Gastric Disease Flashcards
What is dyspepsia?
- A complex of upper GI tract symptoms which are present for 4+ weeks
- including upper abdominal discomfort, heartburn, acid reflux, N+V
Symptoms of gastro-oesophageal reflux disease
- heart burn
- acidic taste > dental erosion
- cough
- asymptomatic
What are the risk factors of gastro-oesophageal reflux disease?
increased intra abdominal pressure
- obesity
- pregnancy
- lower oesophageal dysfunction
- hiatus hernia
- delayed gastric emptying
What is a hiatus hernia?
Lower oesophageal sphincter herniates through diaphragm into thorax
What are the complications of gastric oesophageal reflux disease?
- oesophagitis
- ulceration
- haemorrhage > anaemia
- strictures > dysphagia
- metaplastic changes > Barrett’s oesophagus
What is gastric oesophageal reflux disease?
Reflux of stomach contents into the oesophagus
What is Barrett’s oesophagus?
- Reversible change of stratified squamous epithelia into gastric columnar
- due to repeated exposure of gastric contents
. - risk of adenocarcinoma due to increased risk of dysplasia
Lifestyle management of gastric oesophageal reflux disease
- weight loss
- avoid trigger foods
- eat smaller meals
- don’t eat right before sleep
- decrease alcohol, caffeine (+smoking)
Drug management of gastric oesophageal reflux disease
- proton pump inhibitors > symptom relief + healing inflammation
- H2 receptor antagonists
Surgical management of gastric oesophageal reflux disease
- Fundoplication
- fundus of stomach wrapped around oesophagus
What is gastritis?
- Inflammation of stomach mucosa
Symptoms of gastritis
Pain
Nausea
Vomiting
Haemorrhage
Causes of acute gastritis
NSAIDs
Excessive alcohol
Chemotherapy
Bile reflux
Causes of chronic gastritis
Infection of H pylori
Autoimmune
Changes in acute gastritis
- epithelial damage
- epithelial hyperplasia
- vasodilation ’angry looking’
- neutrophil response
Changes in chronic gastritis
- lymphocyte response
- glandular atrophy
- fibrotic changes
Outline autoimmune chronic gastritis
- antibodies damage parietal cells
- decreased acid production
- decreased intrinsic factor > reduced B12 absorption in terminal ileum
- atrophy of stomach body > gastritis
Symptoms of autoimmune gastritis
- Megaloblastic anaemia
- neurological symptoms
- anorexia + loss of appetite
- glossitis
Why does Helicobacter pylori cause gastritis?
- H pylori produces ammonia > damage to cells
- cytotoxin associated gene A > expresses protein into stomach epithelia > stimulates interleukin 8 > inflammation > ^ stomach cancer risk
- vacuolating toxin A: protein which increases paracellular permeability + toxin
- secretes mucinases > damages mucus layer
Describe Helicobacter pylori
- gram negative bacteria
- helix shape
- microaerophilic > needs some O2
- faecal-oral / oral-oral
features: - produces urease > produces ammonia from urea
- flagellae for movement
- chemotaxis to find area of lower acididty
- adhesions > adhere to gastric epithelium > resists peristalsis
Consequence of H pylori in stomach antrum
- stimulates G cells to release gastrin
- ^ number of parietal cells + acid secretion
- ^ pH of chyme > damages duodenum > ulceration
Consequences of H pylori in stomach body or fundus
- atrophy of parietal cells
- increases risk of stomach cancer
Diagnosis of H pylori
- urease breath test
- stool antigen test
- endoscopy with biopsy
Outline urease breath test for H pylori
- patient injects urea enriched with carbon 13
- if H pylori is present, urea > CO2 + ammonia
- C13 isotope can be detected in CO2 on expiration
Treatment for H pylori
Proton pump inhibitor + 2 antibiotics
e.g. Lansoprazole + clarithromycin + metronidazole/amoxicillin
- check if successful with urease breath test
What is peptic ulcer disease?
Defect in the gastric or duodenal mucosa that extends through the musclaris mucosa
Where does peptic ulcer disease occur in the stomach?
Lesser curve (most common)
Antrum
Compare gastric vs duodenal ulcers:
- incidence
- age
- social class
- blood group
- acid levels
- H pylori
Gastric
- incidence: v
- age: increases with age
- social class: higher in lower
- blood group: A
- acid levels: normal/low
- H pylori: 70%
Duodenal
- incidence: x3 as common as gastric
- age: increases with age up to 35
- social class: X
- blood group: O
- acid levels: normal/high
- H pylori: almost 100%
Risk factors for peptic ulcer disease
- H pylori
- NSAIDS > decrease prostaglandin synthesis
- smoking > contributes to relapse of ulcer
- massive physiological stress
Where do chronic ulcers normally occur?
Mucosal junctions
What is malaena?
- Black stool due to slow upper GI tract bleed
- Haem component is oxidised
Symptoms of peptic ulcer disease
- epigastric pain: burning/gnawing pain
- pain at night
- haematemesis
- malaena
- early satiety due to scar tissue
- weight loss
What is haematemesis?
Vomiting blood
Management of peptic ulcer disease with no active bleeding
H pylori present
- eradicate H pylori > proton pump inhibitor + 2 antibiotics
H pylori absent
- stop NSAIDs
Management of peptic ulcer disease with active bleeding
- adrenaline injection
- cauterisation
- test for H pylori after stopping bleeding
Where are peptic ulcers most likely to occur?
Duodenum
What blood vessel can be damaged by peptic ulcer disease and cause internal bleeding?
Gastroduodenal artery
What part of the stomach is most prone to ulceration?
Lesser curve
How does H pylori produce ammonia?
- produces urease
. - catalyses urea +CO2 > ammonia + CO2
How does H pylori resists peristalsis?
Forms adhesions to gastric epithelium
