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Gwen - GI and General surgery > GI: Gastric ulceration and H. Pylori > Flashcards

GI: Gastric ulceration and H. Pylori Flashcards

1
Q

Differential of dyspepsia

A
  • Oesophagus
    • GORD
    • Oesophagitis
  • Stomach/duodenum
    • Peptic ulcer
    • Gastritis
    • Duodenitis
    • Gastric cancer
    • Hiatus hernia
  • Gall bladder
    • Gallstones
  • Non ulcer dyspepsia
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2
Q

What are risk factors for the development of gastric ulcers?

A
  • H. Pylori
  • NSAID use
  • Smoking
  • Reflux of duodenal contents
  • Delayed gastric emptying
  • Stress
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3
Q

What is a peptic ulcer?

A

Break in the lining of the GI tract, extending through to the muscular layer.

Includes: Gastric ulcer, Duodenal ulcer, NSAID ulcer

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4
Q

What is the difference between an ulcer and an erosion?

A

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter, with depth to the submucosa. Ulcers smaller than this or without obvious depth are called erosions.

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5
Q

How do peptic ulcers occur?

A

Result from an imbalance between factors promoting mucosal damage (gastric acid, pepsin, Helicobacter pylori infection, non-steroidal anti-inflammatory drug use) and those mechanisms promoting gastroduodenal defense (prostaglandins, mucus, bicarbonate, mucosal blood flow).

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6
Q

What type of bacteria is H. Pylori?

A

Slow-growing spiral gram-negative bacteria

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7
Q

Where is h. pylori most commonly found?

A

Gastric antrum

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8
Q

How is H. Pylori protected from gastric acid?

A

By juxtamucosal mucous layer which traps bicarbonate secreted by antral cells, and ammonia produced by bacterial urease.

(The H. Pylori itself decreases somatostatin levels leading to excessive acid production)

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9
Q

What enzyme does H. pylori possess which enables it to convert area to ammonium and chloride?

A

Urease

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10
Q

What results from infection with H. Pylori?

A
  • Antral gastritis
  • Peptic ulceration (duodenal and gastric)
  • Gastric cancer
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11
Q

Investigations for H. Pylori

A

Non invasive

  • Urea breath test
  • Stool antigen test
  • Blood test - serum antibody detection

Invasive

  • OGD and biopsy
  • Rapid urease test
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12
Q

What are features of gastric ulcers?

A

Can be asymptomatic, but can have:

  • Recurrent, burning epigastric pain - relieved by antacids, pain occurs soon after eating
  • Nausea
  • Weight loss
  • Symptoms of anaemia
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13
Q

What are features of duodenal ulcers?

A

Can be asymptomatic, or:

  • Burning epigastric pain - relieved by antacids, pain ocurs several hours after eating or when hungry and classically at night (can be reversed by eating)
  • Weight loss
  • Signs of anaemia
  • Epigastric tenderness

Occur most commonly on the lesser vurvature of the proximal stomach or first part of the duodenum

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14
Q

What are risk factors for the development of duodenal ulcers?

A
  • H. pylori (95% with DU and 70% GU)
  • Drugs - NSAID’s, Steroids, SSRI’s
  • Increased gastric acid secretion
  • Increased gastric emptying
  • Smoking
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15
Q

Why does chronic antral gastritis cause increased gastric acid secretion?

A

Causes hypergastrinaemia due to gastrin release from antral G cells

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16
Q

What might back pain in someone with dyspeptic symtpoms, weight loss and anaemia suggest?

A

Penetration of a posterior ulcer

17
Q

What investigations would you consider going in someone with suspected peptic ulcers?

A
  • Blood tests - FBC, H. pylori serology, fasting gastrin levels
  • Urea breath test
  • H. Pylori stool antigen test
  • Upper GI endoscopy
18
Q

What is involved in the urea breath test for investigating H. Pylori?

A

Give the patient <span>13</span>C or 14C labelled urea -> Measurement of 13CO2 in the breath after ingestion (requires mass spectrometer). The test is sensitive (90%) and specific (96%).

So the H. pylori convert urea to ammonia (using urease), where the ammonia neutralises stomach acid so bacterium can create an alklaine microbacterium. urea labelled with isotope to detect whether this change is ocurring.

19
Q

What is important to tell people to do before performing Urea breath test?

A
  • Stop antibiotics for 4 weeks prior
  • Stop PPIs 2 weeks prior
20
Q

What staining is used on biopsy samples for investigating for H. pylori?

A

Giemsa staining

21
Q

How would you manage someone with confirmed H. Pylori?

A

Eradication Therapy - Triple therapy for 7 days

  • Clarithromycin 500mg bd
  • Amoxycillin 1g bd (or Metronidazole 400mg bd)
    • Tetracycline is given if penicillin allergy
  • PPI: e.g. omeprazole 20mg bd

Remember no alcohol with metronidazole

22
Q

If someone was found to be negative for H. pylori as the cause of their peptic ulcer, how would you manage them?

A

Acid suppression alone

23
Q

What would be your differential diagnosis for someone with features of peptic ulceration?

A
  • Non-ulcer-dyspepsia
  • Duodenal crohn’s
  • TB
  • Lymphoma
  • Pancreatic cancer/pancreatitis
  • Gastric reflux
  • Gastric malignancy
25
Q

What is important to exclude on endoscopy in someone with suspected peptic ulcer disease in older patients?

A

Gastric cancer

26
Q

What are alarm symptoms of someone with gastritis?

A
  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset
  • Malaena/haematemesis
  • Swallowing difficulty
27
Q

What are complications of peptic ulceration?

A
  • Haemorrhage
  • Perforation
  • Gastric outlet obstruction/Pyloric stenosis
28
Q

What are features of gastric outlet obstruction?

A
  • Vomiting - infrequent, projectile, large in volume, contains particles of previous meals.
  • Succussion splash
29
Q

When is surgery considered as an option in peptic ulceration?

A
  • Recurrent uncontrolled haemorrhage
  • Perforation
30
Q

What neoplastic disorders can occur due to H. Pylori infection?

A
  • Gastric adenocarcinoma
  • Gastric B cell lymphoma (MALT)
31
Q

What might you consider giving someone with NSAID associated ulcers which were refractory to PPI administration?

A

Misoprostol

32
Q

What tests could you perform on histological samples taken from the stomach to look for H. Pylori?

A
  • Rapid urease test
  • Histology
  • Culture
33
Q

What is Zollinger-Ellison syndrome?

A

Syndrome caused by gastrin-secreting tumour called gastrinomas or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid, resulting in recurrent peptic ulcers.

Triad of severe peptic ulcer disease, gastrinoma and gastric acid hypersecretion.

Gastrin level >1000, MEN1 linked

34
Q

Histological changes in peptic ulcer:

A

Erosion of mucosal layer,

Necrotic depbris of ulcer base,

Non specific acute inflammation,

Granuloma tissue,

Fibrosis

35
Q

Age >55 with new onset dyspepsia or anyone with alarm symtpoms investigation

A

OGD and biopsy

Rapid urease

36
Q

Age <55 with ulcer type symptoms and no alarm symtpoms investigation

A

Urea breath test

Stool antigen test

Blood serology

Gwen - GI and General surgery (44 decks)

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