Dyspepsia and Peptic Ulcer Disease Flashcards
what is dyspepsia
an epigastric pain or burning
postprandial fullness
early satiety
different from reflux
epidemiology of dyspepsia
very common (seen with H.pylori infection)
no associations with sex/age/smoking etc.
overlaps with IBS/GORD
causes of dyspepsia
organic function (idiopathic)
organic causes of dyspepsia
peptic ulcer disease
drugs - NSAIDS, COX2 inhibitors)
gastric cancer
functional causes of dyspepsia
same as organic causes but no evidence of culprit structural disease
associated with other functional gut disorders
signs of dyspepsia
epigastric tenderness
alarm symptoms of dyspepsia
dysphagia evidence of GI blood loss persistent vomiting unexplained weight loss upper abdominal mass
treatment for non-alarming dyspepsia
non-invasive test and treat;
lifestyle modifications
drug therapy
check H.pylori status - treat accordingly
drug therapy for non-alarming dyspepsia
symptoms relief;
antacids/H2 receptor antagonists
what is functional dyspepsia
presence of at least one of the following; bothersome postprandial fullness early satiation epigastric pain epigastric burning
no evidence of structural disease
causes of functional dyspepsia
visceral hypersensitivity disrupted gut-immune interactions abnormal upper GI motor and reflex functions psychosocial factors genetic factors altered brain-gut interactions
describe peptic ulcer disease pain
predominant dyspepsia (to back) and often nocturnal aggravated or relieved by eating
describe peptic ulcer disease
a relapsing and remitting chronic illness
epidemiology of peptic ulcer disease
seen more in lower socio-economic groups
family history common
causes of peptic ulcer disease
H.pylori
NSAIDs use
describe H.pylori
acquired in infancy - consequences of infection do not arise until later in life
gram negative flagellated bacillus
oral-oral/faecal oral spread
increases pH of its microenvironment
consequences of H.pylori infection
majority of people have no consequences
peptic ulcer disease
gastric cancer (1%)
duodenal ulcers caused by H.pylori infection
no atrophy increase in; duodenal acid load gastrin release (decreased somatostatin) acid secretion (increased parietal cell mass)
consequences of increased duodenal acid load due to H.pylori infection
gastric metaplasia
H.pylori colonisation
ulceration
tests for H.pylori infection
gastric biopsy
urease breath test
faecal antigen test
serology (IgA) - not accurate with older patients
treatment for peptic ulcer disease
anti secretory therapy - proton pump inhibitors
test for presence of H.pylori - treat accordingly
withdraw NSAIDs
lifestyle modifications
surgery - infrequent
lifestyle modification for peptic ulcer disease
nutrition (no form dietary recommendations) and optimise co-morbidities
treatment of H.pylori infeciton
1 week therapy;
proton pump inhibitors
amoxicillin
clarithromycin
treatment of H.pylori infection - penicillin allergic
1 week therapy;
proton pump inhibtor
metronidazole
clarithromycin
complications of peptic ulcer disease
anaemia
bleeding
perforation
gastric outlet/duodenal obstruction - fibrotic scar