This document discusses drug treatment for acid peptic disease. It classifies drugs into those that reduce acid activity like proton pump inhibitors and H2 receptor blockers, mucosal protectants like sucralfate, and prostaglandin analogs like misoprostol. It describes the mechanisms, clinical uses, and adverse effects of representative drugs in each class. Regimens for H. pylori eradication involving combinations of drugs are also outlined.
8. REGIMENS FOR H. PYLORI ERADICATION
TRIPPLE REGIEMEN
OMEPRAZOLE
METRONIDAZOLE FOR 14 DAYS
CLARITHROMYCIN
QURADIPLE REGIEMEN
OMEPRAZOLE
BISMUTH SUBSALICYLATE
TETRACYCLINE FOR
METRONIDAZOLE 14
DAYS
9. H2RECEPTOR BLOCKERS
MECHABISM OF ACTION
MOA –
COMPETITIVE INHIBITIOR OF HISTAMINE ON HISTAMINE
RECEPTORS
SUPPRESSION OF NOCTURNAL SECRETION – 90%
SUPPRESSION OF MEAL TIME SECRETION – LESS THAN PPIs
Famotidine is more potent than Ranitidine
12. ANTACIDS –
1. Suspension has more effect than tab
2. Acid neutralizing capacity
SODIUM BICARBONATE
RAPID ACTION (most rapid)
A/R: BELCHING, DISTENSION & FLATULENCE—CO2
CALCIUM CARBONATE
LESS RAPID THAN NaHCO3
A/R: BELCHING
ALUMINIUM & MAGNESIUM HYDROXIDE
SLOW IN ACTION BUT MORE COMPLETE NEUTRALIZATION
13. MUCOSAL PROTECTIVE AGENTS
SUCRALFATE – SALT OF SUCROSE WITH SULFATED Al(OH)3
MOA –-
1-It is a tenacious viscous base that is negatively charged and
binds with ulcer crator that is positively charged, protecting
ulcer from effect of HCL
2-STIMULATES SECRETION OF MUCOSAL PGs & HCO3
CLINICAL USES :
STRESS ULCERS
ADVERSE EFFECTS
1. CONSTIPATION DRUG INTERACTIONS
14. MISOPROSTOL
MOA: ↑ Production of mucus rich in HCO3
Directly acting on parietal cells and ↓ production of HCL by
acting on EP3 receptors
USES: Only for NSAIDs associated ulcers
SIDE EFFECTS:↑ abdominal cramps, diarrhea, ↑ uterine
contractions