Peptic Ulcer
● Stomach ulcer - open sores that develop on the lining of the stomach
● Bacteria - helicobacter pylori infection which impairs the protective mechanisms of the GI
tract against low pH and digestive enzymes and lead to ulceration of the mucosa
● Other causes - stress, injury or death of mucus producing cells, chronic use of NSAIDs,
smoking, alcohol and diet, hypercalcemia
Symptoms
● Burning or gnawing pain in abdomen
● Epigastric tenderness
● Dyspepsia - indigestion
● Nausea/vomiting
● Belching, bloating
● Heartburn
Diagnosis
● Urea breath test
● Stool antigen test
● Blood test
Management
● Tummy pain - antacids to relieve pain but is temporary
● Eating healthy
● Avoid spicy foods
● Eat regularly in small portions
● Avoid trigger foods
● Eating the evening meal 3-4 hours before going to bed
● Raising the head of the bed
● Smoking cessation
● Reducing alcohol consumption
Antacids
MOA: weak bases which reacts with gastric hydrochloric acid to form salt and water and
reduces intragastric acidity
Systemic antacid - Sodium bicarbonate, Sodium citrate
● Reacts rapidly with HCl to produce CO2 and NaCl
● Formation of CO2 leads to gastric distension
● Unreacted alkali is readily absorbed and can cause metabolic alkalosis
● NaCl absorption may exacerbate the fluid retention in certain patients
Non systemic - Magnesium hydroxide, Magnesium trisilicate, Aluminium hydroxide gel and
Calcium carbonate
● Formulations containing magnesium hydroxide or aluminium hydroxide react slowly with
HCl to form Magnesium chloride, Aluminium chloride and water
● No gas is generated - hence, belching and metabolic alkalosis does not occur
, ● Unabsorbed magnesium can cause osmotic diarrhoea and aluminium cause
constipation - therefore, both are given together to minimize the impact on bowel
function
IDEAL ANTACID - insoluble and neutralize acid, should not produce CO2 and should not
disturb acid-base balance
Proton pump inhibitor (PPI)
Omeprazole, Esomeprazole, Lansoprazole
MOA: irreversibly inhibits H+/K+ ATPase, suppressing gastric acid productions; the H+/K+
ATPase membrane-bound enzyme plays an essential role in the final step of gastric acid
secretion
Side effects: constipation, headache, diarrhoea, abdominal pain, skin rashes, arthralgia (joint
pain), may decrease vitamin B12 absorption, increases the rate of infection and fracture of
bones, low magnesium levels, C. diff infection
Caution: risk of osteoporosis and hypomagnesaemia
Interactions: Omeprazole can inhibit the metabolism of phenytoin, warfarin and diazepam; PPIs
decrease the bioavailability of itraconazole, iron salts etc
H2R antagonists
Cimetidine, Ranitidine, Famotidine
MOA: competitively blocks H2 receptors on parietal cells; suppresses basal and meal-simulated
acid secretion in a linear dose-dependent fashion, most effective in suppressing nocturnal acid
secretion
Side effects: diarrhoea, headache, rash, dizzy, constipation, fatigue,
Caution: renal impairment
● Stomach ulcer - open sores that develop on the lining of the stomach
● Bacteria - helicobacter pylori infection which impairs the protective mechanisms of the GI
tract against low pH and digestive enzymes and lead to ulceration of the mucosa
● Other causes - stress, injury or death of mucus producing cells, chronic use of NSAIDs,
smoking, alcohol and diet, hypercalcemia
Symptoms
● Burning or gnawing pain in abdomen
● Epigastric tenderness
● Dyspepsia - indigestion
● Nausea/vomiting
● Belching, bloating
● Heartburn
Diagnosis
● Urea breath test
● Stool antigen test
● Blood test
Management
● Tummy pain - antacids to relieve pain but is temporary
● Eating healthy
● Avoid spicy foods
● Eat regularly in small portions
● Avoid trigger foods
● Eating the evening meal 3-4 hours before going to bed
● Raising the head of the bed
● Smoking cessation
● Reducing alcohol consumption
Antacids
MOA: weak bases which reacts with gastric hydrochloric acid to form salt and water and
reduces intragastric acidity
Systemic antacid - Sodium bicarbonate, Sodium citrate
● Reacts rapidly with HCl to produce CO2 and NaCl
● Formation of CO2 leads to gastric distension
● Unreacted alkali is readily absorbed and can cause metabolic alkalosis
● NaCl absorption may exacerbate the fluid retention in certain patients
Non systemic - Magnesium hydroxide, Magnesium trisilicate, Aluminium hydroxide gel and
Calcium carbonate
● Formulations containing magnesium hydroxide or aluminium hydroxide react slowly with
HCl to form Magnesium chloride, Aluminium chloride and water
● No gas is generated - hence, belching and metabolic alkalosis does not occur
, ● Unabsorbed magnesium can cause osmotic diarrhoea and aluminium cause
constipation - therefore, both are given together to minimize the impact on bowel
function
IDEAL ANTACID - insoluble and neutralize acid, should not produce CO2 and should not
disturb acid-base balance
Proton pump inhibitor (PPI)
Omeprazole, Esomeprazole, Lansoprazole
MOA: irreversibly inhibits H+/K+ ATPase, suppressing gastric acid productions; the H+/K+
ATPase membrane-bound enzyme plays an essential role in the final step of gastric acid
secretion
Side effects: constipation, headache, diarrhoea, abdominal pain, skin rashes, arthralgia (joint
pain), may decrease vitamin B12 absorption, increases the rate of infection and fracture of
bones, low magnesium levels, C. diff infection
Caution: risk of osteoporosis and hypomagnesaemia
Interactions: Omeprazole can inhibit the metabolism of phenytoin, warfarin and diazepam; PPIs
decrease the bioavailability of itraconazole, iron salts etc
H2R antagonists
Cimetidine, Ranitidine, Famotidine
MOA: competitively blocks H2 receptors on parietal cells; suppresses basal and meal-simulated
acid secretion in a linear dose-dependent fashion, most effective in suppressing nocturnal acid
secretion
Side effects: diarrhoea, headache, rash, dizzy, constipation, fatigue,
Caution: renal impairment
