s4. gastric diseases Flashcards
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
what is peptic ulcer disease?
defect in the gastric or duodenal mucosa that extends through the muscular mucosa
common sites of peptic ulcer
First part of duodenum
lesser curve of stomach
- can occur anywhere in stomach tho
describe the layers beyond epithelia (that ulceration could pass through)
epithelia lamina propria muscular mucosa sub mucosa muscular externa
compare gastric and duodenal ulcers
gastric: less common 1:3 ratio incidence increases with age (only up until 35 with duodenal) social class bias (none with duo) blood group A normal/low acid levels
duodenal
blood group O
normal/high acid levels
almost 100% due to Helicobacter pylori
how do NSAIDS affect stomach defences?
DECREASE prostaglandins so less stimulation of blood flow
risk factors for peptic ulcer disease
- H. Pylori
- NSAIDS
- smoking > contributes to relapse of ulcer
- massive physiological stress e.g. extensive burns
difference between acute and chronic ulcers
acute
- develop as part of acute gastritis
> transient. healing.
chronic
- occur at mucosal junctions e.g. where Antrim meets body/ small int.
implications of ulceration through muscular externae
muscularis externae replaced by scar tissue
> can narrow stomach lumen (pyloric stenosis)
> excessive vomitting
perforate gut wall and cause leakage into peritoneal cavity > peritonitis
/ erosion into adjacent structures e.g. liver/ pancreas
complications if duodenal ulcer erodes posteriorly?
erosion into blood vessels - Gastroduodenal artery or splenic artery
- stomach/duodenum fill with blood
> haematemesis (vom blood)
> melana (black tarry stools)
what is melana
indicative of slow upper GI bleed
haem component oxidised when pass through GI tract
> produce black tarry stools
symptoms of peptic ulcer disease PUD
- Epigastric pain, back pain > following meals
- pain at night > duodenal ulcers
- haematemesis
- melana
- early satiety > from scar tissue. can’t expand as much so get full quicker
- weight loss
how does pain present differently following a meal with duodenal and gastric ulcers?
duodenal:
food initially makes it better as LOS contracts
> transiently
> pain when chyme leaves
gastric
food makes it immediately worse
management of PUD when no active bleeding
- investigate H. pylori presence
- eradicate H. pylori via PPI, 2x abx (usually Clarithromycin and Metronidazole)
> promotes ulcer healing
if no H. pylori > stop taking exacerbating medications e.g. NSAIDs
management of PUD when ACTIVE bleeding
endoscopic treatments
- adrenaline injected at base of ulcer and cautery
if perforated > open surgery
