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Medicine (Year 5) > Gastroenterology (Oesophagus and Stomach) > Flashcards

Gastroenterology (Oesophagus and Stomach) Flashcards

1
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A
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2
Q

Barretts oesophagus

A

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.

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3
Q

causes of Barrets

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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
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4
Q

RF for Barretts

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Risk Factors

  • Acid reflux or GORD
  • Increased age
  • Caucasian ethnicity
  • Male sex
  • Obesity
  • Smoking
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5
Q

presentation of Barretts oesophagus

A

Barrett’s oesophagus itself does not tend to have any particular symptoms, however, patients often present with symptoms associated with GORD:

  • Dyspepsia
  • Regurgitation
  • Dysphagia
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6
Q

Investigations for barretts

A

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

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7
Q

management of Barretts

A

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

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8
Q

complications of Barretts

A

Complications

  • Dysplasia and oesophageal adenocarcinoma (60 times greater chance)
  • Oesophageal structures
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9
Q

Mallory-Weiss syndrome (MWS)

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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.

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10
Q

RF for MW syndrome

A

Risk factors for MWS include conditions predisposing to retching and vomiting:

  • Excessive alcohol consumption
  • Gastroenteritis
  • Hyperemesis gravidarum (most common cause)
  • Bulimia nervosa
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11
Q

Presentation of Mallory Weiss tear

A
  • Haematemesis following retching or vomiting.
  • Light-headedness or dizziness – due to bleeding reducing blood pressure
  • Orthostatic hypotension
  • Melaena
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12
Q

MW tear vs Oesophageal varices

A

Oesophageal varices

Patients may have a history or signs of chronic liver disease such as jaundice, ascites, splenomegaly etc.

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13
Q

investigations for MW tear

A

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

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14
Q

management of MW tear

A
  • 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.
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15
Q

Boerhaave syndrome

A

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.

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16
Q

RF for Boerhaave Syndrome

A

Risk factors include conditions predisposing to retching and vomiting:

  • Excessive alcohol consumption
  • Gastroenteritis
  • Hyperemesis gravidarum
  • Bulimia nervosa
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17
Q

Presentation of Boerhaave syndrome

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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
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18
Q

investigations for boerhaave syndrome

A

Chest x-ray:
* May show a widened mediastinum
May show free mediastinal or peritoneal air

CT scan with contrast swallow:
* The diagnostic test

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19
Q

management of Boerhaave syndrome

A

Treatment involves surgery with antibiotics to prevent sepsis. Even with early intervention, the mortality rate is as high as 25%.

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20
Q

Achalasia

A

describes the failure of the smooth muscle fibres of the lower oesophageal to relax, leading to the closure of the lower oesophageal sphincter (LOS).

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21
Q

types of achalasia

A

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
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22
Q

presentation of achalasia

A

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
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23
Q

investigations for achalasia

A

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
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24
Q

management of achalasia

A

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

25
Q

Complications of achalasia

A
  • Aspiration pneumonia
  • Oesophageal squamous cell carcinoma
  • GORD may develop following treatment
  • This is because treatment is aimed at relaxing the LOS, allowing acid reflux
26
Q

Pharageal pouch

A

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.

27
Q

presentation of pharyngeal pouch

A

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
28
Q

investigations for oesophageal pouch

A

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

29
Q

oesophageal varices

A
  • 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.
30
Q

pathophysiology of Oesophageal varices

A

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.

31
Q

presentation of oesophageal varices

A

Patients typically have features of an upper gastrointestinal bleed, particularly vomiting fresh blood and passing black stool (melaena).

32
Q

management of acute variceal haemorrhage

A
  • 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
33
Q

prophylaxis of oesophageal varices

A

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
34
Q

most common cause of dyspepsia

A
  • Gastro-oesophageal reflux disease
  • Peptic ulcer disease
  • Functional dyspepsia

Other causes include:

  • Barrett’s oesophagus
  • Upper gastrointestinal malignancy
35
Q

dyspepsia presentation

A
  • Epigastric pain or discomfort
  • Bloating
  • Heartburn
  • Feeling full earlier when eating
  • Nausea and vomiting
  • Loss of appetite
36
Q

red flags for dyspepsia

A

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
37
Q

dyspepsia management

A

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:

38
Q

H. Pylori test and treat

A

Test: Carbon-13 urea breath test

Treat: Omeprazole, metronizaole ad amoxicillin

39
Q

dyspepsia student advice

A
  • 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
40
Q

RF for GORD

A
  • Smoking and alcohol
  • Obesity
  • Pregnancy
  • Hiatus hernia
  • Family history
  • Stress and anxiety
  • Trigger foods:
  • For example, chocolate and fatty foods delay gastric emptying
41
Q

GORD presentation

A

The key features of GORD are heartburn and regurgitation, typically after meals. Other associated features may be:

  • Cough
  • Sore throat
  • Asthma
  • Tooth erosion
42
Q

GORD red flags

A

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
43
Q

GORD- who should get an OGD

A
  • 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
44
Q

management of: endoscopically negative reflux disease

A

1st-line: full-dose proton pump inhibitor (PPI, such as omeprazole or lansoprazole) for 1 month

45
Q

endoscopically proven oesophagitis

A
  • 1st-line: full-dose PPI for 8 weeks
  • Offer full-dose PPI long-term as maintenance treatment
46
Q

peptic ulcers

A
  • gastric and duodenal uclers
  • can lead to upepr GU bleeds or perforation
47
Q

RF for peptic ulcers

A

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

48
Q

Presentation: Uncomplicated peptic ulcer

A

Patients present with dyspepsia.

49
Q

when do duodenal ulcers cause pain in relation to eating food

A

Duodenal ulcers tend to have epigastric pain that is relieved when eating

50
Q

when do gastric ulcers cause pain in relation to eating food

A

Gastric ulcers tent to have epigastric pain that is worse when eating

51
Q

presentation of perforated peptic ulcer

A

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.

52
Q

investigation for uncomplicated peptic ulcer

A

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

53
Q

investigation for Bleeding peptic ulcer

A

Immediate same-day referral for endoscopy:
* Endoscopy is the gold-standard test for peptic ulcer disease and can also be used in treatment

54
Q

investigations for Perforated peptic ulcer

A
  • Immediate admission to hospital
  • Erect chest x-ray:
  • May show pneumoperitoneum – free air under the diaphragm
55
Q

complications of peptic ulcer

A
  • upper GI bleed
  • perforation- can perforate into gastroduodenal artery
56
Q

Zollinger-Ellison syndrome (ZES)

A
  • 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.
57
Q

presentation of ZES

A

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
58
Q

Investigations for ZES

A

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

59
Q

management of ZES

A

Management involves the use of proton pump inhibitors (e.g. omeprazole) and H2-receptor antagonists to suppress acid secretion and surgical resection.

Medicine (Year 5) (34 decks)

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