Dyspepsia & peptic ulcer disease Flashcards
(40 cards)
what is dyspepsia?
indigestion
what are 3 symptoms of dyspepsia?
- epigastric pain or burning (epigastric pain syndrome)
- post-prandial fullness (post-prandial distress syndrome)
- early satiety (post-prandial distress syndrome)
what are 5 foregut structures?
- oesophagus
- stomach
- duodenum
- pancreas
- gallbladder
= cico-pharyngeus to ampulla of Water
when is dyspepsia more common?
1) if H. pylori infection
2) if NSAID drugs are used
what are 3 causes of dyspepsia?
1) peptic ulcer disease
2) drugs (esp NSAIDs, COX2 inhibitors)
3) gastric cancer
what are the causes of functional dyspepsia?
- no evidence of culprit structural diseases
= associated with other functional gut disorders e.. IBS
what are the 2 other possible differential diagnosis of dyspepsia?
- heartburn or reflux
- GORD
what might you find on examination of dyspepsia?
Uncomplicated;
= epigastric tenderness only
Complicated;
- cachexia
- mass
- evidence gastric outflow obstruction
- peritoneum
in the absence of alarm symptoms how would you treat dyspepsia?
test and treat method;
- check H. pylori status
- eradicate if infected
= cure ulcer disease
= remove risk of gastric cancer
if HP is negative in dyspepsia what would you treat it with?
= acid inhibition as required
what is the diagnostic criteria for functional dyspepsia?
Presence of at least one of the following;
- bothersome post-prandial fullness
- early satiation
- epigastric pain
- epigastric burning
and
no evidence of structural disease that is likely to explain symptoms
= criteria must be fulfilled for past 3 months, with symptom for at least 6 months before diagnosis
what are peptic ulcers?
break in the inner lining of the stomach, 1st part of the small intestine or lower oesophagus.
what are peptic ulcers a common cause of?
= organic dyspepsia
describe the symptoms of peptic ulcers?
- pain predominant dyspepsia (to back)
- often nocturnal
- aggravated or relieved by eating
= relapsing & remitting chronic illness
+ family history common
what are the causes of peptic ulcers?
1) H. pylori infection
2) NSAIDSs (COX1, COX2, PGE)
+ gastric dysmotility, outflow obstruction
when is H. pylori commonly acquired and when do consequences of infection arise?
acquired = in infancy
consequences arise = later in life
what type of bacteria is H, pylori and how is it spread?
= gram negative microaerophilic flagellated bacillus
Spread
= oral-oral/faecal oral spread
what are the 2 main consequences of H. pylori infections?
1) peptic ulcers
- 95% duodenal ulcers
- 75% gastric ulcers
2) gastric cancers
- almost all = non-cardia gastric adenocarcinoma
- low grade B cell gastric lymphoma (MALT-oma)
what cells are involved in acid secretion?
G cells, parietal cells and gastrin
describe the 2 different outcomes of H. pylori infection.
OUTCOME 1 1) Acid in stomach increases (gastrin increases) 2) no atrophy 3) duodenal ulcer
OUTCOME 2
1) Acid in stomach decreases (gastrin increases)
2) atrophy
3) gastric cancer
what is the Cag A gene?
= cytotoxin associated gene A (oncogene)
describe what happens in duodenal ulcers.
1) duodenal acid load increases
- gastric metaplasia
- H. pylori colonisation
- ulceration
2) gastrin release increases
= gastrin increases
- due to decreased somatostatin
- Cag +ve > Cag -ve
3) acid secretin increases
- due to increase parietal cell mass
= no body gastritis
how would you diagnose H. pylori infection?
= gastric biopsy
- urease test
- histology
- culture/sensitivity
= urease breath test
= FAT (faecal antigen test)
= serology (IgA antibody) - not accurate with increasing patient age
what does H. pylori do to the pH of its microenvironment?
- look at equations on slide 32
= increases the pH
- look t equations on slide 32
