Gastroenterology Flashcards
What is dyspepsia
Symptoms including:
Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice
Plan investigating dyspepsia
- H.pylori urea breath test/stool antigen test
- Immediate endoscopy if evidence eg GI bleed (melena, coffee ground vomit)
- 2ww referral for endoscopy if concerning features of malignancy or over 55
referral criteria 2ww upper gastrointestinal endoscopy
Urgent, direct access upper gastrointestinal endoscopy (2ww) to assess for oesophageal cancer in people:
with dysphagia or
aged 55 and over with weight loss and any of the following:
upper abdominal pain
reflux
Dyspepsia
Non-urgent if over 55 and:
treatment‑resistant dyspepsia or
upper abdominal pain with low haemoglobin levels or
raised platelet count
management of undiagnosed dyspepsia
- Lifestyle advice
- Acid neutralising medications
1. Full dose PPI for 4 weeks
2. If symptoms return after treatment, step down to lowest dose that controls dyspepsia
3. H2 receptor antagonist eg Ranitidine
4. Laparoscopic fundoplication
Pathophysiology of GORD
The oesophagus has a squamous epithelial lining making it more sensitive to the effects of stomach acid. The stomach has a columnar epithelial lining that is more protected against stomach acid.
causes:
- dysfunction of lower esophageal sphincter (LES)
- hiatus hernia
- delayed gastric emptying
Typical history of GORD
PC: heartburn, regurgitation, retrosternal or epigastric pain, bloating, nocturnal cough, hoarse voice
SHx: obesity, high caffeine intake, smoking, alcohol, meal soon before bed
Typical history peptic ulcer
PC: Epigastric discomfort or pain, Nausea and vomiting, Dyspepsia, Bleeding causing haematemesis, “coffee ground” vomiting and melaena, Iron deficiency anaemia (due to constant bleeding), eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers
MHx:
DHx: NSAIDs, steroids
FHx:
SHx: Stress, Alcohol, Caffeine, Smoking, Spicy foods
Pathophysiology h.pylori
H. pylori is a gram negative aerobic bacteria. It damages the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it creates in the mucosa exposes the epithelial cells underneath to acid.
It also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells. Other chemicals produced by the bacteria also damage the epithelial lining.
Plan investigating ?peptic ulcer
- Endoscopy with rapid urease test (CLO test) to check for H. pylori, biopsy ?ulcer to exclude malignancy
Management of h.pylori
triple therapy with a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.
management of peptic ulcer not caused by h.pylori
Stop/reduce causative agent
Full course PPIs (4 or 8 weeks)
H2 receptor antagonist Ranitidine
Can monitor healing using endoscopy
complications of peptic ulcers?
- Bleeding from the ulcer is a common and potentially life threatening complication.
- Perforation resulting in an “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).
- Scarring and strictures of the muscle and mucosa. This can lead to a narrowing of the pylorus (the exit of the stomach) causing difficulty in emptying the stomach contents. This is known as pyloric stenosis. This presents with upper abdominal pain, distention, nausea and vomiting, particularly after eating.
Pathophysiology hepatic encephalopathy
Hepatic encephalopathy may be seen in liver disease of any cause. The aetiology is not fully understood but is thought to include excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut.
pathophysiology barrets oesophagus
risk % of developung cancer?
chronic reflux → metaplasia from a squamous to a columnar epithelium
A “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus (3-5% lifetime risk with Barretts).
Plan barrets oesophagus
Plan
Investigation: regular endoscopy
Management:
PPI
Ablation therapy if progressed to low grade/high grade dysplasia
ddx dyspepsia
GORD
peptic ulcer: gastric or duodenal, h.pylori or drug related or lifestyle or idiopathic
oesopahgeal cancer
ddx upper GI bleeding:
Oesophageal varices :may have ascites, jaundice
Mallory-Weiss tear, which is a tear of the oesophageal mucous membrane
Ulcers of the stomach or duodenum :may have dyspepsia, epigastric pain
Oesophagitis
Cancers of the stomach or duodenum
Presenting complaints upper GI bleeding
Haematemesis
Coffee ground vomit
Melena (tar like stool (digested blood))
Haemodynamic instability (low bp, tachycardia, signs of shock)
initial management ?upper GI bleed
A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 large bore cannula)
T – Transfuse
E – Endoscopy (arrange urgent endoscopy within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)
assessment tool ?upper GI bleed
Glasgow-blatchford score
Drop in Hb
Rise in urea
Blood pressure
Heart rate
Melaena
Syncopy
Score >0 means high risk
Plan invetsigation and management ?upper GI bleed
Invetigation
1. Bloods
Haemoglobin (FBC)
Urea (U&Es)
Coagulation (INR, FBC for platelets)
Liver disease (LFTs)
Crossmatch 2 units of blood
2. Endoscopy with treatment
Management
1. stabilise ie transfusion
2. Endoscopy with banding (varices), cauterization (bleeding vessel)
3. If oesophageal varices: prophylactic broad spectrum abx and Terlipressin
HoPC upper gi bleed oesophageal varices
Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.
HoPC upper GI bleed oesophagitis
Small volume of fresh blood, often streaking vomit. Malena rare. Often ceases spontaneously. Usually history of antecedent GORD type symptoms.
