peptic ulcer disease and acid reflux Flashcards
why should you not give meds on empty stomach
stomach lumen is shrunk when empty
hiatus hernia
hole in the diaphragm which the oesophagus goes through the the oesophagogastric mucosal junction may move
acid may come up and damage the squamous epithelium of the oesophagus
G cells release
gastrin
gastrin stimulates
parietal cells
parietal cells make
acid
antrum senses
pH
D cells secrete
somatostatin
somatostatin
switch of G cells
helicobacter
causes inflammation and somatostatin is suppressed
therefore G cells are always uninhibited so gastrin is constantly produced and acid is excessively produced
GORD
gastro-oesophageal reflux disease
peptic ulcers occur where
acid is present
toxins produced by helicobacter pylori
CagA and VacA
make inflammation
duodenal ulcer and adenocarcinoma may result from toxin producing helicobacter
H pylori non toxin producing
regardless of toxin status, H pylori infection is always associated wth a degree of histological gastritis (inflammation)
pepto-bismol
contains bismuth which is kills spirochetes (helicobacter) and heals ulcers
bismuth
same group in the periodic table as arsenic
bismuth citrate
used in Australia
intestinal metaplasia
sign of chronic inflammatory
sign of gastric cancer risk
cancer probably develops at the edge of islands of intestinal metaplasia
H pylori does not grow
where there is intestinal metaplasia
chronic inflammation due to HH pylori causes formation if
intestinal metaplasia
distribution of helicobacter
wisespread infection - lower acid secretion
antrum only infection - acid secreting part of the stomach is minimally inflamed and overproduces acid due to excessive gastrin secretion
widespread helicobacter infection
not likely to experience excessive acid secretion
antrum only infection symptoms
may have duodenal ulcer
hiatus hernia
heartburn /acid reflux
Proton pump inhibitor
reduces acid
if acid is not reduced the cure rate is low
if acid is not removed in duodenal ulcer patients
cure rate is low
must treat with antibiotic and also proton pump inhibitor
antacids
most common acid reduction therapy
- need too much to heal ulcers
- eg. mylanta
- cause calcium/aluminium salts with constipates the patient
- magnesium salts loosen stools
- interferes with gastric absorption of many drugs e.g antibiotics
- can interfere with absorption and cause malnutrition
gaviscon granules
1-2 tablets prn, bedtime
- alginic acid, aluminium hydroxide, Na bicarbonate
antacid tablets
1-2 tabs chewed prn
quick-eye, tums, mylanta
- chew, leave antacid in the oesophagus, quick relief
mucosal protective agents
thickens/strengthens mucus
antacid which makes the mucus less permeable
can cause black stool
proton pump inhibitors act on
H+ K+ ATPase
histamine stimulates
H2 receptor
H2 receptor is located
on a parietal cell
when H2 receptor is stimulates
gastric acid is secreted
H2 receptor antagonists
cimetidine, ranitidine, famotidine
competitive inhibitors of the H2 receptor
well absorbed with few side effects
renal excretion dn liver metabolism, short half life
cimetidine
competitive H2 receptor inhibitor
inhibits c-P450
why does it take a lot of acid suppression to rate pH
99.9% acid suppression needed to raise pH 1.5-4.5 due to logarithmic scale
ulcer therapy
acid reduction heals 90%
but will relapse unless the underlying problem is treated
duodenal ulcer most often occur in
younger people, high acid secretion, replapse quickly
gastric ulcers occur in
older people, slower to heal
proton pump inhibitor examples
esomeprazole - Nexium bind to -SH groups in the ATPase non-competitive binding - total inhibition of acid secretion - long action
P-cab based acid blocker
potassium competitive acid blockers
long half life
more complete acid blockade than proton pump inhibitors
more effective in resistant H pylori
drugs used to eradicate H pylori - those that can never cause resistance
amoxicillin, bismuth, tetracycline
drugs used to eradicate H pylori - those that always cause resistance
clarithromycin, metronidazole
acid lowering and mucosal drugs to use with the antibiotic
proton pump inhibitor
H2-blocker
mucosal agents
most commonly used triple therapy for H pylori
esomeprazole
amoxicillin
clarithromycin
when H pylori triple treatment fails
usually due to clarithromycin resistance
