H-2 Receptor Antagonist and
Proton Pump inhibitor is prescribed
to deal with adverse effect of
systemic corticosteroid which is
peptic ulcer
Thank You