Upper Gastrointestinal Disorders

Upper Gastrointestinal Disorders Module 4 Nausea and Vomiting • Nausea-conscious desire to vomit • Vomiting-ejection of emesis from upper GI tract Nausea and Vomiting—Etiology • GI disorders – Non GI disorders • • • • • • • • Pregnancy Infections CNS disorders Cardiovascular disorders Metabolic disorders Stress Medications Motion Nausea and Vomiting Pathophysiology • Vomiting center in brainstem • Chemoreceptor zone (CTZ) stimulated • Autonomic nervous system is activated – Sympathetic • • • • Tachycardia Diaphoresis Parasympathetic Relaxation of LES Nausea and Vomiting Clinical Manifestations • Nausea-subjective • If vomiting prolonged – Dehydration – Water, electrolytes lost – Loss of extracellular fluid leading to circulatory collapse – Metabolic alkalosis can occur-gastric loss or – Metabolic acidosis if small intestine contents lost (less common) Characteristics of Vomiting • Regurgitation-Partially digested food • Projectile-forceful expulsion without nausea • Fecal/intestinal-can be result of obstruction Characteristics of Vomiting • Color – ―Coffee grounds‖-bleeding in stomach – Blood changes to dark brown as result of interaction with HCL – Bright red blood-active bleeding – Green-bile Medications to Alleviate Nausea/Vomiting • Antimuscarinics – Scopolamine-patch • Antihistamines – Benadryl-can be given IV • Phenothiazines – Compazine-given IM Medications to Alleviate Nausea/Vomiting • Antimuscarinics – – – – Antihistamines Phenothiazines These classes have anitcholinergic effects Common contraindications with these classes: • Do not give to client with glaucoma, BPH (urinary retention), pyloric/bladder neck obstruction, biliary obstruction • Common side effects: Dry mouth, constipation, hypotension, sedative effects Medications to Alleviate Nausea/Vomiting • Metroloperamide (Reglan) and Domperidone (Motilium) – Antiemetics – Act on Dopamine receptors – Enhance release of acetylcholine – Increased gastric emptying (prokinetics) – Side effects of Reglan: hallucinations, tremors, dyskinesias Medications to Alleviate Nausea/Vomiting • 5-HT receptors-antagonists to serotonin receptors – Work peripherally and centrally to reduce vomiting – Used for Chemotherapy/radiation, migraine induced vomiting • Ondansetron (Zofran), granisetron (Kytril), dolasetron (Anzemet) Oral Inflammations and Infections • Primary • Secondary – Chemotherapy – Good oral hygiene important Oral Inflammations and Infections • • • • • • • Gingivitis Vincent’s infection (trench mouth) Oral candidiasis (thrush) Herpes Simplex (cold sore) Aphthous stomatitis (canker sore) Parotiditis Stomatitis (inflammation of the mouth) Gingivitis • Etiology– Neglected oral hygiene – Stress • Manifestations – Bleeding during tooth brushing – Pus – Loosening of teeth (peridonitis) – Treatment • Prevention, Dental care, dental rinses, flossing Vincent’s Infection (Trench Mouth) • Etiology– Bacteria/Neglected oral hygiene – Stress • Manifestations – – – – Ulcerations that bleed Increased saliva with metallic taste Halitosis Treatment • Prevention, Dental care, dental rinses H2O2, topical antibiotics, stress management Oral Candidiasis (Thrush) • Etiology– Candidiasis albicans – Immunosuppression • Manifestations – White patches in oral cavities – Treatment • Nystatin swish and swallow • Amphotericin B Herpes Simplex (Cold Sore) • Etiology– Herpes simplex I or II – Stress exacerbates • Manifestations – Vesicle formation – Treatment-antivirals • Zovirax Aphthous Stomatitis (Canker Sore) • Etiology– Chronic form of infection secondary to trauma, stress • Manifestations – Painful ulcers of lips – Treatment • Topical/systemic corticosteroids • Topical antibiotic Parotiditis • Etiology– Staph, Strep • Manifestations – – – – Pain in gland/ear Lack of saliva Purulence Treatment • Antibiotics • Mouthwashes • Lollipops to stimulate saliva production Stomatitis (Inflammation of the Mouth) • Etiology– Side effect of chemotherapy – Trauma – pathogens • Manifestations – – – – Excessive salivation Halitosis Sore mouth Treatment • Remove cause • Soothing mouth wash solutions • Bland diet Oral Cancer • Common sites – Lower lip – Lateral border of tongue – Buccal mucosa – Etiology • Tobacco use • Chronic irritation • UV light-Cancer of the lip Manifestations of Oral Cancer • • • • Leukoplakia—‖Smoker’s patch‖ Erthroplakia Sore that does not heal Late – Pain especially moving jaw – Dysphagia – Cancer of the lip-induration – Pain in tongue when eating Diagnostic/Treatment of Oral Cancer • Diagnosis – History and Physical – Biopsy of lesion/cytology – Toluidine test-blue dye is taken up by the cancer – Treatment – Chemo – Radiation – Surgery Surgery for Oral Cancer • Radical Neck dissection – Involves removal of lymph nodes – Need tracheostomy – JP drains Nursing Care of the Radical Neck Dissection Client • Airway monitoring • Monitor for bleeding • Nutritional considerations – Parenteral – Feeding tube – Tracheostomy care – Psychosocial – Pain management Gastroesophageal Reflux (GERD) • Not a disease, but a syndrome • Clinically symptomatic condition resulting in reflux of gastric contents into lower esophagus Gastroesophageal Reflux (GERD)-Etiology • Combination of factors – Hiatal hernia – Incompetent LES – Decreased esophagus clearance – Decreased gastric emptying – Medications – Results in esophageal irritation and inflammation Gastroesophageal Reflux (GERD) Clinical Manifestations • Varies from individual – – – – – – – – – – – Heartburn (pyrosis) Burning, tight sensation Can spread to jaw May wake person from sleep R/O cardiac causes first Heartburn usually relieved with milk, alkaline substances Wheezing, coughing, dyspnea, hoarseness Lump in throat Regurgitation-hot, bitter, sour liquid coming from mouth Stomatitis N/V Gastroesophageal Reflux (GERD) Complications • Esophagitis • Esophageal stricture/scarring • Barrett’s Esophagus—precancerous lesion for esophageal cancer/adenocarcinoma • Bronchospasm • Aspiration pneumonia • Dental erosion Gastroesophageal Reflux (GERD) Diagnostic Studies • • • • History and Physical Barium swallow EGD Use of Proton pump inhibitors as trial Nursing Considerations for the Client with GERD • Smoking cessation • Avoid food that decrease LES pressure – – – – – – – – fatty foods Chocolate Peppermint Coffee Tea Milk Avoid late night snacks Small, frequent meals Nursing Considerations for the Client with GERD • • • • • HOB 30 degrees IV therapy Weight reduction Medication education Advance diet Pharmacological Intervention for GERD • Medications to: – Improve LES function – Increase esophageal clearance – Decrease volume and acidity of reflux – Protect esophageal mucosa – Two approaches • ―Step up‖—from antacids, H2blockers, PPI • ―Step down‖ from PPI, H2 blockers, antacids Antacids Maalox, Mylanta, Milk of Magnesia • Partially neutralizes gastric acid • Does not coat stomach • Usually mixture of aluminum (causes constipation) and magnesium (causes diarrhea) • Caution: magnesium solutions with renal disease • Decrease absorption of Digoxin, tetracycline, INH • May have to separate medication admin and antacids by one hour • Give 1 to 3 hours after meals and at bedtime for maximum effect H2 Blockers • Rantidine (Zantac),Cimetidine (Tagamet), Famotidine (Pepcid), Nizatidine (Axid) • Decrease secretion of HCl acid by stomach • May increase toxicity of Coumadin, Theophylline, Dilantin • Side effects: confusion Proton Pump Inhibitors (PPI) • Omeprazole (Protonix), Esomeprazole (Nexium) • Inhibit proton pump mechanism responsible for secretion of H ion • May increase effects of Dilantin, Coumadin • Give on empty stomach Antiulcer Medication • Sucralfate (Carafate) – Cytoprotective agent – Adheres to an ulcer site – Give 1 hour before meals and at bedtime – Do not crush/Liquid form available – Side effect: constipation, dizziness Prokinetic (Reglan) • Facilitates gastric emptying • Side effect: Hallucinations, anxiety, restlessness, insomnia Surgical/Endoscopic Therapy for GERD • Surgical – Antireflux procedures – Nissen fundoplication • Endoscopic – Stretta procedure-induces collagen formation, forms barrier against reflux Hiatal Hernia • Herniation of portion of stomach into esophagus through opening in diaphragm • Types – Sliding – Paraesophageal/rolling Etiology of Hiatal Hernia • Factors – Structural changes – Obesity – Pregnancy – Heavy lifting Clinical Manifestations of Hiatal Hernia • • • • • May be asymptomatic Heartburn Dysphagia Reflux with lying down Pain, burning when bending over Hiatal Hernia • Diagnostic studies – Barium swallow – Endoscopy – Surgical intervention • Nissen fundoplication Complications of Hiatal Hernia • • • • • • • GERD Hemorrhage Stenosis of esophagus Ulcerations Strangulation of hernia Regurgitation Increased risk for respiratory disease Esophageal Cancer • Rare malignancy • Barrett’s Esophagus-risk for malignancy • Etiology – Unknown – Risk factors • • • • Smoking Excessive ETOH Achalasia (delayed emptying of lower esophagus) Majority of tumors located in middle and lower portions of esophagus Clinical Manifestations of Esophageal Cancer • Usually late – Progressive dysphagia – Pain – Sore throat – Hoarseness – Weight loss – Regurgitation of blood tinged esophageal contents Complications of Esophageal Cancer • Hemorrhage • Esophageal perforation • Esophageal obstruction Diagnostic Studies Esophageal Cancer • • • • • Barium swallow with fluoroscopy Endoscopy Bronchoscopy CT MRI Nursing Considerations for the Client with Esophageal Cancer • • • • Poor prognosis Combination of surgery, chemotherapy, radiation Surgery Esophagectomy– Remove esophagus, graft to resect – Esophagogastrostomy • • • • • • Resect esophagus to stomach Esophagoenterostomy Resect esophagus to colon Dilation of esophagus Parenteral fluids for nutrition Pain management Post-op Nursing Considerations for the Client with Esophageal Cancer • NGT-bloody drainage 8 to 12 hours then turns to greenish • Do not reposition NGT • Airway assessment-T,C,D,B • Semi-Fowler’s Esophageal Diverticula • Saclike outpouching of one or more layers of the esophagus • Zenker’s diverticulum – Most common of esophageal diverticulum – Located above the upper esophageal sphincter – Symptoms • • • • • Dysphagia Weight loss Regurgitation Chronic cough Aspiration Esophageal Diverticula • Treatment Clients learn to empty esophagus by applying pressure – Limit foods (blenderize) – Endoscopic Surgery Esophageal Stricture • Most common-formation of scar tissue from: – Strong acid/alkaline ingestion – Reflux – Treatment • Dilation via endoscopy using bougies • Balloon dilation • Calcium Channel blockers can help to relax smooth muscle Achalasia • Peristalsis of the lower two thirds of the esophagus resulting in: – Dilation of the lower esophagus – Symptoms • • • • Dysphagia Halitosis Regurgitation of sour foods Symptoms similar to GERD Achalasia • Diagnosis – Endoscopy – Treatment • • • • • • • • Dilation Surgery Bland diet Esophageal dilation Heller myotomy (reduces LES pressure) Anticholinergics Calcium channel blockers Botox? Disorders of the Stomach and Small Intestine • Gastritis • Upper GI bleed • Peptic Ulcer disease – Gastric ulcers – Duodenal Ulcer • Gastric Cancer • Food Poisoning Gastritis • Inflammation of gastric mucosa • Acute or Chronic • Three types of chronic – Autoimmune – Diffuse antral – Multifocal Etiology of Gastritis • Breakdown in normal gastric mucosa from: – Medications i.e. ASA, steroids, NSAID’s – Diet i.e. spicy, ETOH – Microorganisms i.e.. H. Pylori, Salmonella, Staph – Smoking – Pathophysiology i.e. burns, stress, renal failure, sepsis, shock – Trauma i.e. NGT, endoscopy H. Pylori Client may be asymptomatic Believed to be acquired in childhood and survives Can play a major role in gastritis, peptic ulcer, duodenal ulcer H. Pylori secretes urease that protects it from being destroyed in acid environment Antibiotics Used to Treat H. Pylori • • • • Amoxicillin Flagyl (metronidazole) Tetracycline Biaxin (Clarithromycin) Manifestations of Gastritis • Acute gastritis – – – – – – – – Anorexia Nausea Vomiting Epigastric tenderness Feeling of fullness Chronic gastritis May be asymptomatic Loss of intrinsic factor lead to s/s of B 12 deficiency-anemia Diagnostic Studies of Gastritis • History and Physical/ Social history – ETOH – Smoking – Endoscope • • • • • • H. Pylori testing CBC Stool for occult blood Cytology Gastric analysis-decreased or absent HCL Antibodies to parietal cells and intrinsic factor Nursing Care of the Client with Acute Gastritis • • • • • • • • May be NPO or NGT IV fluids Antiemetics VS, check for bleeding Antacids H2 blockers Proton pump inhibitor Tritec-Proton pump inhibitor plus bismuth Nursing Care of the Client with Chronic Gastritis • Eliminate specific cause i.e. ETOH • Eradicate H. Pylori – Different protocols – Antibiotics i.e. Amoxicillin – Proton pump inhibitor – Antiinfectives i.e. Flagyl – Six small meals a day – Antacids – No Smoking Upper GI Bleed—Pathophysiology • Can be sudden or gradual • Severity depends on what type of bleed • Arterial – Bright red (not in contact with stomach) – Large amounts – ―Coffee ground‖-In stomach for some time – Longer the passage of blood through intestine, the darker the stool Upper GI Bleed—Pathophysiology • Massive GI bleed – 1500 ml or 25% of intravascular blood volume – Hematemesis-bright red blood or ―coffee grounds‖ – Melena-Black, tarry stools, slow bleeding from upper GI – Occult bleed-small amounts of blood in vomit, stool, etc. not detectable by sight Upper GI Bleed—Etiology • Medications-ASA, NSAID’s, steroids • Esophagus-Esophageal varicies, Esophagitis, Mallory-Weiss tear • Gastric Cancer • Hemorrhagic gastritis • Peptic ulcer disease • Polyps • Stress ulcer • Blood dyscrasias • Renal failure Esophageal Bleeding • Mallory-Weiss tear – Caused by severe retching and vomiting – Tear occurs at the junction of the esophagus and stomach • Esophageal varicies – Usually secondary to cirrhosis of the liver – Anything that increase pressure i.e. coughing can start massive bleed Stomach and Duodenal Bleed • Bleeding ulcers-majority of upper GI bleeds • Physiological stress ulcers – Burns – Surgery – Medications Emergency Treatment for the Client with an Upper GI Bleed • VS (frequent), cap refill, urinary output • Abdominal assessment – Presence/absence of bowel sounds – Rigid, boardlike abdomen-emergency, can indicate perforation – H&P – CBC, BUN, Chemistry, ABG’s, coagulation studies, liver studies – Multiple IV lines with large guage – Fluids (LR) Emergency Treatment for the Client With an Upper GI Bleed • • • • • • Type and cross/transfuse O2 Foley CVP line Gastric lavage To OR or Endoscopy Diagnostic Studies/Treatment for Upper GI Bleed • Endoscopy – Can coagulate/thrombose area – Surgery • Angiography • Medications – Proton pump inhibitors – H2 blockers – Pitressin – Sandostatin Pharmacological Intervention for Upper GI Bleed • Pitressin – Creates vasoconstriction – Continuous IV drip – Titrate for effectiveness – Sandostatin • Suppresses secretion of HCL Peptic Ulcer Disease • Erosion of the GI mucosa from the digestive action of HCL acid and pepsin • Types – Acute-superficial erosion/minimal inflammation – Chronic-Long duration, erosion through muscular wall, fibrous tissue formation • Both gastric and duodenal ulcer fall into this category Peptic Ulcer Disease—Etiology • Peptic ulcers only develop in acid environments • Cause of disease same as for upper GI bleed Peptic Ulcer Disease Pathophysiology • Pesinogen converts to pepsin in acid environment • Mucosal barrier impaired from previously mentioned causes • H. Pylori can also destroy mucosal barrier • As mucosal layer is impaired, increase in bloodflow • Increased vasodilation • Tissue damage occurs • Emotions increase secretion of HCL Gastric Ulcers • Most commonly found on less curvature of stomach • Superficial lesion • Gastric secretion normal to low • Greater in women 50-60 years old Clinical Manifestations/Complications of Gastric Ulcers • Burning or gastric pressure in high epigastrum • Pain 1-2 hours after meals • N/V • Weight loss • Complications – Hemorrhage – Perforation Duodenal Ulcer • • • • Majority of all peptic ulcers More in men 35-45 years High acid secretion Disease that increase risk of developing duodenal ulcers – – – – – – COPD Cirrhosis Pancreatitis Renal Failure Hyperparathyroidism Zollinger-Ellison syndrome Duodenal Ulcer • Penetrating lesion usually found in first 1-2 cm of duodenum • Greater in men • Associated with stress • Increase with ETOH, smoking Zollinger-Ellison Syndrome • • • • Severe peptic ulceration Gastric acid hypersecretion Increased serum gastrin levels Gastrinoma of the pancreas/duodenum Clinical Manifestations of Duodenal Ulcers • Clinical manifestations – Burning, cramping across midepigastrum and upper abdomen – Back pain – Pain 2-4 hr after meals and midmorning, middle of night – Relief with food antacids – N/V Complications of Peptic Ulcer Disease • Hemorrhage • Perforation-most lethal, severe abdominal pain that spreads throughout abdomen, shoulder pain, absent bowel sounds • Obstruction Diagnostic Studies of Peptic Ulcer Disease • Endoscopy • Tests for H.Pylori – Invasive • Tissue specimens • Rapid urease test – Nonivasive • IgG • Urea breath test (by product of H.Pylori) • Barium swallow/X-rays- not accurate Treatment of Peptic Ulcer Disease • Discontinue medications if possible that exacerbate condition • No smoking/ETOH • Avoid spicy/acid foods, black pepper, small frequent meals • Medications – – – – – – – – H2 Blockers Cytotec (antisecretory and cytoprotective) Cytoprotective agents (Carafate) Antacids Antibiotics for H. Pylori Treat stress Antidepressants? Surgery Treatment of Peptic Ulcer DiseaseSurgery • Not usual course of treatment • Gastroduodenostomy (Biliroth I)-Partial gastrostomy • Gastrojejunostomy (Biliroth II) –antrum and pylorus removed, preferred method for duodenal ulcer • Vagotomy-sever Vagal nerve • Pyroplasty-enlarge pyloric sphincter Peptic Ulcer Disease Post op Complications • Avoid Dumping syndrome by: – Small meals, no liquids with meal – Dry foods, low carbs, moderate protein, fats • Avoid Postprandial hypoglycemia by: – If hypoglycemic occurs, candy – Follow diet for dumping syndrome • Bile reflux gastritis – Notify Health care provider if epigastric distress similar to pre op Gastric Cancer • Adenocarcinoma of the stomach wall • Usually men in advanced stage • Etiology – Unknown – ? High spice, high smoked foods – Pathophysiology • Nonspecific mucosal injury • Predisposing factors – – – – – Atropic gastritis H.Pylori at early age Gastric Polyps Pernicious anemia Achlorhydria Clinical manifestations of Gastric Cancer • Usually late in disease process • Signs/symptoms of anemia – – – – – – – – Pallor SOB Fatigue Signs/symptoms of peptic ulcer disease Burning pain, alleviated by antacids Weight loss Dysphagia Later • Papable mass in abdomen • Enlarged hard lymph nodes Acute exacerbation of Peptic Ulcer Disease • • • • • • • • • Frequent VS NGT Several IV lines (Large bore) Crystalloid/colloid solutions (LR) CBC, Chemistries, ABG’s O2 Type and Cross Match Emergency care as per client needs Perforation-OR Diagnostic Studies of Gastric Cancer • • • • • H&P Upper GI barium Endoscopy-biopsy/cytology/US CBC, Chemistries, Stool specimens Tumor markers-CEA, CA 19-9 Treatment of Gastric Cancer • Surgery removal of tumor • Chemo/radiation ? Success • Treat symptoms – Pain – Correct anemia Food Poisoning • Types – Acute gastroenteritis – Neurological symptoms from botulism Responsible Microorganisms of Food Poisoning – Staph • Onset-30 min-7hr • Symptoms-N/V, diarrhea • Prevent: Refrigerate foods – Clostridium • Onset-8-24 hr • Symptoms-Nausea with no vomiting, diarrhea • Prevent: Correct preparation of meat Responsible Microorganisms of Food Poisoning • Salmonella – Onset-8hr-days – Symptoms-n/V fever – Prevent: Proper preparation of poultry, pork, beef • Botulism – Onset: 12-36 hr – Symptoms: GI, CNS symptoms – Prevent: Correct processing of canned foods Responsible Microorganisms of Food Poisoning • E. Coli – Onset: 8hr-1wk – Symptoms: Bloody stools, hemolytic uremic syndrome, profuse diarrhea