Gastrointestinal Disorders ( part 1) N250, Spring 2015 CSULB School of Nursing

What We Will Cover Part 1 GERD, Hiatal Hernia, PUD Cholecystitis Pancreatitis Appendicitis Part 2 Inflammatory Bowel Diseases Diverticular Disease Colorectal Cancer Bowel Obstruction

Clinical Manifestations Of Gastrointestinal Disorders Pain Anorexia Nausea and vomiting Bleeding Diarrhea Belching and flatulence Indigestion

GERD Epidemiology, Etiology, and Risk Factors Backward flow of stomach contents into esophagus Decreased lower esophageal sphincter (LES) pressure (with or without increased acid production) Causes: obesity, pregnancy, hiatal hernia, certain foods and medications Incidence increases after age 50 years Prevalence equal across gender, ethnic, cultural groups

GERD Clinical Manifestations Heartburn: mild to severe Sour taste in morning, regurgitation, coughing, belching, chest pain Atypical symptoms: asthma or cough Long-term consequences can be serious: esophageal strictures, Barrett's epithelium, esophageal cancer

GERD: Diagnostic Procedures and Treatment Upper endoscopy (persistent symptoms for more than 4 weeks) Other procedures: ambulatory esophageal pH, barium studies Medications can be purchased over-the- counter (OTC) or prescribed Most common medications: antacids, histamine 2 receptor-blockers, proton pump inhibitors

GERD Patient Teaching Importance of eating 4 to 6 small meals daily Eliminate foods that decrease LES or increase acid production Instruct patient not to lie down after eating Educate patient about medication regimen and possible side effects

Hiatal Hernia Involves herniation of upper portion of stomach into thorax through esophageal hiatus Two types:  Sliding  Rolling

Epidemiology, Etiology, and Pathophysiology More prevalent in Western countries; increases with age More common in women Causes of sliding hernia: obesity, pregnancy, intra-abdominal pressure Rolling hernia can result in gastritis and ulceration

Laboratory and Diagnostic Procedures Upper endoscopy Ambulatory esophageal pH monitoring Barium swallow Esophageal manometry Computed tomography (CT) Magnetic resonance imaging (MRI)

Clinical Manifestations Generally both types are asymptomatic Primary symptoms: reflux and heartburn; feeling full, belching, indigestion Some patients may complain of substernal chest pain

Medical & Surgical Management Same medical management as GERD Surgery involves increasing LES pressure Most common procedure: Nissen fundoplication

Peptic Ulcer Disease (PUD) Includes gastric and duodenal ulcers PUD develops most often in antrum Occurs between ages of 55 and 70 years Equal frequency in men and women

Etiology and Pathophysiology Erosions of the gastric or duodenal lining from hypersecretion of acid and pepsin and H. pylori infection  Responsible for 70% of gastric ulcers Decreased prostaglandin secretion by the mucosa Hypersecretion disorders (Zollinger-Ellison syndrome; hyperthyroidism, CF)

Etiology and Pathophysiology Cigarette smoke stimulates acid production Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit prostaglandins, increasing acid levels Duodenal ulcers found most often in young adults (ages 30 to 55 years), patients with type O blood Caffeine, alcohol, stress

Clinical Manifestations Pain located in upper abdomen; intermittent; gnawing, burning, aching, hunger-like Older adults may have chest pain or anemia Gastric ulcers:  Pain worse with eating  Relieved by antacids Duodenal ulcers:  Pain occurs 2-3 hours after eating  Pain often awakens the patient at night

Laboratory & Diagnostic Tests Testing for organism (H pylori) Direct visualization of the mucosa in esophagus, stomach, duodenum with endoscope (EGD)

Medical Management Relieving symptoms, eradicating infection, preventing complications Drug therapy on complete physical assessment Avoid irritating foods, no NSAIDs, smoking cessation, proper hygiene Gastrectomy for complications of PUD if therapy fails

Complications Hemorrhage, perforation, pyloric or gastric outlet obstruction Bleeding most common complication of PUD; usually with dark, tarry stools Pyloric obstruction: result of edema, inflammation, scarring of the pylorus or combination Most serious complication: perforation  Triggers inflammatory response and peritonitis

Disorders of the Gallbladder Gallbladder: saclike structure concentrates and stores bile

Cholelithiasis Gallstones – causing obstructed bile flow  Biliary stasis  Gallbladder inflammation  Abnormal bile composition and reabsorption  Cholesterol and pigmented gallstones

Cholelithiasis: Incidence & Risk Factors More common in women Incidence in both men and women increases with age Risk factors:  Ethnicity  Obesity, diabetes, hyperlipidemia, cirrhosis, Crohn's disease  Rapid weight loss, bariatric surgery  Medications

Cholelithiasis: Clinical Manifestations Asymptomatic Epigastric and/or RUQ pain Nausea; fatty food intolerance Flatulence, bloating, abdominal distention, diarrhea, light-colored stool, chest pain Jaundice

Cholecystitis (Inflammation of the gallbladder) Acute or chronic Most common cause is gallstone lodged in the cystic duct Other causes: infectious organisms, gallbladder irritation Can result in necrosis, gangrene, perforation, peritonitis Manifestations similar to cholelithiasis Identify and treat cause

Acute and Chronic Cholecystitis Acute cholecystitis Chronic cholecystitis Cholelithiasis Acalculous cholecystitis -- inflammation can occur in the absence of gallstones.

Placement of a T tube. The surgeon ties off the cystic duct and sutures the T tube to the common bile duct with the short arms of the T tube toward the hepatic duct and duodenum. The long arm of the T tube exits the body near the incision site. Skin suture and tape secure placement T tube for bile collection

ERCP for stone removal

Acute Pancreatitis Serious and possibly life-threatening inflammatory process of the pancreas Necrotizing hemorrhagic pancreatitis  Enzyme activation  Lipolysis, Proteolysis  Necrosis of blood vessels  Inflammation Many cases mild and self-limiting Severe pancreatitis can lead to necrosis of the pancreas

Pathophysiology Most cases associated with biliary tract obstruction or heavy alcohol use Activated pancreatic enzymes (trypsin) causes autodigestion Autodigestion causes edema, vascular leakage, hemorrhage, necrosis Can damage nearby organs leading to respiratory or cardiac disorders

Clinical Manifestations Sudden, severe, steady epigastric pain Nausea and vomiting In some cases, abdominal distention, decreased bowel sounds, and rigidity Turner's sign (ecchymosis in the flanks) may appear 3 to 6 days after onset Cullen's sign (bruising around the umbilicus) may appear 3 to 6 days after onset

Laboratory & Diagnostic Tests History and physical exam Elevated levels of serum amylase, lipase, ALT Serum bilirubin and serum alkaline phosphatase Imaging tests

Medical Management Treatment focus is resting the pancreas Patient is kept NPO  Frequent insertion of a nasogastric tube  Prevents release of pancreatic enzymes Bed rest Large amounts of IV fluids may be required

Medical Management Clear liquid diet  After pain subsides and bowel sounds return Slow transition to low-fat diet Pain management with narcotic analgesics Surgery for infected necrotizing pancreatitis  Pancreas and surrounding area are debrided

Chronic Pancreatitis Progressive irreversible destruction of the pancreas, characterized by remissions and exacerbations Causes:  Chronic alcohol use  Smoking  Stones  Cystic fibrosis  Malnutrition  Heredity  No identifiable cause

Clinical Manifestations Recurrent epigastric and left upper quadrant pain  Pain may be referred to the left lumbar region Pain less severe than acute pancreatitis Tender abdomen with mild muscle guarding over the pancreas

Clinical Manifestations Other symptoms can include:  Anorexia  Nausea  Vomiting  Weight loss  Flatulence  Constipation  Steatorrhea—bulky, fatty, and foul stools

Laboratory & Diagnostic Tests Similar to those of acute pancreatitis Amylase and lipase levels may be normal Stool samples Endoscopic retrograde cholangiopancreatography (ERCP) Magnetic resonance cholangiopancreatography (MRCP) Endoscopic ultrasonography with tissue sampling

Medical Management Analgesic administration  Narcotics not used due to addiction risk  NSAIDs Enzyme replacement Insulin therapy Nutrition therapy Surgery needed with biliary tract disease Lifelong lifestyle changes required:  Alcohol abstinence  Low-fat diet

Appendicitis Primary cause: obstruction Intramural pressure increases, causes thrombosis and occlusion of small vessels Wall becomes necrotic leading to bacterial overgrowth and rupture

Clinical Manifestations & Diagnostic Tests Pain is most common symptom Right lower quadrant abdominal pain, nausea, vomiting; rebound tenderness, guarding WBC count, abdominal x-ray, abdominal CT Rupture poses high risk for peritonitis

Medical & Surgical Management Surgical removal: laparoscopy or open laparotomy Patient with perforation should receive broad-spectrum antibiotics

Nursing Management Management of fluid and electrolyte balance, pain, infection Antiemetics for postoperative nausea and vomiting Early postoperative ambulation