Peptic ulcer disease (PUD)

Peptic ulcer disease (PUD)

Discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin.


Etiology

Helicobacter pylori infection:

Gram-negative, motile spiral rod found in 90% of duodenal ulcers and 70% to 90% of gastric ulcers
Acid secretion and the associated pattern of gastritis play an important role in disease outcome in H. pylori infection. The figure displays the correlations between the pattern of H. pylori colonization, inflammation, acid secretion, gastric and duodenal histology, and clinical outcome. | Kusters, J. G., van Vliet, A. H., & Kuipers, E. J. (2006). Pathogenesis of Helicobacter pylori infection. Clinical microbiology reviews, 19(3), 449–490. https://doi.org/10.1128/CMR.00054-05

Non-steroidal anti-inflammatory drugs (NSAIDs):

#2 M/C cause of PUD. The secretion of prostaglandin normally protects the gastric mucosa. NSAIDs block prostaglandin synthesis by inhibiting COX-1 enzyme resulting in a decrease in gastric mucus and bicarbonate production and a decrease in mucosal blood flow.
Non-steroidal anti-inflammatory drugs induced mucosal injury | Prabhu, V., & Shivani, A. (2014). An overview of history, pathogenesis and treatment of perforated peptic ulcer disease with evaluation of prognostic scoring in adults. Annals of medical and health sciences research, 4(1), 22–29. https://doi.org/10.4103/2141-9248.126604

Hypersecretory environments:

Multiple gastroduodenal, jejunal, or esophageal ulcers
  • Zollinger Ellison syndrome
  • Systemic mastocytosis
  • Cystic fibrosis
  • Hyperparathyroidism
  • Antral G cell hyperplasia

Social factors:

  • Smoking
  • Alcohol (irritate gastric mucosa and induce acidity)

Malignancy:

  • Gastric cancer
  • Lymphomas
  • Lung cancers

Stress:

  • After acute illness
  • Multiorgan failure
  • Ventilator support
  • Extensive burns (Curling’s ulcer)
  • Head injury (Cushing’s ulcer)

Pathophysiology

Mucosal break of the upper gastrointestinal tract due to acid peptic digestion resulting in ulcer formation which extends beyond the muscularis mucosae into the submucosa.

Modified Johnson Classification system:

Based on location of the ulcer
  • Type I (M/C): Lesser curvature; Associated with acid hypersecretion:
    • Type II: Prepyloric + duodenal
    • Type III: Prepyloric only
  • Type IV: Proximal gastroesophageal ulcer
    • M/C bleeds, usually from left gastric artery
  • Type V: Diffuse occurrence. Associated with the chronic use of NSAIDs (such as ibuprofen)
Modified Johnson Classification of Peptic Ulcer | Accessmedicine.mhmedical.com. (2017). Chapter 26. Stomach | Schwartz’s Principles of Surgery, 9e | AccessMedicine | McGraw-Hill Medical . [online] Available at: http://accessmedicine.mhmedical.com/Content.aspx?bookId=352&sectionId=40039768 [Accessed 14 Jul. 2017].

Presentation

Signs and symptoms of peptic ulcer disease may vary depending upon the location of the disease and age.

Epigastric pain:

Usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer; on the other hand, the pain with a duodenal ulcer tends to occur 2-3 hours after a meal.
Gastric and Duodenal Ulcer Differences. | Incorporated Approach towards Development of… New Herbal Drugs for Peptic Ulcer Disease Biomedical Sciences and Herbal Medicines – Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/1-Gastric-and-Duodenal-Ulcer-Differences_tbl1_331674440 [accessed 8 Nov, 2020]

Duodenal ulcers:

Duodenal ulcers are more common than gastric ulcers.
  • M/C site: 1st part of duodenum
  • Anterior duodenal ulcer presentation: Perforation
  • Posterior duodenal ulcer presentation: Bleeding (M/C presentation)
    • Usually due to gastroduodenal artery

Associated features:

  • Loss of appetite
  • Weight loss

Alarming features:

  • Evidence of overt or occult gastrointestinal bleeding: Hematemesis, melena, anaemia, heme-positive stool
  • Symptom of impending perforation: Severe persistent epigastric pain
  • Symptom of obstruction: Persistent vomiting
  • Malignancy: anorexia, unintended weight loss

Complicatoins

  • Upper GI bleeding (15–20%): Manifests as bloody or coffee-ground emesis and/or bloody or tarry stools
  • Perforated peptic ulcer (PPU) (2–10%): Manifests as a sudden, severe, piercing epigastric pain followed by rapidly developing symptoms of diffuse peritonitis
  • Gastric outlet obstruction (GOO): Results from permanent scarring/edema and inflammation associated with an ulcer located in the pylorus or duodenal bulb manifesting as gastric retention, nausea, and profuse vomiting; some patients develop hypokalemia and alkalosis.

Diagnosis

Non-invasive Helicobacter pylori testing:

  • Urea breath test: A solution containing portions of 13C-labeled or 14C-labeled urea are consumed by the patient. The urea is hydrolyzed by bacterial urease to labeled CO2, which is measured in the expired air after 30 minutes.
  • Stool antigen test

Esophagogastroduodenoscopy (EGD):

Gold standard
  • Sharply demarcated circular mucosal defect or an irregular cavity with infiltrated edges
    • Gastric ulcers: Lesser curvature or in prepyloric region
    • Duodenal ulcers: Anterior wall of bulb
Cascade of histologic changes induced by Helicobacter pylori at level of gastric mucosa. | Mégraud, F., Bessède, E., & Varon, C. (2015). Helicobacter pylori infection and gastric carcinoma. Clinical Microbiology and Infection, 21(11), 984–990. https://doi.org/10.1016/j.cmi.2015.06.004

Differential diagnosis:

Other causes of dyspepsia, nausea and vomiting, and epigastric pain
Differential diagnosis of Peptic Ulcer Disease | Fashner, J., & Gitu, A. C. (2015). Diagnosis and Treatment of Peptic Ulcer Disease and H. pylori Infection. American family physician, 91(4), 236–242.

Management

Medical management:

Schematic presentation of main pathophysiological mechanisms involved in the development of peptic ulcer disease, and the sites of action of the most commonly used pharmacological options in the treatment of peptic ulcer disease. | CCK2 = Cholecystokinin Receptor; PGE2 = Prostaglandin E2; PGI2 = Prostaglandin I2; EP3 = Prostaglandin E receptor 3; HIST = Histamine. | Kuna, L., Jakab, J., Smolic, R., Raguz-Lucic, N., Vcev, A., & Smolic, M. (2019). Peptic Ulcer Disease: A Brief Review of Conventional Therapy and Herbal Treatment Options. Journal of clinical medicine, 8(2), 179. https://doi.org/10.3390/jcm8020179
  • Triple therapy: Proton pump inhibitor (PPI) + clarithromycin + amoxicillin/metronidazole (7-14 days)
    • PPIs work synergistically with antibiotics to eradicate H. pylori
    • Due to increasing antibiotic resistance, the efficacy of triple therapy has fallen below 70% in many countries.
  • Bismuth-containing quadruple therapy (for clarithromycin resistance):
    • PPI + bismuth + tetracycline + nitroimidazole (metronidazole/tinidazole) for 14 days
      or
      PPI + clarithromycin + amoxicillin + nitroimidazole

Surgical management:

Indicated if the patient is unresponsive to medical treatment, noncompliant, or at high risk of complications
  • Duodenal ulcers:
    • Highly selective vagotomy or truncal vagotomy with antrectomy
  • Pyloric stenosis:
    • Truncal vagotomy + pyloroplasty or vagotomy + antrectomy
  • Gastric ulcers:
    • Gastric body: Partial gastrectomy + gastroduodenal anastomosis without vagotomy
    • Prepyloric region or gastric + duodenal ulcers: Vagotomy + antrectomy
    • Subcardial region: Partial gastrectomy including pyloric region

Complications of vagotomy & gastric reconstruction:

Highly selective vagotomy has least amount of complications but the highest recurrence rate, whereas truncal vagotomy + antrectomy has the highest reduction in acid secretion with the most vagal complications
  • Nutritional complications: Iron deficiency (M/C complication overall), vitamin B12, calcium deficiency
  • Internal hernia: Stemmer’s hernia, Peterson’s hernia
  • Dumping syndrome (postgastric surgery syndrome)

Summary:

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