Peptic Ulcer Disease
What You Need To Know
What Is Peptic Ulcer Disease?
- Gastric Ulcers: occur on the inner lining of the stomach
- Esophageal Ulcers: occur on the inner linings of the esophagus
- Duodenal Ulcers: occur on the inner lining of the upper part of the small intestine
How it Occurs
FIRST: Some Background on Gastric Cells and Digestion
When the enteric nervous system is stimulated from eating the release of the neurotransmitter acetylcholine acts on the parietal cells in the gastric lumen to stimulate the release of gastric acid also known as hydrochloric acid for digestion and bactericidal properties.
Hormonal stimulation occurs as food arrives in the stomach. The paracrine (cell to cell) stimulation is activated by the secretion of the hormone gastrin from G cells in the mucosa. This stimulates ECL cells to secrete histamine, which directly stimulates parietal cells to secrete hydrochloric acid.
The chief cells of the stomach lining secrete pepsinogen that becomes pepsin a proteolytic enzyme (protein digestion) when in contact with gastrin and hydrochloric acid.
The last cell is the D (delta) cell and it is the inhibitory regulator of the digestive juices. This cell releases somatostatin, which inhibits the secretion of gastric acids.
How Does The Mucosa Protect Itself From The Harmful Secretions?
- Fovealar cells of the stomach make a mucus barrier to the highly acidic enzymes and secretions. This mucus produces a special gastric surfactant containing bicarbonate that protects the epithelial cells from hydrogen ion (acid) penetration. The esophagus has its own mucal barrier and resistance as well as the duodenum.
- Regulation of acid production by somatostatin.
- Epithelial repair made possible by the well perfused tissue.
Pathogenesis: The Two Main Causes
H. Pylori
NSAIDs
Duodenal Ulcers
- continued stimulation of gastric acid well after digestion is complete
- failure in the negative feedback in which acid is inhibited from being released
- overwhelming of the buffering ability of the pancreatic secretions
- necrosis of mucosal epithelium and elevated levels of gastrin and pepsin
- toxins promoting inflammation
NSAID factors:
- inhibition of prostaglandins, reducing barrier resistance and decreases bicarbonate secretion.
Other factors:
- smoking stimulates the production of acid
With duodenal ulcers, acid concentrations increase and penetrate the mucosa!
Gastric Ulcers
- disrupt the gastric mucosa by all of the same mechanisms as in a duodenal ulcer.
- Gastric secretions however, may be normal or even decreased
NSAID factors:
- disrupt the mucosal barrier and reduce its resistance to the acidic contents of the stomach
- decreased synthesis of prostaglandins
- ulcerogenic drugs
Other factors:
- increased bile salt concentration
- gastritis
- reflux of juices from the duodenum
With gastric ulcers the main problem is abnormality that allows increased permeability of hydrogen ions into the mucosa.
It is a vicious cycle because of the stimulation of histamine in response to inflammation causing stomach acid to continuously be recreated!
Esophageal Ulcers
Main affecting factors:
- Acid Reflux: stomach contents coming back up through the esophagus from anything including indigestion, GERD or vomiting irritates the esophageal lining
- Smoking damages the protective barrier mechanisms by harming the mucous barrier and irritating the cells with toxin exposure
- NSAIDs irritate the mucosa of the esophagus as well and make ulcerations worse if they are present there.
Other Causes
Zollinger-Ellison Syndrome: Gastrinoma and or hyperplasia of pancreatic islet cells causes overproduction of gastric acid that causes recurrent peptic ulcers especially in unusual areas. This is a rare occurrence.
Genetics: nearly half the people who develop ulcers say that someone in the family has had them before.
Ischemia: is a very rare case because the stomach and duodenum are perfused very well
Alcohol: in excess increases the production of stomach acid
Diagnosis
- Radiological Diagnosis- Barium x-ray or upper gastrointestinal series- This is a less invasive procedure that allows you to diagnose ulcer disease in the stomach or duodenum; however, it is very difficult to interpret and produces many false positives/negatives. Barium is swallowed by the patient, which will coat the inside of the organs. This coating will allow them to show up on an x-ray.
- Laboratory Testing- Blood, stool sample, urea breath, stomach tissue test are done to detect the presence of H. pylori. Detecting the presence of this bacteria will help guide doctors to different treatments. This test can have many false-positives, especially if patient was recently on an antibiotic.
- Endoscopic Diagnosis- Allows for the esophagus, stomach, and duodenum to be visualized. A scope is placed into the patients mouth and pharynx, and then into the esophagus, stomach, and duodenum to conduct an image to the doctor. This is the most accurate method for establishing a diagnosis for the reason that it allows you to locate the ulcer, determine its size, and figure out if there are other lesions present.
Risk Factors
- Infection from H. Pylori in the gastric mucosa
- Alcohol use
- Smoking
- Increased age
- Chronic diseases (obesity, diabetes, emphysema, cirrhosis, etc.)
- Family history
- Physical stress
- Hypersecretory condition
Treatments
Lifestyle Changes- Smoking can delay healing and is linked to reoccurence. Smoking should be heavily discouraged,
Medications- commonly used in combinations
- Antibiotics- will kill H. pylori
- H2-Blockers- reduce amounts of acid in stomach
- Acid pump inhibitors- will cutoff the stomach-acid pump, which will completely stop the stomach acid production
- Mucosal protective agents- protect stomach's mucous lining from acid by creating a shield.
Surgery- People who do not respond well to medications, have complications arise, or have a cancerous ulcer will require surgery.
- Vagotomy- Will reduce acid secretion by cutting part of the vagus nerve. The vagus nerve transmits impulses from the brain to the stomach.
- Antrectomy- The antrum of the stomach is removed. This will prevent the production of the hormone that triggers the stomach to secrete digestive enzymes. Vagotomy is usually done with this procedure
- Pyloroplasty- The opening to the duodenum and small intestine are enlarged to allow substances to easily pass from the stomach. This is also usually done with a vagotomy.
Manifestations
Pain in the abdomen, specifically the upper left quadrant, is the most common of manifestations. Depending on which kind of ulcer (consequently where it is located) the timing in which pain occurs after eating will vary. Gastric ulcers will be painful almost immediately while duodenal ulcers take until the stomach no longer contains food to emit pain. This is because the lack of contents in the stomach leaves it vulnerable to its own acidic secretions. Additionally, duodenal ulcers will experience pain during sleep while it is less common for those with gastric ulcers. Referred pain in the back also occurs, but is not nearly as prevalent.
Indigestion (dyspepsia) is typical with peptic ulcers. This can be present with general discomfort in the chest and bottom of the throat. This can also be reported as “heart burn” from the sufferer.
Other manifestations include:
- Fatigue
- Dyspnea
- Changes in appetite
The following are manifestations that elicit urgent medical attention
- Dark blood in stool with tarry texture (melena)
- Blood in vomit/emesis (hematemesis)
- Anemia