Upper GI Tract Disorders Flashcards
Gastric acid is produced by parietal cells under:
- autonomic and hormonal influences
- direct and indirect
Effect of acid suppression medication (omneprazole):
(side effects too)
- proton pump inhibitor
- direct inhibition of the proton pump
- reduction in acid secretion
- side effects rare:
- diarrhoea
- increased risk of GI infection - H2 receptor antagonist: reduces histamine
stimulation
Gastro-oesophageal reflux disease (GORD)
- reflux of gastric contents into the oesophagus
- very common
- caused by:
- failure of gatekeeper:
- lower oesophageal sphincter not closing fully
(or frequent non-physiological temporary
relaxations)
- diaphragmatic sphincter - increased intr-abdominal pressure
Risk factors for GORD
GORD symptoms:
- many are asymptomatic
- dyspepsia “acid reflux”“heartburn”
- burning discomfort in chest/trhoat
- reflux of acid into mouth
- upper abdo/chest pain
- globus sensation
- respiratory symptoms
- persistent nausea
- poor dentition
Diagnosis of GORD:
- mostly clinical
- endoscopy
- oesophageal manometry and pH studies
- faeces or breath testing for H.pylori
- Xray contrast swallow/meal
Management of GORD:
- lifestyle advice
- acid suppresion therapy:
- mainly PPI
- H2 receptor antagonist
- reduces acid but do not reduce reflux
- heliobacter pylori eradication if relevant
- surgery reserved for medical failure or where long
term medical treatment is undesirable - proof of reflux usually required pH studies
- restore normal anatomy
Fundoplication = wrap fundus around oesophagus to
stop reflux
hernia
protrusion of all or a part of a viscus through its coverings and into an abnormal position
hiatus hernia
protrusion of the stomach through the diaphragm and into the chest
can be sliding or rolling
sliding hiatus hernia
- 85-95%
- Gastrooesophageal junction is mobile:
- part or all of stomach enters the chest
- loss of diaphragmatic sphincter effect
- negative thoracic pressure pulls gastric contents
into the oesophagus
presentation of a sliding hiatus hernia:
- mostly symptomatic
- GORD symptoms
- dysphagia
what type of hernia is depicted below?
sliding hiatus hernia
Rolling Hiatal hernia (paraoesophageal)
- 5-15%
- gastrooesophageal junction fixed in normal position
below diaphragm:
- gastric fundus is lead part of hernia
- diaphragmatic and lower oesophageal sphincter
working
Presentation of rolling hiatal hernia (paraoesophageal):
- often asymptomatic
- chronic, non-specific, difficult to diagnose
- abdo pain, early satiety, anaemia, dysphagia
- strangulation (1% risk)
Management of hiatus hernia:
- conservative
- medical
- surgical:
- reduce the hernia
- close the defect
- often combined with fundoplication hence
increases the bulk of gastrooesophageal junction
so improves the reflux symptoms
Barrett’s oesophagus:
- metaplastic replacement of normal oesophageal
squamous epithelium with columnar epithelium
(intestinal metaplasia) - 1-2%
Barrett’s oesophagus: causes:
- chronic reflux
Barrett’s Oesophagus: Diagnosis:
columnar epithelium identified at lower oesophagus
Barrett’s oesophagus is a malignant condition.
True or False?
False
is a pre-malignant condition
metaplasia leads to dysplasia which is the adenocarcinoma sequence
Risk Factors for Barrett’s Oesophagus:
- male
- age
- history of reflux: but symptoms may improve as
Barrett’s develops due to metaplastic columnar
mucosa being more acid resistant - obesity
- smoking
- family history
Natural History of Barrett’s:
- metaplasia = replacement of one type of specialised
cell with another - dysplasia = disordered cell development/precursor to
cancer - Low grade dysplasia = some will progress to HGD and
cancer, most will not progress
or will revert to non-dysplastic
mucosa - High grade dysplasia = upto half already have
invasive cancer if HDG
detected, risk of developing
cancer
Management of Barrett’s Oesophagus:
- metaplasia without dysplasia is surveillance only
- LGD is surveillance mostly
- HGD:
- complex MDT management
- radiofrequency ablation
- endoscopic removal +/- ablation
- surgery - PPI therapy may reduce progression
Gastritis is a ——- gastric mucosal injury
multifactorial
Causes of Gastritis:
- ingested irritants: NSAIDs, alcohol, caustics
- Non heliobacter pylori infections eg EBV
- inflammatory conditions can be multisystem eg
Crohns - stress
- smoking
main cause: heliobacter pylori infection
Gastritis symptoms
- gnawing or burning stomach pain
- abdo bloating
- loss of appetite
- frequent belching
- indigestion
- vomiting
- hiccups
- nausea or recurrent upset stomach
Chronic gastritis can lead to
ulceration or even cancer
Management of Gastritis:
- remove causal agent if possible
- acid suppression therapy (PPI)
NSAIDs
- reversible inhibition of cyclo-oxygenase (COX)
enzymes:
- COX 1 produces GI tract protective prostaglandins
- COX 2 produces prostaglandins which mediate
pain and inflammation - Loss of protective prostaglandins:
- reduced gastric mucous and bicarb production
- reduced gastric mucosal blood flow: reduce
protection of gastric mucosa and ability to repair
after injury - always consider need for gastric protection (PPI) with long term NSAID use
Peptic ulceration: causes:
- H. pylori involvement is high
- NSAIDs account for most other causes
- decreasing incidence with advent of H2 receptor
antagonists and PPIs - Rarer causes:
- stress ulceration
- malignancy
- Zollinger-Ellison syndrom
- medications
Zollinger-Ellison Syndrome
- rare neuroendocrine tumour of G cells
- most often of the pancreas
- 1:100,000 people
- secretes uncontrolled and excessive gastrin
- excessive activity of gastric parietal cells
- multiple UGI ulcers
- detected by imaging pancreas and measuring gastrin
levels
What is a peptic ulcer?
A perforation or hole in the lining of the small intestine, lower oesophagus or stomach.
Types of peptic ulcers (2):
- Gastric ulcers
- duodenal ulcers
Gastric Ulcers:
- most commonly lesser curve of stomach
- more likely to be associated with cancer
Duodenal Ulcers:
- usually 1st part (superior)
- four times more common than gastric ulcers
Chronic ulcer presentation:
- upper abdo pain
- gastric ulcer pain often increases 2-3 hours after a
meal due to increased gastric acid - duodenal ulcer pain often reduces after eating
(increased pancreatic juices results in increased bicarb
in duodenum which neutralises acid) - iron deficiency anaemia
- weight change due to association between pain and
food
Acute ulcer presentation:
- acute UGI bleeding:
- haematemesis “coffee-ground” (vomiting blood)
- melaena: dark sticky faeces due to internal
bleeding so contains partially digested blood - sometimes rectal bleeding
- perforation of ulcer:
- peritonitis
- systemically unwell
Diagnosis of ulcers:
- history and examination
- endoscopy
- H.pylori testing: stool/rapid urease test with gastric
biopsy CLO test
Treatment of ulcers:
- PPI +/- H.pylori eradication (antibiotics?)
- remove causal agents if possible
Acute UGI bleeding:
- bleeding from oesophagus, stomach, duodenum
- mortality 2-10%
- Variceal bleeding (11%):
- aim to stop bleeding and reduce portal pressure:
- beta blockers, endoscopic intervention - Non-Variceal bleeding (89%):
- aim to stop bleeding and treat cause:
- medication (PPI)
- radiological or endoscopic intervention
Duodenal ulcer and UGI bleeding:
- gastroduodenal artery passes behind the 1st part of
the duodenum - posterior ulcer can erode into the gastro-duodenal
artery causing bleeding - if seen endoscopically can be treated, else radiological
embolisation or surgery
Management of perforated peptic ulcers:
- occasionally can be managed without surgery:
- omentum spontaneously seals hole
- posterior duodenal ulcer? - otherwise surgery needed:
- closure of ulcer is possible
- omental patch
- high dose PPI
Heliobacter Pylori
- gram negative
- most common in childhood
- cannot live in acidic conditions:
- express urease
- converts urea to ammonia plus CO2
- raises surrounding pH - most colonised humans show no symptoms >70%
Pathogenicity of CagA
- cytotoxin-associated gene A (CagA) produced by some
strains are associated with inflammation, increased
risk of ulcers and cancers - vacuolating toxin A (VacA) causes cell damage
- multiple other factors causing:
- gastritis
- peptic ulceration:
- 70-85% gastric ulcers
- 90-95% duodenal ulcers - gastric cancer:
- adenocarcinoma
- mucosa-associated lymphoid tissue lymphoma
92-98%
Testing for H. pylori:
- uncomplicated but unresponsive dyspepsia
- prior to NSAID use if pervious ulcers
- unexplained iron deficiency anaemia if malignancy
excluded
do not routinely tested:
- predominantly GORD symptoms
- within two weeks of PPI treatment
- following treatment, bar certain contexts
What type of hernia is depicted below?
Rolling hiatal hernia
