Peptic Ulcers and Gastroesophageal Reflux Disease
Hi, and welcome to this review video on peptic ulcer disease. The integrity of the gastric mucosa (the mucous membrane layer of the stomach) is maintained when a balance exists between the acid secreted and the mucosal protective functions of the stomach and duodenum. A peptic ulcer is an erosion or crater in a segment of the GI mucosa. There are two types of peptic ulcers – a gastric ulcer, occurring in the stomach; and a duodenal ulcer, occurring in the first few centimeters of the duodenum.
Nearly all ulcers are caused by Helicobacter pylori infection or NSAID use. H. Pylori and NSAIDs disrupt normal mucosal defense and repair, making the mucosa more susceptible to acid. H. Pylori bacteria degrades the gastric mucosa, causes inflammatory changes in mucosa, epithelial cell injury and death, and penetrates gastric cells, weakening the mucous layer. Most NSAIDs are weak acids that can cause local mucosal irritation and inflammation, but their primary adverse effect involves the inhibition of cyclooxygenase (COX) enzyme, which is needed to produce prostaglandins that maintain normal mucosal defenses. A decrease in prostaglandin production results in decreased mucus and bicarbonate secretion, decreased mucosal blood flow, inability to form mucous cap after injury, and failure to inhibit acid secretion. All of these factors lead to decreased mucosal defenses and an increased acid load, leading to ulcer formation. Cigarette smoking is a risk factor for ulcer development and their complications. Smoking also impairs ulcer healing and increases recurrence.
Signs and symptoms depend on ulcer location and patient age. Many ulcers are asymptomatic, but pain is most common. Epigastric pain is usually described as gnawing, burning or aching, or sometimes a sensation of hunger, often relieved by food or antacids. The symptoms of a gastric ulcer often do not follow a consistent pattern; eating sometimes exacerbates the pain rather than relieving it. They may also cause bloating, nausea, or vomiting.
Duodenal ulcers tend to cause more consistent pain. Often appearing mid-morning, the pain is relieved by food but recurs 2 to 3 hours after a meal, and often awakens the patient at night. In infancy and early childhood, repeated vomiting, abdominal pain and/or hemorrhage may be the first signs of a duodenal ulcer.
The diagnosis of peptic ulcer disease cannot be made from symptoms alone because they are often nonspecific. Several tests can be done to detect H. pylori, including an ELISA blood test, stool test, and urea breath test. Endoscopy with biopsy must be done to do a Steiner’s stain of biopsy, which is considered the gold standard to diagnosis H. pylori. Endoscopy with biopsy must also be done to differentiate between a benign ulcer and stomach cancer.
The major complications of peptic ulcer disease include hemorrhage, perforation, and obstruction of the pyloric outlet. The most common complication is mild to severe GI hemorrhage. ….Symptoms include hematemesis (vomiting of blood, either bright red or dark ‘coffee ground’ in appearance), melena (black tarry stools), hematochezia (bright red bloody stool); and weakness, syncope, orthostasis, thirst, and sweating caused by blood loss. A peptic ulcer may erode through the wall of the stomach or duodenum, spilling gastric secretions into the abdominal cavity. It may occur spontaneously or from a complication of an endoscopy. The patient presents with severe, sharp abdominal pain, rigid abdomen with rebound tenderness, decreased bowel sounds, and tachycardia, tachypnea, and diaphoresis. An X-ray, CT or MRI confirms the diagnosis. An NG tube is inserted for drainage of the GI tract, IV antibiotics are given, and immediate surgery is required. Gastric outlet obstruction can result from scarring, inflammation from an ulcer, spasm, or muscle obstruction. Obstruction usually develops slowly, as the patient is experiencing symptoms of dyspepsia, including nausea and anorexia, as the stomach fails to empty completely. Diagnosis can be made by abdominal x-ray or aspiration of stomach contents. Treatment includes gastric decompression with an NG tube, acid suppression for the ulcer, and fluid and electrolyte replacement.
Peptic ulcers are more likely to recur if H. pylori is not completely eliminated, and if the patient continually uses NSAIDs or smokes. Patients with H. pylori-associated ulcers have an increased risk of gastric cancer later in life.
The main goal of treatment for peptic ulcers includes eliminating H. pylori when present and reducing gastric acidity. Drug therapy is intended to eliminate symptoms, facilitate healing, and prevent complications and recurrences. Antacids are weak bases that neutralize gastric acid and are used to relieve symptoms, promote ulcer healing, and reduce recurrence. There are absorbable antacids (such as sodium bicarbonate and calcium carbonate), that provide quick neutralization, but should only be used for 1 to 2 days. Nonabsorbable antacids (such as aluminum or magnesium hydroxide) have fewer adverse effects and are preferred. H2 blockers inhibit histamine at the H2 receptor, suppressing acid secretion and reducing gastric juice volume. Examples include Zantac, Pepcid, Tagamet, and Axid, which are all available over the counter. Even more effective than H2 blockers, are the proton pump inhibitors, which can completely inhibit acid secretion as well as have a long duration of action. Examples of proton pump inhibitors include Nexium, Prevacid, Protonix, and Prilosec. Sucralfate is a mucosal protective agent that forms a protective barrier over the ulcer crater, protecting it from irritation. If the patient tests positive for H. pylori, then it must be eradicated with antibiotics along with a proton pump inhibitor. Typically triple therapy is prescribed – a proton pump inhibitor with two antibiotics, such as clarithromycin and either amoxicillin or metronidazole. If resistance to clarithromycin is a problem, then quadruple therapy is given, which includes a proton pump inhibitor, bismuth subsalicylate, metronidazole, and tetracycline. Patients are tested after treatment to ensure H. pylori is eradicated; if not, treatment is repeated. Due to the effectiveness of drug therapy, surgery has declined drastically, and is primarily used for the management of complications, such as perforation, obstruction, and uncontrolled or recurrent bleeding.
Let’s take a look at some questions for review…
Causative factors for peptic ulcer disease include:
Mucosal irritation and inflammation, & inhibition of COX enzyme
Acute illness, trauma, or sepsis
H. pylori, NSAIDs, & cigarette smoking
Both 1 and 3
All of the above
If you chose 4, for both answers 1 and 3, you’re correct! H. pylori, NSAIDs, & smoking are all factors in the development of peptic ulcer disease; and NSAIDs cause mucosal irritation, inflammation & inhibition of COX enzyme. Acute illness, trauma, and sepsis are causative factors in stress ulcers. Let’s try another…
The nurse recognizes the following symptoms as a sign of a duodenal ulcer:
Appearing mid-morning, the pain is relieved by food but recurs 2 to 3 hours after a meal, and often awakens the patient at night.
In infancy and early childhood, repeated vomiting, abdominal pain and/or hemorrhage may be the first signs.
All of the above
If you chose 4, all of the above, you’re right! All of the choices are symptoms of a duodenal ulcer.
That’s all for now. Thanks for watching!