Download Peptic Ulcers

The Digestive System
 Also known as the gastrointestinal (GI)
tract or the alimentary system, it is
responsible for breaking down the
complex food into simple nutrients the
body can absorb and convert into energy.
This process is known as digestion.
Major GI Function Organs
 Mouth
 Pharynx
 Esophagus
 Stomach
 Small intestine
 Large intestine
Accessory GI Organs
 Liver
 Gallbladder
 Pancreas
Figure 24-1 The gastrointestinal tract and accessory organs of digestion. (Source: Pearson Education/PH College)
Mouth
 Teeth chew and grind food into smaller
parts
 Moistened with saliva for tasting,
chewing, and swallowing
Pharynx
 Muscles that propel the food from the
mouth
Esophagus
 Carries food through peristalsis
 Cardiac/lower esophageal sphincter
 Closes
after food leaves esophagus
Figure 24-2 Structures of the stomach and duodenum, including the common bile duct and pancreatic duct. The
relationship of the pancreas and gallbladder to the stomach also are shown.
Stomach
 Holds the food
 Pyloric sphincter: controls the emptying
of the stomach
Small Intestine
 Approximately 20 to 25 feet long and is
responsible for absorbing nutrients from
the chyme (semi-liquid mass of partially
digested food).
 Small intestine divided into: duodenum
(first 10-12 inches); jejunum (the middle
8-10 feet) and the ileum (the distal 12
feet).
Large Intestine
 Begins at ileocecal valve, terminates at
the anus
 5 feet long
 Includes the appendix
 Nutrients absorbed and indigestible
materials eliminated
Large Intestine
 Also known as the colon, the large
intestine is responsible for absorbing
water, electrolytes, and salts.
 The last 5 inches of the large intestine
comprise the rectum. The distal end of
the rectum forms the anal canal
composed of muscles that control
defecation. The opening to the anal canal
is called the anus.
Large Intestine (continued)
 Parts:
 Ascending
 Transverse
 Descending
Sigmoid colon
 Rectum

Liver
 Largest gland in the body
 Located in the right side of the abdomen
 Has four lobes
 Encased in a fibrous capsule
 Hepatocytes produce bile, which aids in
digestion
Gallbladder
 Stores bile
 Located on the inferior surface of the
liver
The liver, gallbladder, common bile duct, and sphincter of Oddi.
Pancreas
 Gland located between the stomach and
small intestines
 Exocrine and endocrine functions
 Produce pancreatic juice to neutralize
food
 Produce enzymes to digest food
Digestion
 Mouth
 The
upper opening of the GI tract
 Lined by mucous membranes
 The teeth chew and grind food into
smaller parts
 Saliva (produced by the salivary
glands) moistens food for tasting,
chewing, and swallowing
Mouth
 Digestive process starts here
 Enzymes in saliva begin the food
breakdown
 Amylase
 Lysozyme
Digestion
 Pharynx
 Muscles
here move the food into the
esophagus
 Esophagus
 Carries the food to the stomach
through peristalsis
Stomach
 Mechanical digestion in the stomach
mixes partially digested food with gastric
juices to produce chyme
Nervous System
 Parasympathetic nervous system signals
vagus nerve to increase gastric secretions
in response to food
 Emotions (anxiety/stress) reduce gastric
secretions and motility
Small Intestine
 Location where food is chemically
digested and most absorbed
 Enzymes break down carbohydrates,
proteins, and fats
 Pancreatic buffers neutralize the stomach
acid
Small Intestine (continued)
 Microvilli enhance absorption
 Most of food, water, vitamins, and
minerals are absorbed here into the
blood or lymph
Liver
 Digestive functions:
 Metabolize
carbohydrates, proteins,
and fats
 Synthesize plasma proteins and
enzymes
 Store blood, vitamins, and minerals
 Produce and secrete bile
Pancreas
 Produces enzymes for digestion
 Secretion is controlled by the vagus nerve
and the hormones secretin and
cholecystokinin
 Lipase promotes fat breakdown and
absorption
 Amylase digests starch
Pancreas (continued)
 Trypsin, chymotrypsin, and
carboxypeptidase digest protein
 Nucleases, which digest nucleic acids, are
also present
Large Intestine
 Major function: eliminate indigestible
food
 Absorbs water, salts, and vitamins
forming it into feces or stool
 Feces move with peristalsis
 Goblet cells secrete mucus to aid with
defecation
 Defecation reflex: sigmoid colon walls
contract and anal sphincter relaxes
Nutrients
 Carbohydrates
 Proteins
 Fats
 Vitamins
 Minerals
 Water
Carbohydrates
 Simple sugars
 Milk
 Sugar
cane
 Sugar beets
 Honey fruits
 Complex starches
 Grains
 Legumes
 Root vegetables
Proteins
 Complete proteins
(all essential AA)






Eggs
Milk
Milk products
Meat
Fish
Poultry
 Plant proteins
 Legumes
 Nuts
 Grains
 Cereals
 Vegetables
Additional Nutrients
 Fats
 Saturated
fats
 Unsaturated fats
 Vitamins
 Minerals
 Water
Assessment for Clients with GI
Complaints
History of present complaint regarding specific symptoms
Medication history including medications
Complete nutritional history
Psychosocial factors
Physical examination including inspection
Bowel elimination patterns
Evaluation and diagnostic data including laboratory tests
and radiologic and endoscopic examinations
Health History
 Current complaints, food intolerance
 Appetite, heartburn, nausea, vomiting
 Abdominal discomfort, diarrhea,
constipation
 Weight changes
 Food allergies
 Pattern and amount of daily food intake
Health History
 Teeth, mouth, ability to chew, swallow,
dentures
 Change in stool frequency, amount, color,
caliber
 Medications
 Chronic diseases
 Previous surgeries
Physical Examination
 Overall health status
 Skin color, hair, nails
 Height and weight
 Inspect mouth, teeth, tongue
 Swallow
Physical Examination
 Inspect abdomen, observe skin,
peristalsis
 Auscultate bowel sounds
 Percuss the abdomen
 Palpate the abdomen
Laboratory Tests
 Serum albumin and total protein
 Serologic H. pylori testing
 Stool specimen
 Liver function tests
 Pancreatic function tests
Diagnostic Tests
 Gastric analysis
 Urea breath test
 Ambulatory pH monitoring
 Esophageal manometry
 Paracentesis
Gastric Analysis
 Gastric analysis consists of a series of tests used to analyze the
contents of the stomach. The complete series involves:
A- collecting residual gastric fluid from a fasting patient
B- collecting basal secretions every 15 minutes for four hours
C- intramuscular administration of a drug that stimulates gastric acid
output
D- collecting stomach secretions every 15 minutes for 90 minutes
 Instruct client to abstain from food, fluids, smoking, chewing gum,
and some medications for 8 to 12 hours before the test
 Insert NG tube and collect samples
Urea Breath Test
 is a rapid diagnostic procedure used to identify infections by
Helicobacter pylori, a spiral bacterium implicated in gastritis,
gastric ulcer, and peptic ulcer disease. It is based upon the ability
of H. pylori to convert urea to ammonia.
 Instruct client to abstain from food and
fluids for 4 hours prior to the test
 Instruct client to abstain from antacids,
bismuth sulfate, antibiotics, and Prilosec
for 2 weeks prior to the test
More Diagnostic Tests
 Ambulatory pH Monitor: is a way for the doctor to see how much acid
is backing up into the esophagus over a 24-hour period.
The test involves placing a small catheter in the esophagus. The catheter is
connected to a small recording device called a Digitrapper.
Instruct client how to care for the electrode and
data recorder
 Esophageal Manometry: is a test to assess motor function of the Upper

Esophageal Sphincter (UES), Esophageal body and Lower Esophageal Sphincter
(LES).

Instruct client to abstain from food and fluids up to 8
hours prior to the test
 Assist with insertion of the tube
 Paracentesis: is a medical procedure involving needle drainage of fluid from
a body cavity, most commonly the peritoneal cavity in the abdomen.
Diagnostic Imaging
Procedures
 Ultrasonography
 Radiologic Studies
Gastroesophageal Reflux Disease
(GERD)
1. Definition
 a. Gastroesophageal reflux is the backward flow of
gastric content into the esophagus.
 b. GERD common, affecting 15 – 20% of adults
 c. 10% persons experience daily heartburn and
indigestion
 d. Because of location near other organs symptoms
may mimic other illnesses including heart problems
Gastroesophageal Reflux Disease
(GERD)
2. Pathophysiology
 a. Gastroesophageal reflux results from transient relaxation
or incompetence of lower esophageal sphincter, sphincter, or
increased pressure within stomach
 b. Factors contributing to gastroesophageal reflux
1.Increased gastric volume (post meals)
2.Position pushing gastric contents close to gastroesophageal
juncture (such as bending or lying down)
3.Increased gastric pressure (obesity or tight clothing)
4.Hiatal hernia
Gastroesophageal Reflux Disease
(GERD)
 c.Normally the peristalsis in esophagus and bicarbonate in
3.





salivary secretions neutralize any gastric juices (acidic)
that contact the esophagus; during sleep and with
gastroesophageal reflux esophageal mucosa is damaged
and inflamed; prolonged exposure causes ulceration,
friable mucosa, and bleeding; untreated there is scarring
and stricture
Manifestations
a. Heartburn after meals, while bending over, or
recumbent
b. May have regurgitation of sour materials in mouth,
pain with swallowing
c. Atypical chest pain
d. Sore throat with hoarseness
e. Bronchospasm and laryngospasm
Gastroesophageal Reflux Disease
(GERD)
4. Complications
 a. Esophageal strictures, which can progress to
dysphagia
 b. Barrett’s esophagus: changes in cells lining
esophagus with increased risk for esophageal cancer
5. Collaborative Care
 a. Diagnosis may be made from history of symptoms
and risks
 b. Treatment includes
1.Life style changes
2.Diet modifications
3.Medications
Gastroesophageal Reflux Disease
(GERD)
6. Diagnostic Tests
 a. Barium swallow (evaluation of esophagus,
stomach, small intestine)
 b. Upper endoscopy: direct visualization;
biopsies may be done
 c. 24-hour ambulatory pH monitoring
 d. Esophageal manometry, which measure
pressures of esophageal sphincter and peristalsis
 e. Esophageal motility studies
Gastroesophageal Reflux Disease
(GERD)
7.Medications
 a.
Antacids for mild to moderate symptoms, e.g.
Maalox, Mylanta, Gaviscon
 b. H2-receptor blockers: decrease acid production;
given BID or more often, e.g. cimetidine, ranitidine,
famotidine, nizatidine
 c. Proton-pump inhibitors: reduce gastric secretions,
promote healing of esophageal erosion and relieve
symptoms, e.g. omeprazole (prilosec); lansoprazole
(Prevacid) initially for 8 weeks; or 3 to 6 months
 d. Promotility agent: enhances esophageal clearance
and gastric emptying, e.g. metoclopramide (reglan)
Gastroesophageal Reflux Disease
8. Dietary and Lifestyle Management
 a.






Elimination of acid foods (tomatoes, spicy, citrus
foods, coffee)
b. Avoiding food which relax esophageal sphincter or
delay gastric emptying (fatty foods, chocolate, peppermint,
alcohol)
c. Maintain ideal body weight
d. Eat small meals and stay upright 2 hours post eating;
no eating 3 hours prior to going to bed
e. Elevate head of bed on 6 – 8 blocks to decrease
reflux
f. No smoking
g. Avoiding bending and wear loose fitting clothing
Gastroesophageal Reflux Disease
(GERD)
9.Surgery indicated for persons not improved
by diet and life style changes
 a. Laparoscopic procedures to tighten
lower esophageal sphincter
 b. Open surgical procedure: Nissen
fundoplication
10. Nursing Care
 a. Pain usually controlled by treatment
 b. Assist client to institute home plan
Hiatal Hernia
1.Definition
 a.
Part of stomach protrudes through the
esophageal hiatus of the diaphragm into thoracic
cavity
 b. Predisposing factors include:
 Increased intra-abdominal pressure
 Increased age
 Trauma
 Congenital weakness
 Forced recumbent position
Hiatal Hernia
 c.
Most cases are asymptomatic; incidence
increases with age
 d. Sliding hiatal hernia: gastroesophageal
junction and fundus of stomach slide through the
esophageal hiatus
 e. Paraesophageal hiatal hernia: the
gastroesophageal junction is in normal place but
part of stomach herniates through esophageal
hiatus; hernia can become strangulated; client may
develop gastritis with bleeding
Hiatal Hernia
2. Manifestations: Similar to GERD
3. Diagnostic Tests
 a. Barium swallow
 b. Upper endoscopy
4. Treatment
 a. Similar to GERD: diet and lifestyle changes,
medications
 b. If medical treatment is not effective or hernia becomes
incarcerated, then surgery; usually Nissen fundoplication
by thoracic or abdominal approach

Anchoring the lower esophageal sphincter by
wrapping a portion of the stomach around it to
anchor it in place
Impaired Esophageal Motility
1. Types
 a.
Achalasia: characterized by impaired peristalsis of smooth
muscle of esophagus and impaired relaxation of lower esophageal
sphincter
 b.
Diffuse esophageal spasm: nonperistaltic contraction of
esophageal smooth muscle
2. Manifestations: Dysphagia and/or chest pain
3. Treatment
 a.
Endoscopically guided injection of botulinum toxin
 Denervates cholinergic nerves in the distal esophagus to stop
spams
 b.
Balloon dilation of lower esophageal sphincter
 May place stents to keep esophagus open
Gastritis
1. Definition: Inflammation of stomach lining from
irritation of gastric mucosa (normally protected
from gastric acid and enzymes by mucosal barrier)
2. Types
 a. Acute Gastritis
1.Disruption of mucosal barrier allowing
hydrochloric acid and pepsin to have contact with
gastric tissue: leads to irritation, inflammation,
superficial erosions
2.Gastric mucosa rapidly regenerates; selflimiting disorder
Gastritis
3. Causes of acute gastritis
 a.
Irritants include aspirin and other NSAIDS, corticosteroids,
alcohol, caffeine
 b.
Ingestion of corrosive substances: alkali or acid
 c.
Effects from radiation therapy, certain chemotherapeutic agents
4. Erosive Gastritis: form of acute which is stress-induced, complication
of life-threatening condition (Curling’s ulcer with burns); gastric
mucosa becomes ischemic and tissue is then injured by acid of
stomach
5. Manifestations
 a.
Mild: anorexia, mild epigastric discomfort, belching
 b.
More severe: abdominal pain, nausea, vomiting, hematemesis,
melena
 c.
Erosive: not associated with pain; bleeding occurs 2 or more days
post stress event
 d.
If perforation occurs, signs of peritonitis
Gastritis
6. Treatment
 a. NPO status to rest GI tract for 6 – 12 hours,
reintroduce clear liquids gradually and progress;
intravenous fluid and electrolytes if indicated
 b. Medications: proton-pump inhibitor or H2receptor blocker; sucralfate (carafate) acts locally;
coats and protects gastric mucosa
 c. If gastritis from corrosive substance: immediate
dilution and removal of substance by gastric lavage
(washing out stomach contents via nasogastric
tube), no vomiting
Chronic Gastritis
 1. Progressive disorder beginning with
superficial inflammation and leads to atrophy of
gastric tissues
 2. Type A: autoimmune component and affecting
persons of northern European descent; loss of
hydrochloric acid and pepsin secretion; develops
pernicious anemia
 Parietal cells normally secrete intrinsic factor
needed for absorption of B12, when they are
destroyed by gastritis pts develop pernicious
anemia
Chronic Gastritis
 3. Type B: more common and occurs with
aging; caused by chronic infection of
mucosa by Helicobacter pylori; associated
with risk of peptic ulcer disease and gastric
cancer
Chronic Gastritis
4. Manifestations
 a. Vague gastric distress, epigastric heaviness
not relieved by antacids
 b. Fatigue associated with anemia; symptoms
associated with pernicious anemia: paresthesias
 Lack of B12 affects nerve transmission
5. Treatment: Type B: eradicate H. pylori infection
with combination therapy of two antibiotics
(metronidazole (Flagyl) and clarithomycin or
tetracycline) and proton–pump inhibitor (Prevacid
or Prilosec)
Chronic Gastritis
Collaborative Care
 a. Usually managed in community
 b. Teach food safety measures to prevent acute
gastritis from food contaminated with bacteria
 c. Management of acute gastritis with NPO state
and then gradual reintroduction of fluids with
electrolytes and glucose and advance to solid
foods
 d. Teaching regarding use of prescribed
medications, smoking cessation, treatment of
alcohol abuse
Chronic Gastritis
Diagnostic Tests
 a. Gastric analysis: assess hydrochloric acid secretion
(less with chronic gastritis)
 b. Hemoglobin, hematocrit, red blood cell indices:
anemia including pernicious or iron deficiency
 c. Serum vitamin B12 levels: determine pernicious
anemia
 d. Upper endoscopy: visualize mucosa, identify areas of
bleeding, obtain biopsies; may treat areas of bleeding with
electro or laser coagulation or sclerosing agent
 5. Nursing Diagnoses:
 a. Deficient Fluid Volume
 b. Imbalanced Nutrition: Less than body requirements
Peptic Ulcer Disease
Definition
A circumscribed ulceration of the
gastrointestinal mucosa
occurring in areas exposed to
acid and pepsin and most often
caused by Helicobacter pylori
infection.
(Uphold & Graham, 2003)
Peptic Ulcer Disease (PUD)
Definition and Risk factors
 a. Break in mucous lining of GI tract comes into contact
with gastric juice; affects 10% of US population
 b. Duodenal ulcers: most common; affect mostly males
ages 30 – 55; ulcers found near pyloris
 c. Gastric ulcers: affect older persons (ages 55 – 70);
found on lesser curvature and associated with increased
incidence of gastric cancer
 d. Common in smokers, users of NSAIDS; familial
pattern, ASA, alcohol, cigarettes
Peptic Ulcer Disease (PUD)
2. Pathophysiology
 a. Ulcers or breaks in mucosa of GI tract occur with
1.H. pylori infection (spread by oral to oral, fecal-oral
routes) damages gastric epithelial cells reducing
effectiveness of gastric mucus
2.Use of NSAIDS: interrupts prostaglandin synthesis
which maintains mucous barrier of gastric mucosa
 b. Chronic with spontaneous remissions and
exacerbations associated with trauma, infection, physical
or psychological stress
Peptic Ulcers:
Gastric & Dudodenal
Peptic Ulcer Disease
 Ulcer development
 Lower
esophagus
 Stomach
 Duodenum
 10% of men, 4% of women
Compare and Contrast the symptoms of
Duodenal and Gastric Ulcers
Duodenal
 Burning upper abd, pain
1-3 hrs after meals
 Worse pain when
stomach empty
 Bleeding occurs with
deep erosion
 Hematemesis
 Melena
Gastric
 Relieved by food but




pain may persist even
after eating
Anorexia, wt loss,
vomiting
Infrequent or absent
remissions
Small % become
cancerous
Severe ulcers may erode
through stomach wall
Subjective Data
 Pain—”gnawing”, “aching”, or “burning”
Duodenal ulcers: occurs 1-3 hours after a meal and
may awaken patient from sleep. Pain is relieved by
food, antacids, or vomiting.
 Gastric ulcers: food may exacerbate the pain while
vomiting relieves it.
 Nausea, vomiting, belching, dyspepsia, bloating, chest
discomfort, anorexia, hematemesis, &/or melena may
also occur.
 nausea, vomiting, & weight loss more common with
Gastric ulcers

Objective Data
 Epigastric tenderness
 Guaic-positive stool resulting from occult blood loss
Diagnostic Plan
 Stool for fecal occult blood
 Labs: CBC (R/O bleeding), liver function test, amylase, and
lipase.
 H. Pylori can be diagnosed by urea breath test, blood test,
stool antigen assays, & rapid urease test on a biopsy sample.
 Upper GI Endoscopy: Any pt >50 yo with new onset of
symptoms or those with alarm markings including anemia,
weight loss, or GI bleeding.
 Preferred diagnostic test b/c its highly sensitive for dx of
ulcers and allows for biopsy to rule out malignancy and
rapid urease tests for testing for H. Pylori.
Peptic Ulcer Disease
 Treatment
 Rest
and stress reduction
 Nutritional management
 Pharmacological management

Antacids (Mylanta)
 Neutralizes acids

Proton pump inhibitors (Prilosec, Prevacid)
 Block gastric acid secretion
Peptic Ulcer Disease
 Pharmacological management




Histamine blockers (Tagamet, Zantac, Axid)
 Blocks gastric acid secretion
Carafate
 Forms protective layer over the site
Mucosal barrier enhancers (colloidal bismuth,
prostoglandins)
 Protect mucosa from injury
Antibiotics (PCN, Amoxicillin, Ampicillin)
 Treat H. Pylori infection
Peptic Ulcer Disease
 NG suction
 Surgical intervention




Minimally invasive gastrectomy
 Partial gastric removal with laproscopic surgery
Bilroth I and II
 Removal of portions of the stomach
Vagotomy
 Cutting of the vagus nerve to decrease acid
secretion
Pyloroplasty
 Widens the pyloric sphincter
Peptic Ulcer Disease
Surgical Therapy
A. Billroth I Procedure
B. Billroth II Procedure
Fig. 40-16
Billroth I
Billroth II
Peptic Ulcer Disease (PUD)
4. Complications
 a. Hemorrhage: frequent in older adult: hematemesis, melena,
hematochezia (blood in stool); weakness, fatigue, dizziness,
orthostatic hypotension and anemia; with significant bleed loss
may develop hypovolemic shock
 b. Obstruction: gastric outlet (pyloric sphincter) obstruction:
edema surrounding ulcer blocks GI tract from muscle spasm or
scar tissue
1.Gradual process
2.Symptoms: feelings of epigastric fullness, nausea,
worsened ulcer symptoms
Peptic Ulcer Disease
 c. Perforation: ulcer erodes through mucosal wall
and gastric or duodenal contents enter peritoneum
leading to peritonitis; chemical at first
(inflammatory) and then bacterial in 6 to 12 hours
1.Time of ulceration: severe upper abdominal
pain radiating throughout abdomen and possibly to
shoulder
2.Abdomen becomes rigid, boardlike with
absent bowel sounds; symptoms of shock
3.Older adults may present with mental
confusion and non-specific symptoms
Peptic Ulcer Disease
Nursing Management
 Overall Goals
 Comply
with prescribed therapeutic
regimen
 Experience a reduction or absence of
discomfort related to peptic ulcer
disease
Peptic Ulcer Disease
Nursing Management
 Overall Goals (cont.)
 Exhibits
no signs of GI complications
 Have complete healing
 Lifestyle changes to prevent recurrence
Peptic Ulcer Disease
Nursing Implementation
 Health Promotion
 Identify
patients at risk
 Early detection and ↓ morbidity
 Encourage patients to take ulcerogenic
drugs with food or milk
 Teach patients to report symptoms
related to gastric irritation to health
care provider
Peptic Ulcer Disease
Nursing Implementation
 Acute Intervention
 Patient
generally complains of ↑ pain,
nausea, vomiting, and some bleeding
 May be maintained on NPO status for
a few days, have NG tube inserted,
fluids replaced intravenously
 Physical and emotional rest are
conducive to ulcer healing
Peptic Ulcer Disease
Nursing Implementation
 Hemorrhage
 Changes
in vital signs, ↑ in amount and
redness of aspirate signal massive
upper GI bleeding
 ↑ amount of blood in gastric contents ↓
pain because blood helps neutralize
acidic gastric contents
 Keep blood clots from obstructing NG
tube
Peptic Ulcer Disease
Nursing Implementation
 Perforation
 Sudden,
severe abdominal pain
unrelated in intensity and location to
pain that brought patient to hospital
Peptic Ulcer Disease
Nursing Implementation
 Perforation (cont.)
 Indicated
by a rigid, boardlike
abdomen
 Severe generalized abdominal and
shoulder pain
 Shallow, grunting respirations
Peptic Ulcer Disease
Nursing Implementation
 Perforation (cont.)
 Ensure
any known allergies are
reported on chart

Antibiotic therapy is usually started
 Surgical
closure may be necessary if
perforation does not heal
spontaneously
Irritable Bowel Syndrome (IBS)
(spastic bowel, functional colitis)
Definition
 a. Functional GI tract disorder without
identifiable cause characterized by
abdominal pain and constipation,
diarrhea, or both
 b. Affects up to 20% of persons in
Western civilization; more common in
females
Irritable Bowel Syndrome (IBS) (spastic
bowel, functional colitis)
Pathophysiology
 a. Appears there is altered CNS regulation of motor and
sensory functions of bowel
1.Increased bowel activity in response to food intake,
hormones, stress
2.Increased sensations of chyme movement through
gut
3.Hypersecretion of colonic mucus
 b. Lower visceral pain threshold causing abdominal pain
and bloating with normal levels of gas
 c. Some linkage of depression and anxiety
Irritable Bowel Syndrome (IBS) (spastic
bowel, functional colitis)
Manifestations
 a. Abdominal pain relieved by defecation; may be colicky,
occurring in spasms, dull or continuous
 b. Altered bowel habits including frequency, hard or watery
stool, straining or urgency with stooling, incomplete
evacuation, passage of mucus; abdominal bloating, excess gas
 c. Nausea, vomiting, anorexia, fatigue, headache, anxiety
 d. Tenderness over sigmoid colon upon palpation
4. Collaborative Care
 a. Management of distressing symptoms
 b. Elimination of precipitating factors, stress reduction
Irritable Bowel Syndrome (IBS) (spastic
bowel, functional colitis)
5.




Diagnostic Tests: to find a cause for client’s abdominal pain,
changes in feces elimination
a. Stool examination for occult blood, ova and parasites, culture
b. CBC with differential, Erythrocyte Sedimentation Rate
(ESR): to determine if anemia, bacterial infection, or
inflammatory process
c. Sigmoidoscopy or colonoscopy
1.Visualize bowel mucosa, measure intraluminal pressures,
obtain biopsies if indicated
2.Findings with IBS: normal appearance increased mucus,
intraluminal pressures, marked spasms, possible hyperemia
without lesions
d. Small bowel series (Upper GI series with small bowel-follow
through) and barium enema: examination of entire GI tract; IBS:
increased motility
Irritable Bowel Syndrome (IBS) (spastic
bowel, functional colitis)
Medications
 a. Purpose: to manage symptoms
 b. Bulk-forming laxatives: reduce bowel spasm, normalize
bowel movement in number and form
 c. Anticholinergic drugs (dicyclomine (Bentyl),
hyoscyamine) to inhibit bowel motility and prevent
spasms; given before meals
 d. Antidiarrheal medications (loperamide (Imodium),
diphenoxylate (Lomotil): prevent diarrhea prophylactically
 e. Antidepressant medications
 f. Research: medications altering serotonin receptors in GI
tract to stimulate peristalsis of the GI tract
Irritable Bowel Syndrome (IBS) (spastic
bowel, functional colitis)
Dietary Management
 a. Often benefit from additional dietary fiber: adds bulk
and water content to stool reducing diarrhea and
constipation
 b. Some benefit from elimination of lactose, fructose,
sorbitol
 c. Limiting intake of gas-forming foods, caffeinated
beverages
8. Nursing Care
 a. Contact in health environments outside acute care
 b. Home care focus on improving symptoms with changes
of diet, stress management, medications; seek medical
attention if serious changes occur
Peritonitis
Definition
 a. Inflammation of peritoneum, lining that
covers wall (parietal peritoneum) and
organs (visceral peritoneum) of abdominal
cavity
 b. Enteric bacteria enter the peritoneal
cavity through a break of intact GI tract
(e.g. perforated ulcer, ruptured appendix)
Peritonitis
 Causes include:
 Ruptured
appendix
 Perforated bowel secondary to PUD
 Diverticulitis
 Gangrenous gall bladder
 Ulcerative colitis
 Trauma
 Peritoneal dialysis
Peritonitis
Pathophysiology
 a. Peritonitis results from contamination of normal
sterile peritoneal cavity with infections or
chemical irritant
 b. Release of bile or gastric juices initially causes
chemical peritonitis; infection occurs when
bacteria enter the space
 c. Bacterial peritonitis usually caused by these
bacteria (normal bowel flora): Escherichia coli,
Klebsiella, Proteus, Pseudomonas
 d. Inflammatory process causes fluid shift into
peritoneal space (third spacing); leading to
hypovolemia, then septicemia
Peritonitis
3. Manifestations
 a. Depends on severity and extent of infection, age
and health of client
 b. Presents with “acute abdomen”
1.Abrupt onset of diffuse, severe abdominal
pain
2.Pain may localize near site of infection (may
have rebound tenderness)
3.Intensifies with movement
 c. Entire abdomen is tender with boardlike
guarding or rigidity of abdominal muscle
Peritonitis
 d. Decreased peristalsis leading to paralytic ileus; bowel
sounds are diminished or absent with progressive
abdominal distention; pooling of GI secretions lead to
nausea and vomiting
 e. Systemically: fever, malaise, tachycardia and
tachypnea, restlessness, disorientation, oliguria with
dehydration and shock
 f. Older or immunosuppressed client may have
1.Few of classic signs
2.Increased confusion and restlessness
3.Decreased urinary output
4.Vague abdominal complaints
5.At risk for delayed diagnosis and higher mortality
rates
Peritonitis
4. Complications
 a. May be life-threatening; mortality rate overall 40%
 b. Abscess
 c. Fibrous adhesions
 d. Septicemia, septic shock; fluid loss into abdominal
cavity leads to hypovolemic shock
5. Collaborative Care
 a. Diagnosis and identifying and treating cause
 b. Prevention of complications
Peritonitis
6. Diagnostic Tests
 a. WBC with differential: elevated WBC to 20,000; shift to left
 b. Blood cultures: identify bacteria in blood
 c. Liver and renal function studies, serum electrolytes: evaluate
effects of peritonitis
 d. Abdominal xrays: detect intestinal distension, air-fluid levels,
free air under diaphragm (sign of GI perforation)
 e. Diagnostic paracentesis
7. Medications
 a. Antibiotics
1.Broad-spectrum before definitive culture results
identifying specific organism(s) causing infection
2.Specific antibiotic(s) treating causative pathogens
 b. Analgesics
Peritonitis
8. Surgery
 a. Laparotomy to treat cause (close perforation,
removed inflamed tissue)
 b. Peritoneal Lavage: washing out peritoneal
cavity with copious amounts of warm isotonic
fluid during surgery to dilute residual bacterial and
remove gross contaminants
 c. Often have drain in place and/or incision left
unsutured to continue drainage
Peritonitis
9. Treatment
 a. Intravenous fluids and electrolytes to maintain vascular
volume and electrolyte balance
 b. Bed rest in Fowler’s position to localize infection and
promote lung ventilation
 c. Intestinal decompression with nasogastric tube or
intestinal tube connected to suction
 1. Relieves abdominal distension secondary to paralytic
ileus
 2. NPO with intravenous fluids while having nasogastric
suction
Peritonitis
10. Nursing Diagnoses
 a. Pain
 b. Deficient Fluid Volume: often on hourly output;
nasogastric drainage is considered when ordering
intravenous fluids
 c. Ineffective Protection
 d. Anxiety
11. Home Care
 a. Client may have prolonged hospitalization
 b. Home care often includes
 1. Wound care
 2. Home health referral
 3. Home intravenous antibiotics
Client with Inflammatory Bowel Disease
Definition
 a. Includes 2 separate but closely related
conditions: ulcerative colitis and Crohn’s disease;
both have similar geographic distribution and
genetic component
 b. Etiology is unknown but runs in families; may
be related to infectious agent and altered immune
responses
 c. Peak incidence occurs between the ages of 15 –
35; second peak 60 – 80
 d. Chronic disease with recurrent exacerbations
Inflammatory Bowel Disease
Ulcerative Colitis
Pathophysiology
 1. Inflammatory process usually confined to
rectum and sigmoid colon
 2. Inflammation leads to mucosal hemorrhages
and abscess formation, which leads to necrosis and
sloughing of bowel mucosa
 3. Mucosa becomes red, friable, and ulcerated;
bleeding is common
 4. Chronic inflammation leads to atrophy,
narrowing, and shortening of colon
Ulcerative Colitis
Manifestations
 1. Diarrhea with stool containing blood
and mucus; 10 – 20 bloody stools per day
leading to anemia, hypovolemia,
malnutrition
 2. Fecal urgency, tenesmus, LLQ
cramping
 3. Fatigue, anorexia, weakness
Ulcerative Colitis
Complications
 1. Hemorrhage: can be massive with severe attacks
 2. Toxic megacolon: usually involves transverse colon which dilates
and lacks peristalsis (manifestations: fever, tachycardia, hypotension,
dehydration, change in stools, abdominal cramping)
 3. Colon perforation: rare but leads to peritonitis and 15% mortality
rate
 4. Increased risk for colorectal cancer (20 – 30 times); need yearly
colonoscopies
 5. Abcess, fistula formation
 6. Bowel obstruction
 7. Extraintestinal complications
 Arthritis
 Ocular disorders
 Cholelithiasis
Ulcerative Colitis
 Diet therapy



Goal to prevent hyperactive bowel activity
Severe symptoms
 NPO
 TPN
Less severe
 Vivonex
 Elemental formula absorbed in the upper bowel
 Decreases bowel stimulation
Ulcerative Colitis
 Diet therapy
 Significant
symptoms
Low fiber diet
 Reduce or eliminate lactose containing foods
 Avoid caffeinated beverages, pepper,
alcohol, smoking

Ulcerative Colitis
Ostomy
 1. Surgically created opening between intestine and abdominal
wall that allows passage of fecal material
 2. Stoma is the surface opening which has an appliance applied
to retain stool and is emptied at intervals
 3. Name of ostomy depends on location of stoma
 4. Ileostomy: opening in ileum; may be permanent with total
proctocolectomy or temporary (loop ileostomy)
 5. Ileostomies: always have liquid stool which can be
corrosive to skin since contains digestive enzymes
 6. Continent (or Kock’s) ileostomy: has intra-abdominal
reservoir with nipple valve formation to allow catheter
insertion to drain out stool
Ulcerative Colitis
 Surgical Management



25% of patients require a colectomy
Total proctocolectomy with a permanent ileostomy
 Colon, rectum, anus removed
 Closure of anus
 Stoma in right lower quadrant
In selected patients an ileoanal anastamosis or ileal
reservoir to preserve the anal sphincter
 J-shaped pouch is created internally from the end of
the ileum to collect fecal material
 Pouch is then connected to the distal rectum
Proctocolectomy
Ulcerative Colitis
 Surgical management
 Total
colectomy with a continent
ileostomy
Kock’s ileostomy
 Intra-abdominal pouch where stool is stored
untile client drains it with a catheter

Kocks pouch
Ulcerative Colitis
 Surgical management
 Total
colectomy with ileoanal
anastamosis
 Ileoanal reservoir or J pouch
 Removes colon and rectum and sutrues
ileum into the anal canal
Ulcerative Colitis
Home Care
 a. Inflammatory bowel disease is chronic
and day-to-day care lies with client
 b. Teaching to control symptoms,
adequate nutrition, if client has ostomy:
care and resources for supplies, support
group and home care referral
Ulcerative Colitis
 Treatment
 Medications
similar to treatment for
Crohn’s disease
Ulcerative Colitis
Nursing Care: Focus is effective management of disease with
avoidance of complications
Nursing Diagnoses
 a. Diarrhea
 b. Disturbed Body Image; diarrhea may control all aspects
of life; client has surgery with ostomy
 c. Imbalanced Nutrition: Less than body requirement
 d. Risk for Impaired Tissue Integrity: Malnutrition and
healing post surgery
 e. Risk for sexual dysfunction, related to diarrhea or
ostomy
Crohn’s Disease (regional
enteritis)
Pathophysiology
 1. Can affect any portion of GI tract, but terminal ileum
and ascending colon are more commonly involved
 2. Inflammatory aphthoid lesion (shallow ulceration) of
mucosa and submuscosa develops into ulcers and fissures
that involve entire bowel wall
 3. Fibrotic changes occur leading to local obstruction,
abscess formation and fistula formation
 4. Fistulas develop between loops of bowel (enteroenteric
fistulas); bowel and bladder (enterovesical fistulas); bowel
and skin (enterocutaneous fistulas)
 5. Absorption problem develops leading to protein loss and
anemia
Crohn’s disease
Crohn’s Disease (regional enteritis)
Manifestations
 1. Often continuous or episodic diarrhea;
liquid or semi-formed; abdominal pain
and tenderness in RLQ relieved by
defecation
 2. Fever, fatigue, malaise, weight loss,
anemia
 3. Fissures, fistulas, abscesses
Crohn’s Disease (regional enteritis)
Complications
 1. Intestinal obstruction: caused by repeated
inflammation and scarring causing fibrosis and
stricture
 2. Fistulas lead to abscess formation; recurrent
urinary tract infection if bladder involved
 3. Perforation of bowel may occur with peritonitis
 4. Massive hemorrhage
 5. Increased risk of bowel cancer (5 – 6 times)
Crohn’s Disease (regional enteritis)
Collaborative Care
 a. Establish diagnosis
 b. Supportive treatment
 c. Many clients need surgery
Diagnostic Tests
 a. Colonoscopy, sigmoidoscopy: determine area and pattern of
involvement, tissue biopsies; small risk of perforation
 b. Upper GI series with small bowel follow-through, barium enema
 c. Stool examination and stool cultures to rule out infections
 d. CBC: shows anemia, leukocytosis from inflammation and abscess
formation
 e. Serum albumin, folic acid: lower due to malabsorption
Crohn’s Disease (regional enteritis)
Medications: goal is to stop acute attacks quickly and reduce
incidence of relapse
 a. Sulfasalazine (Azulfidine): salicylate compound that
inhibits prostaglandin production to reduce inflammation
 b. Corticosteroids: reduce inflammation and induce
remission; with ulcerative colitis may be given as enema;
intravenous steroids are given with severe exacerbations
 c. Immunosuppressive agents (azathioprine (Imuran),
cyclosporine) for clients who do not respond to steroid
therapy alone
 Used in combination with steroid treatment and may
help decrease the amount of steroid use
Crohn’s Disease
 d. New therapies including immune
response modifiers, anti-inflammatory
cyctokines
 e. Metronidazole (Flagyl) or Ciprofloxacin
(Cipro)
 For the fistulas that develop
 f. Anti-diarrheal medications
Crohn’s Disease (regional enteritis)
Dietary Management
 a. Individualized according to client; eliminate
irritating foods
 b. Dietary fiber contraindicated if client has strictures
 c. With acute exacerbations, client may be made NPO
and given enteral or total parenteral nutrition (TPN)
Surgery: performed when necessitated by complications
or failure of other measures
removal of diseased portion of the bowel
Crohn’s Disease
a. Crohn’s disease
 1. Bowel obstruction leading cause; may
have bowel resection and repair for
obstruction, perforation, fistula, abscess
 2. Disease process tends to recur in area
remaining after resection