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- Y6 Gastrointestinal > Peptic ulcer disease and gastritis > Flashcards

Peptic ulcer disease and gastritis Flashcards

1
Q

Define gastritis.

A

The histological presence of gastric mucosal inflammation. Usually dyspepsia which is not caused by an ulcer.

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2
Q

What are the 3 most common causes of gastritis?

A
  • H pylori infection - non-erosive gastritis predisposing to atrophic gastritis and autoimmune gastritis
  • NSAID use - acute erosive gastritis
  • Alcohol - acute erosive gastritis
  • Autoimmune e.g. pernicious anaemia
  • Bacterial - phlegmonous gastritis due to staph aureus, strep, E coli, enterobacter etc.
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3
Q

What are the risk factors for gastritis?

A
  • H pylori infection
  • NSAID use
  • Alcohol use/toxic ingestions
  • Previous gastric surgery
  • Critically ill patients
  • AI disease -increased risk of AI gastritis in thyroid disease, idiopathic adrenocortical insufficiency, vitiligo, type 1 diabetes mellitus, and hypoparathyroidism.
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4
Q

Describe how NSAIDs cause gatritis.

A

NSAIDs inhibit prostaglandin production. This in turn decreases gastric mucosal blood flow with loss of the mucosal protective barrier

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5
Q

What is the pathophysiology of autoimmune gastritis?

A

Antiparietal cell antibodies cause immune infiltration and loss of parietal and chief cells in the gastric corpus

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6
Q

Describe the pathophysiology of phlegmonous gastritis.

A

Damage to the gastric mucosa may allow ingested bacteria to become invasive causing phlegmonous gastritis.

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7
Q

What are the signs and symptoms of gastritis?

A

Features are non-specific; check for presence of risk factors.

  • Epigastric pain/dyspepsia
  • Epigastric tenderness
  • Vomiting, nausea, anorexia

No: features suggestive of malignancy e.g. anaemia, weight loss >10%, progressive dysphagia etc.

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8
Q

What investigations would you do for gastritis?

A

Urea breath test OR faecal antigen test- can be used first line if no features of malignancy and <60yrs; may be used to monitor therapy too.

Endoscopy +/- biopsy- 1st line if _>_60yrs or alarming features in younger patients. May show evidence of gastric erosions and/or atrophy +/- H pylori.

Other:

  • FBC -may show low Hb and Hct and increased MCV in autoimmune gastritis; leucocytosis with left shift in phlegmonous gastritis
  • Serum B12 (N or low in AI gastritis), parietal cell and IF antibodies (+ve in autoimmune gastritis)
  • Intrinsic factor antibodies - highly specific for pernicious anaemia
  • UGI contrast series - may show presence of gas which can confirm phlegmonous gastritis
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9
Q

How long should you withhold PPIs before non-invasive H pylori tests?

A

7-14 days

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10
Q

What is the management of gastritis?

A

Depends on type of gastritis:

H pylori - Eradication therapy - triple therapy/2Abx+PPI

  • e.g. CAP: clarithromycin 500mg BD + amoxicillin 1g BD + omeprazole 20mg BD

Stress/erosive gastritis e.g. in ITU patients -

  • Discontinue causative agents
  • H₂ antagonists or PPI e.g. ranitidine/famotidine or pantoprazole

Autoimmune gastritis -

  • B12/cyanocobalamin 1000mcg IM OM

Phlegmonous gastritis -

  • ICU admission +
  • Supportive care
  • Broad spectrum Abx (ampicillin AND cirpofloxacin)
  • +/- gastrectomy (but NG drainage and Abx should be sufficient)
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11
Q

What are the complications of gastritis?

A
  • Gastric carcinoma/carcinoid/lymphoma
  • Achlorhydria post atrophic gastritis (decreased/absent production of hydrochloric acid)
  • Vit B12 deficiency
  • Peptic ulcer disease → GI bleed
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12
Q

What is the prognosis with gastritis?

A

Erosive - symptoms improve after reduction of offending agent

Helicobacter pylori - initial triple therapy may sometimes be inadequate, so may require alternative quadruple bismuth-based regimen

AI gastritis - excellent prognosis with B12 treatment

Phlegmonous gastritis - mortality rate for surgically treated patients ~20% and for medically treated patients is ~50%

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13
Q

Describe the bacteria H.pylori. Where does it reside?

A

Gram negative, motile, microaerophilic bacterium

Resides in human GI tract – exclusively colonising gastric-type epithelium

It is a commensal

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14
Q

How do ulcers form?

A
  • Increased gastric acid formation – through increased gastrin or decreased somatostatin production – this shifts the balance to more acid production
  • Gastric metaplasia of epithelial cells– cell transformation due to excessive acid exposure
  • Downregulation of defence factors - reduces epidermal growth factor & reduces bicarbonate production(which increases acidity)
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15
Q

What are the two virulence factors produced by H.pyroli and what responses does each cause?

A
  • CagA -> antigenic response
  • VacA -> cytotoxic response
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16
Q

What are the main virulent components of H pylori?

A

_Urease* enzyme production_ – (20% of the dry weight of this bacteria is the urease enzye) catalyses urea into ammonium chloride (which is toxic) & monochloramine–> damage epithelial cells

Urease is antigenic–> evokes immune response à damage to epithelial cells

Certain virulent strains produce CagA (antigenic) or VacA (cytotoxic) – more intense tissue inflammation

17
Q

Describe the pathophysiology of a complicated peptic ulcer.

A
  • Dissolves mucus layer: urease enzyme
  • Causes epithelial cell death: exotoxins & inflammation
  • Increased acidity –> peptic ulcer
18
Q

Define peptic ulcer disease.

A

A break in the mucosal lining of the stomach or duodenum >5 mm diameter, with depth to the submucosa. Smaller ulcers are called erosions.

Usually gastric or duodenal due to exposure to gastric acid or pepsin.

19
Q

Name 2 common and 1 rare cause of peptic ulcer disease.

A

Common:

  • Hpylori (in 95% of duodenal and 70-80% of gastric ulcers),
  • NSAID use

Rare: Zollinger-Ellison syndrome

20
Q

How common is peptic ulcer disease?

A
  • Duodenal > gastric
  • H pylori causes 95% of duodenal ulcers and 75% of gastric ulcers
  • Common - ~5% prevalence
  • M>F
  • Duodenal usually present in 30s
  • Gastric usually present in 50s-70s

NB: H pylori is usually acquired in childhood and prevalence is roughly equivalent to the age in years.

21
Q

What are the risk factors for PUD?

A
  • Helicobacter pylori infection - present in >90% of patients with duodenal ulcer and >70% with gastric ulcer.
  • NSAID use
  • Smoking
  • Increasing age
  • Personal or family history of peptic ulcer disease
  • An intensive care stay.
22
Q

List 3 drugs which may cause or exacerbate dyspepsia.

A
  • Alpha blockers
  • Anticholinergics
  • Aspirin
  • Benzodiazepines
  • Beta blockers
  • Bisphosphonates
  • CCB
  • Corticosteroids
  • Nitrates
  • NSAIDs
  • Theophyllines
  • TCAs
23
Q

What is a typical presentation of peptic ulcer disease?

A

Dyspepsia - commonly related to eating and experienced at night

Relieved by antacids

Discomfort

Chronic or recurrent nature

Pointing sign - patient can point to where the pain is exactly

Nausea, anorexia, and vomiting - uncommon, but if present may be relieved by eating.

Variable relationship to food:

  • if worse after eating then more likely gastric
  • if symptoms worse several hours after eating OR symptoms relieved by eating then duodenal

May present with complications e.g. haematemesis, melaena → urgent referral to secondary care

24
Q

What investigations would you do for peptic ulcer disease?

A

Endoscopy is the gold standard diagnostic test but urea breath test or H pylori stool antigen test may be done instead if no suspicion of malignancy.

Bloods:

  • FBC - anaemia
  • Amylase - exclude pancreatitis
  • U&Es, clotting screen (if GI bleeding)
  • LFT
  • Cross-match if actively bleeding
  • Secretin test - If zollinger-Ellison suspected then IV secretin causes rise in gastrin in SE patients but not controls

Tests for H pylori

Endoscopy - 4 quadrants need to be sampled to rule out malignancy, duodenal ulcers need not be biopsied

25
Q

What is the secretin test used for and what is it?

A

Secretin test - If zollinger-Ellison suspected then IV secretin causes rise in gastrin in SE patients but not controls

26
Q

What tests are available for H pylori?

A

13C-urea breath test - radio-labelled urea given by mouth and detection of C13 in the expired air is tested

Serology - IgG antibody against H pylori confirms exposure but not eradication

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

27
Q

Are histologies of biopsies useful for finding H pylori?

A

Difficult to visualise H pylori so no

28
Q

How do you manage peptic ulcer disease? (acute/endoscopic/surgical)

A

Acute:

Resuscitation if perforated or bleeding (IV colloids/crystalloids), close monitoring of vital signs and proceeding endoscopic or surgical treatment

Patients with upper GI bleeding should be treated with IV PPI (e.g. omeprazole or pantoprazole) at presentation until the cause of bleeding is confirmed. Patients with actively bleeding peptic ulcers with high-risk stigmata (e.g. visible vessel or adherent clot) should ocntinue IV PPI. Switch to oral PPI if there is no rebleeding within 24hrs.

Endoscopy - haemostasis by injection sclerotherapy, laser or electrocoagulation

Surgery - if perforated or ulcer-related bleeding cannot be controlled

29
Q

How do you manage peptic ulcer disease?

A

H pylori eradication:

  • Triple therapy 2 weeks = one PPI and 2 antibiotics e.g. clarithromycin, amoxicillin + PPI (all BD for 2 weeks
  • Quadruple therapy = a bismuth salt (subsalicylate or subcitrate potassium) + metronidazole + tetracycline, (all QDS) + PPI (BD)

H pylori excluded:

  • PPI until ulcer healed - 4-8 weeks OR Famotidine - 40mg PO OD at night
  • Reduce risk factors
30
Q

What is the management of a an active bleeding ulcer?

A

ABCDE

NBM

Urgent surgical referral

+/- Blood transfusion - if Hb <70g/L

Endoscopy - clips +/- adrenaline; thermal coagulation; fibrin/thrombin + adrenaline.

31
Q

What score is used to assess for risk of rebleeding?

A

Rockall score - after endoscopy to estimate the risk of rebleeding or death

32
Q

What are the complications of peptic ulcer disease?

A

Rate of major complication is 1% per year including

  • Haemorrhage (haematemesis, melaena, iron deficiency anaemia)
  • Perforation
  • Obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)
33
Q

What is the prognosis with peptic ulcer disease?

A
  • Overall lifetime risk ~10%
  • Generally good as peptic ulcers associated with H pylori can be cured by eradication
34
Q

Define dyspepsia.

A

Complex UGI symptoms for _>_4 weeks including upper abdo pain discomfort, heartburn, acid reflux, nausea +/- vomiting.

35
Q

What are the most common causes of dyspepsia?

A
  • GORD
  • PUD
  • Functional dyspepsia - i.e. symptoms but normal endoscopy, usually post-prandial or intermittent epigastric burning.
36
Q

When might the urease test be falsely negative?

A

UGI bleed

PPI use

Antibiotic use

37
Q

When should you refer a patient for UGI endoscopy immediately vs within 2 weeks?

A

Immediate if:

Dyspepsia

AND GI bleeding

Within 2 weeks if:

_>_55yrs AND weight loss AND any one of the following:

  • +/- Dyspepsia
  • +/- Upper abdo pain
  • +/- Reflux
38
Q

How is gastric acid secretion regulated?

A
  1. ACh released from neurones (vagus / enteric) acts on muscarinic (M3) receptors -> increased ­ [Ca2+]i
  2. Prostaglandins released from local cells act on EP3 receptors -> ­increased cAMP
  3. Histamine released from enterochromaffin-like cells (ECL) act on H2 receptors -> ­increased cAMP
  4. Gastrin released from blood stream acts on cholecystokinin B receptors -> increased ­ [Ca2+]i

NB increased Ca2+ –> increased cAMP which cayse transloaction of proton pumps to the apical surface of parietal cells–> acid secretion

- Y6 Gastrointestinal (70 decks)

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