Peptic Ulcer: Types, Symptoms, Diagnostic tests and Treatment

peptic Ulcer



An ulcer is a sore on the skin or a mucous membrane, accompanied by the disintegration of tissue such as peptic ulcer, anal fissure, mouth ulcer, a venous ulcer, etc.

  • Ulcers can result in complete loss of the epidermis and often portions of the dermis and even subcutaneous fat.
  • Ulcers are most common on the skin of the lower extremities and in the gastrointestinal tract.
  • Complication associated with the ulcer i.e peptic ulcer is that when left untreated the internal bleeding may occur which leads to anemia.
  • Internal bleeding occurs when the sore on the mucous membrane becomes deep and fully rapture the defensive layer, thus damage the membrane and tiny capillaries of the vascular network.

Type of ulcer:

  • Pressure ulcers:

Also known as bedsores/pressure sore

  • Genital ulcer:

An ulcer located on the genital area

  • Anal fissure:

An ulcer or tear near the anus or within the rectum.

  • Diabetic foot ulcer

A major complication of diabetic patients is the diabetic foot.

  • Mouth ulcer

It is an open sore inside the mouth.

  • Aphthous ulcer

It is a specific type of oral ulcer also known as a canker sore.

  • Venous ulcer

A wound thought to occur due to improper functioning of valves In the veins.

  • Peptic ulcer

A peptic ulcer is a break in the gastric or duodenal mucosa. It arises when the normal mucosal defensive factors are impaired or are overwhelmed by aggressive luminal factors such as acid and pepsin.

  • Ulcers extend through the muscularis mucosae and are usually over 5 mm in diameter.

Peptic Ulcer

Sites Affected:

  • Duodenum (1st portion 75%)
  • Stomach (20%)
  • Gastroesophageal junction(1%)
  • Gasteroenterostomy stroma <1%
  • In jejunum <1%


Two Australian scientists:

  • Robin Warren
  • Barry Marshall
  • Discovered that stomach ulcers can be caused by a bacterial infection.
  • Helicobacter pylori play a key role in the development of ulcers. They were awarded Nobel prize in 2005.


  • In the United States, there are about 500,000 new cases per year of peptic ulcer and 4 million ulcer recurrences;
  • The lifetime prevalence of ulcers in the adult population is approximately 10%.
  • Ulcers occur five times more common in the duodenum.

Over 95% are in the bulb or pyloric channel.

  • Ulcers occur slightly more commonly in men than in women (1.3:1)
  • Ulcers can occur in any age group.
  • Duodenal ulcers most commonly occur in patients between the ages of 30 and 55 years.
  • Gastric ulcers are more common in patients between the ages of 55 and 70 years.
  • Ulcers are more common in smokers and in patients taking NSAIDs on a long-term basis.

Etiology of Peptic Ulcer disease

  • Helicobacter pylori
  • Non-steroidal Anti-Inflammatory Drugs (NSAIDs)
  • Gastrinoma (Zollinger-Ellison Syndrome)
  • Hypercalcemia
  • Smoking
  • Stress
  • Alcohol and Diet


  • Peptic ulcers occur when the balance between aggressive factors and mucosal defensive mechanisms are disrupted.
  • Increased acid secretion may occur in patients with duodenal ulcer, but most patients with gastric ulcer have normal or reduced rates of acid secretion.
  • When aggressive factors alter mucosal defense mechanisms, then the subsequent mucosal injury has occurred. This leads to an ulcer.

Types of Peptic Ulcer

  • On the basis of location
    • Esophageal ulcer
    • Gastric ulcer
    • Duodenal ulcer
  • On the basis of cause
    • Pylori induced
    • NSAID induced
    • Stress mucosal Damage

A-   Esophageal ulcer

Esophageal Ulcer usually occurs in the lower end of a patient’s esophagus. The patient may feel difficulty in swallowing and may not eat normally.

B-   Gastric Ulcer

Gastric ulcers, also known as Stomach ulcers are open sores that develop on the lining of the stomach.

The symptom of stomach Ulcer:

  • Burning
  • Indigestion
  • Heartburn

C-    Duodenal Ulcer

A duodenal ulcer is a type of peptic ulcer that occurs in the duodenum.

The most common cause of duodenal ulcer is Helicobacter pylori (H pylori) bacteria.


  • Abdominal pain
  • Bleeding

Peptic Ulcer

H. Pylori Induced Ulcer

  • The pylorus is a Gram-negative microaerophilic bacterium found primarily in the gastric antrum of the human stomach.
  • Pylori involves the production of CagA proteins and vac A, which activate the inflammatory cascade.
  • Enzymes produced by H. pylori that causes tissue damage are:
  • Urease
  • Haemolysins
  • Neuraminidase

NSAID Induced Ulcer

Three patterns of mucosal damage are caused by NSAIDs:

  • Superficial erosions
  • Hemorrhages
  • Silent ulcers
  • Acute superficial erosions may produce by inhibition of COX.
  • The major systemic action of NSAIDs that contributes to the formation of ulcers is the reduction of mucosal prostaglandin production
  • The presence of NSAID-induced ulcers does not correlate with abdominal pain.
  • NSAIDs themselves often mask ulcer pain.
  • NSAIDs have a four-fold increase in the risk of ulcer complications compared with non-users.

Risk factors for NSAID ulcers

  1. Age greater than 65 years
  2. Previous peptic ulceration/bleeding
  3. High dose of NSAID or more than one NSAID (including aspirin)
  4. Short-term history of NSAID use (<1month)
  5. Concomitant corticosteroid or anticoagulant use Cardiovascular disease

How NSAIDs Act?

NSAIDs act

Stress-Induced Ulcer

Severe physiological stress may induce gastro-duodenal ulcerations. These may lead to hemorrhage or perforation.

Causes  of  stress  ulcer:

  • Diminished blood flow to the gastric mucosa
  • Decreased cell renewal
  • Diminished prostaglandin production
  • Acid hypersecretion


Peptic Ulcer mechanism

Comparison of Types of Ulcer

Characteristics H. pylori-induced

Peptic ulcer

Peptic ulcer
Stress-related mucosal damage
Condition Chronic Chronic Acute
Site of damage Duodenum > stomach Stomach > duodenum Stomach > duodenum
Ulcer depth Superficial Deep Most superficial
GI bleeding Less severe, single vessel More severe, single vessel More severe, superficial mucosal capillaries


Signs & Symptoms

  • Epigastric pain (dyspepsia)
  • Pain localized to the epigastrium
  • Nocturnal pain
  • Nausea & Vomiting
  • Anorexia
  • Weight loss
  • Oral flatulence, bloating, distension
  • Heartburn
  • Pain radiating to the back

Diagnostic Tests

  • Laboratory Findings
  • Endoscopy
  • Imaging
  • Test for H. pylori

1)   Laboratory Tests

  • Laboratory tests are normal in uncomplicated peptic ulcer disease
  • Leukocytosis suggests ulcer penetration or perforation.
  • An elevated serum amylase suggests ulcer penetration into the pancreas.

2)   Endoscopy

The endoscope allows visualization of at least 50% of the small intestine, including most of the jejunum and different degrees of the ileum.

An endoscope is:

  • A thin, flexible, lighted tube
  • passed through the mouth
  • Pharynx and into the esophagus.
  • The forward-viewing scope transmits an image of the esophagus, stomach, and duodenum to a monitor visible to the physician.
  • Air may be introduced into the stomach, expanding the folds of tissue and enhancing examination of the stomach.

Fig: Endoscopy visualization


3)   Imaging

  • Abdominal CT imaging is obtained in patients with suspected complications of peptic ulcer disease
  • Because barium upper gastrointestinal series is less sensitive for the detection of ulcers.

Test for H. Pylori

Many methods for detection of H.pylori like:

  • Serological tests
  • Urea breath tests
  • Stool antigen tests

Serological tests:

  • Serological tests are based on the detection of anti-H. pylori IgG antibodies.
  • Not able to distinguish between active or previous exposure to infection.

Urea breath test:

  • Simple and non-invasive
  • have a sensitivity and specificity over 90%
  • Accurate for both initial diagnosis and confirmation of eradication.
  • based on the principle that urease activity in the stomach of infected individuals hydrolyzes urea to form ammonia and carbon dioxide.
  • a breath test is preferable and more convenient

Stool antigen tests:

  • It uses an enzyme immunoassay to detect H.pylori antigen in stool.
  • This test also has a sensitivity and specificity over 90%
  • Accurate for both initial diagnosis and confirmation of eradication.


Treatment Objectives

  • To relieve pain and reduce gastric acid secretion
  • To promote healing of the ulcer
  • To eradicate  pylori if present
  • To prevent recurrence of the ulcer
  • To avoid complications

Medication Selection

Treatment of Peptic Ulcer

  • Triple therapy is given for 1 weak
  • PPI (drug of choice is omeprazole)
  • Macrolides (clarithromycin )
  • Penicillin’s (amoxicillin ) or metronidazole
  • Triple therapy is given for 2 weeks
  • Quadruple therapy is given for 2 weeks
  • Triple therapy + antisecretory agent (bismuth subsalicylate).

Active ulcer not attributable to H pylori

Consider other causes: NSAIDs, Zollinger-Ellison syndrome, gastric malignancy. Treatment options:

  •    Proton pump inhibitors:

Uncomplicated duodenal ulcer: treat for 4 weeks

Uncomplicated gastric ulcer: treat for 8 weeks

  •   H2 -receptor antagonists:

Uncomplicated duodenal ulcer: cimetidine 800 mg, ranitidine or nizatidine 300 mg, famotidine 40 mg, orally once daily at bedtime for 6 weeks

Complicated ulcers: proton pump inhibitors are the preferred drugs.

Treatment of Stress Ulcer

The most commonly used regimen:

  • Ranitidine 50 mg IV every 8 hr.
  • Reducing to 25mg in severe renal impairment


  • People who do not respond to medication, or who develop complications:
  • Antrectomy – remove the lower part of the stomach (antrum)
  • Vagotomy – cutting the vagus nerve to interrupt messages sent from the brain to the stomach to reducing acid secretion.


The opening into the duodenum and small intestine (pylorus) is enlarged

Complications of peptic ulcer disease

  1. Gastrointestinal hemorrhage
  2. Ulcer Perforation
  3. Gastric Outlet Obstruction

Gastrointestinal Hemorrhage

Patients with bleeding ulcers may report :

  • Melena
  • Weakness
  • Orthostatic syncope
  • vomiting blood(hematemesis)
  • Initial treatment
  • replacement of fluids
  • severe bleeding
  • blood transfusions


  • Perforation occurs when an ulcer eats through the wall of the stomach or intestine into the abdominal cavity.
  • When perforation occurs, partially digested food, bacteria, and enzymes from the digestive tract may spill into the abdominal cavity, causing inflammation and infection (peritonitis).
  • Peritonitis usually causes sudden and severe pain.
  • Treatment usually requires urgent hospitalization and surgery.

Gastric outlet obstruction  

In some cases, an inflamed or scarred stomach ulcer can obstruct the normal passage of food.

 Symptoms can include:

  • Vomiting
  • bloating or fullness
  • Weight loss
  • Endoscopy can be used to confirm the obstruction.
  • Proton pump inhibitors (PPIs) or H2-receptor antagonists can be used.

Drug Food Interactions

  • Sucralfate with enteral food
  • Food with erythromycin
  • Tetracycline’s with dairy products
  • PPIs when given with
  • Acidic food and citrus fruits
  • Morning cup of coffee or afternoon soda
  • Spicy foods

Role of Pharmacist

  • Should assess patient allergies, NSAIDs, Patient use of alcohol and oral birth control medications, the likelihood of noncompliance
  • Should monitor the patient for adverse effects, drug interactions, Salicylate toxicity.
  • Should guide the patient about to take PPIs as the whole capsule, do not crush
  • Take omeprazole and lansoprazole at bedtimes
  • Take misoprostol with food and to avoid Mg containing antacids.

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