Summary Ionisation Explained

H2-receptor antagonists  Cimetidine  Well absorbed orally  Very safe (plac
 Inhibit acid secretion by blocking H2-  Famotidine  Peak serum levels = 1-3 hours  Cimetidine: gyn
receptors on parietal cell  Ranitidine  Antacids ↓ absorption by 10-20% Impotence (pro
 Less effective than PPI  Nizatidine  NOT by food  Idiosyncratic m
 Useful for acid reduction, preventing  Cross bbb and breast milk  Cytopenias
NSAIDS induced ulcers and healing CIMETIDINE INTERACTS with  Renal & hepatic elimination  Hemolytic ane
peptic ulcers CISAPRIDE and THIORIDAZINE  QT  Nizatidine = minimally metabolized = 100% BA  Cimetidine: CN
 Category B, safe in lactation PROLONGATION  Cimetidine T1/2 ↑ with liver failure reversible)
 Rare ↑LFT – ca
Adverse effect
Proton pump inhibitor  Omeprazole (esophagitis, category  Weak bases in acidic parts of PC  Rebound gastr
 Effectively block acid secretion by C)  Pro-drug activated by acid & binds to cysteine  Dose tapering
irreversibly binding to and inhibiting  Lansoprazole - FECAL residue in a disulfide bond  Safe
the K+H+ATPase (on luminal surface of  Dexlansoprazole  To inactivate K+H+ATPase  Infections = clo
the parietal cell membrane)  Esomeprazole (esophagitis)  ONLY work in parietal cells stimulated by FOOD to & pneumonia (
 Category B  Pantoprazole have ACIDIC COMPARTMENTS suppression)
 Peptic ulcers  Rabeprazole  Take 30-60 minute BEFORE a meal, so they are  Hypomagnesem
 H. pylori eradication present in blood when food stimulates the parietal  Hip fractures &
 GERD (maintenance) OMEPRAZOLE interacts with cells in older smoke
 NSAID associated ulcers WARFARIN, DIAZEPAM, DIGOXIN,  Hepatic metabolism by Cyt p450 (esp.CYP2C19)  Vit B12 and Fe
CARBAMAZEPINE and PHENYTOIN  Primary URINE excretion  Atrophic gastri
Reduces GLOPIDOGREL efficacy

Mucosal protective agents  Antacids  
 sucralfate
i. Antacids  AlOH   Depends on vo
 Neutralizes gastric acid  MgOH duration
 Bind growth factors  Ca2+  Mg: diarrhea &
 Enhance their binding to ulcers  Milk-alkali synd
 Promote angiogenesis in injured alkalosis and re
mucosa  Al3+
 Bind bile acids anemia (in ren
 Inhibit (NOT eradicate) H. pylori
ii. Sucralfate  Sucrose octasulfate complexed   Aluminium tox
with AlOH  Binds other dru
Significance)
 Heals ulcers
 Prevents mucosal damage (NO altering
In acid secretion or buffering significantly)
 Angiogenesis (GF binding)
 Binds to injured tissue  prevent access to
acid and pepsin
iii. Bismuth  Bismuth subsalicylate  Salicylate toxic
 Suppresses H. Pylori  NOT with Aspir
 NOT ACTIVE in H. pylori negative ulcers
 NO acid neutralization  CI in RENAL FAILURE and ASPIRIN