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Care of Patient with GERD & Peptic Ulcer
63-273
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GERD: Background Gastroesophageal reflux is a normal physiologic phenomenon in most people, particularly after a meal. Gastroesophageal reflux disease (GERD) occurs when the amount of gastric juice that refluxes into the esophagus exceeds the normal limit
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Causes of GERD
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GERD: Symptoms Typical symptoms: Heartburn (Pyrosis): Regurgitation:
Most common Felt as a retrosternal sensation of burning or discomfort Occurs usually after eating or when lying down or bending over. Often relieved with milk or water Regurgitation: Effortless return of gastric and/or esophageal contents into the pharynx. It can induce respiratory complications if gastric contents spill into the tracheobronchial tree. Atypical symptoms Cough, dyspnea, hoarseness, and chestpain
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Diagnosis Role out other potential causes for the heartburn:
Cardiac Peptic ulcer Esophagitis Esophageal Endoscopy: The gold standard as a definitive diagnosis Barium swallow Not as definitive in mild cases
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Collaborative Care Lifestyle modifications Nutritional therapy
Decrease high-fat foods, avoid milk products at night, and avoid late snacking or meals Drug Therapy Surgical therapy Endoscopic therapy
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GERD: Complications Are related to HCl effect on the esophageal mucosa
Esophagitis Can complicate to esophageal ulceration Barrett’s esophagus (esophageal metaplasia) Pre-cancerous lesion
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Nursing Management Avoid factors that cause reflux Elevate HOB ~30°
Stop smoking Avoid acid or acid producing foods Elevate HOB ~30° Do not lie down 2 to 3 hours after eating Patient teaching (see Table in textbook) Drug therapy Evaluate effectiveness Observe for side effects
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Peptic ulcer Erosion or excavation of mucosal wall of the esophagus, stomach, pylorus, duodenum (most common). “Autodigestion” Requires acid environment to develop Mucosal defenses impaired; cannot protect from effects of acid/pepsin Result from infection with H. pylori or Zollinger-Ellison syndrome Risk factors: Alcohol, smoking, and stress, medications
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Three types of peptic ulcer
Gastric Duodenal Stress
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Gastric ulcer Most common in the lesser curvature of stomach near the pylorus Mucus and bicarb. generally protect mucosal barrier from acid H. pylori plays a role Break in gastric mucosal barrier allows HCl to damage epithelium via “back diffusion” Bile reflux from duodenum may break integrity Decreased blood flow
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Duodenal ulcer Results from excessive acid
Associated with protein-rich meals, Ca++, and vagal stimulation) Rapid emptying of food from stomach large acid load in duodenum H. pylori infection plays key role in development produces substances that damage the mucosa, and contributes to higher acid concentrations
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Stress ulcer Occurs after acute medical crisis, surgery, or trauma
Proximal portion of stomach and duodenum are most common sites Ischemia and elevated HCl contribute to evolution of erosions ulcerations May progress to hemorrhage
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Duodenal versus Gastric ulcers
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Diagnostic tests Esphagogastroduodenoscopy
Fiberoptic endoscope allows direct visualization of esophagus, stomach and duodenum
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Diagnostic tests: Upper GI series
Patients ingests barium, a thick, white, milkshake-like liquid, then multiple X-rays. Can detect structural disorders After the exam, provide plenty of liquids for 24 to 48 hours. The barium may make the stool white for several days. If constipation occurs, the doctor may recommend a mild laxative.
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Complications of ulcers: Hemorrhage
Manifested by: Orthostatic hypotension, BP, HR, cool, clammy skin overt bleeding Hematemesis (bloody vomit) – bright red or coffee ground (more likely with gastric ulcer) Melena (bloody or tarry [black] stool) – more likely with duodenal ulcer Hgb, Hct
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Remember: Management during Haemorrhage includes
Monitor S/S Determine rate amount of blood loss (Hct/hct), NGT Replace blood, fluid and electrolyte loss saline lavage via NGT NGT to low intermittent suction Prevents distension Assess amount/rate of bleeding, Medications, oxygen, possible surgery
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Complications: Perforation
GI contents empty into peritoneal cavity Manifested by: Sudden, sharp mid-epigastric pain which can shortly spread to all abdomen Rigid, tender, board-like abdomen Patient assumes the fetal position to reduce tension on muscles Can lead to shock It is a surgical emergency
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Remember: Management during perforation includes
NGT to prevent additional spillage of GI contents in peritoneum Replace blood, fluid, electrolytes Antibiotics I & O, NPO SURGERY: Urgent
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Complications: Pyloric obstruction
Caused by inflammation or edema of the pylorus Stomach cannot empty abdominal bloating, N & V Persistent vomiting Hypokalemia and metabolic alkalosis
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Medical Management of ulcers
Conservative therapy: Rest: Both physical and emotional Dietary modifications Elimination of smoking Long term follow up care Pharmaceutical: Antibiotics To eradicate H. Pylori infections Recurrence of ulcer is 75-90% as high with infection Antiacids Initial drugs of choice Histmaine H2 receptor antagonists Histamine is the final intracellular activator of HCL secretion Anticholinergic: Stop the cholinergic stimulation of HCl secretion and slow gastric motility Not commonly used, if used need to be used with caution in pts with Glaucoma
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Surgical Management of ulcerations
Gastroduodenostomy (Billroth I) Removal of the lower portion of stomach and small portion of duodenum and connects remaining of stomach to duodenum
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Surgical Management of ulcerations
Gastojejunostomy Removes lower stomach and small portion of duodenum. Reconnects stomach to jejunum. Subtotal gastrectomy - removal distal third of stomach, reconnecting to duodenum or jejunum Total gastrectomy removal of stomach; connects esophagus to jejunum
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Dumping syndrome A complication of gastric surgery S&S
vertigo, sweating, palpitations, syncope, pallor, tachycardia occurs after eating D/t rapid emptying of hypertonic stomach contents into small intestine fluid shifts into gut abd. distention and cramps and S/S of plasma volume. Later get rapid elevation of blood glucose followed by insulin secretion and hypoglycemia Management Small frequent meals fat, protein, CHO meals liquid between (not with) meals Lie down after meals
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Nursing diagnoses Pain r/t mucosal injury Anxiety Knowledge deficit
Risk for fluid volum deficit r/t hemorrhage or vomiting
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Intervention: Pain Medications
Give antacids after meals and at bedtime to decrease gastric acidity; buffers the acid. Give H2 receptor antagonists as prescribed to decrease acid secretion Diet therapy Effectiveness controversial Avoid caffeinated beverages Exclude foods that cause discomfort Provide frequent, small, bland meals Avoid smoking, alcohol
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Intervention: Anxiety & Knowledge deficit
Provide emotional support Teach and provide relaxation techniques Identify and manage sources of stress Knowledge deficit Teach re diet, medications, Teach the risks associated with continued smoking Teach S/S of complications
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