GIT - gastritis Flashcards
Agents that reduce gastric acidity
Antacids (anti-acid): neutralise acid
H2 receptor antagonist: famotidine
Proton pump inhibitors (PPI): omeprazole
Mucosal protective agents
Sulcralfate
Misoprostol
Bismuth
Agents that eradicate H pylori
Clarithromycin
Amoxicillin
Omeprazole
Factors cause PUD (peptic ulcer disease)
Increase damage: H.pylori, NSAID, Aspirin, Cigarettes, Alcohol, Gastric hyperacidity, Duodenal-gastric reflux
Impaired defence: Ischemia, shock, delayed gastric emptying
Antacids: 4 examples + arrange in rate of neutralisation
NaHCO3 > CaCO3 > MG(OH)2 > Al(OH)3
Products of antacid + side effects
form H2O + salt
NaHCO3: produce CO2 (also metabolic acidosis)
feeling of bloatedness (flatulence), belching, abdominal discomfort
Na+ and Ca2+ retention = fluid retention, hypercalcemia
metabolic alkalosis
affects absorption of other drugs - 2hrs gap**
RENAL CLEARANCE
what comes with antacids to reduce ADR
simethicone - anti-foaming agent
helps to release the gas through burping
Mg(OH)2 ADR
MG2+ : gives osmotic diarrhoea (effect cancels out when given with Al3+
Al(OH)3 ADR
Al3+ : gives constipation (effect cancels out when given with Mg2+
H2 receptor antagonists mechanism of action
- competitive inhibitors of H2 (histamine) receptors on parietal cells -> suppress gastric secretion
- block amplification of gastrin + cholinergic signals through ECL cells (in gastric mucosa) - makes it potent
H2 antagonist drugs
-tidine
famotidine - most potent, but safe
cimetidine
ranitidine
cimetidine ADR
inhibit cytochrome p450 = decrease metabolism of other drugs
mental confusion
anti-androgenic effects: males - gynaecomastia, females - galactorrhea (nipple discharge)
PPI MOA
protonated in gastric lumen, forming thiophilic sulphenamide
concentrated in parietal cell canaliculi
irreversibly inhibit H+/K+ATPase in parietal cells - by forming covalent disulphide bonds -> increase pH -> less favourable for pathogens to grow
+ direct anti-microbial activity against H.pylori
PPI 2 drugs
-prazole
omeprazole** -> most potent gastric acid inhibitor!!
esomeprazole
are PPIs active?
inactive prodrug
tablet covered by coating so that it will not be activated before reaching - activated drug is not able to be absorbed
SI
how to take PPIs
bioavailibity decreased by 50% when taken with food = need to be taken on an empty stomach - 1hr before breakfast
+ need to be present during meal time (when proton pumps are active) - 1hr half life
(proton pumps activated better with a high protein meal - meat)
takes 3-4 days to fully inhibit gastric acid secretion, continue taking for 4-6wks
high efficacy
PPI ADR
generally quite safe
Ca def -> osteoporosis
headache, diarrhoea, nausea, constipation, flatulence
3 agents for gastric mucosal protection
sucralfate
bismuth compounds
misoprostol
sucralfate MOA
sulphate (-ve charge) binds to +ve charge proteins at the ulcer, forms viscous, tenacious gel preventing further acid attack
stimulates mucosal prostaglandin and bicarbonate secretion
how to take sucralfate + used for what circumstances
empty stomach - 1hr before meals
prevention of stress-related bleeding in critically ill patients
not used for ulcers - use H2 antagonist and PPI
sucralfate ADR
constipation
impairs other drug absorption
Bismuth MOA
forms a protective layer protecting ulcers from acid and pepsin
Stimulates mucus and bicarbonate secretion
Directly anti-microbial activity against H. pylori
Bismuth: used under what circumstances
dyspepsia (indigestion)
acute diarrhoea
eradication of H pylori (quadruple therapy: PPI + metronidazole + tetracycline + bismuth subcitrate)
Bismuth: what to take note
generally safe for short term
prolonged use may cause bismuth toxicity -> encephalopathy
warn patients of harmless blackening of stool and reversible darkening of tongue
avoid in RENAL patients
