Dyspepsia and Peptic Ulcer Disease Flashcards
what is dyspepsia
indigestion
what are the symptoms in romes criteria of dyspepsia
epigastric pain/ burning, postprandial fullness, early satiety
where does the foregut start and end
cricopharyngeus to ampulla of vater
what structures are in the foregut
oesophagus, stomach, duodenum, pancreas, gallbladder
what is dyspepsia more common with
if H pylori infected, NSAID use, overlap with IBS/GORD
what are the causes of dyspepsia
organic causes;
peptic ulcer disease, drugs, gastric cancer
idiopathic causes (75%)
what is the difference between dyspepsia and heartburn/ relfuc
heartburn/ reflux is a burning sensation in the epigastric region
what is GORD
gastro- oesophageal reflux disease
what should be found on exam of uncomplicated dyspepsia
epigastric tenderness only
what might be found on examination of uncomplicated dyspepsia
cachexia, mass, evidence of gastric outflow obstruction (vomiting, splish and splash of gastric content around blockage), peritonism
how is dyspepsia treated
check H pylori status- eradicate if infected which will cure ulcer disease and remove risk of gastric cancer
if HP -ve treat with acid inhibItion
what lifestyle factors could cause dyspepsia
diet (spicy food, drink, infrequent meals)
what is functional dyspepsia
when there in no evidence of structural disease that explain the symptoms- idopathic
what can cause functional dyspepsia
visceral hypersensitivity, disrupted gut-immune interactions, abnormal upper GI motor and reflex functions, physiological factors, genetic factors, altered brain- gut interactions
what is peptic ulcer disease
a common cause of dyspepsia- pain predominant dyspepsia (which radiates to back) cause by gastric or duodenal ulcers
what is the onset/ aggravating factors of peptic ulcer disease
often nocturnal, relapsing and remitting chronic illness- aggravated/ relieved by eating
who is peptic ulcer disease more common in
lower socio-economic groups, people with FH of it
what are the causes of peptic ulcer disease
H pylori, NSAIDs (COX1, COX2, PGE),
gatric dysmobility and outflow obstruction thought to be associated
describe H pylori
gram -ve microaerophilic, flagellated bacillus
how is H pylori aquired
in infancy by oral-oral/ faecal oral spread
what gastric cancers area associated with peptic ulcer disease
almost all non-cardia gastric adenocarcinoma
low grade B-cell gastric lymphomas
is H pylori more common in develop/ developing world?
developing- possibly reflect sanitation
what effect does food have on the acidity of the stomach
food increases pH which stimulates G cells to release gastrin which stimulates parietal cells of the fundus to produce HCL
what happens when H pylori affects the distal stomach
If affects distal stomach G cells stimulated which lead to over stimulation of parietal cells which creates hyper acidic state which creates gastric metaplasia.
Duodenal mucosa cant be infected with h pylori but the gastric metaplasia can cause duodenal ulcer. Will move proximally causing an increased amount of gastrin but acid making ability defect so excessive amount of gastrin= alkaline stomach+ hypertrophy= risk of gastric cancer
what is somatostatin
inhibitor of gastrin release (and insulin and glucagon)
what happens when the acidity of the the stomach increases
gastrin release decreased due to increased somatostatin
what does an increased duodenal acid load result in
gastric metaplasia, H Pylori colonisation, ulceration
how is H pylori infection diagnosed
gastric biopsy (urease test, histology, culture/ sensitivity)
urease breath test
faecal antigen test (FAT)
serology (IgA antibodies)- not accurate with older patients
how does H pylori affect the pH of its microenvironment
increases pH- via the enzyme urease, splits urea and produces ammonium bicarbonate
how is are all PUD treated
anti secretory therapy (PPI)
tested for presence of H pylori
withdraw NSAIDs
lifestyle
surgery (infrequent)
what does a +ve H pylori test mean for management
eradication needed
how are non HP and non NSAIds ulcers treated
nutrition and optimise comorbidities
what are the anti-secretory therapies
PPIs; omeprazole, esomeprazole, lansoprazole, dexlansoprazole, pantoprazole and rabeprazole (OLEs)
histamine 2 receptor antagonists (H2RAs); cimetidine, ranitidine, famotidine and nizatidine (TIDINE)
what is the H pylori eradication treatment
triple therapy for 1 week;
PPI + amoxycillin 1g bd + clarithromycin 500mg bd
or
PPI + metronidazole 400mg bd + clarithromycin 250mg bd
bd= twice a day
what are the common S/E of eradication therapy and the consequences of this
nausea and diarrhoea- reduces patient compliance
what are the complications of PUD
amaemia, bleeding, perforation, gastric outlet. duodenal obstruction- fibrotic scar, malignancy
what are the symptoms of gastric cancer
dyspepsia + alarm symptoms: wight loss, anaemia, mass, recurrent vomiting
what is achlorhydria and how is it associated with gastric cancer
loss of HCL in gastric secretions caused by e.g pernicious anaemia, previous gastric surgery
what causes pernicious anaemia
The most common cause of pernicious anemia is the loss of stomach cells that make intrinsic factor. Intrinsic factor helps the body absorb vitamin B12 in the intestine
what is the pathway from normal stomach to neoplasia (correa’s hypothesis)
normal- (h pylori, salt, antioxidants, N- nitroso compounds)- chronic gastritis, atrophy- (smoking)- intertestinal metaplasia- dysplasia- neoplasia
what does H pylori do to gastric acid secretion
inhibits it- effect of body inflammation cause by infection, direct effect of bacterial product
what gene disposes patients to having a hypochlorhydric response to H pylori
IL- IB gene (powerful acid inhibitor and IB associates with pro inflammatory responses)
what determines whether mucosal inflammation from H pylori infection develops into cancer
IL-1B pro-inflammatory Host genotype
if Yes: Acid hyposecretion Body predominant gastritis Atrophic gastritis Cancer
if No
Normal or high acid
Antral predominant gastritis
DU or No Disease
