Gastroenterology (Oesophagus and Stomach) Flashcards
Barretts oesophagus
METAPLASIA of the lower oesophageal mucosa
- stratified squamous epithelium -> coumnar epithelium with goblet cells present
Barrett’s oesophagus is considered a pre-malignantcondition as the normal cells may become dysplastic, leading to oesophageal adenocarcinoma.
causes of Barrets
consequence of chronic gastro-oesophageal reflux disease (GORD).
- Chronic inflammation due to stomach acid damages lower oesophageal cells.
- Cells that are more resistant to inflammation displace normal squamous cells.
- The degree of GORD and degree of metaplasia do not seem to correlate, therefore, it is difficult to predict who will go on to develop Barrett’s oesophagus
RF for Barretts
Risk Factors
- Acid reflux or GORD
- Increased age
- Caucasian ethnicity
- Male sex
- Obesity
- Smoking
presentation of Barretts oesophagus
Barrett’s oesophagus itself does not tend to have any particular symptoms, however, patients often present with symptoms associated with GORD:
- Dyspepsia
- Regurgitation
- Dysphagia
Investigations for barretts
Upper gastrointestinal endoscopy and biopsy:
* Endoscopy may show darker epithelium proximal to the gastro-oesophageal junction
* A biopsy is essential to confirm the diagnosis and degree of metaplasia/dysplasia
management of Barretts
Lifestyle changes:
* Losing weight, reducing alcohol intake, stopping smoking etc.
Proton-pump inhibitors:
* To manage co-existing GORD
Endoscopic surveillance:
* Patients with metaplasia and no dysplasia are offered endoscopic surveillance every 3-5 years
* Biopsies are also taken with each endoscopy
If dysplasia of any degree is present:
- Radiofrequency ablation or endoscopic mucosal resection is offered
complications of Barretts
Complications
- Dysplasia and oesophageal adenocarcinoma (60 times greater chance)
- Oesophageal structures
Mallory-Weiss syndrome (MWS)
describes non-variceal bleeding due to mucosal tearing at the gastro-oesophageal junction. The tearing involves the mucosa and submucosa, but not the muscular layer. It is caused by severe vomiting and retching, and many patients present with haematemesis. MWS is generally self-limiting in around 80% of patients.
RF for MW syndrome
Risk factors for MWS include conditions predisposing to retching and vomiting:
- Excessive alcohol consumption
- Gastroenteritis
- Hyperemesis gravidarum (most common cause)
- Bulimia nervosa
Presentation of Mallory Weiss tear
- Haematemesis following retching or vomiting.
- Light-headedness or dizziness – due to bleeding reducing blood pressure
- Orthostatic hypotension
- Melaena
MW tear vs Oesophageal varices
Oesophageal varices
Patients may have a history or signs of chronic liver disease such as jaundice, ascites, splenomegaly etc.
investigations for MW tear
Glasgow-Blatchford score:
* Guides whether the patient is managed as an outpatient or not
Upper gastrointestinal (GI) endoscopy:
* Urgently after resuscitation if the patient is unstable with upper GI bleeding
* Within 24 hours of admission for all other patients
Rockall score after endoscopy:
* Determines risk of re-bleeding
management of MW tear
- Initial action: gain IV access. Fluid resuscitation if haemodynamically compromised (followed by blood)
- Prescription: there is no evidence for giving PPI before the endoscopy, but this may be indicated post-endoscopy
- Definitive treatment: Discuss with the gastroenterology team. Dependent on the pathology found there are various different endoscopic treatments possible. If the bleeding cannot be stopped by endoscopy, radiological embolization or surgery may be possible. The Endoscopist will advise on the need for any medications (such as PPI to treat ulcers) after the endoscopy.
Boerhaave syndrome
describes the rupture of the oesophagus due to vomiting. Oesophageal ruptures may also occur following endoscopy or surgery in adjacent areas. Unlike Mallory-Weiss syndrome, in Boerhaave’s syndrome, the mucosa, submucosa, and muscular layer of the oesophagus are affected. The rupture generally occurs at the lower 1/3 of the oesophagus.
RF for Boerhaave Syndrome
Risk factors include conditions predisposing to retching and vomiting:
- Excessive alcohol consumption
- Gastroenteritis
- Hyperemesis gravidarum
- Bulimia nervosa
Presentation of Boerhaave syndrome
Patients classically present with severe retrosternal/epigastric pain following retching and vomiting. The pain may be confused with cardiac causes such as myocardial infarction. Other features may be:
- Subcutaneous emphysema – crepitations under the skin due to free gas
- Signs of shock – tachycardia, tachypnoea
- Cyanosis
investigations for boerhaave syndrome
Chest x-ray:
* May show a widened mediastinum
May show free mediastinal or peritoneal air
CT scan with contrast swallow:
* The diagnostic test
management of Boerhaave syndrome
Treatment involves surgery with antibiotics to prevent sepsis. Even with early intervention, the mortality rate is as high as 25%.
Achalasia
describes the failure of the smooth muscle fibres of the lower oesophageal to relax, leading to the closure of the lower oesophageal sphincter (LOS).
types of achalasia
Primary achalasia occurs due to inflammation and destruction of the Auerbach plexus which consists of inhibitory neurones that ordinarily promote LOS relaxation.
This is similar to Hirschsprung’s disease as they both describe aganglionic segments in the gut, however, primary achalasia differs as it is acquired, not congenital.
Achalasia can also occur secondary to other conditions such as:
- Infection (e.g. Chagas disease)
- Autoimmunity
- Oesophageal cancer
presentation of achalasia
Dysphagia is a red-flag symptom that always raises suspicion of malignancy.
Achalasia cannot be diagnosed based on clinical features alone.
- Dysphagia – the main presenting complaint: This often tends to be to both food and drink from the start
- Regurgitation
- Heartburn
investigations for achalasia
Upper gastrointestinal endoscopy:
- The first-line investigation to rule out malignancy
Barium swallow:
- Shows a dilated oesophagus that narrows down into a bird-beak-like narrowing
Oesophageal manometry:
- The gold-standard test to diagnose achalasia
- Shows incomplete LOS relaxation and increased resting pressure
management of achalasia
First line: pneumatic dilation
* Can be done on an outpatient basis with conscious sedation
* An inflated balloon stretches the LOS and tears its muscle fibres
If recurrent/persisting symptoms:
* laparoscopic Heller cardiomyotomy- thicker outer muscle tissue is cut
For patients that are unsuitable for surgery:
* Isosorbide dinitrate
* Nifedipine or verapamil
* Botulinum toxin A injections
Complications of achalasia
- Aspiration pneumonia
- Oesophageal squamous cell carcinoma
- GORD may develop following treatment
- This is because treatment is aimed at relaxing the LOS, allowing acid reflux
Pharageal pouch
Also known as Zenker’s diverticulum, a pharyngeal pouch is a diverticulum (outpouching) of the pharyngeal mucosa through Killian’s dehiscence, which is superior to the cricopharyngeus muscle and inferior to the thyropharyngeus muscle.
Killian’s dehiscence is where there is least resistance and it is thought that pharyngeal pouches develop due to herniation secondary to increased pressures in the distal pharynx. These pressure increases can occur due to uncoordinated swallowing and impaired relaxation of the surrounding muscles.
presentation of pharyngeal pouch
The main presenting complaint is dysphagia. As always, dysphagia is a red-flag symptom that always raises suspicion of malignancy. Other features may be:
- Regurgitation
- Aspiration
- Neck swelling:
- This tends to gurgle when palpated
- Halitosis
- Due to food decaying in the pouch
- Chronic cough
investigations for oesophageal pouch
Oesophagogastroduodenoscopy:
* To rule out malignancy
* There may be a risk of pouch perforation
Barium swallow:
* The gold-standard test
* Shows a pool of contrast within the pouch
* Serial x-rays are taken and since the barium pools in the pouch, it remains in situ between each film
oesophageal varices
- Oesophageal varices are dilated submucosal veins in the oesophagus and develop secondary to portal hypertension which commonly occurs due to liver cirrhosis.
- Varices are abnormally dilated blood vessels.
pathophysiology of Oesophageal varices
The portal vein drains blood from the gastrointestinal tract, gallbladder, pancreas, and spleen to the liver. Liver cirrhosis leads to increased resistance to blood flow which leads to hypertension in the portal vein (portal hypertension). This then leads to increased pressure in the veins draining into the portal vein, including those from the oesophagus.
It is important to note that varices can form in other parts of the body, particularly the stomach, duodenum, and rectal.
presentation of oesophageal varices
Patients typically have features of an upper gastrointestinal bleed, particularly vomiting fresh blood and passing black stool (melaena).
management of acute variceal haemorrhage
- 1st-line: ABCDE approach, resuscitate, and correct any clotting abnormalities
- Terlipressin should be offered as soon as possible, along with prophylactic IV antibiotics then patients should have endoscopic treatment, which is typically via endoscopic band ligation
- If there is uncontrollable bleeding, a Sengstaken-Blakemore tube should be used
- If these measures fail, then consider a transjugular intrahepatic portosystemic shunt – this is generally very effective but can precipitate hepatic encephalopathy
prophylaxis of oesophageal varices
Prophylaxis
- If varices are small: non-selective beta-blockers (e.g. propranolol)
- If varices are medium/large: non-selective beta-blockers or endoscopic band ligation
most common cause of dyspepsia
- Gastro-oesophageal reflux disease
- Peptic ulcer disease
- Functional dyspepsia
Other causes include:
- Barrett’s oesophagus
- Upper gastrointestinal malignancy
dyspepsia presentation
- Epigastric pain or discomfort
- Bloating
- Heartburn
- Feeling full earlier when eating
- Nausea and vomiting
- Loss of appetite
red flags for dyspepsia
Alarm symptoms are features that are associated with underlying malignancy and warrant an urgent referral via a suspected cancer pathway to gastroenterology. These features can be remembered using VBAD:
- Recurrent vomiting
- Bleeding, such as melaena (black, tarry stools)
- Anaemia, abdominal mass, or unintended weight loss
- Dysphagia
dyspepsia management
Patients that do not meet the referral criteria are treated as follows:
1st-line:
- review medications and give lifestyle advice
- some drugs may be causing dyspepsia such as NSAIDs, steroids, nitrates, and bisphosphonates and should have their doses adjusted or stopped if possible
- This avoids unnecessary over-prescribing of treatment
2nd-line:
- trial full-dose proton pump inhibitor (PPI) for one month
- or test and treat for H. pylori which involves:
H. Pylori test and treat
Test: Carbon-13 urea breath test
Treat: Omeprazole, metronizaole ad amoxicillin
dyspepsia student advice
- Losing weight if patients are overweight or obese
- Avoid trigger foods if possible, typically fatty foods as they slow gastric emptying
- Eat smaller regular meals, with the last meal 3-4 hours before going to bed
- Stop smoking
- Reduce alcohol consumption
RF for GORD
- Smoking and alcohol
- Obesity
- Pregnancy
- Hiatus hernia
- Family history
- Stress and anxiety
- Trigger foods:
- For example, chocolate and fatty foods delay gastric emptying
GORD presentation
The key features of GORD are heartburn and regurgitation, typically after meals. Other associated features may be:
- Cough
- Sore throat
- Asthma
- Tooth erosion
GORD red flags
Red flags
Alarm symptoms are features that are associated with underlying malignancy and warrant an urgent referral via a suspected cancer pathway to gastroenterology. These features can be remembered using VBAD:
- Recurrent vomiting
- Bleeding, such as melaena (black, tarry stools)
- Anaemia, abdominal mass, or unintended weight loss
- Dysphagia
GORD- who should get an OGD
- Aged >55 years
- Symptoms lasting >4 weeks
- Symptoms persisting despite treatment
- Relapsing symptoms
- New symptoms that emerge during treatment
- Any of the aforementioned alarm symptoms
management of: endoscopically negative reflux disease
1st-line: full-dose proton pump inhibitor (PPI, such as omeprazole or lansoprazole) for 1 month
endoscopically proven oesophagitis
- 1st-line: full-dose PPI for 8 weeks
- Offer full-dose PPI long-term as maintenance treatment
peptic ulcers
- gastric and duodenal uclers
- can lead to upepr GU bleeds or perforation
RF for peptic ulcers
Presentation
Uncomplicated peptic ulcer
Patients present with dyspepsia. The nature of epigastric pain can help narrow down the likely diagnosis:
Duodenal ulcers tend to have epigastric pain that is relieved when eating
Gastric ulcers tent to have epigastric pain that is worse when eatingPresentation
Uncomplicated peptic ulcer
Patients present with dyspepsia. The nature of epigastric pain can help narrow down the likely diagnosis:
Duodenal ulcers tend to have epigastric pain that is relieved when eating
Gastric ulcers tent to have epigastric pain that is worse when eating- H. pylori (95% of duodenal ulcers and 80% of gastric ulcers)
- Drugs e.g. aspirin and NSAIDs
- Smoking
- Alcohol
- Stress and anziety
- Zollinger -Ellison
Presentation: Uncomplicated peptic ulcer
Patients present with dyspepsia.
when do duodenal ulcers cause pain in relation to eating food
Duodenal ulcers tend to have epigastric pain that is relieved when eating
when do gastric ulcers cause pain in relation to eating food
Gastric ulcers tent to have epigastric pain that is worse when eating
presentation of perforated peptic ulcer
Patients have an acute abdomen characterised by severe epigastric pain that may become more generalised. Features of peritonitis may be present such as rigidity and guarding.
investigation for uncomplicated peptic ulcer
Full blood count:
* To rule out iron-deficiency anaemia due to bleeding
H. pylori testing:
* The test of choice is a carbon-13 urea breath test
investigation for Bleeding peptic ulcer
Immediate same-day referral for endoscopy:
* Endoscopy is the gold-standard test for peptic ulcer disease and can also be used in treatment
investigations for Perforated peptic ulcer
- Immediate admission to hospital
- Erect chest x-ray:
- May show pneumoperitoneum – free air under the diaphragm
complications of peptic ulcer
- upper GI bleed
- perforation- can perforate into gastroduodenal artery
Zollinger-Ellison syndrome (ZES)
- is an endocrinopathy caused by gastrin-secreting tumours which cause the stomach to produce excess acid, leading to multiple and recurrent peptic ulcers.
- The tumours usually occur in the duodenum or pancreas. ZES is associated with multiple endocrine neoplasia type 1 (MEN 1) in around 30% of cases.
presentation of ZES
Patients present with recurrent and/or refractory peptic ulcers and ZES is often treated as simple peptic ulcers. Features include:
- Epigastric pain – due to peptic ulcers, often described as burning
- Gastro-oesophageal reflux disease
- Gastrointestinal bleeding
- Diarrhoea – peptic ulcer disease and diarrhoea suggests ZES
Investigations for ZES
Fasting serum gastrin:
* Used as initial screening and is increased due to tumour production
Secretin stimulation test:
* Secretin normally inhibits gastrin release, however, gastrinoma cells release gastrin in response to secretin
Upper gastrointestinal endoscopy:
* May identify peptic ulcers
Endoscopic ultrasound:
* May identify ulcers
Other tests
If ZES is confirmed, tests for MEN1 should be considered:
Serum calcium:
May be elevated
Serum parathyroid hormone (PTH):
May be elevated
Serum prolactin:
May be elevated
management of ZES
Management involves the use of proton pump inhibitors (e.g. omeprazole) and H2-receptor antagonists to suppress acid secretion and surgical resection.
