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lower gastro problem

Chapter 43

Gastroesophageal Reflux Disease ( GERD) chronic symptoms or mucosal damage secondary to reflux of gastric contents into the lower esophagus
Causes of GERD No single cause >results when the defenses of the esophagus are overwhelmed by the reflux of acidic gastric contents into the lower esophagus
Predisposing conditions of GERD >Obesity >Pregnancy >Smokers >Alcoholics >Foods (coffee, tea, chocolate)
Clinical Manifestation of GERD >Heartburn -most common - burning tight, sensation felt beneath sternum >dyspepsia- pain/discomfort centered upper abdomen >Otolaryngologic symptoms - hoarseness, sore throat, globus sensation > regurgitation - hot, bitter, sour coming into mouth
What is globus sensation? Sense of lump in throat
Complications of GERD >Esophagitis >Barret's esophagus >Respiratory >Dental Erosion
Esophagitis complication cause (GERD) If inflammation occurs repeatedly scar tissue may form & decrease distensibility
Barret's esophagus complication (GERD) Esophageal Metaplasia Metaplasia is the reversible change from one type of cell to another type & is generally cause by some sort of abnormal stimulus. -Flat epithelial in distal esophagus change to Columnar epithelial cells
Respiratory complication (GERD) includes cough, bronchospasms, laryngospasm, & circopharyngeal due to irritation of the upper airway by gastric secretions
Dental Erosion complication (GERD) result from acid reflux into mouth
Diagnostic Studies for GERD Diagnosed by S & S and how they respond to medication >Barium Swallow >Endoscopic evaluation > Biopsy for Barrets (if endoscopy is done)
Barium Swallow (GERD) can detect if there is a protrusion of the upper part of the stomach (gastric funds) NPO for 6 hrs -Contrast Media
Endoscopic evaluation (GERD) Assessing LES competence & inflammation (if present potential scarring and stricture) -Direct visualization of GI Tract
Collaborative Care: Lifestyle modifications (GERD) -Avoid factors that trigger symptoms >Eliminate smoking >Weight loss to reduce intrabdominal pressure >Elevate HOB
Collaborative care: Nutritional Therapy (GERD) -Avoid Food that decrease LES pressure (chocolate, peppermint, tea, coffee, tomatoes) -Avoid milk (increase gastric acid secretion -Small frequent meals help prevent over distention of stomach -Certain foods may irritate esophagus (OJ, red wine, Cola)
Collaborative Care: Gum and Lozenges GERD increase saliva which decrease acid level (minor symptoms of GERD)
Drug Therapy: Proton Pump Inhibitors (PPI's) GERD >decrease gastric HCL acid secretion >promote esophageal healing up to 90% >Decrease esophageal stricture >SE: Headaches (fracture risk) Drugs: Omeprazole (prilosec), esomeprazole (Nexium), pantoprazole (protonix) lansoprazole (prevacid)
Drug therapy: Antacids GERD >quick but short lived >HCL acid secretion >taken 1 to 3 hours after meal/bedtime Drugs: Maalox, Mylanta
Drug therapy: Histamine (H2) receptor blockers GERD >HCl acid secretions >reduce symptoms and promote esophageal healing >few side effect Drugs: cimetidine (tagamet), ranitidine (Zantac), famotidine (Pepcid), nizatidine (Axid)
Drug Therapy: Acid Protective GERD >used for cytoprotective properties >Paints the wall of stomach and protects it Drugs: Sucralfate (Carafate)
Drug Therapy: Cholinergic GERD >increase LES pressure >improve esophageal emptying in supine position >increase gastric emptying Drugs: Bethanechol (Urecholine)
Drug Therapy: Prokinetic GERD >promote gastric emptying >decrease risk of gastric acid reflux Drug: metoclopramide (reglan)
Surgical Therapy GERD >Goal is to decrease reflux by enhancing the integrity of LES >Nissen & Toupet fundoplication (Fundus of the stomach is wrapped around the lower portion of the esophagus to reinforce & repair the defective barrier)
Surgical therapy performed if: GERD >esophagitis >Medication intolerance >Stricture
Nursing management: Patient Education GERD 1. Nutrition 2. Medication 3. Raise HOB to 30 degrees or 4-6 in. blocks.
Nursing Management: Post Op care GERD -respiratory -maintenance of fluids/electrolytes -prevent infection
Hiatal Hernia Herniation of a portion of the stomach into the esophagus through an opening, or hiatus, in the diaphragm
Types of Hernias -Sliding (most common) -Paraesophageal (rolling)
Sliding hernia junction of stomach & esophagus is above the hiatus of diaphragm, & a part of stomach slides through the hiatal opening in the diaphragm
Paraesophageal Hernia the fundus & greater curvature of the stomach roll up through the diaphragm
Cause of hernia >Structural changes (weakening of muscles in diaphragm around esophagogastric opening) >Increased intrabdominal pressure (obesity, pregnancy, tumors, heavy lifting) -Others: elderly women, decreased nutrition, bed rest
Diagnostic studies of Hiatal Hernia -Barium swallow->show protrusion of gastric mucosa through the esophageal hiatus -Endoscopies ->provide information on the degree of mucosal inflammation or other abnormalities
Clinical manifestation of hiatal hernia >maybe asymptomatic >heartburn esp. after meal or laying supine >pain caused by large meals, smoking, alcohol >Nocturnal symptoms of heartburn >dysphagia >reflux
Complications of Hiatal Hernia -GERD -esophagitis -hemorrhage from erosion -stenosis (narrowing of esophagus) -ulceration of the herniated portion of stomach -strangulation of the hernia (narrow & twisted) -regurgitation with tracheal aspiration
Objective for surgical therapy of hiatal hernia reduce hernia, provide acceptable LES pressure & prevent movement of gastroesophageal junction
Surgical therapy types for Hiatal Hernia >Herniotomy ->excision of hernia sac >Herniorraphy ->closure of hiatal defect (narrow it) >Gastropexy -attachment of the stomach subdiaphragmatically to prevent reherniation Fundoplication-Nissen & Toupet technique _antireflux surgery
Conservative therapy for Hiatal hernia >decrease intrabdominal pressure by: -removing constricting garments - avoid lifting & straining - eliminating smoking and alcohol -elevating HOB -decrease body weight Use antisecretory agents (PPIs, H2RB) and antacids
Gerontologic considerations of hiatal hernia >increase w/age >meds taken all decrease LES pressure (nitrates, calcium channel blockers, antidepressants) >NSAIDs and potassium irritate esophageal mucosa (medication induced esophagitis) >Asymptomatic
Peptic Ulcer Disease (PUD) condition characterized by erosion of GI mucosa resulting from the digestive action of HCl acid & pepsin -anything w/ gastric secretin is susceptible to ulcers -Meds (NSAIDS) can cause ulcers
Types of Ulcers -Acute and Chronic -->depends on duration and degree -Gastric -Duodenal -Stress related -Medication induced
Pathophysiology of PUD (Acid Environment) peptic ulcers develop only in the presence of an acid environment. However, an HCL acid may not be necessary for ulcer development. Pepsinogen the precursor of pepsin, is activated to pepsin in the presence of HCl acid & a pH of 2 to 3
Pathophysiology of PUD (Gastric Mucosal Barrier) ulcerogenic drugs, such as aspirins & NSAIDs, inhibit synthesis of prostaglandins, increase gastric acid secretion & reduce the integrity of the mucosal barrier
Incidence for Gastric Ulcer -Greater in women -Peak age 50-60 year old -increase with smoking, drug use (aspirin & NSAID) & alcohol use -increase w/ incompetent pyloric sphincter & bile reflux
Clinical manifestation of gastric ulcer -burning or gaseous pressure in high left epigastrium & back & upper abdomen -Pain 1-2 hours after meal; if penetrating ulcer, aggravation of discomfort w/ food -nausea and vomitting -weight loss
Gastric Ulcers (lesion, location, gastric secretion, recurrence rate) -Lesion: superficial; smooth margins; round, oval or cone shaped -Location: antrum, also in body & fundus of stomach -Gastric secretion: normal to decreased -Recurrent rate: High
Duodenal Ulcers (Lesions, location, gastric secretion, recurrence rate) -Lesions: penetrating (assoc. w/deformity of duodenal bulb from healing of recurrent ulcers) -Location: first 1-2 cm of duodenum -Gastric Secretion -increased -Recurrence rate - high
Clinical manifestation of Duodenal Ulcers -burning, cramping, pressure-like pain across midepigastrium & upper abdomen, back pain & posterior ulcers -Pain 2-4 hrs after meal & midmorning, mid afternoon, middle of night, periodic & episodic -Pain relief w/antacids & food -Nausea & Vomitting
Incidence of Duodenal Ulcers -greater in men -peak age 35-45 years old -increase with smoking, drug use, alcohol use -Assoc. w/ other diseases (H. pylori is a factor)
Other causes of ulcers (Medication induced injury) -Aspirin & NSAIDS inhibit synthesis of prostaglandin, increase gastric secretion and decrease integrity of mucosal barrier -Corticosteroids (affect mucosal cell renewal & protective effects) & SSRIs, anticoagulants increase risk
Other causes of ulcers (Lifestyle factors) -increase alcohol intake is assoc. w/ acute mucosal lesions, also stimulates acid secretion -coffee increases gastric acid secretion -delay in healing with smoking
Other causes of Ulcer (Stress related mucosal damage) stress secretes more gastric acid
Diagnostic Studies (Laboratory Analyse) -CBC-anemia secondary to ulcer bleeding -Liver enzymes-determine any liver problems (cirrhosis) that complicate ulcer treatment -Stool-blood presence -Serum amylase-determine pancreatic function when posterior duodenal ulcer penetration of pancreas
Collaborative care for ulcers -Adequate rest -Drug therapy (PPI's, antacids, H2R Blockers, Avoid NSAIDS) -Eliminate smoking -Diet (anything that irritate GI mucosa)
Histamine 2 receptor blockers -End in -dine --PUD treatment -Ulcer Healing Drugs: cimetidine, ranitidine, famatodine
Proton Pump Inhibitor (PPI) End in -Prazole -Reducing gastric acid secretion -promote ulcer healing Drugs: omeprazole, lansoprazole, pantaprazole
Antibiotic therapy -Treatment of H. Pylori -Most important element of treating PUD in patient positive w/ H. Pylori -Prescribed w/ H2R blockers & PPIs
Antacids -adjunct therapy for PUD -increase gastric pH by neutralizing the HCl acid -acid content of chyme reaching the duodenum is reduced
Cytoprotective Drugs -Sucralfate (Carafate) -Short term use of ulcers -provides cytoprotection for the esophagus, stomach & duodenum -protects mucosa from erosion caused by pepsin, acid & bile salts
Tricyclic antidepressants drugs -contribute to overall pain relief through their affects on afferent pain fibers transmission -some anticholinergic properties->reduced acid secretion
H. Pylori Drug Therapy (Triple Drug Therapy) Duration & Eradication Rate -Proton Pump Inhibitor -Amoxicillin ->Antibiotic -Clarithomycin ->Antibiotic Duration -7-14 days Eradication rate - 70-85%
H. Pylori Drug Therapy (Dual Therapy) Duration and eradication rate -Proton pump inhibitor -Clarithromycin Duration - 7-10 days Eradication rate - 45-505
H. Pylori therapy (Quadruple therapy) Duration & eradication rate - Proton pump inhibitor -Bismuth (decrease antibiotic resistance) -Tetracycline -Metronidazole (Flagyl) Duration - 10-14 days eradication rate - 85%
Objective for collaborative care decrease gastric acidity & enhance mucosal defense mechanisms
Therapy for Acute Exacerbation -Concern regarding potential complication (Bleeding & Perforation) -Accompanied by pain, N/V, and bleeding -Rest stomach (NG, IV fluids, transfusion, VS's, laboratory studies) -Endoscopic evaluation (visualize what's going on) -Diet, activity, drugs
Complications (Hemorrhage) place an NG tube, administer blood, O2, NPO, IV fluids, monitor VS
Complications (Perforation) Pain management, NG tube (NPO)(monitor output) pressure can radiate to back, monitor VS -Prepare patient for surgery w/antibiotics
Complications (Gastric Outlet Obstruction) ulcers located in antrum or pyloric area (bottom) due to edema & inflammation-scar tissue narrows pyloric retaining acid in stomach causing vomiting -NG tube, IV fluids, pain relief, prepare patient for pyloric ballooning dilation
Surgical intervention -Uncommon -Gastroduodenostomy (Billroth I) partial gastrectomy (part stomach) remove 2/3rd distal of stomach & Connecting to duodenum -Gastrojejunostomy (Billroth II) -Vagotomy or selective vagotomy -Pyloroplasty
Postoperative Complication Dumping Syndrome Define & education -Loss of control of gastric chyme entering small intestine educate: small meals, fluids after meal, low carbs, no more than 1 hour after meal
Postoperative Complication Postprandial Hypoglycemia Define & educate -uncontrolled gastric emptying of a bolus of fluid high in carbohydrate content into the small intestine educate; less carbs or sugar rich foods
Postoperative Complication Bile Reflux Gastritis Define and educate -back diffusion of hydrogen ions through the gastric mucosa Educate: administer Bustran (med for bile)
Post-op care Check VS, pain management, output, NG tube, bowel sounds, NPO, start with small meals
Gerontologic Considerations teach about NSAIDs
Patient and Family education for Discharge -no smoking -no alcohol intake -continue GI meds after surgery -Increase risk of ulcers -intrinsic fact loss so administer B12 injection Any signs of nausea report to doctor
Created by: ygwallace