GASTROINTESTINAL SMALL INTESTINE

SYSTEM Longest segment of the GI tract where the

process of absorption of nutrients takes place
DEFINITION Consisting of three parts:
23-26 foot long pathway that the: Duodenum
Mouth Jejunum
Esophagus Ileum
Stomach
Small intestines
Large intestines
Rectum
Anus
ESOPHAGUS
Located in the mediastinum, anterior to the spine
and posterior to the trachea
Approximately 25cm in length LARGE INTESTINE
Tube connecting the mouth to the stomach The portion of the GI tract into which waste
material from the small intestine passes as
absorption continues and elimination begins
Consists of several parts:
Ascending colon
Transverse colon
Descending colon
Sigmoid colon
Rectum

STOMACH
Distensible pouch into which the food bolus
passes to be ingested by gastric enzymes
Hollow muscular organ with a capacity of
approximately 1500mL
Stores food during eating
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FUNCTIONS OF THE DIGESTIVE SYSTEM Food remains in the stomach for variable length
Digestion of time, from 30 minutes to several hours,
depending on the:
Occurs when digestive enzymes and secretions Volume
mix with ingested food and when proteins, fats
and sugars are broken down into their component Osmotic pressure
smaller molecules. Chemical composition of the gastric contents.
Absorption Small Intestine Function
Occurs when small molecules, vitamins, and Secretions contain digestive enzymes:
minerals pass through the walls of the small and
large intestine and into the bloodstream Amylase
Aids in digesting starch
Elimination
Occurs after digestion and absorption, when waste
Lipase
products are evacuated from the body Aids in digesting fats
Chewing and swallowing Trypsin
1st process of digestion Aids in digestion of protein
Approximately 1.5 L of saliva is secreted daily Bile
from the parotid, the submaxillary, and the Secreted by the liver and stored in the
sublingual glands
gallbladder
Salivary amylase
Is an enzyme that begins the digestion of Aids in emulsifying ingested fats
starches Making them easier to digest and absorb.
Swallowing begins as a voluntary act that is Intestinal secretions total approximately 1L/day of
regulated by the swallowing center in the pancreatic juice, 0.5 L/day of bile, and 3 L/day of
medulla oblongata of the central nervous secretions from the glands of small intestine.
system.
Two types of contractions occur regularly in the
Gastric Function small intestines:
Secretes highly acidic fluid in response to the Segmentation contractions
presence of anticipated ingestion of food
(hydrochloric acid) Produce mixing waves that move the intestinal
Intrinsic Factor contents back and forth in a churning motion.
Secreted by the gastric mucosa, combines w/ Intestinal peristalsis
dietary vitamin B12 Propels the contents of the small intestine
Pepsin toward the colon
An important enzyme for protein digestion. Colonic Function
End-product of the conversion of pepsinogen Bacteria assist in completing the breakdown of
from the chief cells.
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undigested or unabsorbed pro and bile salts. Spleen
The slow, weak peristaltic activity along the tract Tail of pancreas
allows for efficient reabsorption of water and Splenic flexure of the colon
electrolytes, which is the primary purpose of the Upper half of the left kidney
colon. Suprarenal gland
Intermittent, strong peristaltic waves propel the
contents and eventually reach the rectum, usually Right Lumbar
in about 12 hours
Ascending colon
Lower half of right kidney
Physical examination Part of duodenum and jejunum
Inspection
Auscultation Umbilical
Percussion Omentum
Palpation Mesentery
Lower part of duodenum
Order of Palpation Part of jejunum and ileum
Right Lower Quadrant Right Inguinal
Right Upper Quadrant
Left Upper Quadrant Cecum
Left Lower Quadrant Appendix
Lower end of the ileum
Right ureter
Right Hypochondriac Right spermatic cord
Right lobe of the liver Right ovary
Gallbladder
Part of the duodenum Hypogastric
Hepatic flexure of colon Ileum
Upper half of the right kidney Bladder (if enlarged)
Suprarenal gland Uterus (if enlarged)

Epigastric Left Inguinal

Aorta Sigmoid colon
Pyloric end of stomach Left ureter
Pancreas Left spermatic cord
Part of live Left ovary
Left hypochondriac
Stomach
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DIAGNOSTIC With introduction of barium enema
The procedure usually takes about 15 to 30
STUDIES minutes, during which time x-ray images are
obtained
UPPER GI SERIES The patient must be assessed for allergy to
iodine or contrast agent.
Delineates the entire GI tract after the
introduction of a contrast agent (Barium swallow)
Enables the examiner to detect or exclude
anatomic or functional derangement of the upper
GI organs or
sphincters.
Also aids in the diagnosis of ulcers, varices,
tumors, regional enteritis, and malabsorption
syndromes

Nursing Interventions
Emptying and cleansing the lower bowel
prior to the procedure
Low residue diet 1 to 2 days before the test
Nursing Interventions Clear liquid diet, NPO after midnight; and
cleansing enemas until returns are clear the
Clear liquid diet with NPO from midnight the following morning.
night before the study. Laxative is given before and after the
procedure.
Smoking, chewing gum, and mints can stimulate
gastric motility, so the nurse advises against Increased fluid intake after the procedure.
these practices Evaluation of bowel movement for evacuation
Increase fluid intake to facilitate evacuation of of barium
stool and the radiopaque liquid
Typically, oral medications are withheld on the
morning of the study and resumed that evening,
but each patient's medication regimen is
evaluated on an individual basis
LOWER GI SERIES
Visualization of the lower GI tract
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ESOPHAGO-GASTRO-DUODENOSCOPY (EGD) Nursing Interventions
Direct visualization The patient should be NPO for 8 hours prior to
Esophageal the examination.
Gastric Before the introduction of the endoscope, the
Duodenal mucosa through a lighted endoscope patient is given a local anesthetic gargle or
spray.
After the patient is sedated, the endoscope is
lubricated with a water-soluble lubricant and Midazolam (Versed), a sedative that provides
passed smoothly and slowly along the back of the moderate sedation and relieves anxiety during
mouth and down into the esophagus the procedure
The procedure usually takes about 30 minutes. Atropine may be administered to reduce
secretions, and glucagon may be administered
The patient may experience: to relax smooth muscle.
Esophageal The patient is positioned in the left lateral
Gastric position to facilitate clearance of pulmonary
Duodenal mucosa through a lighted endoscope secretions and provide smooth entry of the
scope.
Use of topical anesthetic agents and moderate
sedation makes it important to monitor and After gastroscopy, assessment includes
maintain the patient's oral airway during and after Level of consciousness
the procedure. Vital signs
Precautions must be taken to protect the scope, Oxygen saturation
because the fiberoptic bundles can be broken if Pain level
the scope is bent at an acute angle. Monitor for signs of perforation
Pain
The patient wears a mouth guard to keep from Bleeding
biting the scope. Unusual difficulty swallowing
Rapidly elevated temperature
After the patient's gag reflex has returned,
lozenges, saline gargle, and oral analgesic
agents may be offered to relieve minor
throat discomfort
Patients who were sedated for the
procedure must remain in bed until fully
alert

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Endoscopic Retrograde Cholangio- LAPAROSCOPY
pancreatography (ERCP)
Direct visualization of the organs and structures
Visualization of the common bile duct, the within the abdomen, permitting visualization and
Pancreatic, hepatic ducts through the Ampulla identification of any growths, anomalies, and
of Vater in the duodenum inflammatory processes.
Uses the endoscope in combination with X-ray
techniques to view the ductal structures of the A pneumoperitoneum (injecting carbon dioxide
biliary tracts. into the peritoneal cavity to separate the
intestines from the pelvic organs) is created
Biopsy samples can be taken from the
structures and organs as necessary
Laparoscopy usually requires general
anesthesia and sometimes requires that the
stomach and bowel be
decompressed

COLONOSCOPY
Direct visual inspection of the large intestine
(anus, rectum, sigmoid, transverse, descending
and ascending colon)
Therapeutically, the procedure can be used to
remove all visible polyps with a special snare
and cautery through the colonoscope.

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ESOPHAGEAL DISORDER PHARMACOLOGIC MANAGEMENT
GERD ANTACIDS - neutralize acid
H2 receptor antagonist
GASTROESOPHAGEAL REFLUX DISEASE Decreases amount of HCI produced by stomach
Excessive back-flow of gastric and duodenal by blocking action of histamine on histamine
contents into the esophagus due to incompetent receptors of parietal cells in the stomach
lower esophageal sphincter Proton Pump Inhibitors
Decreases gastric acid secretion by slowing
the ATPase pump on the surface of the
parietal cells
More potent than H2 receptor antagonists
Prokinetic agents
Enhancing colonic transit by increasing
propulsive motor activity
NURSING MANAGEMENT
Teaching the patient to avoid actions that
decrease lower esophageal sphincter pressure
or cause esophageal irritation
CLINICAL MANIFESTATIONS Low fat diet
Burning sensation in the esophagus (Pyrosis) Maintain normal body weight
Dyspepsia (Indigestion) Avoid caffeine, tobacco, beer, milk, and
Dysphagia carbonated drinks, spicy foods
Hypersalivation Avoid eating/drinking 2hours before bedtime.
Esophagitis Avoid tight fitting clothes
NOTE: Elevate head of bed on 6 to 8 inches.
The symptoms may mimic those of a heart attack. Avoid lying after meals
The patient's history aids in obtaining an accurate
diagnosis. SURGICAL MANAGEMENT
Nissen Fundoplication
DIAGNOSTIC PROCEDURES Wrapping of a portion of the gastric fundus
Endoscopy or barium swallow Ambulatory 12 to around the sphincter area of the esophagus.
36 hour esophageal pH monitoring
Bilirubin Monitoring (Bilitec)
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ESOPHAGEAL DISORDER MANAGEMENT
BARRETT'S
ESOPHAGUS
Photodynamic therapy
Laser thermal ablation; destroy the metaplastic
cells
Esophagectomy
A condition in which the lining of the esophageal Total resection of the esophagus with removal
mucosa is altered. of the tumor plus a wide tumor-free margin of
Associated with GERD the esophagus and the lymph nodes the area.
Reflux causes changes in the lining of the lower
esophagus.
The cells that are laid to cover the exposed area
are no longer squamous in origin
Precursor to esophageal cancer

CLINICAL MANIFESTATIONS
Burning sensation in the esophagus (Pyrosis)
Dyspepsia (Indigestion)
Dysphagia
Hypersalivation
Esophagitis

DIAGNOSTIC PROCEDURES
Esophagogastroduodenoscopy (EGD)
Biopsy

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ESOPHAGEAL DISORDER MANAGEMENT
HIATAL
HERNIA
Same pharmacological management with GERD
Small frequent feedings
Patient is advised not to recline for 1 hour
after eating
The opening in the diaphragm through which the
esophagus passes becomes enlarged and part of Elevate head of bed
the upper stomach tends to Move up into the lower Surgery is indicated in about 15% of patients.
portion of the thorax.
SURGICAL MANAGEMENT
Nissen Fundoplication

TYPES
Sliding
Upper stomach and the gastroesophageal junction
are slide displaced upward and out of the thorax.
Paraesophageal
All or part of the stomach pushes through the
diaphragm beside the esophagus

CLINICAL MANIFESTATION
Heartburn
Regurgitation
Dysphagia
Sense of fullness after eating or chest pain

DIAGNOSTIC PROCEDURE
Xray studies
Barium swallow
Fluoroscopy
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ESOPHAGEAL DISORDER
GASTRITIS
Pain occurs 2-3 hrs Pain occurs 1⁄2 -1 hr
after meal after meals

Vomiting uncommon Vomiting common

Inflammation of the gastric mucosa
Hemorrhage less likely Hemorrhage more likely
than gastric ulcer to occur
Relieved by eating Aggravated by eating
MALIGNANCY POSSIBILITY -occasionally
-rare
RISK FACTORS
-alcohol -H. pylori
-smoking -gastritis
-stress -alcohol
-H. pylori -use of NSAID’s
-stress
CLINICAL MANIFESTATIONS
CAUSES Abdominal discomfort
Repeated exposure to irritating agents (e.g. Headache
highly seasoned foods) Lassitude
Overuse of aspirin and other non-steroidal N/V and hiccupping
anti-inflammatory drugs Excessive alcohol Heartburn after eating
intake Intolerance to spicy or fatty foods
Bile reflux Vitamin deficiency (Vit. B12)
Radiation therapy Belching
Ingestion of strong acid or alkali ASSESSMENT AND DIAGNOSTIC
Bacteria (helicobacter pylori)
Achlorhydria or hypochlorhydria (Absence or
DUODENAL ULCER GASTRIC ULCER low levels of HCI)
INCIDENCE Can be determined by an upper GI series or
-Age 30-60 -usually 50 and over endoscopy
-80% of peptic ulcers -15% of peptic ulcers Tissue specimen (Biopsy)
SIGNS, SYMPTOMS, AND CLINICAL FINDINGS
Hypersecretion of HCI Normal to hyposecretion MEDICAL MANAGEMENT
of HCI H2 blockers
May have weight gain Weight loss may occur Antibiotics (Amoxicillin, Clarithromycin)
Proton Pump Inhibitors
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SURGICAL MANAGEMENT
Gastrojejunostomy
Anastomosis of jejunum to stomach to detour
around the pylorus.

NURSING MANAGEMENT
Avoidance to gastric irritating agents
Alcohol
Spicy
Fatty foods
Aspirin
NSAID's until symptoms subside.
Discourage caffeinated beverages.
Be alert for indicator of hemorrhagic gastritis
(hematemesis, tachycardia, hypotension.)
Notify the physician if signs of hemorrhagic gastritis
are present.

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ESOPHAGEAL DISORDER
PUD
Creates a viscous substance in the presence
of gastric acid that forms a protective barrier,
binding to the surface of the ulcer, and
prevents digestion by pepsin
PEPTIC ULCER DISEASE Misoprostol, Sucralfate
Excavation that forms in the mucosa wall of the
stomach, in the pylorus, or in the duodenum. SURGICAL MANAGEMENT
Vagotomy and Pyloroplasty
Transecting nerves that stimulate acid secretion
and opening the Pylorus
Billroth I (Gastroduodenostomy)
Removal of the lower portion of the antrum of
the stomach (which contains the cells that
secrete gastrin) as well as a small portion of the
duodenum segment.
Upper portion of stomach anastomosed to
duodenum.

CAUSES Billroth II (Gastrojejunostomy)

Removal of lower portion (antrum) of stomach
Gram-negative bacteria (H. Pylori) with anastomosis to jejunum. A duodenal stump
Excessive secretion of HCL in the stomach due remains and is oversewn.
to ingestion of caffeinated beverages, spicy
foods, smoking, and alcohol
Zollinger-Ellison Syndrome
Consists of severe peptic ulcers, extreme gastric
hyperacidity, and gastrin-secreting benign or
malignant tumors.
MEDICAL MANAGEMENT
Pharmacologic Therapy
H2 Blockers (Ranitidine, Cimetidine)
NURSING MANAGEMENT
Antibiotics Stress reduction and rest
Smoking cessation
Proton Pump Inhibitors (Omeprazole)
Dietary modification
Antacid Avoidance to the food and beverages that
Cytoprotectants irritate the gastric mucosa (alcohol, coffee, milk
spicy foods, soft drinks, tea, NSAID's, Aspirin)
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ESOPHAGEAL DISORDER
DUMPING
SYNDROME
It is partially the result of rapid gastric emptying,
which prevents adequate mixing with pancreatic
and biliary secretions.
It is an unpleasant set of and GI symptoms that
sometimes occur in patients who have had
gastric surgery or a form of vagotomy.

CLINICAL MANIFESTATIONS
Symptoms occurring 30 minutes after eating
Nausea and vomiting
Feelings of abdominal fullness and
Abdominal cramping
Diarrhea
Palpitations and tachycardia
Perspiration
Weakness and dizziness
Borborygmi Sound
Steatorrhea- "fats in the stool"
MANAGEMENT
Lie down after meals
Avoid sugar, salt, and milk
Take anti-spasmodic medications as prescribed
to delay gastric emptying
Fluid intake with meals is discouraged, instead
fluids may be consumed up to 1 hour before or 1
hour after mealtime.
Meals should contain more dry items than liquid
items.
The patient can eat fat as tolerated but should
keep carbohydrate intake low and avoid
concentrated sources of carbohydrate
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INTESTINAL AND RECTAL DISORDER DIAGNOSTIC PROCEDURE
DIVERTICULAR Colonoscopy
Barium enema
DISEASE CT Scan (test of choice for diverticulitis, and
can also reveal fiber abscesses)
A sac-like herniation of the lining that of the Abdominal x-rays
bowel that extends through a defect in the
muscle layer MANAGEMENT
Most commonly occur in the sigmoid colon. Antibiotics, analgesics and anticholinergics to
reduce bowel spasms as prescribed
DIVERTICULOSIS An opioid (eg, Meperidine [Demerol]) is
Multiple diverticula are present w/o inflammation or prescribed for pain relief.
symptoms Morphine is contraindicated because it can
increase intraluminal pressure in the colon,
DIVERTICULITIS exacerbating symptoms.
Instruct the client to refrain from lifting,
Diverticulosis with inflammation straining, coughing, or bending to avoid
Results when food and bacteria retained in a increased intra-abdominal pressure
diverticulum produce infection. DIET
For diverticulosis, soft, high fiber foods are
indicated for diverticulosis.
For diverticulitis, a low fiber diet may be
necessary until signs of infection decrease.
Monitor for perforation, hemorrhage, fistulas,
and abscesses
Avoid gas forming foods
SURGICAL INTERVENTIONS
Colon resection with primary anastomosis
CLINICAL MANIFESTATIONS Temporary or permanent colostomy may be
Bowel irregularity with intervals of diarrhea required for increased bowel inflammation
Nausea and anorexia
Bloating or abdominal distention
Narrow stools
Increased constipation or at times intestinal
obstruction
Signs and symptoms of infection
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INFLAMMATORY BOWEL DISEASE
CROHN'S
DISEASE (REGIONAL ENTERITIS)
DESCRIPTION
Subacute and chronic inflammation of the GI
tract wall that extends through all layers,
(transmural lesion)
Most common in ileum and colon but can occur
anywhere along the GI tract.
Leads to thickening and scarring, a narrowed
lumen, fistulas, ulcerations, and abscesses
(Classic cobblestone appearance)

CLINICAL MANIFESTATIONS
Fever and leukocytosis
Cramp-like and colicky pain after meals
Diarrhea (Semi solid), which may contain mucus or pus
Abdominal Distention
Anorexia, nausea, and vomiting
Weight loss
Anemia
Dehydration
Electrolyte imbalances
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INFLAMMATORY BOWEL DISEASE
ULCERATIVE
Sigmoidoscopy
Barium Enema
CBC
Abdominal X-ray
COLITIS Stool Examination
Recurrent ulcerative and inflammatory disease of
the mucosal and submucosal layers of the colon MANAGEMENT
and rectum Pharmacologic Therapy
(Priority: Relieve inflammation)
Salicylate Compounds
Effective for mild or moderate inflammation and
are used to prevent or reduce Recurrences in
long-term maintenance regimens
Corticosteroids
Are used to treat severe and fulminant disease
and can be administered orally in outpatient
treatment or parenterally in hospitalized patients
RISK FACTORS Immunosuppressants
Prevalence is highest in Caucasians and Jewish Have been used to alter the immune response.
NSAIDs exacerbate IBD The exact mechanism of action of these
medications in treating IBD is unknown
CLINICAL MANIFESTATIONS Anti—diarrheal drugs
Anorexia
Weight loss Are used to minimize peristalsis to rest the
inflamed bowel. They are continued until the
Diarrhea (10 to 20 liquid stools per day) patient's stools approach normal frequency and
Malaise consistency.
Left lower quadrant abdominal NURSING INTERVENTIONS
Tenderness and cramping
Rectal Bleeding NPO status and administer fluids and electrolytes
for acute episodes
Dehydration and electrolyte imbalances Diet
Anemia and hypocalcemia Low residue
Vitamin K deficiency High protein
High calorie diet
DIAGNOSTIC PROCEDURES Supplemental vitamin therapy
Colonoscopy Iron replacement.
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 IV or via parenteral nutrition as prescribed
Monitor for bowel perforation, peritonitis, and
hemorrhage
Avoid gas-forming food

SURGICAL INTERVENTIONS
Proctocolectomy with permanent ileostomy
An ileostomy, the surgical creation of an opening
into the ileum or small intestine (usually by
means of an ileal stoma on the abdominal wall),
is commonly performed after a total colectomy
(ie, excision of the entire colon).
Continent Ileostomy (Kock ileostomy)
Creation of a continent ileal reservoir (ie, Kock
pouch) by diverting a portion of the distal ileum to
the abdominal wall and creating a stoma
Restorative Proctocolectomy
Surgical procedure of choice in cases where the
rectum can be preserved in that it eliminates the
need for a permanent ileostomy. It establishes an
ileal reservoir that functions as a "new" rectum,
and anal sphincter control of elimination is retained
Ileoanal Anastomosis (Ileorectostomy)
Involves connecting the ileum to the anal pouch
(made from a small intestine segment), and the
surgeon connects the pouch to the anus in
conjunction with removing the colon and the rectal
mucosa

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APPENDICITIS Rovsing's sign
may be elicited by palpating the left lower
quadrant; this paradoxically causes pain to be
Inflammation of the appendix felt in the right lower quadrant
Appendix
- Small, fingerlike appendage about 10 cm (4
in) long that is attached to the cecum just
below the ileocecal valve.

DIAGNOSTIC PROCEDURES
Complete blood cell count- Increase WBC
Abdominal x-ray films
Ultrasound studies
CT scans- right lower quadrant density
RISK FACTORS Pregnancy test- to rule out ectopic pregnancy
Between the ages of 10 and 30 years
COMPLICATIONS
CAUSES Perforation of the appendix
Kinked or occluded by a fecalith Peritonitis
Tumor Abscess formation (collection of purulent
Foreign body material)
Portal pylephlebitis- septic thrombosis of the
CLINICAL MANIFESTATIONS portal vein caused by vegetative emboli that
Vague epigastric or periumbilical pain Right arise from septic intestines
lower quadrant pain (ie, parietal pain that is
sharp, discrete, and well localized) PHARMACOLOGIC MANAGEMENT
Low-grade fever
Nausea and Vomiting IV fluids are administered
Loss of appetite Antibiotic therapy to prevent infection
Rebound tenderness (ie, production or
intensification of pain when pressure is Morphine sulfate: prescribed to relieve pain.
released)
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SURGICAL MANAGEMENT
Appendectomy
(ie, surgical removal of the appendix) is performed
as soon as possible to decrease the risk of
perforation
Low abdominal incision (laparotomy)
Laparoscopy
Perforation- place a drain in the abscess

NURSING MANAGEMENT
Post-operatively, the nurse places patient in a
high- Fowler's position.
Reduces the tension on the incision and
abdominal organs, helping to reduce
DISCHARGED TEACHINGS
Have the surgeon remove the sutures between
the 5th and 7th days after surgery.
Incision care
Heavy lifting is to be avoided postoperatively
Normal activity can usually be resumed within 2 to
4 weeks.

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HEMORRHOIDS PHARMACOLOGIC MANAGEMENT
Hydrophilic bulk-forming agents (Psyllium)
Dilated portions of veins in the anal canal. Analgesic ointments and suppositories
Astringents (eg, witch hazel)
CAUSES
50 years of age NON-SURGICAL AND SURGICAL MANAGEMENT
Shearing of the mucosa during defecation Infrared photocoagulation
Increased pressure in the hemorrhoidal Bipolar diathermy
tissue due to pregnancy Laser therapy
Injection of sclerosing agents
TYPES Rubber-band ligation procedure
Internal hemorrhoids Cryosurgical hemorrhoidectomy
Above the internal sphincter Hemorrhoidectomy
External hemorrhoids NURSING MANAGEMENT
Appearing outside the external sphincter
Good personal hygiene
Avoiding excessive straining during defecation
High-residue diet that contains fruit and bran
Increase fluid intake
Warm compresses/Sitz baths
Bed rest

CLINICAL MANIFESTATIONS
Itching
Pain
Bright red bleeding
External hemorrhoids severe pain from the
inflammation and edema caused by thrombosis
Internal hemorrhoids are not usually painful until
they bleed or prolapse when they become
enlarged.
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HEPATOBILIARY PANCREAS
SYSTEM A slender, fish-shaped organ, that lies
horizontally in the abdomen behind the stomach
and extends roughly from the duodenum to the
spleen
Endocrine and exocrine functions Has
pancreatic juice:
Amylase
Lipase
Trypsin

LIVER
Largest gland of the body
Divided into four lobes
Left
Right
Caudate
Quadrate
Contains several cell types, including
hepatocytes and Kupffer's cells
Regulating blood glucose level by
Making glycogen, which is stored in hepatocytes
Converting ammonia produced from
gluconeogeneticby- products and bacteria to
urea

GALLBLADDER
Pear-shaped organ attached to the liver under
the right lobe.
Normally holds 30-50m1 of bile and can hold up
to 70 ml when fully distended

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HEPATITIS Post- Icteric Stage
Convalescent stage lasting a few weeks
Inflammatory disorder of the liver parenchyma Fatigue decreases
Occurring in Hepatitis A, B, C, D, E, and toxic or Appetite returns
drug-induced hepatitis
Hepatocellular damage results from the body's VIRAL HEPATITIS
immune response to the virus or toxin and is
characterized by diffuse inflammatory infiltration Hepatitis A
with local necrosis Mode of transmission: Fecal-oral route
Incubation: In: 15-50 days
Outcome: Usually mild with recovery

Hepatitis B
Mode of transmission: Parenterally;
perinatal: sexual
Incubation: In: 28-160 days
CLINICAL MANIFESTATIONS Outcome: May be severe
Pre-Icteric Stage Hepatitis C
Earliest symptoms are not specific
Flu-like symptoms Mode of transmission:
Malaise Blood transfusion: sexual transmission
Fatigue Incubation: In: 15-160 days
Headache Outcome:
Myalgias Frequent occurrence of chronic hepatic cancer
Anorexia carrier state and chronic liver disease.
Nausea & vomiting
Diarrhea Hepatitis D
Icteric Stage Mode of transmission: Same as HBV
Few days to weeks after pre-icteric stage Incubation: In: 21-140 days
Jaundice
Dark-colored urine Outcome:
Light-colored stool Similar to HBV but greater likelihood of carrier
Steatorrhea state
Enlarged liver
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Hepatitis D
Mode of transmission: Fecal-oral route
Incubation: In: 15 to 65 days
Outcome:
Similar to HAV except very severe in pregnant
women

DIAGNOSTIC PROCEDURES
Liver function test results are elevated
Serum bilirubin level is increased
Urinalysis reveals increased bilirubin levels

MANAGEMENT
Administer prescribed medications, which may
include:
Immunoglobulins
Immunizations
Antiviral
Prevent transmission of infection
Promote adequate rest without complications
Encourage proper nutrition

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LIVER
CIRRHOSIS
LABORATORY AND DIAGNOSTIC FINDINGS
Liver biopsy
Liver Scan
DESCRIPTION Liver function test (ALT, AST)
Serum protein levels
Chronic liver disease marked by diffuse destruction Prothrombin time
and fibrotic regeneration of hepatic cells
MANAGEMENT
Administer diuretics to decrease ascites.
Promote adequate nutrition (Vitamins and
nutritional supplements promote healing of
damaged liver cells.)
Prevent threats to skin integrity
Minimize risk of bleeding
CLASSIFICATIONS Antacid/ H2 antagonist to minimize possibility
Laennec’s Cirrhosis of GI bleeding
Commonly caused by alcoholism and Limit visitors, and orient the client to date, time,
Chronic nutritional deficiencies and place
Biliary cirrhosis Avoid drinking alcoholic beverages Institute
safety measures, such as raising side rails and
Caused by bile duct disorders that suppress bile assisting with ambulation
flow
Post- hepatic cirrhosis DIET
Caused by various types of hepatitis Early Phase:
High protein diet- to promote healing of the liver
CLINICAL MANIFESTATION Late Phase:
Enlarged, firm liver Low protein diet- to decrease ammonia levels
Chronic dyspepsia
Constipation or diarrhea
Gradual weight loss
Ascites
Splenomegaly
Spider telangiectasis
Caput Medusae
Dilated abdominal blood vessels
Portal Hypertension
Mental deterioration
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PORTAL
HYPERTENSION
DESCRIPTION
Elevated pressure in the portal vein associated with
increased resistance to blood flow through the
portal venous system
Obstruction of portal venous flow through the liver
lead to: Enlarged, palpable spleen
Formation of esophageal, and hemorrhoidal Fluid and electrolyte imbalance
varicosities due to
Increased venous pressure
Accumulation of fluid in the abdominal cavity MANAGEMENT
Bed rest
Administering medications which may include
diuretics
Measure & record abdominal girth & body
weight daily
Promote measures to prevent or reduce edema
Assist the health care provider with
paracentesis
Monitor serum ammonia and electrolyte levels.

MNEMONIC!
ABCDE
CLINICAL MANIFESTATION
Ascites
A scites
Rapid weight gain
Shortness of breathing
B leeding; hematomesis/piles
Fluid wave on abdominal percussion
Liver dullness
C aput medusae
Dilated abdominal vessels radiating from D iminished liver (atrophy)
umbilicus (caput medusa)
E nlarged spleen (spleenomegaly)
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ESOPHAGEAL Provide nursing care for the client undergoing

VARICES prescribed tamponade to control bleeding

balloon
Sengstaken-Blakemore Tube
DESCRIPTION Four openings:
Hemorrhagic process involving dilated, tortuous Gastric aspirations
veins in the submucosa of the lower esophagus Esophageal aspiration
Caused by portal hypertension Gastric balloon inflation
Esophageal balloon inflation

CLINICAL MANIFESTATIONS
Hematemesis and melena
Massive hemorrhage occurs
Signs of hepatic encephalopathy
Dilated abdominal veins
Ascites Instrument at the bedside- Scissors (Cut the
History of Alcohol Abuse tube in case of respiratory distress.)
The patient being treated with balloon
DIAGNOSTICS tamponade must remain under close observation
in the ICU because of the risk of serious take
Endoscopy complications. Precautions must be taken to
Lab. Tests: ALT, AST, Bilirubin (increased) ensure that the patient not pull on or
Portal Hypertension Measurements inadvertently displace the tube.

MANAGEMENT Vasopressin
initial mode of therapy
Assess for ecchymosis, epistaxis, petechiae,
and bleeding gums Sclerotherapy
Monitor level of consciousness, vital signs, and After treatment for acute hemorrhage, the
urinary output to evaluate fluid balance patient must be observed for bleeding,
perforation of the esophagus, aspiration
Monitor the client during blood transfusion pneumonia, and esophageal stricture
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 Variceal Band Ligation
A modified endoscope loaded with an elastic
rubber band is passed through a band directly
onto the varix (or varices) to be banded.
Complications:
Superficial ulceration
Dysphagia
Transient chest discomfort
Esophageal strictures

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HEPATIC The patient is asked to hold the arm out with
ENCEPHALOPATHY the hand held upward (dorsiflexed). Within a
few seconds, the hand falls forward
involuntarily and then quickly returns to the
DESCRIPTION dorsiflexed position.
Neurologic syndrome that develops as a complication
of liver disease
It may be acute and self –limiting and progressing or
chronic
Incidence is similar to cirrhosis
DUE TO: Fetor hepaticus
Severe liver damage A sweet, slightly fecal odor to the breath that
Hepatocellular failure is presumed to be of intestinal origin,
Increased serum ammonia levels from: Constructional Apraxia
GI bleeding Deterioration of handwriting and inability to
High-protein diet draw a simple star figure occurs with
Bacterial growth in the intestine Uremia progressive hepatic encephalopathy.
Serum ammonia level is elevated
PATHOPHYSIOLOGY Serum bilirubin level is elevated
Prothrombin time is prolonged

MANAGEMENT
Administer prescribed medications which may
include laxatives (Lactulose)
Ammonia is kept in the ionized state,
resulting in a decrease in colon pH
Evacuation of the bowel takes place, which
decreases the ammonia absorbed from the
colon
The fecal flora are changed to organisms
CLINICAL MANIFESTATIONS that do not produce ammonia from urea
Neurological dysfunction progressing from minor Administer antibiotics (Neomycin)
mental aberrations and motor disturbances to Reduce levels of ammonia-forming bacteria
coma in the colon
Closely monitor neurologic status for any
Flapping tremors/Liver flap (Asterixis) changes
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Evaluate serum ammonia values daily
Monitor for signs of impending coma.
Reduce or eliminate the client's dietary
protein intake if you detect evidence of
impending coma.
Monitor the client closely, and administer a
conservative dose of prescribed sedative or
analgesic medication, because liver damage
alters drug metabolism.

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GALLBLADDER CAUSES
DISORDERS Obstruction of the cystic duct by impacted
gallstone
RISK FACTORS Tissue damage due to trauma, massive burns,
Obesity or surgery
Women especially who have had Gram-negative septicemia
Overuse of opioid analgesics
Multiple pregnancies or who are of Native
American or U.S. Southwestern Hispanic Ethnicity
Frequent changes on weight
CLINICAL MANIFESTATIONS
Cholelithiasis
Rapid weight loss
Episodic, cramping pain in the RUQ of the
High dose estrogen abdomen or the epigastrium, possibly
Ileal resection or disease radiating to the back near the right scapular
Cystic Fibrosis tip
Diabetes mellitus Nausea and vomiting
Fat intolerance
Cholelithiasis Fever and leukocytosis
Formation of calculi in the gallbladder Jaundice
Epigastric distress
CAUSES Cholecystitis
Result from changes in bile components or bile
stasis, which may be associated with such Biliary colic
factors as infection, cirrhosis, and pancreatitis Tenderness and rigidity in the RUQ elicited on
palpation
Cholecystitis Murphy’s Sign
Acute or chronic inflammation of the gallbladder Pain on taking a deep breath when the
examiner's fingers are on the approximate
location of the gallbladder.

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 Fever Stones in the gallbladder or common bile duct may
Nausea and vomiting be fragmented by means of laser pulse technology
Fat intolerance Extracorporeal Shockwave Lithotripsy
Heart burn Non-invasive procedure; uses repeated shock
Flatulence waves directed at the gallstones in the gallbladder
Vitamin deficiency or common bile duct to fragment the stones.
DIAGNOSTIC TESTS Surgical Approach
Laparoscopic Cholecystectomy
Abdominal X-ray
Ultrasonography Performed through a small incision or puncture
made through the abdominal wall at the umbilicus
diagnostic procedure of choice
Cholescintigraphy
radioactive agent is administered intravenously
Cholecystography
iodide containing contrast agent is administered
before xray
Endoscopic Retrograde
Permits direct visualization of structures that
previously could be seen only during laparotomy
A fiberoptic duodenoscope, with side-viewing
apparatus is inserted into the duodenum. The Cholecystectomy
ampulla of Vater is catheterized, and the biliary Gall bladder is removed through an abdominal
tree is injected with contrast agent incision after the cystic duct and artery are
ligated.
MANAGEMENT A drain is placed close to the gall bladder if
Pharmacologic Management there is a bile leak, removed after 24 hours
Ursodeoxycholic acid (UDCA [URSO, Actigall]) - Bile duct injury-serious complication
dissolve small radiolucent gall stone Choledochostomy
Administer prescribed medication, which may
include analgesic {morphine sulfate} and antacids Making an incision in the common bile duct for
removal of stones.
Nutritional therapy
Maintaining skin integrity and Promoting
Low-fat liquids Biliary Drainage
High in protein and carbohydrates
If bile is not draining properly, an obstruction
Non-surgical Approach is probably causing the bile to be forced back
Intra-corporeal Lithotripsy into the liver or bloodstream

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Every 24 hours, the nurse measures the bile collected
and records the amount, color and character of
drainage.
After several days of drainage, the tube may be
clamped for 1 hour before and after each meal to
deliver bile to the duodenum to aid in digestion
Within 7 to 14 days, the drainage tube is removed.

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ACUTE Turner's sign
PANCREATITIS Discoloration lateral of the trunk or posteriorly

DESCRIPTION
Self- digestion of the pancreas by its own
proteolytic enzymes, principally trypsin
Inflammation of the pancreas ranging from a
relative mild, self-limiting disorder to rapidly fatal,
acute hemorrhagic pancreatitis
Cause: DIAGNOSTIC TESTS
Alcoholism Elevated amylase
Cholecystitis Lipase
Surgery involving or near the pancreas
Increase WBC Levels
CLINICAL MANIFESTATIONS Hypocalcemia
Abdominal Tenderness with back pain MANAGEMENT
GI problems, such as nausea, vomiting, diarrhea, Administer prescribed medications, which
and steatorrhea include opioid or non-opioid analgesics
Fever histamine receptor antagonist
Jaundice proton pump inhibitors
Mental confusion Drug of Choice for pain: Morphine sulfate
Flank or umbilical bruising The client should avoid oral intake to inhibit
pancreatic stimulation and secretion of
Hypotension pancreatic enzymes
Signs of hypovolemia Maintain fluid and electrolyte balance
Internal bleeding: Promote adequate nutrition
Cullen's sign
Bluish discoloration around the umbilicus

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CHRONIC ASSESSMENT AND DIAGNOSTICS
PANCREATITIS Serum lipase and amylase elevated
WBC elevated
DESCRIPTION Endoscopic retrograde
Cholangiopancreatography
Progressive pancreatic inflammation resulting in Detects pancreatic calcification
permanent structural damage to pancreatic tissue Glucose tolerance test values are abnormal
Results from repeated episodes of acute
pancreatitis MANAGEMENT
More than half of chronic pancreatitis cases are Administer prescribed medications, which
associated with alcoholism include pancreatic enzymes,
Long term alcohol consumption causes Non-opioid pain medications, antacids,
hypersecretion of protein in pancreatic secretions, histamine receptor antagonist, and proton-
resulting in protein plugs and calculi within the pump inhibitors
pancreatic ducts. Provide symptomatic treatment focusing on
relieving pain, promoting comfort, and treating
new attacks
Emphasize the importance of avoiding alcohol,
caffeine, and foods that tend to cause
abdominal discomfort
Manage any endocrine insufficiency such as
Diabetes Mellitus, by initiating dietary and
insulin or oral hypoglycemic therapy.

SURGICAL MANAGEMENT
Pancreatic jejunostomy (Roux-en-Y)
Joining of the pancreatic duct to the jejunum.
Allows drainage of the pancreatic duct to the
CLINICAL MANIFESTATIONS jejunum.
Recurring attacks of severe upper abdominal A Whipple resection (pancreaticoduodenectomy)
and back pain
Weight loss Can be carried out to relieve the pain of
chronic pancreatitis
Steatorrhea
Stools become frequent, frothy, and foul-smelling
because of impaired fat digestion, which results
in stools with a high fat content
Anorexia

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PERITONITIS Anorexia
Nausea and vomiting
Pyrexia
DESCRIPTION Increased pulse rate
Inflammation of the peritoneum, the serous membrane
lining the abdominal cavity and covering the viscera. DIAGNOSTIC FINDINGS
Increase WBC
Altered levels of Potassium, Sodium and Chloride
Abdominal Xray- distended bowel loops

MANAGEMENT
Fluid, colloid, replacement
Analgesics are prescribed for pain
Antiemetics
Intestinal intubation and suction
Relieves abdominal distention and promotes
intestinal function
CAUSE Oxygen therapy by nasal cannula or mask
Antibiotic therapy
Bacterial infection
Injury or trauma SURGICAL MANAGEMENT
Inflammation that extends from an organ outside Removing the infected area
the peritoneal area Excision (ie, appendix)
Appendicitis Resection (ie, intestine)
Perforated ulcer Correcting the cause
Diverticulitis Repair (ie, perforation)
Bowel perforation Drainage (ie, abscess).
Abdominal surgical procedures
Peritoneal dialysis NURSING MANAGEMENT
Positioning the patient for comfort are helpful
CLINICAL MANIFESTATIONS in decreasing pain
Diffuse pain, becomes constant localized and more Patient is placed on the side with knees
intense on the site of maximal peritoneal irritation flexed- decreases tension on the abdominal
Muscles become rigid and tender organs
Rebound tenderness Drains are frequently inserted during the
surgical procedure.
Paralytic ileus
Prevent dislodging of the drain
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