5. Gastric Diseases Flashcards
What anti-reflux mechanisms prevent reflux of gastric acid into the lower oesophagus?
Lower oesophageal sphincter, oesophagus enters the stomach in the abdominal cavity, pressure in the abdominal cavity is higher than that of the thoracic cavity, right crus of the diaphragm acts as a sling around the lower oesophagus.
How is the normal amount of acid reflux dealt with?
Secondary peristaltic waves, gravity, and salivary bicarbonate.
When do clinical features of gastro-oesophageal reflux disease (GORD) occur?
When antireflux mechanisms fail and there is prolonged contact of gastric juices with lower oesophageal mucosa.
What is the key clinical feature of GORD?
Dyspepsia (heartburn).
When is dyspepsia from GORD made worse?
On lying down, bending over, and drinking hot drinks.
How is GORD investigated and diagnosed?
Usually made based on clinical features alone and there is no need to investigate unless alarming symptoms or hiatus hernia is suspected.
How is GORD managed?
Lifestyle adaptations - lose weight, stop smoking, reduce alcohol consumption, reduce consumption of food groups that aggravate it. Medication - simple antacids, raft antacids, PPIs, H2 antagonists.
How do PPIs act to manage GORD?
Reduce acid secretion by parietal cells.
How do H2 antagonists act to manage GORD?
Block H2 receptors which reduces acid secretion.
What is Barrett’s oesophagus?
Metaplastic change of lower oesophageal epithelium from normal stratified squamous epithelium to simple columnar epithelium (normally found in lower GI tract).
What is a peptic ulcer?
Break in the superficial epithelial cells penetrating down into the muscularis mucosa of the stomach or duodenum.
Where are duodenal ulcers most commonly found?
In the duodenal cap.
Where are gastric ulcers most commonly found?
In the lesser curve of the stomach.
What causes peptic ulcers in the developed world?
The use of NSAIDs primarily. These inhibit production of prostaglandins and so prevent production of protective unstirred layer.
How prevalent are duodenal ulcers in the adult population?
10% of the adult population have them.
How much more common are duodenal ulcers than gastric ulcers?
2-3 times as common.
How is prevalence of peptic ulcers changing in different age groups?
Younger people - prevalence is falling, especially in men.
Older people - prevalence is increasing, especially in women.
How has prevalence of NSAID-associated duodenal ulcers changed?
Increased in developed countries.
How has prevalence of H pylori-associated ulceration changed in developed countries?
Decreased.
What are the clinical features of peptic ulcers?
Recurrent, burning epigastric pain. Nausea, vomiting. Or asymptomatic.
What is a clinical feature of peptic ulcers specific to gastric ulcers?
Weight loss and anorexia.
When is pain worse with duodenal ulcers?
Worse at night and when hungry.
How is duodenal ulcer pain relieved?
With eating. Also with the use of antacids.
What does persistent, sever pain from peptic ulcers suggest?
Penetration of ulcer into other organs.
What does back pain from peptic ulcers suggest?
Penetrating posterior ulcer.
How are peptic ulcers investigated?
investigate H pylori infection. In older patients or those with alarming symptoms, endoscopy to exclude cancer.
How are ulcers due to H pylori infection managed?
Triple therapy - proton pump inhibitory (omeprazole), antibiotics (clarithromycin or amoxillin), and H2 antagonist (cimetidine).
What is an example of a proton pump inhibitor?
Omeprazole.
What is an example of an H2 antagonist?
Cimetidine.
What are some complications of peptic ulcer disease?
Haemorrhage of blood vessel which ulcer has eroded, perforation of the ulcer, gastric outlet obstruction.
How does peptic ulcer eroding into a blood vessel and causing haemorrhage present?
With haematemesis and melena.
Which peptic ulcer type more commonly has perforation?
Duodenal ulcers.
Where do duodenal ulcers commonly perforate?
Into the peritoneal cavity.
Why does gastric outlet obstruction occur?
Active ulcer with oedema or from healing of an ulcer with associated fibrosis.
How does gastric outlet obstruction present?
Vomiting without pain.
What type of bacteria is helicobacter pylori?
Gram negative, helical, aerobic, urease producing bacteria.
How does H pylori survive in the acidic conditions of the stomach?
It produces urease from ammonia so neutralises the local acidic environment, allowing it to survive.
Where does H pylori colonise?
In the mucous layer of the gastric epithelium or just beneath.
How does H pylori damage the gastric epithelia?
Through enzymes released and through induction of apoptosis. Also inflammatory response to infection - inflammatory cells and mediators.
How is H pylori infection diagnosed?
IgG detection in serum. Also 13C-urea breath test. Gastric sample from endoscopy - then use histology and culture.
How effective is the triple therapy treatment of H pylori?
It eradicates infection in 90% of patients.
How long is the treatment for H pylori?
7-14 days.
Why do some patients not complete the 14 day course of treating H pylori?
The side-effects put them off.
How does H pylori cause gastritis?
Usual effect of infection, normally asymptomatic.
What does chronic gastritis cause?
Hypergastrinaemia from gastrin release from astral G cells. The increased acid production is normally asymptomatic but can lead to duodenal ulcers.
What can chronic gastritis lead to?
Duodenal ulceration.
What factors may contribute to duodenal ulceration?
Genetic predisposition, bacterial virulence, increased gastrin secretion, and smoking.
Gastric ulcers are associated with gastritis affecting which parts of the stomach?
The body and antrum.
What can gastritis in the body and antrum cause?
Gastric ulcers and parietal cell loss so reduced acid production.
How does H pylori cause gastric ulcers?
Reduced gastric mucosal resistance due to cytokine production as a result of infection.
What gastric diseases can H pylori cause?
Gastritis, peptic ulcer disease, and gastric cancer.
How are peptic ulcers treated?
If from H pylori, triple therapy to treat. If taking NSAIDs, stop or review and use alternative that have low risks or use prophylactic PPI as well as the NSAID.
Which two drug types can reduce gastric acid secretion?
Histamine at H2 receptors and proton pump inhibitors.
How can histamine reduce gastric acid secretion?
Removes amplification of gastrin and ACh signals to trigger more gastrin release.
How can proton pump inhibitors reduce gastric acid secretion?
Prevent H+ ions being pumped into the parietal cell canaliculi.
