Stomach acid then gets through to the lining. NSAIDs nonsteroidal anti-inflammatory drugs. These are over-the-counter pain and fever medicines such as aspirin, ibuprofen, and naproxen. Over time they can damage the mucus that protects the lining of your stomach. What are the symptoms of peptic ulcers? Less common ulcer symptoms may include: Feeling full after eating a small amount of food Burping Nausea Vomiting Not feeling hungry Losing weight without trying Bloody or black stool Vomiting blood Peptic ulcer symptoms may look like other health problems.
How are peptic ulcers diagnosed? Imaging tests used to diagnose ulcers include: Upper GI gastrointestinal series or barium swallow. This test looks at the organs of the top part of your digestive system. It checks your food pipe esophagus , stomach, and the first part of the small intestine the duodenum. You will swallow a metallic fluid called barium. Barium coats the organs so that they can be seen on an X-ray. Upper endoscopy or EGD esophagogastroduodenoscopy.
This test looks at the lining of your esophagus, stomach, and duodenum. It uses a thin lighted tube called an endoscope.
The tube has a camera at one end. The tube is put into your mouth and throat. Then it goes into your esophagus, stomach, and duodenum. Your health care provider can see the inside of these organs. A small tissue sample biopsy can be taken. This can be checked for H. You may also have the following lab tests to see if you have an H. These check for infection-fighting cells antibodies that mean you have H. Stool culture. A small sample of your stool is collected and sent to a lab.
In 2 or 3 days, the test will show if you have H. Urea breath test. This checks to see how much carbon dioxide is in your breath when you exhale. You will swallow a urea pill that has carbon molecules. If you have H. You will have a sample taken of your breath by breathing into a bag.
It will be sent to a lab. If your sample shows higher than normal amounts of carbon dioxide, you have H. How are peptic ulcers treated? Lifestyle changes may include: Not eating certain foods. Avoid any foods that make your symptoms worse. Quitting smoking. Smoking can keep your ulcer from healing.
The bacteria has the ability to withstand the strong stomach acid and digestive enzymes. It burrows into the stomach wall tissue and can penetrate deeper into it. In the process it weakens and even destroys the blood vessels in the stomach wall. This results in a bleeding ulcer. The severity of the bleed depends on the blood vessels that is affected and the severity of the damage.
Read more on causes of stomach bleeding. Vomiting does not always occur but when it does, blood may be visible in the vomitus. This is more likely to occur with an acute bleed where there is extensive bleeding. Vomiting may be associated with the ulcer itself or occur due to other reasons where the blood is then noticed. The vomit may be stained with fresh blood or degraded blood may appear as black coffee grounds in the vomit.
Blood in the stool is a more common symptom. However, most of the time the blood is degraded by the time it passes from the stomach down the intestines to the rectum. The stool may appear dark and tarry. This is known as melena. However, there are instances where fresh blood may be visible in the stool particularly when wiping after a bowel movement. This is more likely to occur when there is a severe bleed or diarrhea. Dizziness is another sign of a bleeding ulcer but is more likely to occur in severe bleeds and particularly in the elderly.
The blood loss can lead to low blood pressure and anemia, both of which contribute to dizziness. Pain may further contribute to it. In severe cases, a person may even have fainting spells. Loss of consciousness is a serious sign, especially in the elderly. Ask a Doctor Online Now! Pain in the epigastric region upper middle abdomen is another common sign. It may even be present before the ulcer starts to bleed. Gisela A. Ocasio Quinones ; Andrew Woolf.
Authors Gisela A. Ocasio Quinones 1 ; Andrew Woolf 2. Duodenal ulcers occur when there is a disruption to the surface of the mucosa of the duodenum. These ulcers are part of peptic ulcer disease, which involves the stomach and first part of the duodenum. This activity reviews the evaluation and treatment of duodenal ulcers and explains the interprofessional team's role in improving care for patients with this condition. Objectives: Summarize the epidemiology of duodenal ulcers.
Outline the dysfunctional mucosal defense mechanisms in the pathophysiology of duodenal ulcers. Review the importance of proton pump inhibitors and H2 receptor blockers in the treatment of duodenal ulcers. Describe the importance of the interprofessional team in the diagnosis and treatment of duodenal ulcers.
Access free multiple choice questions on this topic. Duodenal ulcers are part of a broader disease state categorized as peptic ulcer disease. Peptic ulcer disease refers to the clinical presentation and disease state that occurs when there is a disruption in the mucosal surface at the level of the stomach or first part of the small intestine, the duodenum.
Anatomically, both the gastric and duodenal surfaces contain a defense system that includes pre-epithelial, epithelial, and subepithelial elements. Ulceration occurs from damage to the mucosal surface that extends beyond the superficial layer. While most duodenal ulcers present with dyspepsia as the primary associated symptom, the presentation can range in severity levels, including gastrointestinal bleeding, gastric outlet obstruction, perforation, or fistula development.
Therefore, the management is highly dependent on the patient's presentation at the time of diagnosis or progression of the disease.
The diagnosis of duodenal vs. Any patient diagnosed with peptic ulcer disease and, most specifically, the duodenal ulcer should undergo testing for H.
Some of these include Zollinger-Ellison syndrome, malignancy, vascular insufficiency, and history of chemotherapy. Most recently, a systematic review of seven studies discovered the rates to be significantly lower. However, the variability was thought to be due to the prevalence of H. In areas with a higher incidence of H. As noted above, duodenal ulcers are the result of the corrosive action of gastric secretions on the surface epithelium of the small intestine that has undergone prior injury.
In duodenal ulcers, there are multiple underlying comorbidities to consider when establishing the diagnosis and underlying cause. The mechanism by which H. However, the thinking is that H. A secondary running theory considers the possibility that H. Prostaglandins play a crucial role in developing the protective mucosa in the gastrointestinal tract, including gastric and small intestine mucosa.
Recurrent use of NSAIDs causes a significant and persistent decrease in prostaglandins leading to susceptibility to mucosal injury. It is thought to be one of the primary predisposing pathophysiologic factors for the development of duodenal ulcers. However, the ultimate result is generally recurrent mucosal injury that predisposes the tissue to ulceration or an elevation in the amount of acid the mucosa is exposed to, which in turn causes tissue damage.
In cases of H. As Giemsa stain is straightforward to use, inexpensive and provides consistent results, it is preferred in many laboratories. The presentation of patients with symptoms consistent with dyspepsia or peptic ulcer disease, and most specifically, duodenal ulcers, can vary highly depending on the degree of disease progression and time when a patient seeks treatment.
Overall, dyspepsia is the most common symptom for patients who do experience symptoms. As noted above, the degree of disease progression before the initial diagnosis can affect the symptoms with which a patient may present.
The location of the disease can also be differentiated based on symptoms. Other common signs and symptoms include epigastric abdominal pain, bloating, nausea and vomiting, and weight gain due to improved symptoms post meals. Patients who initially present with ulcer-related complications may present with symptoms suggestive of upper GI bleed, including melena, hematemesis, elevated BUN, and anemia of varying degrees in severity with associated fatigue.
Patients who present with more alarming symptoms such as anemia, melena, or hematemesis, which may represent perforation or bleeding, will likely require more invasive forms of evaluation. The patient's history and age should also be considered when considering duodenal ulcers as part of the differential diagnosis, especially when patients present with more non-specific symptoms such as epigastric abdominal pain.
Duodenal ulcers may occur in any age group. However, they are most commonly diagnosed in patients aged 20 to 45 and are more common in men than women.
Most patients will have a history of presenting symptoms consistent with peptic ulcer disease PUD associated with a previous diagnosis of H. Other elements of the history to consider include smoking history, daily aspirin use, and history of GI malignancy. On physical examination, patients may have epigastric abdominal tenderness, and if presenting with complications, they may demonstrate signs of anemia such as pale skin and positive fecal occult blood test. Once the diagnosis of H.
In simple terms, the diagnosis of peptic ulcer disease in general and, more specifically, duodenal ulcers can be made directly by the visualization of the ulcer on upper endoscopy.
The evaluation process will depend on what studies the patient may have had completed for the previous assessment of their symptoms. Computed tomography performed for the evaluation of abdominal pain can identify non-perforated peptic ulcers.
However, the majority of patients will need a referral for esophagogastroduodenoscopy EGD for further evaluation. Barium endoscopy is an option for patients with contraindications to EGD. Once the diagnosis of peptic ulcer disease has been made, it is vital to establish the etiology of the disease as this will help develop a treatment plan for the patient, not only acutely but also a long-term plan to help prevent a recurrence.
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