Dyspepsia & peptic ulcer disease Flashcards
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
how would you treat peptic ulcer disease?
- ALL anti-secretory therapy (Proton pump inhibitor - PPI)
- ALL test for H. pylori
= H. pylori +ve eradicate
= H. pylori -ve anti-secretory therapy - withdraw NSAIDS
- lifestyle
- non-HP/non-NSAIDS ulcers
= nutrition & optimise co-morbidities
(surgery is infrequent)
what are 4 H2 receptor antagonists (H2RAs) used as anti-secretory therapy?
1) cimetidine
2) ranitidine
3) famotidine
4) nizatidine
what are 6 examples of effective PPIs?
1) omeprazole
- 20-40mg/daily
2) esomeprazole
3) lansoprazole
4) dexlansoprazole
5) pantoprazole
6) rabeprazole
what heals duodenal and gastric ulcers faster - omeprazole or ranitidine?
duodenal ulcers are healed faster by = omperazole
gastric ulcers = omperazole but difference is not as great as for duodenal ulcers
what else can be used to help healing other duodenal ulcers - that has not yet been established for Gastric ulcers, NSAIDS or non.H.pylori/ non-NSAID ulcers?
1) anti-acids
2) sucralfate
what else enhances duodenal healing, but no advantage over PPIs or H2RAs?
misoprostol
how would you treat H. pylori infections - with the aim to eradicate it?
1) triple therapy for 1 week
= PPI + amoxycillin 1g bd + clarithromycin 500mg bd
= PPI + metronidzole 400mg bd + clarithromycin 250mg bd
- 2 week regimens
+ higher eradication rates
+ poor compliance
2) Dual therapy
= PPI + 1 antibiotic not recommended
3) quadruple therapy + culture directed therapy
Side effects are common = nausea and diarrhoea.
what are 4 complications of peptic ulcer disease?
1) anaemia
2) bleeding
3) perforation
4) gastric outlet/duodenal obstruction - fibrotic scar
describe the post-therapy follow up in duodenal and gastric ulcers?
Duodenal ulcers
= uncomplicated DU requires no f/u
- only if ongoing symptoms
gastric ulcers
= f/u endoscopy at 6-8 weeks
= ensure healing and no malignancy
what are the alarm symptoms of gastric cancer?
- dyspepsia
- weight loss
- anaemia
- mass
- recurrent committing
what increases the risk of getting gastric cancer?
= achlorhydria (absence of HCL in gastric secretions)
- pernicious anaemia, previous gastric surgery
+ family history
what are 3 histological, 2 physiological features and bacteriology of gastric cancer?
Histology
= body predominant or pangastritis
= atrophy
= intestinal metaplasia
Physiology
= deceased of no acid secretions
= increased gastrin
Bacteriology
= H. purloined disappear
= mixed bacterial overgrowth
True or False.
those with H. pylori who develop peptic ulcer disease are somehow protected from developing gastric cancer.
Yes.
how does H. pylori inhibit gastric secretions?
1) direct effect of bacterial product
- ammonia
- caves factor
- alpha methyl histamine
2) effect of body inflammation induced by H. pylori
- IL-1B = increased in H. pylori gastritis
- powerful inhibitor of acid secretion
(1B = recognised polymorphisms of IL- gene with different pro-inflammatory activities)
how does inflammation, induced by H. pylori, inhibit gastric secretion?
= IL-1 beta production is stimulated by H. pylori
= IL-1 is a powerful inhibitor of acid secretion
describe the progression that happens as a result of H. pylori infection, mucosal inflammation and then IL-1B pro-inflammatory host-genotype?
IL-1B pro-inflammatory host genotype = acid hypo-secretion = body predominant gastritis = atrophic gastritis = cancer
NO IL-1B pro-inflammatory host genotype
= normal or high acid
= antral predominant gastritis
= duodenal ulcer or no disease
