GI Acid Controlling Drugs (antiulcers and antacids) Flashcards
Control of gastric acid secretion
Blocks the Ca2+ dependent and cAMP dependent pathway of the parietal cell in the stomach → Inhibition of H+, K+ ATPase
Pharmological therapy
To inhibit secretion
To provide cytoprotective effects
Stomach secretion
Hydrochloric acid (HCl)
Bicarb, pepsinogen, intrinsic factor, mucus, PGs
Glands of the stomach
Cardiac
Gastric** important, where drugs target
Pyloric
Gastric acid secretion
Secretion of H+ ions by parietals →
Stimulate receptors → Activates H+, K+ ATPase proton pump exchange →
PGE inhibits gastric acid by blocking cAMP production
Gastric acid secretion receptors
Neuronal: ACh (M3)
Endocrine: gastrin (CCK) → ↑ cystolic Ca2+
Paracrine: histamine (H2) → ↑ cAMP
Indirects effects by ACh on gastric secretion
↑ gastrin from G cells and histamine from enterochromaffin cells
Drugs that inhibit acid production
Proton pump inhibitors
Histamine H2 receptor blockers
Anti-cholinergics
PG analogues
Drugs that neutralize gastric acids (antacids)
Systemic: sodium bicarb, sodium citrate
Non systemic: Magnesium hydroxid, etc.
Ulcer protectives
Sucralfate
Colloidal bismuth sulfate
Antacids
Neutralize stomach acid and reduce GI pain → treating ulcers
Raising pH 1 point neutralizes 90% of acid
Different antacids
Al(OH)3, Mg(OH)2, CaCO3 inactivates pepsin and binds bile salts
Adverse effect of antacid:
Constipation
Antacid drug interactions
Interferes with gastric absorption of concurrently administered drugs: digoxin, tetracyclines, fluroroquinolones
H2 Receptor antagonists MOA
↓ gastric acid secretion via reversible competitive inhibition of H2 receptors on gastric parietal cells
Different H2 receptor antagonists
Cimetidine (1st gen), nizaridine, famotidine
Reduce H+ and pepsin (70-90% ↓ in acid)
_______ is the preffered H2R antagonist
Famotidine due to high potency and less drug interaction
H2 receptor antagonist uses
Gastric and duodenal ulcers from stress, uremic gastritis
Hypersecretory conditions like gastrinoma
H2 recptor antagonists are not effective in preventing _______________ ulcers
NSAID induced
Proton pump inhibitors
Most potent suppressors of gastric acid secretion
Inhibits gastric H+, K+ ATPase
Diminish daily production of acid by 80-90%
Different proton pump inhibitos
Omeprazole, pantoprazole, lansoprazole, rabeprazole
Prodrugs requiring activation, inactive @ neutral pH
PPI uses
Gastroesophageal reflex disease (GERD)
NSAID- associated gastric ulcers
Peptic ulcer
Adverse effects of PPI
Nausea, loose stools, abdominal pain, constipation
Gastrin levels elevated → gastrin neoplasia
Comparing PPI with H2
Omeprazole > cimetidine 30x more potent
PGE1 Analog (Misoprotosol)
Prevents NSAID-induced gastric ulcers
MOA: ↑ Bicarb secretion, mucus production, mucosal blood flow, epithelial cell growth and ↓ gastric acid secretion
Misoprotosol should not be used around ______________ may causes ___________
Pregnant animals, abortion
Cytoprotective agents (sucralfate)
Sucrose octosulfate and aluminum sulfate
Binds and protects the ulceration site from BA and pepsin activity
Effects of sucralfate
↑ mucosal synthesis of PGE and epidermal GF
Helps with ulcer healing
Sucralfate indications
Treating ulcers
Prevents gastritis caused by NSAIDs
Needs acid environment so give at least an hour before other acid drugs
Sucralfate drug interactions
Interferes with absorption and ↓ bioavailability of H2 antagonists, phenytoin, tetracycline, fluoroquins, digoxin and fat soluble vitamins
Gastroduodenal ulceration and erosion (GUE)
PPIs superior to H2 antagonists
Misoprostol for humans
