Peptic Ulcer Disease(PUD)

Definition:

An excavation (hollowed-out area) that forms in the mucosal wall of the stomach, in the

pylorus (the opening the stomach and duodenum), in the duodenum (the first part of

small intestine), or in the esophagus. Erosion of a circumscribed area of mucous membrane is

the cause. This Erosion may extend as deeply as the muscle layers or through the muscle to the

peritoneum.

Classifications: Stomach (called gastric ulcer)

Duodenum (called duodenal ulcer) Esophagus (called esophageal ulcer) Meckel's Diverticulum (called Meckel's Diverticulum ulcer)

Types:

Type I: Ulcer along the lesser curve of stomach Type II: Two ulcers present - one gastric, one duodenal Type III: Prepyloric ulcer Type IV: Proximal gastro esophageal ulcer Type V: Anywhere along gastric body, NSAID induced

Causes: Helicobacter Pylori Nonsteroidal Anti-inflammatory Drug (NSAID) Tobacco Smoking Stress Caffeine

Helicobacter Pylori:

A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion can either be decreased (most cases) resulting in hypo- or achlorhydria or increased. Gastrin stimulates the production of gastric acid by parietal cells and, in H. pylori colonization responses that increase gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation.

Nonsteroidal Anti Inflammatory Drug:

Another major cause is the use of NSAIDs. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration. As the prevalence of H. pylori-caused ulceration declines in the Western world due to increased medical treatment, a greater proportion of ulcers will be due to increasing NSAID use among individuals with pain syndromes as well as the growth of aging populations that develop arthritis.

Tobacco Smoking:

Tobacco smoking leads to atherosclerosis and vascular spasms, causing vascular insufficiency and promoting the development of ulcers through ischemia. Nicotine contained in cigarettes can increase parasympathetic nerve activity to the gastrointestinal tract by acting on the nicotinic receptors at synapses - increased stimulation to the enterochromaffin-like cells and G cells increases the amount of histamine and gastrin secreted and therefore increases the acidity of the gastric juice. Similarly, glucocorticoids lead to atrophy of all epithelial tissues. However, these factors, along with diet or spices, blood type, and other factors suspected to cause ulcers until late in the 20th century, are actually of relatively minor importance in the development of peptic ulcers.

Stress:

Researchers also continue to look at stress as a possible cause, or at least complication, in the development of ulcers. There is debate as to whether psychological stress can influence the development of peptic ulcers. Burns and head trauma, however, can lead to physiologic stress ulcers, which are reported in many patients who are on mechanical ventilation.

Caffeine seems to stimulate acid secretion in the stomach, which can aggravate the pain of an existing ulcer. However, the stimulation of stomach acid cannot be attributed solely to caffeine.

Caffeine:

Signs & Symptoms: abdominal pain, classically epigastric with severity relating to mealtimes, after around 3 hours of taking a meal (duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it); bloating and abdominal fullness;

waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus);

nausea, and copious vomiting;

loss of appetite and weight loss;

hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.

melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin);

rarely, an ulcer can lead to a gastric or duodenal perforation. This is extremely painful and requires immediate surgery.

Risk Factors:

Helicobacter Pylori

Use of Nonsteroidal Anti-Inflammatory Drug (NSAIDs)

Alcohol

Tobacco Smoking

Cirrhosis

Stress

Gastritis

Different Laboratory and Diagnostic Procedures

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described.

The diagnosis of Helicobacter pylori can be made by:

Urea breath test (noninvasive and does not require EGD); Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform H. pylori cultures; Direct detection of urease activity in a biopsy specimen by rapid urease test; Measurement of antibody levels in blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;

Stool antigen test;

Histological examination and staining of an EGD biopsy.

Macroscopic appearance

Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irregular in the acute form of peptic ulcer, regular but with elevated borders and inflammatory surrounding in the chronic form. In the ulcerative form of gastric cancer the borders are irregular. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.

Microscopic appearance

A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.

Differential diagnosis of epigastric pain

Peptic ulcer Gastritis

Stomach cancer

Gastroesophageal reflux disease

Pancreatitis

Hepatic congestion

Cholecystitis

Biliary colic

Inferior myocardial infarction

Referred pain (pleurisy, pericarditis)

Superior mesenteric artery syndrome

Pathophysiology:

Damage to mucosa with

alcohol abuse, smoking, use of

aspirin and NSAIDs

Acid and pepsinogen release with chronic vagal response to

increased stress

Infection with Helicobacter

Pylori

Damaged mucosal barrier

Imbalance of aggressive and defensive factor

Low of mucosal cells; Low quality of mucous; Less of tight juntion between cells

A damage mucosa could not secrete enough mucus to act as a barrier against

gastric acid

Mucosal ulcerations, possible bleeding and

scarring

Erosive gastritis inflammation >> decreased

acid and intrinsic factor

Severe Ulcerations:

Signs and Symptoms: Epigastric pain Hematemesis

Dsypepsia Pyrosis

Infection gives increased gastrin and decreased

somatostation production

Medical Management:

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