Peptic Ulcer Disorder – Causes, Symptoms, Treatment

Peptic Ulcer Disorder(PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve the lower esophagus, distal duodenum, or jejunum. 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. Today, testing for Helicobacter pylori is recommended in all patients with peptic ulcer disease. Endoscopy may be required in some patients to confirm the diagnosis, especially in those patients with sinister symptoms. Today, most patients can be managed with a proton pump inhibitor (PPI) based on triple-drug therapy.

Causes of Peptic Ulcer Disorder

Peptic ulcer disease (PUD) has various causes; however, Helicobacter pylori-associated PUD and NSAID-associated PUD account for the majority of the disease etiology.

Causes of Peptic Ulcer Disease

Common

  • H. pylori infection
  • NSAIDs
  • Medications

Rare

  • Zollinger-Ellison syndrome
  • Malignancy (gastric/lung cancer, lymphomas)
  • Stress (Acute illness, burns, head injury)
  • Viral infection
  • Vascular insufficiency
  • Radiation therapy
  • Crohn disease
  • Chemotherapy

Helicobacter Pylori-Associated PUD

  • H. pylorus is a gram-negative bacillus that is found within the gastric epithelial cells. This bacterium is responsible for 90% of duodenal ulcers and 70% to 90% of gastric ulcers. H. pylori infection is more prevalent among those with lower socioeconomic status and is commonly acquired during childhood. The organism has a wide spectrum of virulence factors allowing it to adhere to and inflame the gastric mucosa. This results in hypochlorhydria or achlorhydria, leading to gastric ulceration.

 Virulence Factors of  Helicobacter pylori

  • Urease  The secretion of urease breaks down urea into ammonia and protects the organism by neutralizing the acidic gastric environment.
  • Toxins CagA/VacA is associated with stomach mucosal inflammation and host tissue damage.
  • Flagella  Provides motility and allows movement toward the gastric epithelium.

NSAID-associated PUD

  • Nonsteroidal anti-inflammatory drugs use is the second most common cause of PUD after H. pylori infection. 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.

Medications

  • Apart from NSAIDs, corticosteroids, bisphosphonates, potassium chloride, steroids, and fluorouracil have been implicated in the etiology of PUD.
  • Smoking also appears to play a role in duodenal ulcers, but the correlation is not linear. Alcohol can irritate the gastric mucosa and induce acidity.

Hypersecretory environments

  • Zollinger Ellison syndrome
  • Systemic mastocytosis
  • Cystic fibrosis
  • Hyperparathyroidism
  • Antral G cell hyperplasia

Symptoms of Peptic Ulcer Disorder

Signs and symptoms of peptic ulcer disease may vary depending upon the location of the disease and age. Gastric and duodenal ulcers can be differentiated from the timing of their symptoms in relation to meals. Nocturnal pain is common with duodenal ulcers. Those with gastric outlet obstruction commonly report a history of abdomen bloating and or fullness.

Common signs and symptoms include

  • Epigastric abdominal pain
  • Bloating
  • Abdominal fullness
  • Nausea and vomiting
  • Weight loss/weight gain
  • Hematemesis
  • Melena
  • Unintentional weight loss
  • Progressive dysphagia
  • Overt gastrointestinal bleeding
  • Iron deficiency anemia
  • Recurrent emesis
  • Family history of upper gastrointestinal malignancy

Diagnosis of Peptic Ulcer Disorder

Diagnosis of PUD requires history taking, physical examination, and invasive/non-invasive medical tests.

History

  • A careful history should be obtained and noted for the presence of any complications. Patient reporting of epigastric abdominal pain, early satiety, and fullness following a meal raise suspicion of PUD. The pain of gastric ulcers increases 2 to 3 hours after a meal and may result in weight loss, whereas the pain of duodenal ulcers decreases with a meal which can result in weight gain. Any patient presenting with anemia, melena, hematemesis, or weight loss should be further investigated for complications of PUD, predominantly bleeding, perforation, or cancer.

Physical Exam

  • A physical exam may reveal epigastric abdominal tenderness and signs of anemia.

Investigations

  • Esophagogastroduodenoscopy (EGD) Gold standard and most accurate diagnostic test with sensitivity and specificity up to 90% in diagnosing gastric and duodenal ulcers. The American Society of Gastrointestinal Endoscopy has published guidelines on the role of endoscopy in patients presenting with upper abdominal pain or dyspeptic symptoms suggestive of PUD. Patients over 50 years of age and new onset of dyspeptic symptoms should get evaluated by an EGD. Anyone with the presence of alarm symptoms should undergo EGD irrespective of age.
  • Barium swallow  It is indicated when EGD is contraindicated.
  • Complete blood work – liver function, and levels of amylase and lipase
  • Serum gastric – is ordered if Zollinger Ellison syndrome is suspected

Helicobacter pylori testing

  • Serologic testing
  • Urea breath test High sensitivity and specificity. It may be used to confirm eradication after 4 to 6 weeks of stopping treatment. In the presence of urease, an enzyme produced by H.pylori, the radiolabeled carbon dioxide produced by the stomach is exhaled by the lungs.
  • Antibodies – to H.pylori can also be measured
  • Stool antigen test
  • Urine-based ELISA and rapid urine test
  • Endoscopic biopsy Culture is not generally recommended as it is expensive, time-consuming, and invasive. It is indicated if eradication treatment fails or there is suspicion about antibiotic resistance. Biopsies from at least 4-6 sites are necessary to increase sensitivity. Gastric ulcers are commonly located on the lesser curvature between the antrum and fundus. The majority of duodenal ulcers are located in the first part of the duodenum.
  • Computerized tomography – of the abdomen with contrast is of limited value in the diagnosis of PUD itself but is helpful in the diagnosis of its complications like perforation and gastric outlet obstruction.

Treatment of Peptic Ulcer Disorder

Medical treatment

Antisecretory drugs used for PUD include H2-receptor antagonists and the proton pump inhibitor (PPIs). PPIs have largely replaced H2 receptor blockers due to their superior healing and efficacy. PPIs block acid production in the stomach, providing relief of symptoms and promote healing.

  • Corticosteroid, bisphosphonates, and anticoagulants should also be discontinued if possible. Prostaglandin analogs (misoprostol) are sometimes used as prophylaxis for NSAID-induced peptic ulcers.
  • First-line treatment for H. pylori-induced PUD is a triple regimen comprising two antibiotics and a proton pump inhibitor. Pantoprazole, clarithromycin, and metronidazole or amoxicillin are used for 7 to 14 days.
  • Antibiotics and PPIs work synergistically to eradicate H. pylori. The antibiotic selected should take into consideration the presence of antibiotic resistance in the environment.
  • If first-line therapy fails, quadruple therapy with bismuth and different antibiotics is used.

NSAIDs induced PUD can be treated by stopping the use of NSAIDs or switching to a lower dose.

Treatment may be incorporated with calcium supplements as long-term use of the PPIs can increase the risk of bone fractures.

Refractory disease and Surgical treatment

Surgical treatment is indicated if the patient is unresponsive to medical treatment, noncompliant, or at high risk of complications. A refractory peptic ulcer is one over 5 mm in diameter that does not heal despite 8-12 weeks of PPI therapy. The common causes are persistent H/pylori infection, continued use of NSAIDs or significant comorbidities that impair ulcer healing or other conditions like gastrinoma or gastric cancer. If the ulcer persists despite addressing the above risk factors, patients can be candidates for surgical treatment. Surgical options include vagotomy or partial gastrectomy.

Differential Diagnosis

The following conditions can present with symptoms similar to peptic ulcer disease and it is important to be familiar with their clinical presentation in order to make the correct diagnosis.

  • Gastritis – an inflammatory process of the gastric mucosa from immune-mediated or infectious etiology presenting with upper abdominal pain and nausea. Clinical presentation is very similar to that of peptic ulcer disease.
  • Gastroesophageal reflux disease (GERD) – Patients usually describe a burning sensation in the epigastrium and lower retrosternal area, excessive salivation, or intermittent regurgitation of food material.
  • Gastric cancer – apart from abdominal pain, patients usually describe alarm symptoms like weight loss, melena, recurrent vomiting, or evidence of malignancy elsewhere in the case of metastasis.
  • Pancreatitis – epigastric or right upper quadrant pain that is more persistent and severe, worse in the supine position and patients usually have a history of alcoholism or gallstones. Elevated serum amylase and lipase are useful in the diagnosis.
  • Biliary colic – intermittent, severe deep pain in the right upper quadrant or epigastrium precipitated by fatty meals.
  • Cholecystitis – right upper quadrant or epigastric pain that usually lasts for hours and is exacerbated by fatty meals and is associated with nausea and vomiting. Fever, tachycardia, positive Murphy’s sign, leukocytosis, and abnormal liver functions help further distinguish this from biliary colic.
  • Myocardial infarction – especially in inferior wall and right ventricular involvement, sometimes patients can present with epigastric pain with nausea and vomiting. The presence of other symptoms like dizziness, shortness of breath, and abnormal vital signs in a high-risk patient should alert the clinician to look for this.
  • Mesenteric ischemia – while acute mesenteric ischemia presents with severe, acute onset abdominal pain; the chronic variant usually presents with ongoing post-prandial epigastric pain and can be mistaken for peptic ulcer disease. Older age, presence of risk factors for atherosclerosis, and weight loss should prompt a workup for the same.
  • Mesenteric vasculitis – unexplained abdominal symptoms with or without lower gastrointestinal bleeding in a patient with other features from underlying systemic vasculitis should raise the suspicion of mesenteric vasculitis.

Prevention Of Peptic Ulcer Disorder

There are a lot of things you can do to prevent the symptoms of GERD. Some simple lifestyle changes include

  • Elevate the head of your bed at least six inches. If possible, put wooden blocks under the legs at the head of the bed. Or, use a solid foam wedge under the head portion of the mattress. Simply using extra pillows may not help.
  • Avoid foods that cause the esophageal sphincter to relax during their digestion. These include:
    • Coffee
    • Chocolate
    • Fatty foods
    • Whole milk
    • Peppermint
    • Spearmint
  • Limit acidic foods that make the irritation worse when they are regurgitated. These include citrus fruits and tomatoes.
  • Excess pounds put pressure on your abdomen, pushing up your stomach and causing acid to reflux into your esophagus.
  • Smoking decreases the lower esophageal sphincter’s ability to function properly.
  • If you regularly experience heartburn while trying to sleep, place wood or cement blocks under the feet of your bed so that the head end is raised by 6 to 9 inches. If you can’t elevate your bed, you can insert a wedge between your mattress and box spring to elevate your body from the waist up. Raising your head with additional pillows isn’t effective.
  • Wait at least three hours after eating before lying down or going to bed.
  • Put down your fork after every bite and pick it up again once you have chewed and swallowed that bite.
  • Common triggers include fatty or fried foods, tomato sauce, alcohol, chocolate, mint, garlic, onion, and caffeine.
  • Clothes that fit tightly around your waist put pressure on your abdomen and the lower esophageal sphincter.
  • Avoid carbonated beverages. Burps of gas force the esophageal sphincter to open and can promote reflux.
  • Eat smaller, more frequent meals.
  • Do not eat during the three to four hours before you go to bed.
  • Avoid drinking alcohol. It loosens the esophageal sphincter.
  • Lose weight if you are obese. Obesity can make it harder for the esophageal sphincter to stay closed.
  • Avoid wearing tight-fitting garments. Increased pressure on the abdomen can open the esophageal sphincter.
  • Use lozenges or gum to keep producing saliva.
  • Do not lie down after eating.

Complications Of Peptic Ulcer 

  • Perforation – A hole develops in the lining of the stomach or small intestine and causes an infection. A sign of a perforated ulcer is sudden, severe abdominal pain.
  • Internal bleeding – Bleeding ulcers can result in significant blood loss and thus require hospitalization. Signs of a bleeding ulcer include lightheadedness, dizziness, and black stools.
  • Scar tissue – This is thick tissue that develops after an injury. This tissue makes it difficult for food to pass through your digestive tract. Signs of scar tissue include vomiting and weight loss.
  • Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
  • Perforation (a hole in the wall of the gastrointestinal tract) often leads to catastrophic consequences if left untreated. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of the stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain; an example is Valentino’s syndrome, named after the silent-film actor who experienced this pain before his death. Posterior wall perforation leads to bleeding due to the involvement of the gastroduodenal artery that lies posterior to the first part of the duodenum.
  • Penetration is a form of perforation in which the hole leads to and the ulcer continues into adjacent organs such as the liver and pancreas.
  • Gastric outlet obstruction is a narrowing of the pyloric canal by scarring and swelling of the gastric antrum and duodenum due to peptic ulcers. The person often presents with severe vomiting without bile.
  • Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.

References

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