Peptic Ulcer Disease (Chapter 59 Pages 1287-1305)

Group 3APeptic Ulcer DiseasePeptic UlcersDefinedThe term 'peptic ulcer' generally refers to an ulcer or erosions in stomach or duodenum. TypesGastricDuodenal

2Peptic ulcer is a mucosal lesion of the stomach or duodenum. The term peptic ulcer is used to describe both gastric and duodenal ulcers. PUD results when gastric mucosal defenses become impaired and no longer protect the epithelium from the effects of acid and pepsin.Peptic Ulcer Disease

Stomach Defense SystemsMucous layerCoats and lines the stomachFirst line of defenseBicarbonateNeutralizes acidProstaglandinsHormone-like substances that keep blood vessels dilated for good blood flowThought to stimulate mucus and bicarbonate productionRisk FactorsLifestyleSmokingAcidic drinksMedications

H. Pylori infection90% have this bacteriumPassed from person to person (fecal-oral route or oral-oral route)AgeDuodenal 30-50Gastric over 60GenderDuodenal: are increasing in older womenGenetic factorsMore likely if family member has HxOther factors: stress can worsen but not the causeGastric UlcersPain occurs 1-2 hours after mealsPain usually does not wake patientAccentuated by ingestion of foodRisk for malignancyDeep and penetrating and usually occur on the lesser curvature of the stomach6When a break in the mucosal barrier occurs, hydrochloric acid injures the epithelium. Gastric ulcers may then develop. With a gastric ulcer the pain occurs 1-2 hours after meals and does not usually wake the patient from sleep. Food worsens the pain. There is an increased risk for malignancy and these ulcers are deep and penetrating and usually occur on the lesser curvature of the stomach. Gastric and Duodenal Ulcers

Duodenal UlcersPain occurs 2-4 hours after mealsPain wakes up patientPain relieved by foodVery little risk for malignancy8Most duodenal ulcers occur in the first portion of the duodenum. With this type of ulcer the pain occurs 2-4 hours after meals, pain wakes up the patient, the pain is relieved with the administration of food and there is very little risk for malignancy.General Peptic Ulcer SymptomsEpigastric tendernessGastric: epigastrium; left of midlineDuodenal: mid to right of epigastriumSharp, burning, aching, gnawing painDyspepsia (indigestion)Nausea/vomitingBelchingComplications of Peptic UlcersHemorrhageBlood vessels damaged as ulcer erodes into the muscles of stomach or duodenal wallCoffee ground vomitus or occult blood in tarry stoolsPerforationAn ulcer can erode through the entire wallBacteria and partially digested fool spill into peritoneum=peritonitisNarrowing and obstruction (pyloric)Swelling and scarring can cause obstruction of food leaving stomach=repeated vomiting10Hemorrhage: With massive bleeding the patient vomits bright red or coffee ground blood. Minimal bleeding from ulcers is manifested by occult blood in a tarry stool (melena). Perforation: Gastric and duodenal ulcers can perforate or bleed. Perforation occurs when the ulcer becomes so deep that the entire thickness of the stomach or duodenum is worn away. The gastroduodenal contents may then empty into the peritoneal cavity. Symptoms of perforation are sudden, sharp pain, the abdomen is tender, rigid, and boardlike. The patient assumes the fetal position, knees to chest. Client can become acutely ill within hours. Peforation is considered a surgical emergency and can be life threatening. If this occurs the physician needs to be notified immediatley.

Diagnostic TestsEsophagogastrodeuodenoscopy (EGD)Endoscopic procedureVisualizes ulcer craterAbility to take tissue biopsy to R/O cancer and diagnose H. pyloriUpper gastrointestinal series (UGI)Barium swallowX-ray that visualizes structures of the upper GI tractUrea Breath TestingUsed to detect H.pyloriClient drinks a carbon-enriched urea solutionExcreted carbon dioxide is then measured11A barium examination of the GI tract can be used to establish a duodenal ulcer. If perforation is suspected the health care provider usually requests an upright abdomen series to demonstrate free air in the peritoneum. Do not use barium where free air is a possibility. Pathophysiology

Peptic ulcers are produced by an imbalance between the gastro-duodenal mucosal defense mechanisms and damaging forces of gastric acid and pepsin, combined with superimposed injury from environmental or immunologic agents.

H. pylori infection is present in almost all patients with duodenal ulcers and 70% cases with gastric ulcers. Duodenal ulcers - Usually associated with gastritis confined to the antrum. Gastric ulcers - Usually associated with pangastritis. Mechanism:H. pylori secretes urease (generates ammonia), protease (breaks down glycoprotein in the gastric mucus) or phospholipases. Bacterial lipopolysaccharide attracts inflammmatory cells to the mucosa. Neutrophils release myeloperoxide. A bacterial platelet-activating factor promotes thrombotic occlusion of surface capillaries.Mucosal damage allows leakage of tissue nutrients in the surface microenvironment , sustaining the bacillus.

Damage of the protective mucosal layer. The epithelial cells are exposed to the damaging effect of acid-peptic digestion.Inflammation of the gastric mucosa.Chronically inflamed mucosa more susceptible to acid- peptic injury and prone to peptic ulceration. Ulcers occur at sites of chronic inflammation . Eg - Antrum - Junction of antral and body- fundic mucosa (division between the inflamed antral mucosa and normal acid secreting mucosa). Pangastritis - When there is extensive gastritis, the ulcers are more proximally situated. In elderly patients gastric ulcers are more proximally situated as there is proximal migration of the antral-body mucosal junction.

12Etiology and Genetic RiskPUD primarily associated with NSAID use and infection with H. PyloriCertain drugs may contribute to cause:Theo-DurCaffeine stimulates hydrochloric acid productionCorticosterioids associated with an increased incidence of PUDGenetic factors

13I added this slide to the presentation so add this to your notes. Drug Therapy/Primary GoalsProvide pain reliefAntacids and mucosa protectorsEradicate H. pylori infectionTwo antibiotics and one acid suppressorHeal ulcerEradicate infectionProtect until ulcer healsPrevent recurrenceDecrease high acid stimulating foods in susceptible peopleAvoid use of potential ulcer causing drugsStop smokingHyposecretory DrugsProton Pump InhibitorsSuppress acid productionPrilosec, PrevacidH2-Receptor AntagonistsBlock histamine-stimulated gastric secretionsZantac, Pepcid, AxidAntacidsNeutralizes acid and prevents formation of pepsin (Maalox, Mylanta)Give 2 hours after meals and at bedtime

Prostaglandin AnalogsReduce gastric acid and enhances mucosal resistance to injuryCytotecMucosal barrier fortifiersForms a protective coatCarafate/Sucralfatecytoprotective15Hyposecretory drugs produce a reduction in gastric acid secretions. Your proton pump inhibitors have emerged as the drug class of choice for treating clients with acid-related disorders. These drugs suppress acid production. They include Prilosec and Previcid. Your H2 receptor antagonists block histamine stimulated gastric secretions. Antacids neutralizes acid and prevents formation of pepsin. The prostoglandin analogs reduce gastric acid and enhance mucosal resistance to injury. The drug Carafate acts as a mucosal barrier by forming a protective coating. These drugs are all listed in Chart 59-3 pages 1286-1287.SurgeryGreatly decreased in the last 20-30 years secondary to the discovery of H. pyloriRequired if ulcer in one of these statesPerforated and overflowed into the abdomenScarred or swelled so that there is obstructionAcute bleedingNon-responsive to medicationsTypes of Surgical ProceduresGastroenterostomyallows regurgitation of alkaline duodenal contents into the stomachCreates a passage between the body of stomach to small intestinesKeeps acid away from ulcerated area

17A simple gastroenterostomy permits neutralization of gastric acid by regurgitation of alkaline duodenal contents into the stomach. The surgeon creates a passage between the body of the stomach and the small bowel. Drainage of the gastric contents diverts acid from the ulcerated area and facilitates healing. Types of Surgical ProceduresVagotomyCuts vagus nerveEliminates acid-secretion stimulus

18A vagotomy eliminates the acid-secreting stimulus to gastric cells and decreases the responsiveness of parietal cells. Surgical Procedure/PyloroplastyPyloroplastyWidens the pylorus to guarantee stomach emptying even without vagus nerve stimulation

19In this procedure the surgeon enlarges the pyloric stricture by incising the pylorus longitudinally and sutures the incision transversely. Types of Surgical ProceduresAntrectomy/ Subtotal GastrectomyLower half of stomach (antrum) makes most of the acidRemoving this portion (antrectomy) decreases acid productionSubtotal gastrectomyRemoves to 2/3 of stomachRemainder must be reattached to the rest of the bowelBillroth IBillroth IIBillroth IDistal portion of the stomach is removedThe remainder is anastomosed to the duodenum

Billroth IIThe lower portion of the stomach is removed and the remainder is anastomosed to the jejunum

Postoperative CareNG tube care and managementMonitor for post-operative complications

23The postoperative plan of care is similar for all of the gastric operative procedures. These patients will have NG tubes in place and attached to low wall suction. Ensure the patency of these tubes. Irrigation or repositioning of the NG tube is not done after gastric surgery unless specifically ordered by the doctor. Post-op ComplicationsBleedingOccurs at the anastomosed siteFirst 24 hours and post-op days 4-7Duodenal stump leakBillroth IISevere abdominal painBile stained drainage on dressingGastric retentionWILL NEED TO PUT NG TUBE BACK INDumping Syndrome (page 1303)Prevalent with sub total gastrectomiesEarly-30 minutes after mealsVertigo, tachycardia, syncope, sweating, pallor, palpatationsLate 90 min-3 hours after mealsAnemiaRapid gastric empyting decreases absorption of ironMalabsorption of fatDecreased acid secretions, decreased pancreatic secretions, increased upper GI mobility24Observe for any bleeding, monitor vital signs and post surgery hemoglobin and hematocrit. If gastric retention occurs once ng tube is removed, it will have to be put back in.