Peptic ulcer disease and gastritis Flashcards

1
Q

What is peptic ulcer disease?

A

Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin (protease).

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2
Q

Where does peptic ulcer disease manifest? (x4)

A

Most commonly gastric and duodenal, but also in oesophagus and Meckel’s diverticulum.

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3
Q

What is the aetiology of peptic ulcer disease?

A

Cause is an imbalance between damaging action of acid and pepsin and mucosal protective mechanisms.

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4
Q

What are the risk factors of peptic ulcer disease? (x2, x3, x3)

A

o Commonly H. pylori (present in 95% of duodenal ulcers and 70-80% of gastric ulcers), NSAID use.

o DUODENAL-SPECIFIC: Rarely smoking, increased gastric acid secretion, Zollinger-Ellison syndrome (gastrinomas in duodenum pancreas – gastrin production stimulates gastric acid production)

o GASTRIC-SPECIFIC: reflux of duodenal contents, stress, Cushing’s ulcers.

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5
Q

What are Cushing’s ulcers?

A

Gastric ulcer arising from high intracranial pressure. Mechanism is thought to be that increased intracranial pressure stimulates the vagus nerve which increased gastric acid secretion.

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6
Q

What is the most common location for duodenal ulcers and why?

A

Duodenal cap (first part of duodenum), as this is where acid enters the duodenum prior to addition of alkaline which neutralises it.

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7
Q

What is the most common location for stomach ulcers and why?

A

Antrum because this is where gastric epithelium begins to transition to duodenal epithelium which is less robust to damage.

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8
Q

What is the epidemiology of peptic ulcer disease: Incidence? Gender? Age? (x2) Prevalence and age? Difference between duodenal and gastric ulcer incidence?

A

Common with annual incidence of 1-4/1000. More common in males. Duodenal ulcers have a mean age of 30s, while gastric ulcers are 50s. Prevalence if roughly equivalent to age in years. Duodenal 4-fold more common than gastric ulcer.

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9
Q

What are the symptoms of peptic ulcer disease? (x3)

A
  • Epigastric abdominal pain, burning and dull, relieved by antacids. Some will describe it as heartburn.
  • ALARM symptoms: anaemia (arising as a complication), loss of weight, anorexia, recent onset/progressive symptoms, melaena/haematemesis (as a complication), swallowing difficulty (dysphagia).
  • Vomiting
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10
Q

How does epigastric pain change according to food intake in peptic ulcer disease? (x2)

A

If worse soon after eating, more likely to be gastric ulcers. If worse several hours later and relieved on eating, more likely to be duodenal.

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11
Q

What are the complications of peptic ulcer disease? (x3 categories)

A

o Haemorrhage: haematemesis, melaena, iron-deficiency anaemia

o Perforation

o Obstruction or pyloric stenosis due to scarring, penetration or pancreatitis

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12
Q

What are the signs of peptic ulcer disease? (x3)

A

o May be no physical findings

o Epigastric tenderness

o Signs of anaemia

o Succession splash in pyloric stenosis

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13
Q

What is succession splash in pyloric stenosis?

A

A succussion splash, also known as a gastric splash, is a sloshing sound heard through a stethoscope during sudden movement of the patient on abdominal auscultation. It reflects the presence of gas and fluid in an obstructed organ.

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14
Q

What are the investigations for peptic ulcer disease? (x5)

A

o BLOODS: FBC (for anaemia), amylase (to exclude pancreatitis), U&Es, clotting screen (if GI bleeding), LFTs, Secretin test (if Zollinger-Ellison syndrome is suspected).

o ENDOSCOPY: gold standard for visualisation of ulcer and carrying out further tests.

o BARIUM MEAL X-RAY: look at photo.

o ROCKALL SCORING: for severity after a GI bleed. Less than 3 carries a good prognosis; more than 8 means high risk of mortality.

o TESTING FOR H. PYLORI.

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15
Q

What can be tested with endoscopy in peptic ulcer disease? (x2)

A

Four quadrant gastric ulcer biopsies to rule our malignancy. Biopsy of ulcer rim and base for H. pylori histology.

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16
Q

What are the tests for H. Pylori? (x3)

A

o 13C-Urea breath test: radio-labelled urea given by mouth and detection of 13C in the expelled air.

o Serology: IgG antibody against H. pylori, confirms exposure but not eradication i.e. can’t tell whether someone is immune or whether they still have the infection

o Stool antigen test: Campylobacter-like organism test: Gastric biopsy is placed with a substrate of urea and a pH indicator. If H. pylori is present, ammonia is produced from the urea and there is a colour change (yellow to red).

17
Q

Why is urea tested in H. pylori investigations?

A

H. pylori survives in gastric acid by secreting urease, breaking down any urea in the stomach into ammonia and CO2. The ammonia neutralises any acid found in the vicinity of the bacteria. The CO2 is absorbed into the blood stream and then released from the lungs.

18
Q

How is peptic ulcer disease managed? (x6 components)

A

o LIFESTYLE CHANGES: less tobacco and alcohol.

o ACUTE MANAGEMENT: resuscitation if perforated or bleeding (IV colloids/crystalloids), and close monitoring.

o H. PYLORI ERADICATION: triple therapy for 1-2 weeks of one PPI and two antibiotics.

o DRUGS TO REDUCE ACID: Patients should also be treated with IV PPI at presentation until the cause of bleeding is confirmed. Switch to oral after bleeding cessation.

o WHEN DISEASE IS NOT H. PYLORI ASSOCIATED: i.e. drug-induced ulcers. Treat with PPIs and H2-antagonists, use misoprostol (e.g. prostaglandin E1 analogue – reduces NSAID-induced ulcer risk)

o Proceeding with endoscopy or surgical treatment if indicated.

19
Q

What are H2 antagonists? Examples? (x2)

A

Affect parietal cells and block histamine production which decreased stomach acid production. Examples include cimetidine and ranitidine.

20
Q

When is endoscopic investigation indicated?

A

Over 55 years old, AND persistent symptoms OR ALARM symptoms.

21
Q

How is peptic ulcer disease managed endoscopically? (x2)

A

To manage active bleeding: by injection sclerotherapy, laser cautery, or electrocoagulation; AND 6-8-week follow-up to confirm healing and exclude malignancy.

22
Q

When is peptic ulcer disease managed surgically? (x2)

A

If perforated, or ulcer-related bleeding cannot be controlled.

23
Q

How is peptic ulcer disease managed surgically? (x2 and x2)

A

HAEMORRHAGE managed by under-running the bleeding ulcer base (stitch under ulcer and tie off) or excision of the ulcer; PERFORATION by excision of the hole for histology, then closure.

24
Q

What is the prognosis of peptic ulcer disease?

A

Overall lifetime risk is 10%, though prognosis is good as H. pylori is generally very treatable (85% effective medically) and this is the main cause.

25
Q

What is gastritis?

A

Inflammation of the lining of the stomach. Can be acute or chronic.

26
Q

What is the epidemiology of gastritis?

A

Affect around 50% of the general population.

27
Q

What is the aetiology of gastritis?

A

Cause is an imbalance between damaging action of acid and pepsin and mucosal protective mechanisms.

28
Q

What are the risk factors of gastritis? (x10)

A

Alcohol, NSAIDs, H. pylori, GORD, hiatus hernia, atrophic gastritis, granulomas (Crohn’s, sarcoidosis etc.), cytomegalovirus, Zollinger-Ellison syndrome, Menetrier’s disease.

29
Q

What are the symptoms of gastritis? (x6)

A

Epigastric pain, vomiting, haematemesis, bloating, loss of appetite, weight loss.

30
Q

What are the investigations for gastritis? Indications?

A

Endoscopy and biopsy, only when over 55 years old, AND persistent symptoms OR ALARM symptoms.

31
Q

How is gastritis managed? (x4)

A

o Antacids are the most common treatment. When these do not work, the following options can be considered:

o H2 blockers and PPIs to reduce secretion of acid.

o Cytoprotective agents such as misoprostol. Indicated when drug-induced e.g. by NSAIDs.

o Treatment regimens when H. pylori is the cause: two antibiotics and one PPI.

32
Q

What are the complications of gastritis? (x3)

A

Peptic ulcer disease, haemorrhage and gastric cancer.

33
Q

What is the prognosis of gastritis?

A

Very good – often does not need treatment.

34
Q

SUMMARY: What are the differentials for dyspepsia?

A

.