Drugs Used In Peptic Ulcer Flashcards
Classification of peptic ulcer drugs
Proton pump inhibitor: Omeprazole, pantoprazole
Hydrogen (H2) receptor inhibitor: Cimetidine, Ranitidine
Prostaglandin: Misoprostol
Antacids: aluminium hydroxide, magnesium hydroxide, sodium bicarbonate, calcium bicarbonate
Mucosal protective agents: bismuth subsalicyclate, sucralfate
Antimicrobial agent (peptic ulcer cause by H. Pylori)
-Metronidazole, Clarithromycin, tetracycline and Amoxicillin
MOA of H2 receptor antagonist
-selectively blocks the binding of the histamine to H2 receptor.
-reversible antagonist of histamine
-decrease intracellular concentration of cyclic AMP
-decrease secretion of gastric acid
Clinical uses/therapeutic uses of H2 receptor antagonist
-inhibit gastric acid secretion induced by histamine or gastrin
-GERD (Gastroesophageal reflux disease)
-ZES (zollinger-Ellison syndrome)
-peptic ulcer
-combine with proton pump inhibitor to treat NSAID induced peptic ulcer.
Ranitidine vs cimetidine
Ranitidine
-longer acting
-more potent
-has minimal side effects
-does not produce antiandrogenic/prolactin stimulating effects of cimetidine
-does not inhibit cytochrome P450
Side effect: headache, dizziness, diarrhea, muscular pain.
Cimetidine
-has more side effects
-side effects: confusion, hallucination, antiadrogenic, gynaecomastia, impotence
*famotidine is more ptent
MOA of proton pump inhibitor (Omeprazole)
-Omeprazole is a prodrug
-enteric coated to prevent degradation by peptic ulcer
-irreversibly bind to H+/K+ ATPase enzyme system (proton pump)
-suppress the secretion of hydrogen ions into peptic lumen.
Therapeutic uses of PPIs
*sodium bicarbonate fastens absorption of omeprazole
*must taken 30 min before breakfast
-suppress acid production
-heal peptic ulcer
-NSAID induced peptic ulcer
-H. Pylori induce ulcer
-erosive esophagitis
-active duodenal ulcer
-non ulcer dyspepsia
Adverse effect of PPIs
-inhibit the metabolism of warfarin & phenytoin
-low of vitamin B12 due to prolongation suppression of gastric acid. Acid is needed to absorp vitamin B12.
-headache
-mild diarrhea
-mild nausea
MOA prostaglandin analog
Misoprostol (PGE1 analog)
-decrease cAMP, decrease gastrin
-bind to prostaglandin receptor on parietal cells
-inhibit HCL secretion
-stimulates secretion of mucus and bicarbonate, Mucosal blood flow
Clinical uses and contraindicated of misoprostol
Clinical use: NSAID induced peptic ulcer
Adverse effects:
-contraction of uterine (contraindicated during pregnancy)
-Diarrhea
-nausea
Anitimuscarinic agent in treatment of peptic ulcer
Drug: Dicyclomine
-relaxing the smooth muscle
-reduce secretion by blocking M3 receptor in parietal cells, block M1 receptor in paracrine cells
Side effect of anitimuscarinic agents
Cardiac arrhythmia
Dry mouth
Constipation
Urinary retention
MOA of antacid
-a weak bases that react with gastric acid to produce water and salt (neutralizer the acid)
-cause decrease in gastric acidity
-reduce pepsin activity (inactive at pH greater than 4)
-stimulate Mucosal prostaglandin production
Therapeutic uses of antacids
-symptomatic relief of peptic ulcer
-GERD
-promote healing of duodenal ulcer except acute gastric ulcer
-used as last line therapy
Adverse effect of antacid
Aluminium hydroxide cause constipation
Magnesium hydroxide cause diarrhea
Sodium bicarbonate liberates CO2 cause belching and flatulence.
Excessive intake of calcium carbonate cause hypercalcemia.
Calcium carbonate stimulate gastrin release & rebound acid production
MOA of sucralfate
*sucralfate cannot be administer with H2 receptor antagonist or antacids
-a complex of aluminium hydroxide and sulfated sucrose
-bind to protein of both normal and necrotic mucosa to form a complex.
-complex creates a physical barrier.
-it impair diffusion of HCL
-prevents degradation of mucus by pepsin & acid
-stimulate prostaglandin release
-stimulate mucus & bicarbonate output
-inhibit peptic digestion
