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Aman Sulehri
Gastric Physiology
Gastroduodenal Mucosal Defense:The mucosal defense system can be divided as a threelevel barrier 1. Preepithelial 2. Epithelial 3. Subepithelial
Definition:An
ulcer is defined as disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation.
Epidemiology
In US, approx 4 million people have PU and 350,000 new cases are diagnosed each year. Around 180,000 patients are hospitalized yearly. And about 5000 people die each year as result of PUD. The lifetime likelihood of developing PU is abt 10% for amercian males and 4% for females. The male-to-female ratio for DU is ant 3:1, and for gastric ulcer abt 1.5 to 2:1. DU more common between ages 30-50 years old and GU more common in people over age 60 years old
Etiology
Helicobacter pylori infection(90%) Drugs - anti-inflammatory(NSAIDs) & Corticosteroids Hyperacidity - e.g.. Zollinger Ellison syndrome. Food habits(Spicy food, diet poor in vitamins, smoking and alcohol) Diabetes may increase your risk of having H. pylori Lifestyle factors, including chronic stress, coffee drinking, may make more susceptible to damage from NSAIDs or H. pylori if one is a carrier of this organism. But these factors do not cause an ulcer on their own. Diseases associated with an increased risk of PUD include cirrhosis, chronic obstructive pulmonary disease, renal failure, and organ transplantation.
Pathogenesis
H. pylori and Acid Peptic Disorders:
The bacterium is a gram-negative microaerophilic rod found most commonly in the deeper portions of the mucous gel coating the gastric mucosa or between the mucous layer and the gastric epithelium. It may attach to gastric epithelium but under normal circumstances does not appear to invade cells. It induces an intense inflammatory & immune response. There is increased production of pro-inflammatory cytokines such as IL-1, IL6 TNF, IL-8. This cytokine is produced by mucosal epithelial cells, and it recruits and activates neutrophils Several bacterial genes products are involved in causing epithelial cell injury and induction of inflammation. H.pylori secrets urease that breaks down urea to form toxic compounds such as ammonium chloride and monochloramine
The organism also elaborate phospholipases that damage surface epithelial cells. Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in gastric mucus, thus weakening 1st line mucosal defense It also enhances gastric acid secretion and impairs duodenal bicarbonate production thus reducing pH in duodenum Several H.pylori are immunogenic, and they cause activation of both T cells and B cells Thromboembolic occlusion of surface capillaries is promoted by bacterial platelet-activating factor.
A specific region of the bacterial genome, the pathogenicity island, encodes the virulence factors cytotoxin-associated antigen(Cag A) associated with more severe epithelial damage, greater acute and chronic inflammation, higher likelihood of PU and gastric cancer One important genes regulated by CagA is vacuolating toxin(VacA) which causes cell injury in vitro and gastric tissue demage.it also act as urea transporter and hence increasing permeability of epithelium to urea
Clinical Features
Epigastric pain (the most common symptom) it is said that gastric ulcers present with pain associated or closely followed by eating ,where-as duodenal ulcer pain is relieved by food. Burning in nature Patient awakens with pain at night. May radiate to the back (consider penetration) Increased salivation(water brash) Nausea Vomiting, which might be related to partial or complete gastric outlet obstruction Dyspepsia, including belching, bloating, distention, and fatty food intolerance Chest discomfort Anorexia, weight loss Hematemesis(this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe vomiting) Melena
Complications
Gastrointestinal bleeding Perforation Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas. Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction
Diagnosis
Oesophagogastroduodenoscopy(OGD):
Ulcer appears as a crater with/without slough or bleeding . In GU, routine biopsy is advised to r/o malignancy while in DU biopsy is done in recurrent cases to r/o H.pylori
DU
GU
Non-invasive:
Antibodies: IgG to H pylori can be measured in serum, plasma, or whole blood.
Urea breath test: Simple; sensitivity and specificity of 90 to 99% Stool antigen: >90 sensitivity, convenient; not established for eradication but promising
D/D
Gastritis Stomach cancer Gastro esophageal reflux disease Pancreatitis Cholecystitis Inferior myocardial infarction Referred pain (pleurisy, pericarditis)
Medical Treatment
Surgical Treatment
Indication:
Intractable pain in spite of treatment with H2 receptor blockers, omeprazole and not responding to anti H.pylori regime Frequent relapses, H.pylori ve Complications of DU: Gastric outlet obs. Hemorrhage
Truncal vagotomy
Anterocolic GJ
Retrocolic GJ
Billroth II gastrectomy
It is indicated when gastric ulcer is located on lesser curvature. Here gasterctomy is done below the ulcer and remnant of stomach is anastomosed to jejunal loop(gastrojejunal anastomosis)