Nursing of Clients With Gastrointestinal Disorders

NURSING CARE OF CLIENTS
WITH GASTROINTESTINAL
DISORDERS
Rhenier S. Ilado, RN
Gastrointestinal System
I. Upper alimentary canal - function for digestion
Mouth – mechanical and chemical digestion, deglutition
Pharynx (throat)
Esophagus – passage of bolus by peristalsis, contains
UES and LES
Stomach- mechanical and chemical digestion, secretion
of gastric juice, gastric emptying
1st half of duodenum
II. Middle Alimentary canal – Function: for absorption
-Complete absorption – large intestine
2nd half of duodenum - for digestion/absorption of most
nutrients
Jejunum
Ileum
1st half of ascending colon
III. Lower Alimentary Canal – Function:
elimination/defecation
2nd half of ascending colon
Transverse
Descending colon
Sigmoid
Rectum
IV. Accessory Organ
Salivary gland
Vermiform appendix
Liver
Pancreas – auto digestion
Gallbladder – storage of bile
DIAGNOSTIC EXAMS
Stool for Occult Blood (Guaic Stool Exam)
• used to check stool samples for hidden (occult) blood.
• detects GI bleeding
• Nursing Intervention before exam:
High fiber diet for 48-72 hours
Avoid Red meats, poultry, fish and dark colored foods
No Iron – because it causes blackish discoloration of
stool
No steroids causes GI irritation
3 stool specimen will be collected
+ Guaic stool exam means peptic ulcer or gastric cancer
Gastric Analysis
• This test measures acid content of
stomach collected through a
nasogastric (stomach) tube.
• Measures secretion of HCL and
pepsin
• NPO for 12 hours
• NGT is inserted
• Gastric contents collected for every
15minutes to 1 hour
• Results: Increase HCL means
duodenal ulcer
Decrease HCL means gastric
cancer, Pernicious anemia
Radiographic Tests
UGIS (Upper GI Series/Barium Swallow) – to
visualize the esophagus, stomach, duodenum
and jejunum
Nursing Interventions Before procedure:
a. NPO for 6-8 hours
b. Barium sulfate (BaSO4) per Orem
c. X-ray will be taken
After procedure:
a. laxative
b. increase fluid intake
c. inform client that the stool is white
for 24-72 hours
d. observe Ba impaction: distended
abdomen, constipation
Radiographic Tests
LGIS (Lower GI Series/Ba Enema) – to
visualize the colon
Before procedure:
a. low residue/clear liquid diet for 2
days
b. laxative for cleansing the bowel
c. cleansing enema in AM
d. BaSO4 per rectum
After procedure:
a. laxative
b. increase fluid intake
c. inform client that the stool is white
for 24-72 hours
d. observe Ba impaction: distended
abdomen, constipation
Endoscopy
UGI Endoscopy – direct visualization of esophagus, stomach and
duodenum
a. Consent
b. NPO for 6-8 hours
c. Anticholinergic - atropine sulfate. To reduce mucus secretion
d. Sedatives, narcotics, tranquilizers. To relax the client
(Diazepam/Meperidine HCL)
e. Remove dentures. To prevent airway obstruction.
f. local anesthetic spray on posterior pharynx. To depress gag
reflex.
After Procedure:
a. Side-lying position. To prevent aspiration
b. NPO until gag reflex returns (2-4 hours)
c. monitor VS
d. NSS gargle. To soothe the throat
e. assess: bleeding, fever, neck/throat pain, dyspepsia, dysphagia
f. advice to avoid driving for 12 hours. If sedative was used
LGI Endoscopy
Proctosigmoidoscopy (Sigmoid, rectum)
a. clear liquid diet 24 hours before
b. laxative
c. cleansing enema
d. knee chest /lateral position
After procedure:
a. supine position. To prevent postural
hypotension.
b. assess for signs of perforation – bleeding, pain,
fever
c. hot sitz bath for discomfort in anorectal area.
LGI Endoscopy
Colonoscopy
• Preparation is the same with
proctosigmoidoscopy
• Sedation is done to relax the
client
• Patient is placed in left lateral
position
After procedure
• Monitor VS – bradycardia
(vasovagal response)
• assess for signs of perforation –
bleeding, pain, fever
Liver Biopsy
1. Consent
2. NPO 2-4 hours
3. Vit K injection; monitor PT
4. Position in left side or supine with pillow under
right shoulder
5. Instruct the patient to exhale deeply, hold breath for
5-10 seconds, during needle insertion to prevent trauma to
diaghpram.
After procedure:
1. Turn to right side for 4 hours to apply pressure and
prevent bleeding
2. Bed rest for 24 hours
3. Monitor VS 30 min.
Liver Biopsy
Paracentesis
• aspiration of fluid in the peritoneal cavity
Indications
• to relieve abdominal pressure from ascites
• to diagnose spontaneous bacterial peritonitis and other infections
• to diagnose metastatic cancer
• to diagnose blood in peritoneal space in trauma
1. consent
2. check initial VS
3. empty bladder to prevent puncture
4. place in sitting or supine pos.
After procedure:
1. assess VS
2. Assess rigidity of the abdomen (peritonitis) and
hypovolemic shock
Paracentesis
Endoscopic Retrograde
Cholangiopancreatography (ERCP)
• direct visualization with radiographic examination of the liver,
gallbladder and pancreas.
• Contrast medium is introduced via the endoscope, x-ray are taken
simultaneously.
1. Consent
2. NPO 10-12 hours
3. Check allergy to iodine/seafoods
4. VS
5. AtSO4, valium
6. Local anesthetic spray into the throat
7. pos. in left side
After procedure:
1. NPO until gag returns
2. Turn to sides to prevent aspiration
3. VS
4. monitor for signs of perforation and sepsis
Endoscopic Retrograde
Cholangiopancreatography (ERCP)
Nasogastric Tube Feeding (NGT)
Nursing responsibilities:
1. Assist patient in semi to high Fowler’s position
2. Assess tube placement and patency
a. Auscultation –introduced 10 ml of air in NGT and auscultate at
epigastric area for gurgling sound
b. Aspiration – gastric contents is aspirated which is
yellowish/greenish in color
c. Immersion – immerse the tip of the tube in the water, no
bubbles should be produced
3. the most effective – X- ray
4. Assess residual feeding contents. To assess absorption of the last
feeding. If 100 or more, verify if the feeding will be given
5. Height of feeding is 12 inches above point of insertion.
6. Instill 30-60 ml of water into NGT after feeding. To cleanse the lumen of
the tube
7. Have client remain in semi to high- Fowler’s position 30-60 minutes after
feeding. To prevent gastric reflux and aspiration
Tube Feeding (NGT)
Administering ENEMA
• Purposes:
To relieve constipation
To relieve flatulence
To administer medication
To evacuate feces in
preparation for diagnostic
procedure or surgery
Administering ENEMA
 Non- retention Enema/Cleansing Enema – stimulates peristalsis by irritating the colon
and rectum
• Solutions:
a. Tap water (500-1000ml)
b. Soap suds
c. NSS (9 ml of NaCl to 1000ml of water)
d. Hypertonic solution/fleet enema (90-120 ml)
 Retention Enema – introduces oil into the rectum and sigmoid colon, oil retained in 1 to 3
hours
• act to soften the feces and to lubricate the rectum and anal canal facilitating the passage of
feces
Nursing responsibilities:
1. Check doctor’s order
2. Provide privacy
3. position – left lateral position. To facilitate flow of solution by gravity
4. Lubrication 2 inches of the rectal tube. To prevent trauma to anorectal mucosa
5. Insert 3-4 inches while asking to inhale deeply
6. If abdominal cramps occur, temporarily stop the flow by clamping the tube.
7. Ask the client who is using the toilet not to flush it. The nurse should actually assess the
return flow of the solution
GASTROINTESTINAL
DISORDERS
GASTROESOPHAGEAL
REFLUX DISEASE (GERD)
Gastroesophageal Reflux Disease
(GERD)
• Backward flow of gastric or duodenal contents into the
esophagus
• Affects 15 to 20% of adults; increasing incidence with
aging
• Etiology:
 Reflux results from transient relaxation or incompetence of the
lower esophageal sphincter; pyloric stenosis
 Increased gastric volume (after meals)
 Positions pushing gastric contents close to gastroesophageal
juncture (i.e. bending or lying down)
 Increased gastric pressure (obesity or tight clothing)
Pathophysiology
• A weak or incompetent LES allows backward movement
of gastric contents into esophagus
• Decreased esophageal peristalsis and salivary function
impair clearance of the refluxed acid, resulting in mucosal
injury to the esophagus
Gastroesophageal Reflux Disease
(GERD)
• Signs and Symptoms:
 Pyrosis – burning sensation in the esophagus
 Dyspepsia – indigestion
 Regurgitation
 Dysphagia – difficulty on swallowing
 Odynophagia – pain on swallowing
 Hypersalivation
 Esophagitis
Complications:
Esophageal strictures progressing to dysphagia
Increased risk for esophageal cancer
Diagnostic Test
• Diagnosis may be made from history of symptoms
• Barium Swallow – evaluation of esophagus, stomach
and small intestine
• Upper endoscopy – for direct visualization
Collaborative Management
• Life style changes
• Diet modifications
 Elimination of acid foods or irritants (tomatoes, spicy, citrus foods,
coffee)
 Avoiding foods which relax esophageal sphincter or delay gastric
emptying (fatty foods, chocolate, alcohol)
 Maintain ideal body weight
 Eat small meals and stay upright for 2 hours after eating; client
should not eat 3 hours prior to going to bed
 Elevate the head of bed on 6 to 8 blocks to decrease reflux
 Eat a low fat, high fiber diet
• Medications
Antacids: mild to moderate symptoms e.g. Maalox,
Gaviscon
H2 receptor blockers: decrease acid production; given
BID or more often e.g. cimetidine, ranitidine
Proton pump inhibitors; reduce gastric secretions,
promote healing of esophageal erosion e.g. omeprazole
Pro-motility agent; enhances esophageal clearance and
gastric emptying e.g. metoclopramide
• Surgical Management
 Nissen Fundoplication – suture fundus around the esophagus;
wrapping a portion of the gastric fundus around the sphincter area
of the esophagus
HIATAL HERNIA
(DIAPHRAGMATIC HERNIA)
HIATAL HERNIA (Diaphragmatic Hernia)
• Part of the stomach protrudes through the esophageal hiatus
of the diaphragm into thoracic cavity
• Most cases are asymptomatic; incidence increases with age
• Types:
Sliding Hiatal Hernia
o protrusion of the esophageal junction into the thoracic cavity and back
into the abdominal cavity in relation to position changes
o Primary cause is muscle weakness in the esophageal hiatus (opening
between the domes of the diaphragm where the esophagus enters the
abdominal cavity)
o Due to aging process, congenital muscle weakness, obesity, trauma,
surgery, prolonged increased in intra-abdominal pressure i.e. heavy
lifting
HIATAL HERNIA (Diaphragmatic
Hernia)
Hernia)
Paraesophageal hernia or rolling hernia
o Protrusion of the fundus of the stomach and the greater curvature
into the thorax next to the esophagus
o Gastric junction remains below the diaphragm
o Due to anatomic defect
Hernia)
Hernia)
• Clinical Manifestations:
Heartburn due to gastroesophageal reflux
Dysphagia (difficulty swallowing) – due to compression of
the esophagus
Dyspnea – due to compression of the lungs
Abdominal pain due to compression of the protruding
portion of the stomach
Nausea and vomiting
Gastric distention, belching, flatulence due to
accumulation of gas in the stomach and abdomen caused
by impaired motility
• Modify diet
 High protein diet to enhance LES pressure and prevent esophageal
reflux
 Small frequent feedings to prevent gastric distention (this prevents
further protrusion of the stomach into the thoracic cavity)
 Instruct client to eat slowly and chew food properly. To reduce gastric
motility
 The client should avoid foods and beverages that decreases LES
pressure like fatty foods, cola beverages, coffee, tea, chocolate, alcohol
 The client should assume upright position before and after eating for 1
to 2 hours (this prevents protrusion of the stomach into the thoracic
cavity)
 Instruct the client to avoid eating at least 3 hours before bedtime (to
prevent night time reflux)
• Administer medications as ordered:
 Antacids to relieve heartburns
 Antiemetics to releive nausea and vomiting e.g. phenergan
(promethazine HCL), Reglan (Metochlopromide)
 Histamine H2 receptor antagonists to suppress secretion of gastric
acid e.g. ranitidine, cimetidine
• Advise client to reduce body weight if obese
• Advise client to promote lifestyle changes
 Elevate head of bed 6-12 inches for sleep
 Avoid factors that increase abdominal pressure like use of
constrictive clothing, straining at stool, heavy lifting, bending,
stooping, vigorous coughing
 Avoid cigaratte smoking. Smoking causes rapid and significant
drop in LES pressure
 Nissen Fundoplication – suture fundus around the esophagus;
wrapping a portion of the gastric fundus around the sphincter area
of the esophagus
GASTRITIS
GASTRITIS
• localized inflammation of the gastric mucosa
which is normally protected from gastric acid
and enzymes by mucosal barrier
• Types:
Acute Gastritis
• short inflammatory process due to ingestion
of chemical agents or food products that
irrigate and erode gastric mucosa
• Disruption of mucosal barrier allowing
hydrochloric acid and pepsin to have contact
with gastric tissue
• Self-limiting
• Erosive Gastritis – a form of acute gastritis,
stressed-induced, complication of a life-
threatening condition i.e. Curling’s ulcer with
burns, gastric mucosa becomes ischemic
and tissue is injured by stomach acid
GASTRITIS
Chronic Gastritis
• Progressive disorder beginning with superficial
inflammation and leads to atrophy of gastric tissues
• Type A – autoimmune component; loss of hydrochloric
and pepsin secretion; patient develops pernicious anemia
• Type B – more common and occurs with aging; caused by
chronic infection of mucosa by helicobacter pylori;
associated with rick of peptic ulcer disease and gastric
cancer
Etiology
• Irritants include aspirin and other NSAIDS,
corticosteroids, alcohol, caffeine
• Ingestion of corrosive substances; alkali or acid
• Effects from radiation therapy, certain chemotherapeutic
agents
GASTRITIS
• Signs and Symptoms:
Acute Gastritis
Mild – anorexia, mild epigastric discomfort, belching
More severe – abdominal pain, nausea, vomiting,
hematemesis, melena
Erosive – not associated with pain; bleeding occurs 2 or more
days post-stress event
Chronic Gastritis
Vague gastric distress, epigastric heaviness not relieved by
antacids
Fatigue associated with anemia; symptoms associated with
pernicious anemia i.e. paresthesia
Diagnostic Tests
• Gastric analysis – assess hydrochloric acid secretion
(les with chronic gastritis)
• Hemoglobin, hematocrit, RBC – anemia including
pernicious anemia or iron deficiency
• Serum vitamin B12 levels – determine presence of
pernicious anemia
• Upper endoscopy – visualizes mucosa; identify areas of
bleeding; obtain biopsies
Collaborative Management (Acute Gastritis)
• NPO status to rest GI tract for 6 to 12 hours; reintroduce clear
liquids gradually; give IV fluid and electrolytes if indicated
• Medical treatment: proton-pump inhibitor (omeprazole) or H2-
receptor blocker (Ranitidine); sucralfate (carafate) acts locally
to coat and protect the gastric mucosa
• Type B: eradicate H. Pylori infection with combination therapy of
two ATBC – (Metronidazole and clarithromycin or tetracycline)
and proton-pump inhibitor
• Teach food safety measures to prevent acute gastritis from food
contaminated with bacteria
• Management of acute gastritis with NPO state and then gradual
reintroduction of fluids with electrolytes and glucose then
advanced to solid foods
• Teach regarding use of prescribed medications, smoking
cessation and alcohol abuse
PEPTIC ULCER DISEASE (PUD)
• excoriation / erosion of
submucosa & mucosal
lining of the
esophagus, stomach
and intestine due to:
 Hypersecretion of acid –
pepsin
 Decrease resistance of
mucosal barrier
• Types:
Duodenal ulcers
Gastric Ulcers
Types:
Duodenal ulcers Gastric Ulcers

• Also called “executive” • Also called “poor man’s or
ulcer because it is “laborer’s ulcer because the
stomach is usually empty
primarily stress-related
• Affect older persons (ages
• most common (80% of 55 to 70)
incidence) • Affects those who are
• affect mostly males ages malnourished
30-55 • Found on lesser curvature
• There is normal HCL
• usually well-nourished secretion
• ulcers found near pylorus • Increased incidence of
• There is increased HCL gastric cancer
secretion
Zollinger-Ellison syndrome
• Peptic ulcer disease caused by gastrinoma (tumor in
pancreas, stomach or intestine which secretes gastrin
• Excess gastric acid lead to ulceration and often bleeding
and perforation
• Etiology:
Stress – SNS/PNS response causes Hypersecretion of HCL
Cigarette smoking – nicotine stimulates increased HCL
secretion and causes vasoconstriction (irritation and damage to
GI mucosa)
Alcohol – irritates gastric mucosa, increases gastric acid
secretion
Caffeine – stimulates increased HCL secretion; causes
vasoconstriction; decreased blood flow to GI mucosa causes
decrease mucous secretion
Drugs – aspirin (ASA), nonsteroidal anti-inflammatory drugs
(NSAIDs) and steroids are ulcerogenic (should be taken with
food to prevent GI irritation)
Irregular, hurried meals – leads to increased gastric
motility and increased HCL secretion
Type A personality (stress personality) – characterized
by “perfectionism”, “workaholism”, inability to concentrate
in one task, very punctual; this individual has increased
gastric motility and HCL secretion
Fatty, spicy, highly acidic foods – stimulants and
increased HCL secretion
H. pylori infection – damages gastric epithelial cells
reducing effectiveness of gastric mucus
Genetics – it has familial pattern
Break in the mucosal lining of GI tract that comes in
contact with gastric juice
Sign and Symptoms
Gastric Ulcers Duodenal Ulcers
• Pain is experienced ½ to 2 • Pain is experienced 3 to 4
hours after eating or during hours after eating
• Pain radiates to the right
meals side of the abdomen
• Pain radiates to the left side • Pain is relieved by food
• Pain is not relieved by food intake
intake • Pain is commonly
experienced between 12MN
• Characteristic manifestation and 3AM (due to increased
are nausea and vomiting acid secretion)
and hematemesis (vomiting • Characteristic
with blood) manifestations is melena
(black, tarry stool)
Complications
Bleeding/hemorrhage – most life-threatening
complication
 Frequent in older adult
 Hematemesis, melena, hematochezia (blood in stool)
 Weakness, fatigue, dizziness, orthostatic hypotension an anemia
 With significant blood loss (hemorrhage), hypovolemic shock
develops
Complications
Obstruction – gastric outlet obstruction; edema
surrounding ulcer blocks GI tract from muscle spasm or
scar tissue
Symptoms; feeling of epigastric fullness, nausea,
worsening of ulcer symptoms
Complications
Perforation – ulcers erodes through mucosal wall and
gastric or duodenal contents enter peritoneum leading to
peritonitis
Severe upper abdominal pain radiating throughout
abdomen and possibly to the shoulders
Abdomen becomes rigid, board like abdomen with absent
bowel sounds; symptoms of shock
Diagnostic Tests
Upper GI Series – detects up to 90% of ulcers
Gastroscopy – visualization of esophageal, gastric and
duodenal mucosa for ulcers
Gastric analysis – analysis of stomach contents
aspirated through NGT; diagnosis of Zollinger-Ellison
syndrome
Medications
Antacids – to neutralize HCL; administered 1 to 2 hours after eating
(this is the peak time of HCL secretion), rapid relief of ulcer
symptoms
o E.g. Amphogel (Aluminum hydroxide gel), Maalox (Aluminum-Magnesium
hydroxide), Gaviscon (Aluminum Magnesium hydroxide)
Histamine H2 Receptor Antagonists – to reduce HCL secretion

o Used for 8 weeks or longer to heal ulcers
o Best taken in the morning and at bed time
o E.g. Ranitidine and Cimetidine
Proton Pump inhibitor – suppress gastric acid secretion

o Heals ulcers in 4 weeks
o E.g. omeprazole
Cytoprotective Drug – to coat ulcers; binds to ulcer base
forming a protective barrier
o Administer on empty stomach (30-60 minutes) before meals
o E.g. Carafate (Sucralfate)
Prostaglandin analogue –suppresses secretion of

gastric acid
o Administered with meals
o Abortifacient, contraindicated in pregnancy
o E.g. Cytotec (Misoprostol)
Anticholinergic – reduce gastric motility (antispasmodic)
and hydrochloric acid secretion
o E.g. atropine sulfate, 2. Prophantheline Bromide (Profanthene)
Helicobacter pylori drug treatment – uses two ATBCs

and proton pump inhibitor
o Clarithromycin, metronidazole, tetracycline
o Advised client to avoid alcohol when on flagyl therapy to prevent
disulfiram like manifestations i.e. headache, hypotension,
nausea/vomiting, tachycardia, palpitations, chest pain, dyspnea
etc.)
Surgical Interventions for PUDs –
recommended for patients with intractable
ulcers; life threatening hemorrhage,
perforation or obstruction
Surgical resection of 50% of the distal part
of the stomach followed by anastomosis
with the duodenum or jejunun
Billroth I (Gastroduodenostomy) – anastomosis
of the gastric stump with the duodenum
Billroth II (Gastrojejunostomy) – anastomosis of
the gasric stump with jejunum; duodenum is
bypassed (not removed) to permit flow of bile
Subtotal Gastrectomy – removal of 75% of the distal
stomach with Billroth I or Billroth II repair
Nursing Interventions
• Relieve pain by administering antacid as prescribed
• Encouraged client to promote a healthy lifestyle
Advise client to eat slowly and to chew food properly
Small, frequent feedings during exacerbation
Bland diet is recommended during exacerbation
• The client should avoid the following:
 Fatty foods, coffee, tea, chocolate, cola drinks, spices, red/black pepper,
alcohol
 Bedtime snacks (night time reflux)
 Large quantities of milk (milk is alkaline, thus stimulates stomach to
increase HCl secretion to neutralize it, causing rebound acidity)
• Encourage client to quit smoking
• Enhance coping through stress therapy
Dumping Syndrome (complication)
• A group of unpleasant vasomotor and GI symptoms caused
by rapid empting of gastric content into the jejunum
• Rapid emptying of hypertonic food from the stomach causes
fluid shift from the bloodstream into the jejunum, resulting to
hypovolemia
• early Manifestations 5 to 30 minutes after meal:
Weakness, tachycardia, dizziness, diaphoresis, pallor,
feeling of fullness or discomfort, nausea, abdominal cramps
and diarrhea
• Late signs and symptoms: occur 2-3 hours after eating
Initially hyperglycemia – this stimulates increased insulin
secretion which leads to HYPOGLYCEMIA
• Includes measures to slow down emptying of gastric
content:
Client should eat in lying position
Place client in left side-lying position 30-60 minutes after meal
Give small, frequent feedings
Provide high protein diet. Protein empties stomach slowly (3
to 4 hours after eating)
Limit carbohydrates, no simple sugars. These foods empty
the stomach rapidly (1-2 hours after eating)
Avoid very hot and cold foods and beverages
Administer anticholinergic or antispamosdic e.g. Pro-banthine
(Propantheline bromide)
GASTRIC CANCER
Gastric Cancer
• Begin as localized lesion that
progresses to mucosa; spreads
to lymph nodes and metastasis
early to liver, lungs, ovaries,
peritoneum
• Often advanced with metastasis
when diagnosed
• Adenocarcinoma is the most
common form from involving
mucus-producing cells of
stomach
Gastric Cancer
• Etiology:
Incidence is highest among African Americans and asian
American
Twice common in males
H. pylori infection
Genetic predisposition
Chronic gastritis, pernicious anemia and history of gastric
ulcers
Diet high in smoked foods i.e. smoked fish or meat
Low in fresh, green, leafy vegetables and fresh fruits
Smoking and alcohol ingestion
Gastric Cancer
• Signs and symptoms
Early symptoms: early satiety (gastric fullness), anorexia,
indigestion, pain induced by eating and relieve by
vomiting
Late symptoms: weight loss, cachexia (wasted
appearance), palpable abdominal mass, positive guaiac
stool exam, hematemesis, melena, anemia, fatigue
Gastric Cancer
• Diagnostic Tests
CBC indicates anemia
Upper GI series - identifies a mass
Upper endoscopy – visualization and tissue biopsy of
lesion
• Surgery (if diagnosis is made prior to
metastasis)
Partial gastrectomy with
anastomosis to duodenum: Bilroth I or
Gastroduodenostomy
Partial gastrectomy with
anastomosis to jejunum; Bilroth II or
gastrojejunostomy
Total gastrectomy with
esophagojejunostomy (esophagus is
anastomosed to the jejunum; duodenum is not
removed to allow common bile duct to
transport bile into the duodenum)
• Radiation and chemotherapy to control
metastatic spread
Complication
• Dumping syndrome
• Anemia: iron deficiency and/or pernicious anemia
APPENDICITIS
Appendicitis
• Appendix is a tube-like pouch attached
to cecum just below the ileoceccal valve
• Common cause of acute abdominal
pain, most common reason for
emergency abdominal surgery
• The most common cause of
appendicitis is obstruction of the
appendix by fecalith (hard mass of
feces); foreign body; tumor;
inflammation or infection
• Other causes: low fiber diet and high
intake of refined carbohydrates
Appendicitis
• Signs and symptoms:
Acute abdominal pain starts in the epigastric
area; in 4 hours, pain intensifies and localizes in
the RLQ of abdomen (McBurney’s point)
aggravated by moving, walking, coughing
Anorexia, nausea and vomiting
Rigid abdomen, guarding
Rebound tenderness (blumberg sign) – relief of
pain with direct palpation followed by pain on
release of pressure
Fever (38-38.5C)
Leukocytosis (wbc level above 10,000/mm3) –
due to inflammatory response, if >20,000/mm3
indicates peritonitis from ruptured appendicitis
Psoas sign (left lateral position with right hip
flexion)
• Bed rest (to reduce peristalsis and prevent rupture of appendicitis)
• Prepare client physically and psychology for emergency surgery
• Maintain NPO to observe pattern of abdominal pain more accurately
and this is also in preparation for emergency appendectomy
• Relieve pain by cold application over the stomach
• Analgesia is limited while diagnosis is established; sudden relief of
preoperative pain may signal rupture of the appendix (presence of
pain means appendix has not yet ruptured)
• Avoid factors that increase peristalsis, thereby preventing rupture of
the appendicitis
 Heat application over the abdomen
 Laxative
 enema
• Intravenous therapy (to maintain fluid-electrolyte balance)
• ATBC therapy (to control infection)
• Surgery: APPENDECTOMY (surgical removal)
Preoperative
Secure consent, do Skin prep, NPO, avoid enema (leads to rupture
of appendix)
Postoperative
If spinal anesthesia was used, position patient flat on bed for 6 to
8hours (to prevent spinal headache)
Maintain NPO until peristalsis returns. Return of bowel sounds and
passing out of flatus indicate return of peristalsis
Ambulate client 24 hours to prevent postop complications
In ruptured appendicitis – client should be placed in semi-fowler’s
position to promote drainage and to localize inflammation within the
pelvic area (at risk for peritonitis)
PERITONITIS
Peritonitis
• Inflammation of peritoneum, lining that covers wall
(parietal peritoneum) and organs (visceral peritoneum) of
abdominal cavity
• Caused by contamination of normal sterile peritoneal
cavity with infections or chemical irritants
• Etiology:
Ruptured appendicitis
Perforated peptic ulcer
Pelvic inflammatory disease
UTI
Trauma
Bowel obstruction
Peritonitis
• Inflammatory process may lead to the following problems:
Adhesions, abscess formation and intestinal obstruction
Decreased peristalsis leading to the following:
o Fluid shifting into the abdominal cavity (300 to 500 ml/hr) – third
spacing
o Bowel distention with gas and fluid
o Hypovolemia, electrolyte imbalance, dehydration and shock
Peritonitis
• Diagnostic Tests:
Elevated WBC to 20,000
Blood culture: to identify bacteria in the blood
Abdominal x-rays – detect intestinal distention, air-fluid
levels (sign of perforation)
Diagnostic paracentesis
Peritonitis
• Clinical manifestations:
Abdominal pain and rebound tenderness
Board like or abdominal rigidity
Abdominal distention (accumulation of gas and fluid in the
abdomen)
Paralytic ileus; diminished to absent bowel sounds
(decrease peristalsis)
Fever, elevated wbc (20,000/mm3) – due to inflammatory
process
Restlessness, tachycardia, tachypnea, weakness,
oliguria, pallor (signs of shock)
Peritonitis
• Complications:
Abscess leading to SEPTICEMIA
Hypovolemic shock (fluid loss into abdominal cavity)
Paralytic ileus (intestinal obstruction)
• Monitor VS, I & O (to assess fluid balance)
• Assists in NGT insertion for intestinal decompression to
relieve abdominal distention
• Bed rest in semi-fowler’s position (to localize inflammatory
process in pelvic cavity)
• Intravenous fluids and electrolytes to maintain vascular
volume and electrolyte balance
• Encourage deep breathing to prevent respiratory
complications (abdominal distention and pain may inhibit
the client from deep breathing)
• Administration of broad spectrum ATBCs an analgesics
• Surgical management: Laparotomy to treat the cause
and remove inflamed tissue
DIVERTICULAR DISEASE
Diverticular disease
Diverticulum – is a single outpouching of the mucosal
lining of the GIT, commonly in the colon
Diverticula (diverticulosis) – are multiple outpouchings
of the mucosal lining of the GIT, especially in the colon
Diverticulitis – is an acute inflammation and infection
caused by trapped fecal material and bacteria in an
outpouching of the mucosal lining of the colon
• Incidence increases with age
• Muscle in bowel wall thickens narrowing bowel lumen and
increasing intraluminal pressure
• Etiology: (related to weakening of the bowel wall and
increased intraluminal pressure leading to formation of
diverticula)
Low fiber diet (most common cause)
Decreased activity levels
Postponement of defecation
Pathophysiology
Low fecal volume in the colon
Increased muscular
contraction to push
Increased intraluminal pressure feces
Decrease muscle strength in the colon wall
Herniation/outpouching of mucus membrane
Entrapment of fecal material and bacteria
Inflammation and infection
Perforation
peritonitis
Clinical Manifestations
• Crampy abdominal pain in the left lower
quadrant worsen with movement,
coughing or straining
• Chronic constipation with episodes of
diarrhea (due to obstruction in the colon)
• Low grade fever (due to inflammation)
• Nausea and vomiting
• Abdominal distention and tenderness
(due to accumulation of gas and fecal
waste)
• Palpable LLQ mass
• Occult bleeding
• Signs and symptoms of peritonitis (due
to perforation)
• Diagnostic Tests
• Barium enema—reveals inflammatory process,
confirmatory
• CBC reveals: decreased hematocrit and hemoglobin
• WBC count – leukocytosis
• Guaiac test – determine presence of occult blood
• High fiber diet – to increase bulk of the feces and promote
peristalsis
• Liberal fluid intake of 2,500-3000ml/day – to prevent constipation
• Avoid nuts and seeds – these can become trapped in the diverticula
• Bulk-forming laxatives (to promote peristalsis and defecation) e.g.
metamucil, fibercon (calcium polycarbophil)
• During acute episodes:
 Bed rest (to reduce peristalsis and relieve pain)
 NPO then clear liquids to rest the bowel
 Avoid high fiber foods to prevent further irritation of the colon
 IV fluids to replace fluid and electrolyte losses due to vomiting, fever
 Broad-spectrum ATBCs to treat infection
 Antispamosdics/anticholinergics – to rest the bowel bowels and relieve pain
e.g. Probanthine
 NGT insertion to releive abdominal distention
CHRONIC INFLAMMATORY
BOWEL DISORDERS
CHRONIC INFLAMMATORY BOWEL
DISORDERS
• Includes two chronic inflammatory gastrointestinal disorders:
Ulcerative colitis and Crohn’s disease (Regional Enteritis)
• Etiology – unknown
 Run in families
 Related to infectious agent
 Altered immune response
 Exacerbations can be precipitated by
o Pesticides
o Food additives
o Tobacco
o Radiation expsure
• Peak incidence occurs between the ages of 15 to 35; second
peak is between ages 60 to 80
• Characterized by exacerbations and remissions
Ulcerative Colitis
• Inflammatory process usually starts to rectum and
sigmoid colon, then ascends until entire lower colon is
affected
• Rectal involvement is 100%
• Inflammation is continuous
• Inflammation leads to mucosal hemorrhages and
abscess formation – leading to necrosis and sloughing
of bowel mucosa
• Mucosa becomes red and ulcerated – bleeding
 Diarrhea with stool containing pus, blood and mucus; 20-30
watery stools/day)
 Fecal urgency; LLQ cramping
 Fatigue, anorexia, weakness
 Abdominal pain
 Weight loss
Crohn’s disease (regional enteritis)
• Can affect any portion of the GI tract, but ileum and
ascending colon are commonly affected
• inflammation is discontinuous (regional)
• Inflammatory lesion of mucosa and sub mucosa
develops into ulcers involving the entire bowel wall
(transmural inflammation)
• Fistula formation – abnormal opening that
connects small and large intestine (contamination
of small intestine content – septicemia); bowel and
bladder fistula
• Absorption problems leading protein loss and
anemia
 Diarrhea (5-6 soft stool/day) – semi-formed or liquid with
pus and mucus
 Abdominal pain
 Tenderness in RLQ relieved by defecation
 Fever, fatigue, malaise, weight loss
 anemia
Complications
• Ulcerative Colitis:
 Hemorrhage
 Toxic megacolon – usually involves transverse colon which
dilates and lacks peristalsis (charac. by fever, tachycardia,
hypotension, dehydration, abdominal cramping)
 Colon perforation leading to peritonitis (15% mortality rate)
 Increased risk for colorectal cancer (20 to 30 times) – need
yearly colonoscopies
Complications
• Crohn’s disease
 Intestinal obstruction cause by repeated inflammation and
scarring/fibrosis
 Fistulas
 Perforation of bowel with peritonitis
 Massive hemorrhage
 Increased risk of bowel cancer (5-6 times)
Diagnostic Tests
• Colonoscopy, sigmoidosopy – determine area and
pattern of involvement; visualize ulcerations
• Upper GI series, Barium enema – most conclusive test;
shows mucosal irregularities; shortening of the bowel and
dilation of bowel loops
• Stool examination and stool culture to rule out infections
and blood
• CBC – anemia, leukocytosis from inflammation and
abscess formation
• low Serum albumin due to mal-absoprtion
• Low fiber diet/low residue, high protein, high
calorie – to rest the bowel
• Promote nursing care for a client who is NPO,
receiving IV fluids or TPN during acute
exacerbations to provide nutritional support
• Total parenteral nutrition –feeding a person
intravenously, bypassing the usual process of
eating and digestion; if severe malnutrition is
present
• Assess for fluid and electrolyte imbalance;
administer IV fluids and electrolytes as ordered
• Medical treatments:
 Corticosteroids – to relieve inflammation
 Sulfasalazine (Azulfidine) – sulfonamide ATBC with
topical effect in the colon
 Metronidazole (Flagyl) and Ciprofloxacin to control
secondary bowel inflammation and infection
Chron’s Disease
o Total colectomy with ileostomy (stoma is found in
the right lower quadrant of the abdomen)
o Segmental colectomy with anastomosis
Ulcerative Colitis
o Proctocolectomy with ileostomy
ANATOMY & PHYSIOLOGY OF
THE LIVER, GALL BLADDER
AND PANCREATIC SYSTEM:
Liver
• Largest glandular organ
• Has 2 lobes
• Located in the RUQ of the abdomen
• 2/3 of blood supply comes from
portal vein (receives mostly
unoxygenated blood)
• Blood supply are portal vein and
hepatic artery
• Functional unit is hepatic lobule
• Contain Kupffer cells – phagocytic
cells which cleansed blood of
bacteria and other foreign
substances
• Contain hepatocytes – liver cells
Liver
• Major Functions:
Metabolism of carbohydrates, proteins and fats
Carbohydrate metabolism
o Glycogenesis (formation of glycogen from glucose)
o Glycogenolysis (breakdown of glycogen to form glucose)
o Gluconeogenesis (production of glucose from non-carbohydrate substance)
Protein metabolism
o Protein catabolism
o Synthesize plasma proteins i.e. albumin, clotting factors, enzymes, globulins
Fat metabolism
o Synthesis of cholesterols and phospholipids
o Formation of lipoproteins
o Ketone formation (from breaking down fatty acids)
Liver
Production of bile salts (hepatocytes) – produces 1L/day;
BILE comprises of water, electrolytes, phospholipids,
cholesterol and bile salts
Bilirubin metabolism; breakdown product of hemoglobin;
being conjugated to be secreted into the bile
Detoxification of endogenous and exogenous substances
e.g. ammonia, steroids and drugs
Converts AMMONIA to urea
Storage of minerals and vitamins – vitamin A, D, E, K,
B12, Iron
Excretion of adrenal cortex hormones e.g. glucocorticoid,
mineralocorticoid i.e. aldosterone, sex hormone
Phagocytosis by Kupffer cells
Liver
• Physiologic changes of the liver with aging:
Decrease in size of the liver
Decrease in enzymes involved in the metabolism with
drugs
Increased propensity to drug toxicity
Gallbladder
• Stores and concentrate bile produced by the liver
• Liver produces 600 to 1200 mls of bile at a time. 90% of this volume
is water, which is absorbed by the mucous membrane lining of
gallbladder
• Stores 50-70 ml of concentrated bile
• Bile is greenish liquid composed of water, cholesterol, bile salts,
electrolytes and phospholipids
• Functions of BILE:
 Bile is important in fat emulsification and intestinal absorption of fatty acids,
cholesterol and other lipids
 Aids in excretion of conjugated bilirubin from liver and prevent jaundice
• Presence of fat in the acidic chyme transported into duodenum
causes secretion of cholecystonin
• Cholecystonin causes gallbladder contraction and relaxation of
sphincter of Oddi, Releasing bile into the common bile duct for
delivery in the duodenum
Pancreas
• A heterocrine gland – perform both
exocrine and endocrine functions
• Exocrine function: secrete
pancreatic juice containing
pancreatic amylase, lipase and
trypsin
• Amylase completes digestion of
carbohydrates; lipase completes
digestion of fats; trypsin completes
digestion of proteins
• Endocrine function: involves the
Islet of Langerhans
• Islet of Langerhans has two types of
cells: Beta and Alpha cells
• Beta cells secrete insulin to promote
carbohydrate metabolism
• Alpha cells secrete glucagon, which
stimulates glycogenolysis in the liver
LIVER CIRRHOSIS
Liver Cirrhosis
• A chronic progressive disease of the liver characterized
by replacement of normal liver tissue with diffuse fibrosis
that disrupts the structure and function of the liver
• Repeated destruction of hepatic cells causes the
formation of scar tissue
• Incidence is twice as high among men than women
• Peak incidence occurs between the ages of 40 and 60
years
Liver Cirrhosis
• Types:
Laennec’s Cirrhosis (alcohol-induced)
o most frequent type caused by chronic alcoholism and chronic
nutritional deficiencies;
o cellular necrosis causes wide spread scar tissue surrounding
portal areas
Posthepatic cirrhosis
o occurs after massive liver necrosis
o occurs as a complication of acute viral hepatitis or exposure to
hepatotoxins;
o scar tissue causes destruction of liver lobules and entire lobes
Biliary cirrhosis
o scarring occur in the liver around the bile ducts and results from
chronic biliary obstruction and infection
Liver Cirrhosis
• Causes:
 Alcohol abuse (most common cause)
 Malnutrition
 Infection
 Drugs
 Biliary obstruction
 Right-sided congestive heart failure
Causes destruction of hepatocytes
Fibrosis/Scarring
Obstruction of blood flow

Increase pressure in the venous channels
Fatty infiltration
PORTAL HYPERTENSION (persistent increase in the

pressure within the portal vein that develops as a result of obstruction to blood flow
Liver Cirrhosis
• Clinical Manifestations:
Anorexia (early sign of liver function impairment),
weakness, Weight loss – due to inability to metabolize
the nutrients and stores FAT soluble vitamins
Fever (response to liver tissue damage)
Jaundice (icterus), Tea-colored urine (due to increase
serum bilirubin level)
Pruritus – accumulation of bile salts in the skin
Bleeding (decreased Vit. K absorption results to reduced
synthesis of clotting factors)
Decreased resistance to infection (due to destruction of
kupffer cells; unable to perform phagocytosis)
Liver Cirrhosis
Portal hypertension leads to:
o Hepatosplenomegaly – liver and spleen
become congested with blood
o Caput medusae – dilated veins over the
abdomen
o Spider angioma (telangiectasia) – dilated
capillaries over the face and anterior trunk
o Palmar erythema – manifested by reddish
palms
o Ascites – accumulation of fluid within the
peritoneal cavity secondary from venous
congestion of hepatic capillaries and due to
hypoalbumenemia
o Esophageal varices – fragile, thin-walled,
distended esophageal vein that may become
irritated and rupture
o Internal hemorrhoids, leg varicosities,
dependent edema – portal hypertension causes
venous stasis
Caput medusae
Spider angioma
Ascites
Esophageal varices
Liver Cirrhosis
Asterixis – is a course tremor characterized by rapid, non-
rhythmic extension and flexion on the wrist and fingers (due
to elevated serum ammonia)
Hepatic encephalocepathy- is end-stage hepatic failure
and cirrhosis caused by elevated serum ammonia
o Confusion/disorientation
o Hallucination
o Fetor hepaticus – fruity, musty breath odor
o Hepatic coma - irreversible
Diagnostics tests
• Liver biopsy detects destruction and fibrosis of liver tissue
• Decrease albumin; serum protein levels reveal
hypoalbuminemia
• Increase alkaline phosphatase (ALT) and alanine amino
transferase (AST) (Liver function test)
• CT scan, liver scan – gives information as to liver size,
hepatic blood flow and obstruction
• Promote bed rest (to reduce metabolic demands on the
liver and maximize liver function)
• Diet – should be high in calorie (2,000-3,000cal/day) and
high in carbohydrates to maintain weight; little protein to
rebuild tissue but not high protein because this may
precipitate hepatic encephalopathy; decrease fat to prevent
fatty liver; provides fat soluble vitamins supplements
• Skin care – to relieve pruritus
 Wash the skin with warm water and mild soap
 Change position at regular intervals
 Keep environment cool. sweating intensifies pruritus
 Apply antipruritic agent on the skin as prescribed such as calamine
lotion
 Administer oral cholestyramine resin (a bile acid sequestrant (a bile
sequestrant – enhances excretion of bile salt via feces
• Prevent trauma or injury (to prevent bleeding)
 Monitor client for bleeding gums, melena, hematoma and
hematemesis
 Avoid or minimize parenteral injection; use small gauge needle
 Apply pressure at injection sites for 5 minutes
 Avoid vigorous nose blowing
Protect client from infection - Practice asepsis
• Relieve ascites
Monitor daily weights, abdominal girth, intake and output
(every shift)
Restrict sodium and fluid intake
Administer diuretic as prescribed. The DOC is aldactone
(spironolactone) – potassium sparing diuretic;
To prevent hyperkalemia due to aldactone therapy; lasix (
furosemide) a potassium wasting diuretic may be prescribed
Albumin per IV may prescribed as ordered to increase
colloidal osmotic pressure and prevent shifting of plasma into
peritoneal cavity and to manage hypoalbuminemia
Assist the client during paracentesis
• Prevent rupture of esophageal varices
Advice the client to avoid the following:
o Screaming, shouting, yelling
o Straining at stool
o Hot spicy, rough foods
o Bending, stooping
o Coughing, sneezing
Administer Inderal (Propanolol) to reduce portal
hypertension)
• Control hemorrhage due to ruptured esophageal
varices:
 Monitor VS and urine output
 Administer IV fluid, plasma expanders and blood transfusions
as prescribed
 Administer vasopressin as prescribed (to lower portal pressure
and promote vasoconstriction)
 Administer beta-adrenergic blocking agents (e.g. Inderal
(Propanol), Lopressor (Metoprolol)
 Balloon tamponade using Sensgtaken-blakemore tube
inserted by the physician into stomach and inflates the
esophageal and gastric balloons
• Balloon tamponade using Sensgtaken-
blakemore tube
 The pressure of the esophageal balloon is
inflated for a maximum of 24 hours at a time
 It is important to release the pressure
periodically to prevent tissue necrosis
 The GASTRIC BALLOON anchors
Sengstaken tube
 Have scissors readily available at the
bedside in order to remove the tube in an
emergency
 If gastric balloon is accidentally punctured,
the esophageal balloon is displaced
upwards, thereby causing airway obstruction
 Appropriate nursing action is to cut the tube
with scissors. Airway is always a priority
• Reduce ammonia formation (to prevent hepatic
encephalopathy)
Interventions to reduce ammonia formation are
as follows:
o Chronulac, Duphalac (Lactulose) – it decreases the pH
of the colon, decreases production of alkaline ammonia
and facilitate the excretion of ammonia (expected side
effects is 2-4 watery stools/day. If more than 4 watery
stools/day- notify the physician)
o Neomycin sulfate – to reduce colonic bacteria which are
responsible for the production of ammonia
• Avoid medications such as narcotics, sedatives,
barbiturates, acetaminophen (hepatotoxic drugs)
• Avoid ASA, to prevent bleeding
• Avoid alcohol
PANCREATITIS
Pancreatitis
• Is an acute or chronic
inflammation of the pancreas with
associated escape of pancreatic
enzyme into surrounding tissue
itself leading to hemorrhage and
necrosis
• Etiology:
 alcohol, biliary obstruction
(cholelithiasis), drugs (ATBCs,
anticonvulsant), abdominal and
pancreatic trauma,
hyperlipidemia, hypercalcemia,
hyperparathyroidism, viral or
bacterial disease, PUD
Pancreatitis
• Pathophysiology
Damage to pancreatic cells
Inflammation
Edema of the pancreas and pancreatic duct
Obstruction to the flow of pancreatic enzymes
Activation of pancreatic enzymes inside Pancreas
Autodigestion of the Pancreas
Fatty necrosis, Ulceration, Hemorrhage, Infection

Pancreatitis
• Acute pancreatitis occurs suddenly
• Chronic pancreatitis is a continual
inflammation and destruction of the
pancreas, with scar tissue replacing
pancreatic tissue
• Damage to the pancreatic cells causes
inflammation. This results to edema of the
pancreas and pancreatic duct
• Obstruction to the flow of pancreatic
enzymes (amylase, lipase, trypsin) occurs.
This causes activation of pancreatic
enzymes inside the pancreas
• AUTODIGESTION of the pancreas
(digestion of pancreatic tissues by the
pancreatic enzymes) – leads to fatty
necrosis, ulceration, hemorrhage and
infection
Pancreatitis
Pain – located in mid-epigastrium or left upper quadrant (LUQ) with
radiation to the back; pain is intensified by a fatty meal, alcohol
Abdominal tenderness and distention due to paralytic ileus that
follows peritonitis
Fever
Anorexia and weight loss (due to inadequate metabolism of nutrients)
Severe dehydration (excessive fluid loss from fever, nausea/vomiting,
blood loss) and signs of hypovolemia
Steatorrhea – fatty/greasy, bulky, foul-smelling stools result from
inadequate fat digestion
Hypocalcemia (calcium is deposited in areas of fatty necrosis; calcium
is lost in the steatorrhea)
Pancreatitis
• Hyperglycemia (hormonal functions of the
pancreas is disrupted from tissue damage
esp. Islet of Langerhans
• Jaundice (caused by common bile duct
obstruction by pancreatic edema and seen in
clients with gallstone-associated pancreatitis)
• Hemorrhagic pancreatitis – produces post-
hemorrhagic necrosis (purplish discoloration)
 Grey-Turner’s sign (left flanks)
 Cullen sign (periumbilical area)
Laboratory Findings
• Elevated urine and serum amylase
• Elevated serum lipase (most specific indicator)
• Elevated WBC, Bilirubin
• Relieve pain; Meperidine is DOC
Morphine is contraindicated because it may cause spasm
of the sphincter of oddi, which potentiate pancreatic tissue
injury)
Pain relief by sitting in bed with knees flexed and pressing
a pillow over the abdomen
Diet. NPO status is maintained during acute phase. Food
ingestion increases pancreatic secretion, which may
increase inflammation and pain
IV therapy to maintain fluid-electrolyte balance
Digestive enzymes (pancreatin) as prescribed. These
medication should be taken with each meal and snack.
Food help buffer stomach acid
o A high fiber diet may enhance efficacy
o Absence of steatorrhea indicates effectiveness
o S.E include abdominal cramps/pain and diarrhea
• Administer fat-soluble vitamins (Vit. A, D, E, K) as prescribed.
Fat-soluble vitamins are lost in the steatorrhea
• Administer antacids to neutralize gastric secretion
• Administer H2 receptor antagonists as prescribed. (to decrease
HCL production and prevent activation of pancreatic enzymes)
• Administer anticholinergic as prescribed (to decrease GIT
motility and inhibit pancreatic enzyme secretion)
• Administer ATBCs as prescribed (to treat infection of the
pancreas)
• Administer calcium supplement and Vit. D as prescribed (to
manage hypocalcemia. Vit D enhances absorption of calcium
• Instruct client on the importance of avoiding alcohol
• Instruct client to notify physician if acute abdominal pain,
jaundice, clay-colored stools or dark urine develops
GALLBLADDER
DISORDERS
Gallbladder disorders
• Cholecystitis – inflammation of gallbladder
• Cholangitis – inflammation of the biliary duct
• Cholelithiasis – presence of gallstones
• Choledocholithiasis – presence of stone in the common
bile duct
• Cholecystitis – inflammation of the gall bladder
Gallbladder disorders
• Cholelithiasis – formation or
presence of gallstones (calculi)
within the gallbladder or biliary
duct system
• Gallstones are crystalline
structures formed by hardening or
adherence of particles of bile
constituents
• Most gallstones are composed
primarily of bile (80%)
• Remainder are composed of a
mixture of bile components
• Excess cholesterol in bile is
associated with obesity, high
cholesterol in the diet
Cholelithiasis
• Bile stones are due to:
Abnormal bile composition
o Bile undergo change in composition
o Bile is saturated with cholesterol but deficient in bile salts (bile salts
normally keep cholesterol in suspension to prevent precipitation)
Biliary stasis
o Bile stasis may change the composition of bile, supersaturate bile
with cholesterol and precipitate some bile constituents
Infection/inflammation of gallbladder
Cholelithiasis
• Risk factors for Cholelithiasis:
5 P’s (Female, Fat, Fair, Forty, Fertile)
Female – over 40 years old, those who have high fat
intake, those who are multigravida and those who using
contraceptive pill
Obesity, hyperlipidemia
Conditions which lead to biliary stasis – pregnancy,
prolong parenteral nutrition
Caucasian race, native Americans, south Americans
Cholecystitis
• Inflammation causes gallbladder wall to become
thickened and edematous and cystic lumen to increase
diameter – leading to submucosal hemorrhage,
mucosal ulceration
• Inflammation may spread to common bile duct –
obstructing bile drainage can lead to jaundice
Cholelithiasis
Gallstone causes pressure within the gallbladder
Gallstone continue to grow in size
Obstruction to bile flow occurs
Bile stasis
Decreased emulsification of fat

Inflammation of the gallbladder
Biliary obstruction
Infection (Cholecystitis)
Cholelithiasis
• Decreased emulsification of fats leads to:
Fat intolerance
Steatorrhea (fatty, foul-smelling stool due to
undigested fats)
Anorexia
Weight loss
Belching
Flatulence, bloating
Cholecystitis
• Inflammation of the gallbladder leads to:
Pain
o Epigastric pain radiates to the scapula 2 to 4 hours after eating fatty
foods and may persist for 4 to 6 hours
o Pain becomes localized in right upper quadrant (RUQ) with
guarding and rigidity
Fever, leukocytosis
Jaundice
Murphy’s sign
o Pt cannot take deep breath when the examiner’s fingers are
passed below the hepatic margin
Cholelithiasis
• Biliary obstruction leads to:
Alcoholic stool (pale/gray/clay – colored
stool)
Decreased Vit. K absorption in the colon
(leads to bleeding tendencies)
Increased serum bilirubin leads to
jaundice, pruritus, tea-colored urine
• Relief of pain
Administer analgesic as prescribed
Demerol (Meperidine HCL) is the DOC
Avoid administration of morphine Sulfate (it
causes spasm of sphincter of Oddi and may
increase pain
Administer antispamodic (anticholinergic) to
relax smooth muscles
• Diet
Maintain NPO with IV fluids administered during nausea
and vomiting episodes
Small frequent feedings
Avoid gas forming foods
Administer anti-emetics for nausea and vomiting
• Administer medications to dissolve gallstone as
ordered:
E.g. Chenix (Chenodiol) – it decreases
cholesterol production, lowering content of bile
and facilitates dissolution of gallstones
E.g. Actigall (Ursodiol) – a bile salt;
suppresses hepatic synthesis of cholesterol and
inhibit intestinal absorption of cholesterol and
facilitates dissolution of gallstone
• Major SIDE EFFECTS: abdominal pain,
diarrhea, nausea and vomiting; Notify the
physician if these SE occurs
• Surgical interventions:
Cholecystectomy – removal of
the gallbladder
Choledochotomy – removal of
stone from the common bile
duct
Laparoscopic
cholecystectomy – involves 3-
4 small incision; gas
insufflation with CO2 of the
abdomen to lift the abdominal
wall (facilitates visualization of
the gall bladder)
Laparoscopic cholecystectomy
• “Lap Chole”
• Laparoscopic Cholecystectomy
After “lap chole”, pt may have fluids as soon as
awake; then may eat lightly for few days
During first 24 hors post op, the client normally
experience belatedness and abdominal pain
that radiates to the shoulders (due to gas
insufflation of the abdomen during the
procedure)
Pt may go back to normal activities of daily
living within 5 to 7 days
• Open Cholecystectomy
Involves right subcostal
incision (below the
diaphragm)
High abdominal incision may
inhibit the client to breathe
deeply and to cough
Preoperative care
emphasizes teaching client
deep breathing, coughing and
turning exercises (DBCT)
Client is at risk for respiratory
complications during postop
period
• During post-op period:
• Since gallbladder is removed, bile directly flows from the liver to
the duodenum via common bile duct
Position the client in Semi-Fowler’s to promote lung expansion
NGT is in place, to drain gastric content and prevent abdominal
distention
Reinforce DBCT exercise to prevent respiratory complications
(atelectasis, pneumonia)
Diet low in FAT for 2-3 months; then gradually introduce fats
according to client’s tolerance
Fat intolerance is common during the first few months postop
Early ambulation is encouraged to prevent postop complications
• Post-op period:
If Common bile duct exploration is done, a
client will have T-tube in place to promote
flow of bile to the outside as area heals
Purpose of T-tube:
o To drain bile from the common bile duct
and minimize amount of bile flowing into
duodenum
o To maintain patency of common bile duct
o To prevent leakage of bile into peritoneum
and prevent peritonitis
• The normal color of drainage from the T-
tube for the first 24 hours is reddish brown
(due to combination of bile and blood)
• After 24 hours, drainage color becomes
greenish brown
• Normal amount of drainage from the T-tube
during the first 24 hours post-op is 300-500
mls; then up to 500-1000 mls per day after
24 hours
• The drainage bottle should be placed in bed,
below the level of the gallbladder (this
allows drainage of excess bile, not all of the
bile)
HEPATITIS
Hepatitis
• Inflammation of the liver caused by a virus, expsoure to
medications or hepatotoxins
• Types of viral hepatitis are:
Hepatitis A (HAV) – “Infectious hepatitis
Hepatitis B (HBV) – “Serum hepatitis”
Hepatitis C (HCV) – “Non A, Non B hepatitis or “Post-
transfusion hepatitis”
Hepatitis D (HDV) – “Delta agent hepatitis”
Hepatitis E (HEV) – Enterically transmitted or “Epidemic
hepatitis”, Non-A, Non-B hepatitis
Pathophysiology
Immune system response to the virus or toxin
Diffuse inflammatory infiltration with local necrosis
Hepatocellular damage
Bile flow is interrupted, bilirubin diffuses into tissues, bile

salts accumulate
Hepatomegaly and splenomegaly

Stages of Viral Hepatitis
• Pre-Icteric phase
Precedes appearance of jaundice
Flu-like symptoms
malaise, fatigue
Anorexia, nausea, vomiting, diarrhea
Pain, headache, muscle aches, polyarthritis
Serum bilirubin and liver enzyme levels are
elevated
• Icteric phase
Occurs few days to weeks after pre-icteric
stage
Jaundice
Pruritus
Tea-colored urine
Light-colored stools
Steatorrhea
Enlarged liver
• Post-icteric phase
Convalescent stage lasting a few weeks
Fatigue decreases, jaundice resolves,
appetite returns
Increased energy levels
Subsiding of pain
Minimal to absent GI symptoms
Serum bilirubin and enzymes return to
normal
Hepatitis A
• High risk groups; young children, international travelers to developing
countries, health care personnel
• Incubation period is 15 to 50 days (2-6 weeks)
• MOT
 Fecal-oral route, contaminated water/food, uncooked shellfish,
contaminated fruits/vegetables, poorly washed utensils, person-
person contact
• Associated with poor sanitation
• Prevention:
 Strict hand washing especially after bowel movement
 Stool precautions
 Safe water and food supply
 Treatment of municipal water supplies
 Immunoglobulin shot for household members within 2 weeks of
exposure to individuals with hepatitis A
Hepatitis B
• Common in young adults
• High risk groups: drug addicts, clients undergoing long-
term hemodialysis, health care personnel
• MOT
 Blood or body fluids through contaminated needles
 sexual contact
 Parenteral – syringes and needles;contaminated instruments
 Perinatal transmission from mother to baby
• Incubation period: 45-160 days, average of 60 to 120
days (6 to 24 weeks)
• Reservoir
 Blood and body secretions, saliva, semen, urine, nasopharyngeal
secretions, feces, pleural fluids
Hepatitis B
• Prevention:
Strict hand washing
Adhere to standard precautions
Screening blood donors
Testing of all pregnant women (HBsAg)
Needle precautions – use of disposable syringes, needles
and lancets
Avoiding intimate sexual contact with person who are HBsAg
positive
Immunization with Hepatitis B vaccine (Engerix-B,
Recombivax HB)
Hepa B Immunoglobulin for individuals exposed to HBV
through sexual contact or through blood and body secretions
Hepatitis C
• The major cause of post-transfusion hepatitis
• Common among client on chronic hemodialysis
• These are the client who frequently received blood transfusion
• Formerly known as NON A, NON B hepatitis
• Common also to drug abusers
• Incubation period: 5 to 10 weeks
• Prevention:
Strict hand washing
Standard precautions
Needle precaution
Instruct IV drug users not to share needles
Screening of blood donors
Hepatitis D
• Co-infection of hepatitis B
• Virus requires hepatitis B surface antigen for
replication
• Only clients with hepa B are at risk for hepatitis D
• High risk groups: drug users, client receiving
hemodialysis, client receiving frequent blood
transfusion
• MOT – same as hepatitis B
• Prevention:
Because hepatitis D co-exist with hepatitis B,
implement precautions that help prevent hepatitis B
Hepatitis E
• Is waterborne virus
• Prevalent in areas where sewage disposal is inadequate
or where communal bathing in contaminated river is
practiced
• Transmitted by fecal-oral route; person to person contact
• MOT: same as hepatitis A
• Incubation period – 15 to 65 days
Client and Family Education for Hepatitis
• Institute enteric and blood and bod secretion standard
precautions
• Handwashing must be strict and frequent after caring for the
client especially after handling personal items from patient
• The client must not prepare food for other family members
• Do not share bathrooms unless the client strictly adheres to
personal hygienic measures
• Individual washcloths, towels, drinking and eating utensils,
toothbrush and razors must be labeled and identified
• The client should avoid alcohol and OTC medications
particularly acetaminophen (Tylenol) and sedatives because
these drugs are hepatotoxic
• Encourage client to decrease activities and stay on bed rest
until enlarged liver and liver enzymes return to normal to
prevent fatigue
Client and Family Education for Hepatitis
• The client should consume small, frequent feedings with
high-carbohydrate, low-fat, high calorie diet
• Proteins are restricted when liver is unable to metabolize
proteins
• The client should not donate blood
• Close personal contact such as kissing should be
discouraged until hepatitis B surface antigen test results
are negative
• The client is to avoid sexual activity, donating blood for
patient with Hepa B, C and D
• Maintain proper personal hygiene and environmental
hygiene
OTHER GASTROINTESTINAL
DISORDERS
Diarrhea
• Increase in frequency, volume and fluid content of stool
• A symptoms rather than a primary disorders
• Types:
Acute: last less than a week; often due to infectious
agent
Chronic: persists longer than 3 to 4 weeks; may be
caused by inflammatory bowel disorders, endocrine
disorders
Diarrhea
• Etiology
Large volume diarrhea: caused by increased
water content of stool from osmotic process
Small volume diarrhea: characterized by small
frequent stool; usually caused by inflammation or
diseases of the colon
Clinical manifestations
• Affected by cause, duration, severity, area of bowel
affected and client’s general health
• Varies from several large watery stools daily to very
frequent small stools containing mucus, blood or exudate
Complications
• Dehydration esp. in very young and elderly
• Severe diarrhea leads to:
Vascular collapse
Hypovolemic shock
Electrolyte imbalances i.e. hypokalemia, metabolic
acidosis
Collaborative Care
• Management focuses on identifying treating the cause and
preventing complications
• Solid food should be withheld for the first 24 hours to rest the
bowel; then begin frequent small feeding to start with soft diet
• IV fluids to replace fluid and electrolyte losses
• Food with roughage, fried and spicy, coffee and alcohol are
avoided
• Antidiarrheal medications may worsen disease if it slows
elimination of toxin from the bowel
• Health education:
 Safe food handling and measures to take if travelling outside countries or
without safe water
 Proper handwashing
 Introduction of foods with constipating effects e.g. crackers, bananas, rice,
potatoes
Constipation
• Infrequent or irregular bowel movements weekly or
difficulty passing stools
• More frequently affects persons > 65 years old
• May be a primary problem or a symptom of a disease
• Types:
Acute constipation
Chronic constipation
• Etiology
Overuse of laxatives can lead to intestinal problems
Fecal impaction: rock-hard mass of feces in rectum
blocking the passage; client may experience abdominal
cramping and rectal fullness and may have diarrhea
passed around the impaction
Collaborative Care
• Determine probable cause by history and physical
assessment
• Patient education and health promotion are important
aspects of management through diet, fluid and exercise
• Foods high with fiber (draws fluid and increases bulk in
the stool which stimulate peristalsis)
• Fluids (6 to 8 glasses daily) necessary to maintain bowel
motility and soft stools
• Administration of mild laxatives to promote stool
evacuation
• Enema for acute situations
GASTROENTERITIS
Gastroenteritis
• Inflammation of stomach and small intestine
caused by bacteria, viruses, parasites, toxins
commonly causing anorexia, nausea, vomiting
and diarrhea
• Food poisoning: usually self-limiting, but can be
severe for the very young, old people
• Major clinical manifestations:
Diarrhea
Abdominal pain and cramping
Nausea, vomiting
Fever and malaise
Distention, tenesmus (straining on defecation)
Borborygmi (hyperactive bowel sounds)
Stool specimen shows leukocytes, blood, mucus
or parasitic ova
Gastroenteritis
• Etiology – gastroenteritis is a generic term for various
common specific and nonspecific intestinal disorders
 Bacterial food poisoning – e.g. Staphylococcus aureus, Salmonella,
Shigella
 Amoebae – e.g. entamoeba histolytica
 Adenoviruses e.g. enteroviruses
 Parasites e.g. Ascaris, Enterobius
 Nonbacterial food poisoning from toxins in plants e.g. mushrooms
or contaminated food
 Side effects of drugs e.g. ATBCs
Pathophysiology
Gastroenteritis irritates and inflames the gastric mucosa
Resulting in vomiting (protective mechanism; empties the

contents of the stomach and portions of the small
intestines)
Diarrhea is produced by toxins that:
• stimulates secretion of water and electrolytes

Destruction of the intestinal epithelial cells and local
inflammation
Gastroenteritis
• Types:
Shigella (Bacillary dysentery)
oSpread by fecal-oral route through
contaminated foods, fomites, vectors
oAbrupt onset of diarrhea that is watery
and contains blood, mucus, exudates
oSevere abdominal cramping, tenesmus
oMay develop secondary infection and
acute blood loss
Gastroenteritis
• Types
Salmonella
oFood poisoning caused by eating raw or
improperly cooked meat, poultry, eggs, dairy
products
oOnset is 8 to 48 hours post bacterial ingestion
oSevere diarrhea with abdominal cramping,
nausea and vomiting
oLow grade fever, chills
Gastroenteritis
• Types:
Traveller’s Diarrhea
o Often persons travelling to other countries
o Develop diarrhea in 2 to 10 days
o Usually with difference in climate, sanitation, food and
drink
o Causes are most often strains of enterotoxin-producing
E coli, Shigella
o Manifestations: diarrhea (up to 10 stools/day),
abdominal cramping resolving in 2 to 5 days
Gastroenteritis
• Etiology
Infection produces inflammation and tissue damage by
two primary mechanisms
o Productions of exotoxins – causes damage and inflammation
o Impaired intestinal absorption – causing diarrhea and fluid loss
Gastroenteritis
• Etiology
Staphylococcus
o Causes food poisoning when food is contaminated and
left at room temperature (meats, dairy)
o Abrupt onset, usually 2- 8 hours
o Last 3 to 6 hours with abdominal cramping, diarrhea,
headache, fever
Gastroenteritis
• Etiology
Clostridium botulinum
o Severe life-threatening from improperly preservation of
foods (home canned vegetables, smoked meats)
o Toxin causes descending weakness and paralysis
o Nausea, vomiting, abdominal cramps occur
o Respiratory muscle paralysis (requires mechanical
ventilation)
o Treatment include administration of Anti-toxin
o Gastric lavage
Gastroenteritis
• Etiology
Vibrio cholera
o Causes cholera
o Often abrupt onset with severe, frequent watery diarrhea
“rice watery stools”
o Significant complications are dehydration, hypokalemia
and metabolic acidosis
Collaborative Care
• Fluid and electrolyte replacement
• Health education:
Proper handwashing
Proper food handling
Thoroughly cooking meat
Prompt refrigeration of meats, eggs, dairy products
Boiling canned foods to destroy potential toxins
Discarding foods that appear spoiled
Avoiding contaminated water; using bottled water
Collaborative Care
• Provide measures designed to allow the gastrointestinal
tract to rest i.e. keeping client in NPO, maintain bed rest
• Promote return to a regular diet
As acute symptoms subside, gradually provide clear
liquids i.e. gatorade and pedialyte to provide oral
replacement therapy;
Followed by a bland diet and gradual resumption of the
client’s regular diet
Closely monitor intake, output and fluid and electrolyte
status
Monitor for dehydration; increased fluid intake with IVF
Collaborative Care
• Administer the following medications:
Antidiarrheals – absorbs excess water from stool;
e.g. Kaolin-pectin mixture (Kaopectate), diphenoxylate
(Lomotil), Loperamide (Imodium)
Antiemetics – releive nausea and vomiting by
inhibitng medullary chemoreceptor triggers – e.g.
promethazine (Phenergan), Scopolamine (Transderm)
HEMORRHOIDS
Hemorrhoids
• Varicose veins or varicosities of veins in
anus, anal canal region
• Types:
Internal hemorrhoids
o Occur above anal sphincter
o Rarely cause pain but present with
bleeding
o May vary in severity but recurrence can
cause anemia
o Associated with portal hypertension
Hemorrhoids
• Types:
External hemorrhoids
o Occur below the anal sphincter
Hemorrhoids
• Etiology:
Constipation (most common)
Pregnancy
Obesity
Prolonged-sitting or standing
Wearing constricting clothing
Liver cirrhosis
Right sided CHF
Low fiber diet
Clinical Manifestations
• Anal irritation and feeling of pressure
• Constipation
• Anal pain
• As hemorrhoids enlarge it may prolapse
and protrude through the anus (painful)
• Rectal bleeding with defecation
Collaborative Care
• High fiber diet, increase fluid intake and stool
softener/bulk forming products (e.g. metamucil) to
prevent constipation (absorb water and increase fecal
bulk; stimulate peristalsis through mucosal irritation)
• Apply cold packs to the area followed by warm sitz bath
• Apply topical anesthetics (Nupercaine) as prescribed
• Treatments
 Sclerotherapy – injecting chemical irritant into a tissue
surrounding hemorrhoid to cause inflammation and fibrosis
and scarring
• Surgery: Hemorrhoidectomy
 Postop: side-lying or prone position (to promote comfort)
 Apply ice packs over dressing site for 12 hours postop to
prevent bleeding
 Warm sitz bath 12 to 24 hours postop to relieve pain
 Administer stool softener i.e. Docusate sodium (Colace) as
prescribed (ease stool passage by facilitating the mixing of
water with fecal mass; retain and increase water in the feces)
 Increased fluids and high fiber diet

Nursing of Clients With Gastrointestinal Disorders

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NURSING CARE OF CLIENTS

Duodenal ulcers Gastric Ulcers

Histamine H2 Receptor Antagonists – to reduce HCL secretion

Proton Pump inhibitor – suppress gastric acid secretion

Prostaglandin analogue –suppresses secretion of

Helicobacter pylori drug treatment – uses two ATBCs

Decrease muscle strength in the colon wall

Herniation/outpouching of mucus membrane

Entrapment of fecal material and bacteria

Inflammation and infection

Causes destruction of hepatocytes

Obstruction of blood flow

PORTAL HYPERTENSION (persistent increase in the

Edema of the pancreas and pancreatic duct

Obstruction to the flow of pancreatic enzymes

Activation of pancreatic enzymes inside Pancreas

Autodigestion of the Pancreas

Fatty necrosis, Ulceration, Hemorrhage, Infection

Gallstone continue to grow in size

Obstruction to bile flow occurs

Decreased emulsification of fat

Diffuse inflammatory infiltration with local necrosis

Bile flow is interrupted, bilirubin diffuses into tissues, bile

Hepatomegaly and splenomegaly

Resulting in vomiting (protective mechanism; empties the

Diarrhea is produced by toxins that:

• stimulates secretion of water and electrolytes

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