NOTE: PLEASE USE YOUR MS BOOK FOR A THOROUGH UNDERSTANDING

ABOUT THE DISEASES.

Gallbladder & biliary tract disorders

I. Gallbladder
a. Storage depot for bile
b. 30 to 50ml of bile.
II. Definition of Terms:
CHOLELITHIASIS – presence of gallstones in the gallbladder.
BILIARY COLIC - pain caused by the obstruction in the cystic duct.
CHOLECYSTITIS – Acute or chronic inflammation of the gallbladder, most
commonly associated with gallstones.
CHOLEDOCHOLITHIASIS – presence of gallstones in the common bile duct.
CHOLANGITIS – inflammation of the biliary tract.
III. Incidence
a. Most often occurs :in women after age 40
In postmenopausal women on estrogen therapy
In women taking oral contraceptives
In the obese
b. Most often occurs :
Caucasians
Hispanic
Native Americans
IV. Predisposing Factors:
a. High-fat diet
b. Advancing age
c. Genetics
V. Signs/symptoms
a. Acute cholecystitis, cholelithiasis, choledocholithiasis
The classic attack with severe midepigastric or RUQ pain – shoulder
(Collins's sign)
Recurring fat intolerance
Dyspepsia- Bloating, Belching
Nausea
Chills and low-grade fever
Possible jaundice
Clay-colored stools
Steatorrhea
Dark amber urine
b. Cholangitis
Abdominal pain
High fever and chills
Possible jaundice and related itching
Weakness and fatigue
c. Cholecystitis
Murphy’s sign –tenderness over the right upper quadrant that increases
on inspiration.
d. Diagnostic Test Findings
e. Elevated WBC
f. Elevated alkaline phosphatase level - are evidence for common bile duct
obstruction.

VI. Diagnostic Test Findings

a. Elevated amylase level - distinguish GBD from pancreatitis
 b. Elevated total bilirubin
c. Urine bilirubin
d. Elevated lipase - is indicative of pancreatitis, the most common causes of
which are alcohol and gallstones.
e. Cholangiogram – stones in the biliary tree.
f. Gallbladder series – stones in the biliary tree
g. Ultrasonography – bile duct distention and calculi
h. Cholescintigraphy – detects obstruction of the cystic duct.
i. Oral Cholecystography – shows calculi in the gallbladder and biliary
obstruction
j. Endoscopic Retrograde Cholangiopancrea-tography (ERCP) – to visualize
biliary structures and pancreas via endoscopy
k. Percutaneous transhepatic cholangiography – calculi in the ducts.
VII. Management
a. Surgery, elective
b. Low-fat diet
c. Ursodiol(Actigall)
d. Antibiotics: Ampicillin/Sulbactam(Unasyn), Levofloxacin(Levaquin)
e. ESWL
f. Endoscopic Sphincterotomy
g. GALLBLADDER SURGERY
Cholecystectomy
VIII. Nursing management
a. Maintain the patient’s diet; withhold food and fluids as ordered.
b. Administer IV fluids as ordered
c. Encourage turning, coughing, deep breathing and incentive spirometry
d. Assess pain level, administer analgesic as prescribed, and evaluate effect.
e. Place the patient in semi-Fowler’s position.
f. Monitor and record vital signs, I/O, laboratory studies, and pulse oximetry
g. Administer medications as prescribed.
h. Provide preoperative and postoperative care.
i. Allay the patient’s anxiety and provide emotional support.
j. Provide skin, nares and mouth care.
k. Have the patient ambulate as tolerated
l. Maintain a quiet environment.
m. Individualize home care instructions.
a. Knowledge
b. Medications
c. Complete skin care daily
d. Recognize the signs and symptoms of renal colic.
PANCREATITIS

HEPATIC DISORDERS
LIVER
• Largest internal organ in the body
• Weighs between 1200 and 1500g and divided into four lobes.
• A thin layer surrounds each lobe extending into the lobe itself and dividing the
liver mass into small, functional units – lobules.
• Produces bile(main function), which emulsifies fats and stimulates peristalsis.
• Conveys bile from the gallbladder, where it’s stored, until it enters the duodenum
at Oddi’s sphincter through the common bile duct.
• Metabolizes carbohydrates, fats and proteins
• Synthesizes coagulation factors VII, IX, X and prothrombin
• Stores fat-soluble vitamins A, D, E, K, B12, copper and iron
• Detoxifies chemicals (such as drugs)
• Excretes bilirubin
• Obtains dual blood supply from the portal vein and hepatic artery
• Produces and stores glycogen
• Promotes eythropoiesis when bone marrow production is insufficient.

Functions
• Glucose Metabolism
• Ammonia conversion
• Protein metabolism
• Functions
• Fat metabolism
• Vitamin and iron storage
• Bile formation
• Drug metabolism

CIRRHOSIS
GENERAL INFORMATION
• Chronic, progressive, inflammation, fibrosis, and degeneration of the liver
parenchymal cells.

Incidence
• Occurs twice as often in men as in women; ages 40-60

Types
 • Laennec’s cirrhosis
– most common form of cirrhosis
– Fibrosis occurs mainly around central veins and portal areas.
– results from chronic alcoholism and malnutrition.
• Post necrotic cirrhosis
– Consist of broad bands of scar tissue
– results from previous acute viral hepatitis or drug-induced massive hepatic
necrosis.

• Biliary Cirrhosis
– Consist of scarring of bile ducts and lobes of the liver and results from
chronic biliary obstruction and infection (cholangitis), and is much rarer
than the preceding forms.
Pathophysiology
Type and Disease Name Causal Mechanism Pathophysiology

Alcoholic Cirrhosis, Laennec Toxic effects of chronic, Fatty liver, inflammation

Cirrhosis, Portal Cirrhosis excessive alcohol intake (alcoholic hepatitis) and
derangement of the lobular
architecture by necrosis
and fibrosis (cirrhosis)
Biliary Cirrhosis (intra- Unknown, possibly an auto- Inflammation and scarring
hepatic or extra hepatic immune mechanism of lobular bile ducts
obstruction of bile flow),
Primary Biliary Cirrhosis
Secondary Biliary Cirrhosis Obstruction by neoplasms, Inflammation and scarring
strictures or gallstones of bile ducts proximal to
the obstruction.
Post-necrotic Cirrhosis Viral hepatitis caused by Replacement of necrotic
HBV, or HCV; drugs or tissue with cirrhosis tissue,
toxins; autoimune particularly fibrous, nodular
destruction scar tissue.
Metabolic Cirrhosis Metabolic defects and Inflammation and scarring
storage disease with specific morphologic
changes related to cause

ASSESSMENT FINDINGS
• Early complaints
– fatigue,
– anorexia,
– edema of the ankles in the evening,
– epistaxis,
– bleeding gums,
– weight loss.
• In later disease:
– Chronic dyspepsia, constipation and diarrhea.
– dilated cutaneous veins around umbilicus (caput medusa); internal
hemorrhoids, ascites, splenomegaly.
– Fatigue, weakness, and wasting caused by anemia and poor nutrition.
– Deterioration of mental function.
– Estrogen-androgen imbalance causing spider angioma and palmar
erythema(reddened palms); menstrual irregularities in women; testicular
and prostatic atrophy, gynecomastia, loss of libido, and impotence in men.
– Bleeding tendencies and hemorrhage.
Compensated S/S: usually found secondary to routine physical examination; vague
symptoms
– Intermittent mild fever
– Vascular spiders
– Palmar erythema
– Unexplained epistaxis
– Ankle edema
– Vague morning indigestion
– Flatulent dyspepsia
– Abdominal pain
– Firm, enlarged liver
– splenomegaly

Decompensated S/S: symptoms of decreased proteins, clotting factors, and other

substances and of portal hypertension
– Ascites
– Jaundice
– Weakness
– Muscle wasting
– Weight loss
– Continuous mild fever
– Clubbing of fingers
– purpura
– Spontaneous bruising
– Epistaxis
– Hypotension
– Sparse body hair
– White nails
– Gonadal atrophy

See Table 39-5 Modified Child-Pugh Classification of the Severity of Liver Disease
• Parameters: ascites, bilirubin, albumin, prothrombin time, encephalopathy
• Points assigned for each parameter.

Diagnostic Tests
• Elevated serum liver enzyme levels, reduced serum albumin.
• Liver biopsy detects cell destruction and fibrosis of hepatic disease.
• Liver scan
– shows abnormal thickening and a liver mass.
• Serum aninotransferases (transaminases)
• Alanine aminotransferase(ALT)
• Aspartate aminotransferase(AST)
• Gamma-glutamyl transferase(GGT) or G-glutamyl transpeptidase
• CT scan
– determines the size of the liver and its irregular nodular surface.
• Percutaneous transhepatic cholangiography differentiates extrahepatic from
intrahepatic obstructive jaundice.
• Paracentesis
– examines ascitic fluid for cell, protein, and bacteria counts.

Pharmacologic Interventions
• Provide asymptomatic relief measures such as pain medications and antiemetics.
• Diuretic therapy, frequently with spironolactone, a potassium-sparing diuretic
 – inhibits the action of aldosterone on the kidneys.
• I.V albumin
– maintain osmotic pressure and reduce ascites.
• Administration of lactulose or neomycin through a nasogastric tube or retention
enema to reduce ammonia levels during periods of hepatic encephalopathy.

Surgical Intervention:
• Transjugular intrahepatic portosystemic shunt (TIPS)
– This approach uses a catheter (a thin tube) that is inserted in the jugular
vein in the neck and threaded through the hepatic vein (which leads to
the liver). A needle is passed through the tube, and a suction device
collects liver samples.
– liver transplantation
Nursing Diagnosis
• Activity intolerance
• Imbalanced nutrition: Less than body requirements
• Impaired skin integrity
• Risk for Injury and bleeding

Planning
• Independence in activities
• Improved nutritional status
• Improved skin integrity
• Decreased potential for injury
• Improved mental status
• Absence of complications

Nursing Interventions:
• Provision of rest
– Position bed for maximal respiratory efficiency
– Initiate efforts to prevent respiratory, circulatory, and vascular
disturbances
– Encourage pt. to increase activity gradually and plan rest with activity and
mild exercise.
• Improving nutritional status
– Nutritious, high protein with B-complex vitamins and others, A,C, K and
folic acid –if no indication of impending coma
– Small frequent meals, protein supplements if indicated
– Provide nutrients by feeding tube or TPN
– Water-soluble forms of fat-soluble vitamins A, D, E (pts with steatorrhea);
folic/iron(anemia)
– Low protein diet (if with signs of impending coma)
• Providing Skin Care
– Change position frequently.
– Avoid using irritating soaps and adhesive tape.
– Provide lotion to soothe irritated skin.
• Reducing Risk of Injury
– Use padded side rails
– Orient to time, place, and procedures
– Instruct pt. to ask for assistance to get out of bed.
– Provide safety measures to prevent cuts, injury
– Apply pressure to venipuncture sites to minimize bleeding.
• Monitoring and managing complications
– Primary concern:
 • Prevent bleeding – due to decreased production of prothrombin
• monitoring for hepatic encephalopathy.
– Observe for melena, check stools for blood
– Take precautionary measures(use padded side rails, avoid sharp objects)
– Use appropriate dietary modification and stool softeners.
– Monitor for GI bleeding
– Keep equipment to treat hemorrhage; IV fluids, medications
– Monitor closely to identify early evidence of condition.
• Promoting home and community-based care
– Sodium restriction
– Provide written instructions
– Encourage rest
– Instruct family about symptoms of impending complications/bleeding
tendencies.
– Assess
• bowel sounds,
• increasing abdominal girth,
• pain,
• nausea and vomiting,
• electrolyte imbalance.
Other Nursing Care:
• If patient has a chronic circulatory problem, provide small, frequent feedings of
light, bland foods.
• Observe stools and emesis for color, consistency, and amount, and test each one
for occult blood.
• Monitor fluid intake and output and serum electrolyte levels to prevent
dehydration and hypokalemia, which may precipitate hepatic encephalopathy.
• Maintain some periods of rest with legs elevated to mobilize edema and ascites.
Alternate rest periods with ambulation.
• Encourage and assist with gradually increasing periods of exercise.
• Encourage the patient to eat high-calorie, moderate protein meals and
supplementary feedings. Suggest small, frequent feedings.
• Encourage oral hygiene before meals.
• Administer or teach self-administration of medications for nausea, vomiting,
diarrhea or constipation.
• Encourage frequent skin care, bathing with soap, and massage with emollient
lotions.
• Keep the patient’s finger nails short to prevent scratching from pruritus.
• Keep the patient quiet and limit activity if signs of bleeding are evident.
• Encourage the patient to eat foods high vitamin C content.
• Protect from sepsis through good handwashing and prompt recognition and
management of infection.
• Pad side rails and provide careful nursing surveillance to ensure the patient’s
safety.
• Stress the importance of giving up alcohol completely.
• Involve the person closest to the patient, because recovery usually is not easy
and relapses are common.

Common Symptoms and Signs Due to Complications of Cirrhosis

PORTAL HYPERTENSION
• is an increase in the blood pressure within a system of veins called the portal
venous system.
 CAUSES
• blood clots in the portal vein
• blockages of the veins that carry the blood from the liver to the heart
• a parasitic infection called schistosomiasis.

S/S:
• Gastrointestinal bleeding : Black, tarry stools or blood in the stools; or vomiting
of blood due to the spontaneous rupture and hemorrhage from varices
• Ascites (an accumulation of fluid in the abdomen)
• Encephalopathy or confusion and forgetfulness caused by poor liver function
• Reduced levels of platelets, structures that help form blood clots, or white blood
cells, the cells that fight infection.

ASCITES
Definition
• Accumulation of fluid in the peritoneal cavity.
• Cirrhosis is the most common cause of ascites.

Signs and Symptoms

• Weight gain
• Abdominal distention
• Increased abdominal girth
• Dyspnea
• If with b. peritonitis(10%):
– Fever
– Chills
– Abdominal pain
– Decreased bowel sounds
– Cloudy ascitic fluid
Diagnostic Tests
• Paracentesis
– Aspiration
– Biochemical analysis
– Microscopic examination
Nursing Management
• Assess and monitor I & O.
• Assess abdominal girth
• Assess daily weight
• Monitor serum ammonia and electrolyte levels
• Promote home and community based care
– Alcohol intake
– Low-sodium intake
– Take medications as prescribed
– Skin care
– Weight monitoring
– Watch out for (WOF) s/s of complications
Management
• Dietary salt restriction
• Potassium-sparing diuretics
• Serum electrolytes monitoring
Hepatic encephalopathy
• Frequent terminal complication in liver disease
• Diseased liver is unable to convert ammonia to urea
Causes:
 • Cirrhosis
• GI hemorrhage
• Hyperbilirubinemia
• Transfusions
• Thiazide diuretics
• Uremia
• dehydration

Assessment Findings
• Early in the course of disease
– Changes in mental functioning(irritability)
– Insomnia
– Slowed affect
– Slow slurred speech
– Impaired judgement
– Slight tremor
– Babinski’s reflex
– Hyperactive reflexes
• Progressive disease
– Asterixis
– Disorientation
– Apraxia
– Tremors
– Fetor hepaticus
– Facial grimacing
• Late in disease:
– COMA, ABSENT REFLEXES

West Haven Criteria

– The severity of hepatic encephalopathy is graded with the West Haven
Criteria; this is based on the level of impairment of autonomy, changes in
consciousness, intellectual function, behavior, and the dependence on
therapy.
• Grade 1 - Trivial lack of awareness; euphoria or anxiety; shortened attention
span; impaired performance of addition or subtraction
• Grade 2 - Lethargy or apathy; minimal disorientation for time or place; subtle
personality change; inappropriate behaviour
• Grade 3 - somnolence to semistupor, but responsive to verbal stimuli; confusion;
gross disorientation
• Grade 4 - coma(unresponsive to verbal or noxious stimuli)

Diagnostic tests
• Increased serum ammonia levels
• PT prolonged
• Hgb and hct decreased
Nursing Interventions
• Conduct ongoing neurologic assessment and report deteriorations
• Restrict protein in diet; provide carbohydrate intake and Vitamin K supplements
• Administer enemas, cathartics, intestinal antibiotics and lactulose as ordered
– Reduces ammonia level
• Protect client from injury: keep side rails up; provide eye care with use of
artificial tears/eye patch.
• Avoid administration of drugs detoxified in liver
• Maintain client on bed rest to decrease metabolic demands on liver.