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