upper GI disorders: dyspepsia Flashcards
symptoms of PUD (peptic ulcer disease)
gastric ulcer pain made worse by food
major cause of PUD
Caffeine 'smoking alcohol NSAID stress H. pylori
why does long term use of NSAID cause peptic ulceration
NSAID block COX enzymes and decrease Prostaglandin production
gastric ulceration is associated with what kind of acid secretion
decreased
duodenal ulceration is associated with what kind of acid secretion
increased
gastic ulcers are normally where
whole gastric area
dudoenal ulcers are normally where
antrial/pyloric region
which ulcer has less acid secreted
gastric
how can gastric damage through NSAID be prevented
use PEG1 analogue
COX-2 is switched on
sometimes
COX-1 is switched on
all the time
disadavantages of systemic anatacids
overload in kidneys
diadvantages of non-systemic antacids
most of dose stays in GI tract
adverse effects of magnesium hydroxide
laxative effect
magnesium antacids should not be used where
renal failure
mechanism of action of alginates
reacts with acids to form raft of alginic-acid gel
how is HCi released from parietal cells
- activate gastric receptors
- activate muscarinic receptors through Ach
- activate H2 receptor through histamine
how can you stop Acid production from parietal cells
PPI
stop histamine receptor
block muscarinic receptor
whih drug isnt used clinically
muscarinic receptor antagonists
PPI act on what cells
parietal
PPI’s end in what
azole
which drugs are enteric coated
PPI
PPI are a type of what
pro drug
how do PPI work
active form irreversibly binds to cysteins of H+/K+ of ATPase inhibitting active proton pump
this prevent H+ movement from parietal cells to stomach
this causes gastric acid secretion to be blocked
