Helicobacter pylori and Gastric Disease Flashcards
Upper GI Tract
Oesophagus
Stomach
Lower GI Tract
Small intestine
Large intestine
dyspepsia symptoms
Epigastric pain
Burning
Fullness
Bloating
Satiety
Nausea
Sickness
Heartburn
Reflux
Discomfort
Dyspepsia greek meaning
dys = bad, pepsis = digestion
what are the collective group of symptoms for dyspepsia
Pain or discomfort in the upper abdomen
upper abdominal discomfort, retrosternal pain, anorexia, nausea, vomiting, bloating, fullness, early satiety and heartburn
For 4 weeks ( 12weeks Rome criteria)
is dyspepsia common
80 % of people, most have no serious underlying disease
GP consultations percentage for dyspepsia patients
When broadly defined, dyspepsia occurs in 40%, leads to GP consultation in 5% and referral for endoscopy in 1% of the population annually.
what can cause symptoms of dyspepsia for upper GI
GORD
Peptic ulcer
Gastritis
Non ulcer dyspepsia
Gastric cancer
What can cause the symptom of dyspepsia in lower GI
Gallstones
Pancreatic disease
IBS
Colonic cancer
Coeliac disease
what may be other causes of dyspepsia
Other systemic disease – metabolic, cardiac
Drugs
Psychological
what do you do if a patient presents with dyspepsia
History & examination are key!!
Drug history – NSAIDs, steroids, bisphosphonates, Ca antagonists, nitrates, theophyllines, remember OTT
Lifestyle – alcohol, diet, smoking, exercise, weight reduction
Examination including BMI
Bloods – FBC, ferritin, LFTs, U&Es, calcium, glucose, coeliac serology/serum IgA
what bloods need to be done for dyspepsia
FBC, ferritin, LFTs, U&Es, calcium, glucose, coeliac serology/serum IgA
when do you refer for endoscopy
ALARMS
Anorexia
Loss of weight
Anaemia – iron deficiency
Recent onset >55 years or persistent despite treatment
Melaena/haematemesis (GI bleeding) or mass
Swallowing problems - dysphagia
what is an upper GI endoscopy
Diagnostic and therapeutic upper GI endoscopy
Local anaesthetic (throat spray) or sedation
Day case
Fasted
Consent
Risks - 1:2000 risk perforation, bleeding, reaction to drugs given
what is helicobacter pylori
Gram negative, spiral-shaped, microaerophilic, flagellated Gram –ve bacteria
how common is helicobacter pylori
Infects 50% world population
Acquired in childhood
what can H.pylori only colonise
only colonise gastric type mucosa
where does H.pylori reside
in the surface mucous layer and does not penetrate the epithelial layer
what does an H.pylori infection do
Evokes immune response in underlying mucosa – dependent on host genetic factors
what is the infection pathway and pathogenesis for Helicobacteria
- enters host and aurvives
- motility and chemotaxis
- adhesin receptor interaction (establish colony)
- toxin release and damage to host
- intracellular replication
what is the clinical outcome of helicobacter pylori for >80%
asymptomatic or chronic gastritis
what is the C
chronic atrophic gastritis
intestinal metaplasia
gastric or duodenal ulcer
what is the the clinical outcome of helicobacter pylori for 1%
gastric cancer
MALT lymphoma
what is the clinical outcome of H.Pylori dependent on
site of colonization
characteristics of bacteria
host factors e.g. genetic susceptibility
environmental factors e.g. smoking
what are the three different types of gastritis caused by chronic H.Pylori infection
Antral predominant Gastritis
Mild Mixed Gastritis
Corpus predominant Gastritis
what does Corpus predominant Gastritis mainly affect
the body of the stomach
Corpus predominant Gastritis effect on acid secretion
decreased acid secretion and Gastric Atrophy
what condition will Corpus predominant Gastritis lead to
gastric cancer
what part of the stomach is predominantly affected by Antral predominant Gastritis
antrum
what effect does Antral predominant Gastritis have on acid secretion
increased acid secretion
low Risk of Gastric Ca
what condition will Antral predominant gastritis lead to
Duodenal ulcer
Mild Mixed Gastritis
Normal Acid producing No significant disease
what are the non invasive diagnostic methods of H.Pylori
Serology: IgG against H. pylori
13C /14C Urea Breath Test
Stool antigen test – ELISA - need to be off PPI for 2 weeks
what are the invasive methods for H.Pylori
requires endoscopy
Histology: gastric biopsies stained for the bacteria
Culture of gastric biopsies
Rapid slide urease test (CLO)
Rapid slide urease test (CLO)
A biopsy is taken from the stomach and is put into the well where the gel is impregnated with urea if there is bacteria in the specimin the ureas reacts with the urea and forms ammonia changing the ph of the well and the colour to pink (positive) yellow (negative)
what colour will a positive Rapid slide urease test (CLO) show
Pink
what colour will a negative Rapid slide urease test (CLO) show
Yellow
what is gastritis
Inflammation in the gastric mucosa
Histological diagnosis
Clinical features seen at endoscopy
what are the causes of Gastritis
Autoimmune (parietal cells)
Bacterial (H. pylori)
Chemical (bile/NSAIDs)
what age groups are most commonly affected by peptic ulcers
Both GU and DU commoner in elderly people
what are the majority of peptic ulcers caused by
Helicobacter pylori infection (50% GU 80% DU)
what are peptic ulcers also caused by
NSAIDs, smoking
Rarely they are caused by other conditions such as Zollinger-Ellison syndrome, hyperparathyroidism, Crohn’s disease
what symptoms are associated with peptic ulcer
pigastric pain is the main feature (pointing sign, may be relieved by antacids)
Nocturnal/hunger pain (more common in DU)
Back pain (may suggest penetration of a posterior DU)
Nausea and occasionally vomiting
Weight loss and anorexia (chronic ulcer)
Only sign may be epigastric tenderness
If the ulcer bleeds, patients may present with haematemesis and/or melaena, or anaemia
If the peptic ulcer bleeds what will the patient present with
haematemesis and/or melaena, or anaemia
how do you treat a peptic ulcer caused by H.Pylori
Ulcers caused by H. pylori are treated by eradication therapy to get rid of the bacteria
Complications are treated as they arise
what are pharmalogical treatments for peptic ulcers
Antacid medication – proton pump inhibitors (omeprazole)or H2 receptor antagonists (ranitidine)
If NSAIDs are also involved, these have to be stopped if possible, or should continue to receive other protective agents following eradication therapy
when is surgery indicated for a peptic ulcer
In a complicated PUD
How do you eradicate H.Pylori
Triple therapy for 7 days
Clarithromycin 500mg bd
Amoxycillin 1g bd (or Metronidazole 400mg bd)
Tetracycline is given if penicillin allergy
PPI: e.g. omeprazole 20mg bd
is eradication of H.pylori effective
In 90% of cases
what are the complications of a peptic ulcer
Acute bleeding – melaena and haematemesis
Chronic bleeding – iron deficiency anaemia
Perforation
Fibrotic stricture (narrowing)
Gastric outlet obstruction – oedema or stricture
gastric outlet obstruction symptoms
Vomiting – lacks bile, fermented foodstuffs
Early satiety, abdominal distension, weight loss, gastric splash
Dehydration and loss of H+ and Cl- in vomit
Metabolic alkalosis
blood results for gastric outlet obstruction
low Cl, low Na, low K, renal impairment
diagnosis for gastric outlet obstruction
UGIE (prolonged fast/aspiration of gastric contents), identify cause – stricture, ulcer, cancer
how do you treat gastric outlet obstruction
endoscopic balloon dilatation, surgery
Gastric cancer
Second commonest malignancy worldwide
Large geographical variation – genetic and environmental factors
Very poor prognosis (5 yr survival <20%)
Presents late in Western countries
Majority are adenocarcinomas (epithelial cells)
what are types of gastric tumours
MALT, GIST
how do patients present with gastric cancer
Dyspepsia, early satiety, nausea & vomiting, weight loss, GI bleeding, iron deficiency anaemia, gastric outlet obstruction
Aetiology of gastric cancer
Smoking has a definite positive association as has some food groups e.g. high salt diet, foods high in nitrates. The major aetiological factor in GC is HP.
Other factors to consider – family history, previous gastric resection, biliary reflux, premalignant gastric pathology
characteristics of majority of gastric cancer
sporadic with no demonstrable inherited component
characteristics of <15% of gastric cancer
familial clustering, most not associated with definitive germline mutation
characteristics of 1-3% of gastric cancer
heritable gastric cancer syndromes
HDGC;AD, CDH-1 gene (E-cadherin)
how do you make a histological diagnosis of gastric cancer
Endoscopy and biopsies
what investigations are done for gastric cancer
Staging investigations – has it spread elsewhere?
CT chest/abdo – lymph nodes and liver/lungs/peritoneum/bone marrow
MDT discussion – imaging/histology/patient fitness
MDT discussion for gastric cancer
imaging/histology/patient fitness
Who is present? gastroenterologist, pathologist, radiologist, upper GI surgeons, oncologists, specialist nurses
treatment of gastric cancer
surgical and chemotherapy
