s4. gastric diseases Flashcards
(38 cards)
what is dyspepsia
a complex of upper GI tract symptoms which are present for 4 or more weeks
- including upper abdominal discomfort, heartburn, acid reflux, nausea/ vom
e.g. GORD, gastritis, PUD
symptoms of GORD (Gastro-oesophageal reflux disease)
heart burn/ chest pain
acidic taste
cough/ sore throat
asymptomatic
reflux of contents into oesophagus
risk factors for GORD
anything increasing intra abdominal pressure e.g. -obesity -pregnancy -lower oesophageal sphincter(LOS) dysfunction -hiatus hernia -delayed gastric emptying
what is hiatus hernia
when LOS herniates through diaphragm into thorax> loses mechanisms like the crural muscles acting as a sling around it > distorted anatomy therefore less useful as a sphincter.
describe the mechanism of LOS
intrinsic muscles > help contract and close
only relaxes when detects food coming down oesophagus
- muscular element of diaphragm - oesophagus pierces through so D muscle is kinda wrapped around oesophagus> right crus > pulls tighter when pressure increases
- acute angle that oesophagus joins stomach
complications of GORD
Oesophagitis- irritation
ulcerations -deeper erosion through muscularis mucosa
bleeding / haemorrhage > anaemia
fibrous strictures> make it hard to swallow=dysphagia
(scar tissue in oesophag)
Barrett’s oesophagus
what is Barrett’s oesophagus
problem?
metaplastic change in the normal epithelia in lower oesophagus (stratified squamous) into gastric columnar epithelia
> repeated exposure of stomach contents causes adaptive change
> reversible
problem- can become dysplastic. risk of oesophageal cancer is higher
adenocarinoma>glandular cancer in oesophagus.
lifestyle management of GORD?
- weight loss to dec obesity
- avoid trigger foods
- eat smaller meals
- don’t eat them sleep
- sit up in bed
- reduce alcohol and caffeine
- stop smoking (less evidence)
drug treatment of GORD
proton pump inhibitors
> provide relief from symptoms
> heal the inflammation
H2 receptor antagonists (blockers) > added if PPI not effective
surgical intervention of GORD name and describe
fundoplication > funds of stomach wrapped round lower oesophagus to help with sphincter mechanism
what is gastritis?
symptoms?
inflammation of stomach mucosa
symptoms: pain nausaea vomiting haemorrhage
endoscopic appearance- angry and inflamed
acute vs chronic gastritis causes
acute
- heavy use of NSAIDs
- alcohol
- chaemotherapy
- bile reflux
chronic
- H pylori bacteria
- autoimmune
acute can go onto be chronic
what is bile reflux
bile delivered to duodenum usually but if it goes back into stomach through pyloric sphincter , causes chemical injury to stomach
pathological changes seen in acute gastritis
- epithelial damage
- epithelial hyperplasia
- vasodilation ‘angry looking’
- neutrophil response
pathological changes in chronic gastritis/ longlasting stimulus
- lymphocyte/plasma cells found in lamina propria
- glandular atrophy
- fibrosis of lamina propria
- metaplastic changes
describe autoimmune chronic gastritis
antibodies to parietal cells >lose parietal cells > dec acid production > dec intrinsic factor > dec absorption of B12
-atrophy of body of stomach> renders defence system less effective
where is B12 absorbed with intrinsic factor
ileum
complications of AUTOimmune chronic gastritis
- megaloblastic anaemia (lack of B12 disturbs DNA synthesis)
- neurological symptoms
- anorexia (loss of appetite)
- glossitis = inflammation of tongue
describe Helicobacter Pylori bacteria
- helix shape
- gram negative
- microaerophilic (needs some o2 but not lots> stomach ideal condition)
- enters GI tract vua faeco oral or oral oral route.
what are the important features of Helicobacter Pylori and how do these aid its survival?
- flagella > can move and advance
- chemotaxis > find areas of lower acidity in stomach (e.g. surface of epithelia under mucosal layer)
- adhesins> adhere to epithelial lining so aren’t washed away can resist peristalsis
- own urease enzyme > converts urea into CO2 and NH4
> de-acidifyies outer membrane creating an env to thrive and survive
how does Helicobacter pylori cause gastritis?
- produced NH4> damage stomach epithelia
- produce cytotoxin associated gene A (CAG A) causes inflammatory response IL8 of stomach epithelia > inc stomach cancer risk
-produce Vacuolating toxin A (Vac A)> inc paracellular permeability
>toxic to stomach epithelial cells
compare the presence of H pylori in antrum of stomach vs in body of stomach
antrum:
- overactivity of gastrin > produce more acid
> makes chyme more acidic. damage duodenum. change in duodenum epithelial cells > colonisation of H pylori in duodenum > ulcers
body: /fundus
cause atrophy and inc cancer risk
*when in both places usually asymptomatic
what investigations are used to determine diagnosis of Helicobacter pylori?
Urease breath test-
Ingest C13 isotope of gastric urea> if H. P present, broken down into NH4 and CO2> C13 isotope detected when exhale.
Stool antigen test
endoscopy with biopsy
how do we eradicate helicobacter pylori colony?
drugs:
proton pump inhibitor AND 2x Abx (usually Clarithromycin and Metronidazole)
side effects: diarrhoea, nausea
7 days
> check success with urease breath test
