Drugs Used for Peptic Ulcer disease Flashcards
Proton Pump Inhibitors
Omeprazole
Lansoprazole
Pantoprazole
MOA of Proton Pump Inhibitors
Irreversible inhibition of proton pump H+/K+ ATPase (final step in gastric secretion from parietal cells) → inhibit basal and stimulated acid secretion
PK of PPI
Prodrug, taken orally
Rapidly absorbed in the intestines, long duration of action
Metabolised in the liver by CYP450
Activated in acidic medium
Given 1 hour before meals or 2 hours after meals
Clinical Use of PPI
Zollinger Ellison Syndrome (drug of choice), severe peptic ulcer, reflux esophagitis
AE of PPI
GIT disturbances:
nausea, vomiting, diarrhoea ;
Hypergastrinemia that lead to gastric hyperplasia ;
Increased bacterial flora
What are the H2 Receptor Inhibitor
Cimetidine (older version)
Ranitidine (new version)
MOA of H2 Receptor inhibitor
Competitively and reversibly block H2 receptor on parietal cells → adenylyl cyclase not activated → protein kinase not activated → inhibits histamine induced gastric secretions
This reduces basal and food stimulated gastric secretions and reduces pepsin activity.
Promote mucosal healing and decrease pain
PK of H2 receptor Inhibitor
Absorbed orally, given before meals
Metabolised in the liver by CYP450
Excreted in urine
Can cross placenta and excreted in milk
Clinical Use of H2 Receptor Inhibitor
Only used when patients cannot tolerate PPIs
Duodenal ulcers, reflux esophagitis, ZES
AE of H2 Receptor Inhibito
Nausea, vomiting,
gynecomastia, impotence, galactorrhea
CNS (if cross BBB): headache, dizziness, confusion
CVS: bradycardia, hypotension
Renal/hepatic dysfunction in elderly
What are the Anticholinergic Drugs
Pirenzepine
What is the MOA of Pirenzepine
Blocks muscarinic M1 receptors on parietal cells → no Ca2+ → protein kinase not activated → PP not activated → inhibits gastric acid secretion
Clinical Use of Pirenzepine
Used together with H2 receptor blockers
Decrease pain in peptic ulcer (spasmolytic effect)
Antacids
Sodium Bicarbonate
Calcium Carbonate
(Aluminium OH + Magnesium OH) Longer duration of action
MOA of Antacids
When antacid bind to HCl → increases the pH → neutralises gastric acid and inhibits pepsin
Clinical uses of Antacids
Used to relieve pain from peptic ulcer and dyspepsia
AE of Sodium Bicarbonate
Rebound hyperacidity, stomach distension, pain, salt and water retention, systemic alkalosis
Stomach distention due to liberation of CO2
AE of Calcium Carbonate
Stomach distension, hypercalcemia, rebound hyperacidity, milk alkali syndrome
AE of Al and Mg hydroxides
No stomach distension and rebound hyperacidity
Constipation, diarrhoea, CNS depression, renal failure
*** Decreases the absorption of tetracycline, digoxin and iron
Drugs for mucosal Protective Agent
Sucrose octaphosphate + Al2(OH)3 (Sucralfate)
Prostaglandin Analogues (Misoprostol)
Colloidal Bismuth (Bismuth)
MOA of Sucralfate
In acidic conditions, sucralfate dissociates into sucrose octaphosphate and an antacid
SO binds to positively charged protein molecules (coats the ulcer) → inhibits pepsin → promotes healing
PK of Sucralfate
Orally, poor systemic absorption
Recommended to take on an empty stomach
Excreted in faeces
Clinical use of Sucralfate
Benign gastric and duodenal ulcers, chronic gastritis
Stimulates mucosal protective mechanisms by secreting mucus and bicarbonates
AE of Sucralfate
Constipation, dry mouth
Do not co-administer with H2 blockers
Interferes with absorption of tetracycline, theophylline and tricyclic antidepressants
