Gastrointestina l Disorders (part 1) N250, Spring 2015 CSULB School of Nursing
Dec 26, 2015
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 OfGastrointestinal 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:SlidingRolling
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 infectionResponsible 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 flowBiliary stasisGallbladder inflammationAbnormal bile composition and
reabsorptionCholesterol and pigmented
gallstones
Cholelithiasis: Incidence & Risk Factors More common in women Incidence in both men and women increases with
age Risk factors:
EthnicityObesity, diabetes, hyperlipidemia, cirrhosis, Crohn's
diseaseRapid weight loss, bariatric surgeryMedications
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 activationLipolysis, ProteolysisNecrosis of blood vesselsInflammation
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 tubePrevents 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 painPain 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:
AnorexiaNauseaVomitingWeight lossFlatulenceConstipationSteatorrhea—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