Gastric Ulcer


Article Author:
Andrew Woolf


Article Editor:
Robert Rose


Editors In Chief:
Wanda Wright
Cynthia Oster


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
1/28/2019 4:30:01 PM

Introduction

Gastric ulcers are a common clinical presentation in the United States and often lead to the expenditure of millions of healthcare dollars. They are a break in the mucosal barrier of the stomach lining that penetrates through the muscularis mucosa and are greater than 5 mm in diameter. It is important to understand this disease process is both preventable and treatable. Patients may be treated differently depending on the etiology of their gastric ulcer. The body has natural ways to protect the stomach mucosa from the harmful acidic environment that is the gastric lumen. When alterations occur to these defenses, it can lead to changes in the gastric mucosa which will eventually cause erosion and then ulceration. Gastric mucosa protection is via prostaglandins, mucous, growth factors, and adequate blood flow. Known damaging factors of this barrier include smoking, hydrochloric acid, ischemia, NSAID medications, hypoxia, alcohol, and Helicobacter pylori infection. 

Etiology

The most common etiologies of gastric ulcers include a bacterial infection with Helicobacter pylori and gastric prostaglandin loss associated with the use of non-steroidal anti-inflammatory medications. Less common etiologies include hypergastrinemia (Zollinger-Ellison syndrome), viral infections such as CMV, chemotherapy and radiation, gastric outlet obstruction, gastric infiltrative disorders such as malignancy, cigarette smoking, and Crohn disease. The common factor in all of these etiologies is that they promote a breakdown in the mucosal barrier and expose the gastric mucosa to the damaging effects of acid.[1]

Epidemiology

Gastric ulcers are a part of peptic ulcer disease, which carries a lifetime prevalence of 5 to 10% of patients, which is likely an underestimation of the disease as some patients may remain asymptomatic. Studies have shown that the prevalence of gastric ulcers increases with age and with the chronicity of NSAID use. Research shows that smoking leads to a relative risk of 2.0 times that of non-smokers for developing gastric ulcers.  There is no difference between men and women in the prevalence of gastric ulcers. The prevalence of Helicobacter pylori infection at age 60 approximates 50% in the US population. Estimates are that 25% of chronic NSAID users will develop gastric ulcers.[2]

Pathophysiology

The pathophysiology of gastric ulcer development depends on the insult. Since about 80 to 90% of gastric ulcers result from either Helicobacter pylori and/or NSAID use, a detailed discussion will focus each in detail.

First, regarding Helicobacter pylori - these bacteria colonize about 45-50% of the stomach mucosa worldwide. It is a bacterium that people are inoculated with at an early age, especially in developing countries with lower socioeconomic status and crowded households. These bacteria induce an inflammatory response in the host that leads to an epithelial response, degeneration, and injury, known as gastritis. Typically, patients with this infection develop pan-gastritis. This damages the antral somatostatin release, which leads to an increase in gastrin secretion which stimulates increased acid production. Patients who develop gastric ulcers are those in whom the bacteria has remained in the antrum. Parietal cells of the more proximal gastric body still have full production capabilities preventing ulcer genesis in this area. Of note, not all patients with this infection are symptomatic; this depends on the virulence of the bacteria and other host risk factors. A common bacterial virulence factor is the production of cagA, which leads to more cytokine cell destruction and mucosal damage.[3]

NSAID medications are the other most common etiology causing gastric ulcers. Patients who use these medications have a relative risk of four for developing gastric ulcers when compared to people who don't. There are multiple mechanisms by which NSAID medications lead to ulceration. The drugs themselves are weak acids when they become exposed to gastric acid. They remain in the epithelial cells and lead to increased cellular permeability, which leads to physical cellular injury. The primary mechanism of NSAID induced ulceration is the decrease in prostaglandin synthesis. NSAIDs inhibit the cyclooxygenase-1 enzyme, which usually increases prostaglandin synthesis which in turn leads to gastric bicarbonate secretion, mucus barrier formation, increased mucosal blood flow, and accelerated epithelial cell restitution and repair after injury or cell death. NSAID medications allow the gastric mucosa to become more vulnerable to gastric acid and pepsin damage. Overall, the most harmful physiological damage results from the decrease in gastric blood flow and the mild ischemia it causes in the gastric mucosa.

Overall, the pathophysiology of gastric ulcer development depends on the etiology, but they all lead to the loss or damage of the gastric mucosal integrity. 

Histopathology

On histopathology, one will see an ulcer base with clear margins that penetrates the muscularis propria and into the submucosa. Inflammatory debris on the epithelial surface is often present. In the submucosa, one will see fibrosis and thickened blood vessels. 

History and Physical

The typical presentation of a patient with gastric ulcers is epigastric pain that is worse with eating. It often correlates with mild nausea and early satiety. They often describe this pain as a sharp or burning type of pain that typically doesn't radiate. The most common finding on the physical exam is epigastric tenderness. These symptoms may continue for weeks or months before patients seek medical help. Patients may present with an upper GI bleeding. The clinician should ask if they are having any black tarry stools, hematemesis, coffee ground emesis, or bright red blood per rectum. It is important to remember that up to 15% of patients who present with bright red rectal bleeding have a brisk upper GI bleed. 

During the interview with the patient, one should definitely ask about use of NSAID, oral anticoagulation, and a history of peptic ulcer disease. 

Evaluation

When a gastric ulcer is suspected, evaluation for hemodynamic stability is critical as they often present with upper GI bleeding and may have hemorrhagic shock. Necessary labs include BMP, CBC, PT/INR, and lipase. Chest X-ray should be obtained to test for other causes of epigastric pain. Many times patients are evaluated for pancreatitis with an abdominal CT scan.

During endoscopy, gastric ulcers are graded using the Forrest classification scheme; this provides the estimated risk of ulcer bleeding and helps to distinguish which ulcers need endoscopic management such as injection therapy, cautery, or hemoclip placement. Below is a representation of the grading system.[3]

Forrest classification:

  • Ia- jet arterial bleeding, 90% rebleeding risk
  • Ib- oozing, 50% rebleeding risk
  • IIa-visible vessel, 25-30% rebleeding risk
  • IIb- adherent clot, 10-20% rebleeding risk
  • IIc- black spot in the ulcer, 7-10% rebleeding risk
  • III- clean based, 3-5% rebleeding risk

Treatment / Management

The goal of treatment and management of gastric ulcers is first to increase the gastric pH and allowing the gastric mucosa to heal, which is possible through administering proton pump inhibitors, such as pantoprazole. A decision to proceed with an EGD should be the next consideration. Alarm symptoms should be recognized which would make the need for an EGD more urgent. Alarm symptoms include unintentional weight loss, bleeding, age over 50, nausea and vomiting. If a gastric ulcer is present on EGD, biopsies of the mucosa surrounding the ulcer will b necessary to rule out gastritis, Helicobacter pylori infection, and malignancy. These patients need to be on PPI therapy twice daily for 8 weeks and then undergo a repeat endoscopy to confirm for healing.[4]

If the patient is on NSAID medications, these require immediate discontinuation. If the biopsies or lab testing are positive for Helicobacter pylori infection, this condition requires treatment with antibiotic therapy and eradication needs to be confirmed. 

If the gastric ulcer is bleeding or has a higher Forrest classification, different modalities to stop and prevent future bleeding can be employed. Epinephrine injection with either cautery or hemoclip placement is usually effective. 

Surgical management may be needed when endoscopic therapy is inadequate or not indicated. Indications for surgical intervention include perforation, uncontrolled bleeding, severe gastric outlet obstruction and ulcers not healed with medical therapy. 

Differential Diagnosis

The differential diagnosis includes other causes of dyspepsia, such as gastritis, chronic pancreatitis, acute pancreatitis, gastric cancer, biliary disease. 

Prognosis

Overall, patients who have gastric ulcers do well when they continue medical treatment and avoid medications that worsen the disease. 

Complications

The most common complications associated with gastric ulcers include GI bleeding, perforation, penetration, and gastric outlet obstruction. 

Consultations

Patients require a gastroenterologist referral for diagnosis and treatment of this disease. 

Deterrence and Patient Education

Patients with gastric ulcers need to know what caused the ulcer and to continue treatment. They need to avoid NSAID medications if this is possible. If positive for Helicobacter pylori, they need to be treated with antibiotics and then have the eradication of the bacteria confirmed. 

Pearls and Other Issues

The most common etiologies of gastric ulcers are Helicobacter pylori infection and NSAID use. Patients often present with epigastric pain that is worse with eating. It frequently correlates with nausea and early satiety. They often present with upper GI bleeding. These patients need to be evaluated to determine when they need an EGD to diagnose ulcers. Recommended treatment is with PPI therapy and avoidance of known triggers. Patients with Helicobacter pylori are at a higher risk of gastric cancer, specifically lymphoma. Ulcers are categorized based on the Forrest classification with Ia having the worse re-bleeding rate and III having the lowest re-bleeding rate. 

Enhancing Healthcare Team Outcomes

To ensure that these patients obtain the best care, they need to receive education about gastric ulcers at all levels. They need to hear it from their healthcare providers, nursing staff, medical assistants and pharmacists. Once their gastric ulcer has healed, they need to avoid the known causes of ulcers and use medications to prevent them. 


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Gastric Ulcer - Questions

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What is the best surgical management of gastric ulcers?



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In which of the following is excess acid secretion sometimes seen?



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Where are benign gastric ulcers most commonly located?



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In which condition would one expect to see a Hampton line?



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A patient was hospitalized after experiencing extensive deep-partial thickness burns. The patient has developed Curling ulcers. Which of the following will most likely be prescribed?



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A patient who has a history of gastric ulcer disease has a sprained ankle and is to receive a medication to relieve pain. Which of the following medications is the better choice given the case history?



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A patient has a proximal gastric ulcer and undergoes a total gastrectomy. Which digestive enzyme would be decreased markedly?



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Which of the following have not been linked to gastric ulcers?



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Besides NSAIDs, which of the following is known to induce gastroduodenal ulcers?



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A 69-year-old male has a gastric ulcer on endoscopy. Which one of the following is the next best initial test to perform for this patient?



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Gastric ulcers have not been related to the intake of which of the following?



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Which organism is associated with the development of gastric ulcers?



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A 55-year-old patient has emesis of bright red blood on 3 occasions over 6 hours. He complains of dizziness but no abdominal pain. He has no significant past medical history. The patient's gastrointestinal bleeding is most likely secondary to to which of the following?



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Which of the following symptoms is NOT common with peptic gastric ulcers?



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A 72-year-old male has an esophagogastroduodenoscopy (EGD) done and has a gastric ulcer. Which of the following statements best describes the role of repeat EGD?



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Which of the following is not associated with a gastric ulcer?



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A patient has pain along the lateral border of the right scapula that is aching in nature and does not change with motion. The pain increases with valsalva. The physical therapist has seen the patient for treatment on 5 occasions and there is no improvement. Select the possible visceral organ causing the pain.



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A patient with a gastric ulcer complains of sharp pain. Which nerve is responsible for the pain?



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A patient is found to have a gastric ulcer. Which of the following should be avoided?



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A 52-year-old female is evaluated for upper abdominal pain with an upper GI X-ray and found to have a single gastric ulcer. The patient is on ibuprofen 600 mg TID for low back pain. Select the next step in management.



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A 60-year-old female is found to have a deep gastric ulcer on the greater curvature measuring 2 x 2 cm and EGD. Biopsies were negative for malignancy or H. pylori. She had been taking H2 blockers at therapeutic doses. Select appropriate management.



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A 59-year-old male presents with a 5-month history of epigastric pain that is associated with early satiety. His past medical history includes hypertension, benign prostatic hyperplasia, and hyperlipidemia. His medications are lisinopril, lovastatin, and a multivitamin. He admits to using ibuprofen 800 mg four times daily for the past two months for knee pain. He denies any weight loss, melena, hematochezia, or hematemesis. Which of the following is a risk factor that would be concerning for a gastric ulcer and would make an EGD (esophagogastroduodenoscopy) more urgent?



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Which of the following best describes the mechanism of injury caused by Helicobacter pylori infection leading to gastric ulcer formation?



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Which of the following is not associated with gastric ulcer formation?



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A 60-year-old male presents to the clinic with a chief complaint of epigastric pain and nausea for the last 8 weeks. He also has been having early satiety with meals and reports a 15-pound weight loss over the last 2 months. His medical history includes hypertension, hyperlipidemia, atrial fibrillation, and osteoarthritis. His medications include rivaroxaban and naproxen. A CBC shows a hemoglobin of 10 mg/dL and a mean corpuscular volume (MCV) of 72. An EGD (esophagogastroduodenoscopy) is done and reveals a 1.3 cm gastric ulcer with a flat, darkly pigmented spot in the pre-pyloric region. Biopsies are taken and are negative for Helicobacter pylori. Which of the following is not an alarm symptom in this patient?



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A patient is diagnosed with multiple 9 mm gastric ulcers in the antrum during an EGD (esophagogastroduodenoscopy) that was performed to evaluate nausea and vomiting. He has been taking ibuprofen 800 mg twice daily for 6 months. How should he be treated at this point?



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Gastric Ulcer - References

References

Scida S,Russo M,Miraglia C,Leandro G,Franzoni L,Meschi T,De' Angelis GL,Di Mario F, Relationship between Helicobacter pylori infection and GERD. Acta bio-medica : Atenei Parmensis. 2018 Dec 17;     [PubMed]
Kayali S,Manfredi M,Gaiani F,Bianchi L,Bizzarri B,Leandro G,Di Mario F,De' Angelis GL, Helicobacter pylori, transmission routes and recurrence of infection: state of the art. Acta bio-medica : Atenei Parmensis. 2018 Dec 17     [PubMed]
Barchi A,Miraglia C,Violi A,Cambiè G,Nouvenne A,Capasso M,Leandro G,Meschi T,De' Angelis GL,Di Mario F, A non-invasive method for the diagnosis of upper GI diseases. Acta bio-medica : Atenei Parmensis. 2018 Dec 17     [PubMed]
Graham DY,Lu H,Dore MP, Relative potency of proton-pump inhibitors, Helicobacter pylori therapy cure rates, and meaning of double-dose PPI. Helicobacter. 2019 Feb     [PubMed]

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