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
misoprostol usage
rapidly absorbed - short T1/2 - 4 times per day
Prevention of NSAID-induced peptic ulcers
misoprostol MOA
(mimics prostaglandin)
Binds to PGE2 receptors
At low dose (cytoprotective): promotes bicarbonate and mucus secretion, enhances mucosal blood flow
At high dose (antisecretory): inhibits gastric acid secretion
misoprostol ADR
Abdominal pain Diarrhoea Abortion (uterine contraction) -> ppl may use as abortifacient Bone pain and hyperostosis (excessive bone growth) not really used nowadays
Eradication of H.Pylori
1st line: triple therapy (2 antibiotics + 1 PPI)
- Clarithromycin
- Amoxicillin/ Metronidazole
2 antibiotics given tgt to prevent buildup of resistance
- Anti-secretory agent (PPI): Omeprazole
triple therapy for 1-2wks -> continue PPI for 4-6wks
2nd line: quadraple therapy:
+ bismuth
H2 inhibitor clinical use (famotidine)
inhibit nocturnal acid secretion
why H2 has less effects for meal induced acid secretion
gastric parietal cell also receives stimulation directly from the vagus nerve and gastrin = blocking H2 receptors cannot fully inhibit gastric acid secretion
esp when not on empty stomach
