Transcript GI Disorders PPT (part one)

Gastrointestinal
Disorders (part 1)
N250, Spring 2015
CSULB School of Nursing
What We Will Cover
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Part 1
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GERD, Hiatal Hernia, PUD
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Cholecystitis
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Pancreatitis
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Appendicitis
Part 2
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Inflammatory Bowel Diseases
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Diverticular Disease
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Colorectal Cancer
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Bowel Obstruction
Clinical Manifestations Of
Gastrointestinal Disorders
Pain
 Anorexia
 Nausea and vomiting
 Bleeding
 Diarrhea
 Belching and flatulence
 Indigestion
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GERD Epidemiology, Etiology,
and Risk Factors
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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
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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
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Long-term consequences can be serious:
esophageal strictures, Barrett's epithelium,
esophageal cancer
GERD: Diagnostic Procedures and
Treatment
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Upper endoscopy (persistent symptoms for
more than 4 weeks)
Other procedures: ambulatory esophageal pH,
barium studies
Medications can be purchased over-thecounter (OTC) or prescribed
Most common medications: antacids,
histamine 2 receptor-blockers, proton pump
inhibitors
GERD Patient Teaching
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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:
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 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
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Laboratory and Diagnostic
Procedures
Upper endoscopy
 Ambulatory esophageal pH
 monitoring
 Barium swallow
 Esophageal manometry
 Computed tomography (CT)
 Magnetic resonance imaging (MRI)
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Clinical Manifestations
Generally both types are asymptomatic
 Primary symptoms: reflux and heartburn;
feeling full, belching, indigestion
 Some patients may complain of substernal
chest pain
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Medical & Surgical
Management
Same medical management as
GERD
 Surgery involves increasing
LES pressure
 Most common procedure:
Nissen fundoplication
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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
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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)
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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
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Clinical Manifestations
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Pain located in upper abdomen; intermittent;
gnawing, burning, aching, hunger-like
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Older adults may have chest pain or anemia
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Gastric ulcers:
 Pain worse with eating
 Relieved by antacids
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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)
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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
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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
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 Triggers inflammatory response and peritonitis
Disorders of the Gallbladder
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Gallbladder: saclike structure concentrates
and stores bile
Cholelithiasis
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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:
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 Ethnicity
 Obesity, diabetes, hyperlipidemia, cirrhosis,
Crohn's disease
 Rapid weight loss, bariatric surgery
 Medications
Cholelithiasis: Clinical Manifestations
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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
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Acute and Chronic Cholecystitis
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Acute cholecystitis
Chronic cholecystitis
Cholelithiasis
Acalculous
cholecystitis -inflammation can
occur in the absence
of gallstones.
T tube for bile
collection
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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
ERCP for
stone
removal
Acute Pancreatitis
Serious and possibly life-threatening
inflammatory process of the pancreas
 Necrotizing hemorrhagic pancreatitis
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 Enzyme activation
 Lipolysis, Proteolysis
 Necrosis of blood vessels
 Inflammation
Many cases mild and self-limiting
 Severe pancreatitis can lead to necrosis
of the pancreas
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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
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Clinical Manifestations
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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
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Medical Management
Treatment focus is resting the pancreas
 Patient is kept NPO
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 Frequent insertion of a nasogastric tube
 Prevents release of pancreatic enzymes
Bed rest
 Large amounts of IV fluids may be required
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Medical Management
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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
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 Pancreas and surrounding area are debrided
Chronic Pancreatitis
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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
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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
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Clinical Manifestations
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Other symptoms can include:
 Anorexia
 Nausea
 Vomiting
 Weight loss
 Flatulence
 Constipation
 Steatorrhea—bulky, fatty, and foul stools
Laboratory & Diagnostic Tests
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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
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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:
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 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
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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
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Medical & Surgical Management
Surgical removal:
laparoscopy or open
laparotomy
 Patient with
perforation should
receive broad-spectrum
antibiotics
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Nursing Management
Management of fluid and electrolyte
balance, pain, infection
 Antiemetics for postoperative nausea and
vomiting
 Early postoperative
ambulation
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