Gastritis, peptic ulcer disease Flashcards
Antacids: Class, names, moa, administration, adr, contraindications
Drugs to reduce gastric acidity
From strongest to weakest,
Sodium, calcium bicarbs, magnesium, aluminium hydroxides
Essentially weak bases, provides symptomatic relief by neutralising gastric acid but does not prevent production
Liquids more effective than tablets, large and frequent doses required
Mg-diarrhoea, Al-constipation (mixtures usually formulated)
Na: fluid retention, CHF, HTN
Renal insufficiency, cation toxicity
Antacids: DDI
Affects absorption of tetracyclines, itraconazole, fluroquinolones, digoxin. Advise patients to take 2-3h before or after other meds
H2 antag: Class, names, moa, adr, contraindications
Drugs to reduce gastric acidity
Ranitidine, famotidine (more potent)
Competitive H2R inhibitors on apical side of parietal cells, targets cAMP pathway which stimulates luminal proton pump
Suppress acid secretion, pepsin concentration
Constipation, headaches
Renal excretion, eliminated slowly in elderly
Can be secreted into breastmilk!!!
Causes of gastric ulcers
Gastric, duodenal ulcers: NSAIDs, H. pylori
GERD
Gastrinoma: Zollinger-Ellison syndrome
Are H2 antagonists more effective in inhibiting nocturnal (fasting) acid secretion or meal-stimulated secretion?
Nocturnal secretion, which is histamine dependent.
Meal-stimulated secretion is Ach-gastrin (vagal pathway) dependent.
Why is cimetidine not a preferred H2 antag?
Antiandrogenic- causes gynaecomastia, not to be taken for males
More DDI, well-known CYP450 inhibitor
PPIs: Class, names, moa, adr, contraindications
Drugs to reduce gastric acidity
-‘prazole’s
Irreversible blocker of apical H+/K+ ATPase proton pump (by covalent bonds), which is the final step of gastric acid secretion. Antagonizes ALL 4 stimulants of gastric secretion. Absorbed in SI to be transported back to stomach, concentrated in parietal cell canaliculi.
Inactive pro-drugs (absorbed well), enteric-coated to prevent gastric digestion
Nausea, diarrhoea
Risk of bacterial overgrowth, vitB12 deficiency and hypergastrinemia long term
Why are PPIs preferred over H2 antagonists?
PPIs used for maintenance therapy also
4 stimulants of gastric acid secretion
Histamine, gastrin, Ach, prostaglandins (negative effect)
Why must PPIs be taken just before meals?
Only inhibits active proton pumps. At fasting state, only 10% of pumps are active.
Sucralfate: Class, moa, adr, contraindications
Mucosal protecting agents Polymerises in acidic solutions to form a paste that binds to ulcer as a barrier Cause constipation DDI: Bind to theophylline, digoxin *Not very clinically useful
Bismuth colloids: Class, names, moa, adr, contraindications
Mucosal protecting agents
Bismuth subcitrate, subsalicylate
ANTIMICROBIAL AGAINST H. PYLORI, used for 2nd line quad therapy
Bind to mucus glycoprotein to form protective coat over ulcer
Stimulates prostaglandin, bicarb secretion
Blackens stool, darkens tongue and teeth
May cause encephalopathy in renal impairment
PG analogues: Class, names, moa, adr, contraindications
Mucosal protecting agents
Misoprostol
More for NSAID-associated ulcers. PGs reduce acid secretion.
Stimulate mucus, bicarb secretion at low doses
Inhibits acid secretion at high doses
CAUSES ABORTION, abdo pain, diarrhoea
What is the ulcer recurrence rate if H. pylori is not eradicated in ulcer treatment?
60-100%
What is the first line therapy for H. pylori eradication?
Triple therapy: 2 antibiotics + PPI for 7-14 days
