Peptic ulcer disease

Defect or injury to mucosa of the stomach or small intestine.

Sequelae ranges from abdominal pain in G.I. bleeding to gastric outlet obstruction and perforation.

Prevalence estimated at 8.4%.

Higher peptic ulcer disease incidence associated with male gender, smoking, and chronic medical conditions.

Associated with increasing age.

There has been a significant decrease in peptic ulcer disease diagnoses throughout the world.

The most common cause of upper G.I. bleeding.

Due to a variety of causes including increased production of stomach acid and digestive enzyme pepsin.

Ulceration results when mucosal defense mechanisms in the upper G.I. tract or overwhelmed by endogenous factors such as acid, pepsin, or bile, or by exogenous factors.

Some stomach acid is necessary for the development of ulcers.

The two most common causes of PUD are nonsteroidal anti-inflammatory drugs and Helicobacter pylori infection, both of which may present with gastric or duodenal ulcerations.

Most ulcers of the small intestine occur in the duodenum.

Two most common causes are Helicobacter pylori and nonsteroidal anti-inflammatory drugs: The relative risk of developing a symptomatic ulcer is 4 for nonaspirin NSAID users and 2.9 for patients taking aspirin.

The majority of PUD cases are known to be associated with age. 

H. pylori creates ulceration by causing inflammation of the stomach and small intestine mucosa and also. increases stomach acid production. Nonsteroidal anti-inflammatory drugs cause irritation of stomach and small intestine mucosa eroding the tissue and can dissolve the protective mucus layer that overlies the mucosa of the stomach.

The strain of H. pylori, genetic variation, exposure to NSAIDs or tobacco may influence ulcer development.

Medications including corticosteroids, potassium chloride and bisphosphonates can cause ulcerations.

Crohn’s disease, infection with Cytomegalovirus or herpes simplex virus, can lead to gastric and small intestine.

Stress ulcers can occur in critically ill hospitalized patients as a result of decreased blood flow to the stomach and small intestine.

Gastrinomas, the Zollinger-Ellison syndrome, can lead to peptic ulcers secondary to excess gastric acid.

Approximately 2/3 of patients found to have peptic also disease are asymptomatic.

The most common presenting symptom is epigastric pain, which may be associated with dyspepsia, bloating, abdominal fullness, nausea, and early satiety.

In many patients there may be intermittent symptoms.

Dyspepsia is the most common symptom with pain or discomfort located in the mid, upper abdomen and may radiate to the back.

Duodenal ulcer pain characteristically improves with eating and worsens with fasting and at night.

Stomach ulcer pain often increases with eating and may be accompanied by poor appetite and weight loss.

Gastrointestinal bleeding, weight loss and persistent vomiting, and anemia may occur.

Diagnosis confirmed by upper gastrointestinal endoscopy or radiographic imaging.

Upper endoscopy is an urgent procedure in patients with dyspepsia and concurrent alarm systems: greater than 60 years of age, family history of upper G.I. tract malignancy, weight loss, early satiety, dysphasia, gastrointestinal bleeding, iron deficiency, or vomiting.

Endoscopy allows for establishing weather and ulcer is benign or malignant.

Physical examination is usually negative except for epigastria tenderness.

Laboratory testing may indicate the presence of anemia and iron deficiency.

A positive serum test for H. pylori may be present.

A positive test for the presence of H. pylori antigen in the stool indicates that a person is currently infected with the organism and is stronger evidence that H. pylori is the cause of an existing peptic ulcer.

The test for urea in a person’s breath is indicative of H. pylori in the stomach.

Diagnostic testing for H. pylori includes urea breath testing, stool antigen testing, rapid urease testing or histology of gastric biopsies

For patients treated for H. pylori in the past, they should undergo testing to demonstrate eradication with either stool antigen testing or urea breath testing.

PPIs are the main medical treatment for PUD related G.I. bleeding.

PPIs promote ulcer healing by acid suppression.

For H. pylori 10 to 14 day triple therapy with bismuth and non-bismuth containing agents including clarithromycin, amoxicillin, or metronidazole.

Peptic also disease complications include: bleeding, perforation, penetration, and gastric outlet obstruction.

Risk factors associated with peptic ulcer complications include: the use of NSAIDs, aspirin, H pylori infection, smoking, acid hypersecretory state, chronic/refractory type ulcers, large size, and location of ulcers.

Complicated peptic ulcer disease risks are also related to concomitant comorbid disease, older age, poor physiological status, metabolic acidosis, acute renal failure, hypoalbuminemia, and delayed treatment.

Upper cash or intestinal hemorrhage is the most common complication of peptoc ulcer  disease and is associated with morbidity and a 10% mortality.

Upper endoscopy is the best initial test in suspected peptic also bleeding as it is both diagnostic and possibly therapeutic.

Endoscopic hemostasis therapies include: injection, thermal, mechanical, or a combination of these modalities.

Endoscopic hemostasis is effective in achieving hemostasis and reducing re-bleeding, the need for blood transfusion, urgent surgery, length of hospitalization, and mortality.

Intravenous PPI should be used for 72 hours post endoscopic hemostasis followed by oral PPI therapy.

Patients who to fail endoscopic hemostasis may benefit from transcatheter angiography and treatment.

The use of surgery in the treatment of peptic ulcer bleeding has significantly diminished in the past two decades.

Perforated peptic ulcer, is a medical emergency, with associated mortality of up to 30%.

The classic clinical triad of sudden onset of abdominal pain, tachycardia, and abdominal rigidity is the hallmark of peptic ulcer perforation.

Peptic ulcer perforation is seen with abdominal distention, tenderness to palpation, guarding and rebound when peritonitis is present.

Peptic ulcer perforation is associated with leukocytosis and x-rays may show sub diaphragmatic free air is up to 15% of patients with bowel perforation.

Abdominal CT is more sensitive to detect small amounts of free air and is the imaging modality of choice in suspected perforated peptic ulcer.

Urgent surgical intervention is imperative to improve patient outcomes for perforated peptic ulcer.

Peptic ulcer penetration is the penetration of an ulcer through the bowel wall into an adjacent organ or an anatomical structure without free air, perforation or leakage of bowel  continents into the peritoneal cavity.

Penetrating ulcers occur more most commonly with gastric antral ulcers and duodenal alters.

Penetration May occur  into the pancreas, biliary tract, omentum, liver, vascular structures, and colon.

Complications of penetrating ulcers include abscess formation, hemorrhage, hemobilia, hyperamylasemia, and rarely, pancreatitis.

Gastric outlet obstruction is most often associated with a duodenal or pyloric channel ulcer.


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