PEPTIC ULCER DISEASE

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 Description 


An ulcer is an open sore in the stomach or intestine. Peptic ulcer is as an excavation that forms in the mucosal wall of the stomach in the pylorus, in the duodenum or in the esophagus (Smeltzer et al, 2014). It is frequently referred to as a gastric, duodenal or esophageal ulcer depending on its location. It is defined by the erosion of a circumscribed area of the mucous membrane.

 Epidemiology

Peptic ulcer disease accounts for approximately 10% of adult admissions into any health facility worldwide. It is more common in people between the ages of 40 and 60 years, and uncommon in women of child bearing age. It has also been observed in children and infants. Duodenal ulcers account for about 80% of peptic ulcer diseases and occurs most often in males aged between 20 and 30 years. Gastric ulcer tends to occur in middle aged and the elderly over 50 years. The risk of peptic ulcer disease increases among chronic users of ulcerogenic drugs such as Non-Steroidal Anti-Inflammatory Drugs (NSAIDS), steroids or alcohol. People with blood group ‘A’ are at risk of developing gastric ulcer and those with blood group ‘O’ are at risk of developing duodenal ulcer. About 10%-15% of people with PUD develop complications that necessitate surgery (Williams & Hopper, 2011).

 Types of peptic Ulcer 

Peptic ulcers are categorized into:

  • Gastric ulcer: Found lying on lesser curvature of the stomach. Gastric ulcers may be acute or chronic. Acute gastric ulcer is also known as gastric erosions or multiple small ulcers. It may occur after severe stress such as trauma or burns (Curling’s ulcer). Chronic gastric ulcers develop from acute ulcers which fail to heal. It is present continuously for many months or intermittently throughout the person’s whole lifetime.

  •  Duodenal ulcers: occur in the first part of the duodenum or on duodenal cap.
  • Anastomotic ulcer: this is due to failure of healing of a wound at where intestinal resection and anastomosis was done.

 Etiology of Peptic Ulcer Disease 

According to Smeltzer and Bare (2014), the etiology of peptic ulcer disease is not fully understood, but recent research has identified that peptic ulcer results from infection with the gram negative bacterium Helicobacter pylori. Chronic usage of ulcerogenic drugs such as aspirin, steroids and NSAIDS can also cause ulcer. These agents interfere with the ability of the stomach to produce mucus, bicarbonate and other protective barriers. They also affect cell repair ability and blood flow to the stomach parenchyma.


Predisposing Factors 

Factors that predisposes one to developing peptic ulcer disease. Some of these factors are:

  1. Aging: people over 65 years are more predisposed to peptic ulcer disease
  2. Genetic makeup: people with blood type ‘A’ and ‘O’ are at risk of getting gastric and duodenal ulcers respectively
  3. High alcohol intake 
  4. Emotional stress: though this is not clear, it may increase gastric secretion thereby increasing the chance of developing peptic ulcer disease
  5. Smoking: this could be to related to diminished bicarbonate secretion by the pancreas
  6. The use of Non-Steroidal Anti-Inflammatory Drugs: this increases the rate of superficial gastric mucosal erosion and gastric ulceration
  7. Certain disease conditions such as chronic lung disease, liver cirrhosis, chronic renal failure (especially after transplantation)
  8. Irregular eating pattern.
  9. Helicobacter pylori infection: as many as 80-90% of peptic ulcer diseases are associated with Helicobacter pylori infection (Williams &Hopper, 2011).


Pathophysiology

Peptic ulcers occur mainly in the gastroduodenal mucosa because the tissue of the gastroduodenal mucosa cannot withstand the digestive action of gastric acid (HCL) and pepsin. The erosion is as a result of the increase in the concentration or activity of acid and pepsin, or by a decrease in the resistance of the mucosa. A damaged mucosa is unable to secrete enough mucous to act as a barrier against HCL. The mucous lining is generally protected from the ulcerative action of the HCL and pepsin due to the presence of the following physiological barriers:

  1. Mucus secreting goblet cells that secrete mucus. Mucus act as a protective coat on the mucosal lining against the corrosive effect of gastric acid.
  2. Rapid cell proliferation rate of the epithelial cells allows damaged cells to be replaced within 36-48 hours 
  3. Layers of alkaline mucous coat and secretion of bicarbonate that help to cover the gastric mucosa and neutralized acid in the duodenum.
  4. Tight junctions between cells prevent gastric acid from leaking back into the submucosa

When there is a break in the physiological barriers due to excessive acid and pepsin secretion or infection, overactive vagus nerves or hypersecretion of gastrin as in tumors, ulceration of the linings, these lead to ulcer formation.The mechanism of HCL production and its release is triggered by sight, smell or food ingestion. This increases the release of gastrin by the stomach and the pancreas. The release of gastrin sends an impulse to the brain and in turn the vagus nerve is stimulated by the neurotransmitter acetylcholine which then triggers the parietal cells of the stomach to secrete gastric acid.Also histamine is released from the stomach linings and the damaged part that causes vasodilation of the capillaries leading to increased blood flow to the ulcer. This will then lead to inflammation, pain, dyspepsia, bleeding, hematemesis, melena, hyper gastric acid secretion and hypoperfusion of the stomach leading to necrosis and ulcer formation.


Clinical Manifestation 

  1. Epigastric pain that can radiate to the back or sternum
  2. Pain may/may not be relieved by food ingestion or antacid
  3. Pain may occur 1-2 hours for gastric ulcer and 2|-3 hours for duodenal ulcer after meals
  4. Nocturnal pain that wakes patient up at night
  5. Epigastric tenderness 
  6. Weight loss may occur in gastric ulcer and weight gain in duodenal ulcer
  7. Heartburns
  8. Nausea and vomiting 
  9. Water brash (sudden flow of saliva into mouth)
  10. Anorexia
  11. Headache
  12. Anxiety
  13. Belching
  14. General body weakness.
  15. Flatulence
  16. Constipation 
  17. Hematemesis
  18. Dizziness 
  19. Melena
  20. Fever may be present if it is caused by H. Pylori.


Complications

  • Perforations 
  • Gastric carcinoma
  • Cancer
  • Septicemia 
  • Shock
  • Peritonitis
  • Hemorrhage 
  • Pyloric stenosis


Diagnostic Investigation of Peptic Ulcer

  1. History and physical examination: this can reveal pains, epigastric tenderness and abdominal distention 
  2. A barium swallow with X-ray of the GI reveal ulcer lesion.
  3. Endoscopy: this is the preferred and appropriate diagnostic procedure because it allows direct visualization of inflammatory changes, ulcer, and lesions on the gastrointestinal tract. This can also be achieved by esophagogastroduodenoscopy (EGD).
  4. Biopsy and histology with culture to determine Helicobacter pylori infections
  5. Urea breath test: this is performed by giving a patient carbon labeled urea to drink. The urea is metabolized rapidly if H. Pylori is present allowing carbon to be absorbed and measure in an exhale carbon dioxide
  6. Serologic test: immunoglobulin G (IgG) detection test for H. Pylori to identify whether the patient is infected or not
  7. Hemoglobin level estimation
  8. Fecal occult blood test


Medical management

Several treatment options are used to cure H. Pylori without recurrence. The first antibiotics treatment for peptic ulcer disease caused by H. Pylori was approved by food and drugs board in 1996. For better and effective outcome, triple therapy with two antibiotics to decrease resistance to bacteria, proton pump inhibitors and histamine receptor antagonist are used to modulate the acidic effect on the GI mucosa (Williams & Hopper, 2011).


Surgical management

Surgical interventions for peptic ulcer is performed when medical therapy has not been successful or when complications arise. Various types of surgical procedures may be used in treating peptic ulcer disease. These include:

  • Vagotomy
  • Gastroduodenostomy (Billroth I)
  • Gastrojejunostomy (Billroth II)
  • Antrectomy 
  • Gastrectomy 


Drug groups used in the treatment of PUD

  1. Antibiotics: these drugs have bactericidal effects that eradicate the bacteria. Examples are Amoxicillin, Metronidazole, Clarithromycin, Ciprofloxacin etc.
  2. Proton Pump Inhibitors (PPI): these groups of drugs reduce the gastric acid secretion by slowing hydrogen, potassium and adenosine triphosphate pump on the surface of the parietal cells, examples are omeprazole, lansoprazole, esomeprazole and rabeperazole. The commonly used PPI is omeprazole and lansoprazole.
  3. Histamine type 2 receptor blockers (H2 antagonist): these drugs decrease the amount of HCL by blocking the histamine receptors on the parietal cells in the stomach. Example Cimetidine (Tagamet), famotidine (Pepcid) and ranitidine (Zantac). These drugs can be given with meals for 6-8 weeks followed by daily maintenance of Cimetidine for another 4 weeks.
  4. Cytoprotective medications: these are synthetic prostaglandins that protect the mucosa lining from ulcerogenic substances and also increase mucus and bicarbonates secretion. Example, misoprostol (cytotec).
  5. Antacid: these drugs have no systemic effects; they act only on the gastric contents by neutralizing acid in the stomach to form alkaline. Examples are Magnesium Trisilicate, Aluminum Hydroxide.
  6. Anticholinergic drugs: these drugs can also reduce output of gastrin by inhibiting the effect of the vagus nerve on acid secretion, example Propantheline.

Prevention of peptic ulcer disease 


To reduce your risk of developing a peptic ulcer:

  1. Avoid tobacco products
  2. Avoid alcohol
  3. Use caution with aspirin and/or NSAIDs
  4. Don’t ignore your ulcer symptoms
  5. Protect yourself from infections by washing hands regularly and consuming foods that have been cooked thoroughly

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