Slide 1

Report
Nursing Care and
Interventions with Diseases
of the Liver, Gallbladder
& Pancreas
Keith Rischer RN, MA, CEN
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Today’s Objectives…
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Review pathophysiology and systemic manifestations of the
inflammatory response.
Compare and contrast pathophysiology & manifestations of
diseases of the liver, pancreas and gallbladder.
Interpret abnormal laboratory test indicators of liver, pancreatic
and gallbladder function.
Identify the diagnostic tests, nursing priorities, and client
education with diseases of the liver, pancreas and gallbladder.
Analyze assessment data from clients with cirrhosis to determine
nursing diagnoses and formulate a plan of care for clients with
diseases of the liver, pancreas and gallbladder.
Prioritize assessment based nursing care for clients experiencing
chronic pancreatic or gall bladder disease.
Integrate nutrition therapy in care of clients with hepatic,
pancreatic or gallbladder disease.
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Inflammatory Response
Occurs in response
to injury
 Localized
 Immediate
 Beneficial
 Appropriate level of
response
 Non Specific
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What is a Mast Cell?
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Bag of Granules
Located in connective tissue
• close to blood vessels
Histamine released
• Increase blood flow
• Increase vascular permeability
• Binds to H1, H2 receptors
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Causes
Bacteria-viral
 Trauma
 Lacerations
 Allergic response
 Bites
 Burns
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Purpose of inflammation
Neutralizes and Dilutes Toxins
 Removes necrotic materials
 Provides an environment for healing
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Systemic Manifestations of Acute
Inflammation
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Fever/chills
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Benefits
 Increased
killing of microorganisms
 Increased phagocytosis by neutrophils
 Increased activity of interferon
Leukocytosis
 Plasma Proteins
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Patho Review
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Liver
• Produces bile…elimination of bilirubin
• Drug/hormone metabolism
• CHO-fat-protein metabolism
• Clotting factor synthesis
• Storage of vitamins & minerals
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Gallbladder
• Store & concentrate bile
Pancreas
• Endocrine
• Exocrine
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Hepatitis
Definition:
 Inflammation of the
Liver
Causes:
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Viral (most common)
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Toxic
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A, B, C, D, E
Amiodorone, Tylenol,
statins
Alcohol
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Hepatitis A
THINK FECAL-ORAL
Etiology: Hepatitis A Virus
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Incubation period: 15-50 days
Duration: 60 days
Young children asymptomatic
No chronic carrier…virus in feces during incubation pd. Before sx
apparent
Transmission:
Fecal-Oral
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Outbreaks occur by contaminated food/drinking water
Male homosexuals
Poor hygiene, improper handling of food, poor sanitary conditions
HAV found in feces 2 or more weeks before onset of sx and up to
10
one week after onset of jaundice
Hepatitis A: Prevention
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Good hygiene
Water treatment
Hepatitis A vaccine
 booster
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6-12 mos after first dose
Immunoglobulin before exposure or within 2
weeks after exposure
 protects
about 2 months
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Hepatitis B
THINK BODY SECRETIONS-BLOOD
Etiology: Hepatitis B Virus
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Incubation period: 48-180 days (mean 56-96)
Chronic & carrier status
Transmission
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Exposure to infected blood, blood products or body
fluids
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Perinatal: mother to baby (10-85% liklihood)
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90% become chronic carrier…25% mortality as adults
Percutaneously (IV drug use, needle sticks)
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Found in most body secretions
Nurses at risk!
STD-30% cases r/t heterosexual activity
Major source of spread are healthy, chronic carriers
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Hepatitis B: Prevention
Hepatitis B vaccine
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series of 3; use of HBIG for post-exposure
prophylaxis
Screening of donor blood
Use of disposable equipment
Sterilization of non-disposable equipment
Abstinence/condom use
Needle exchange programs
Use of standard precautions and PPE
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Hepatitis C
THINK BLOOD-IV DRUG USE
Etiology: Hepatitis C Virus
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Incubation period: 14-180 days (mean 56)
Sx persist 2-12 weeks
Most common cause of chronic hepatitis, cirrhosis, liver CA
Most are asymptomatic carriers-spread to others
Transmission
 Percutaneous-contaminated needles
 Bloodborne pathogen
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Before 1990 most cases due to contaminated blood
IV drug use, needle sticks (tattoo/body piercing)
Perinatal/sexual contact uncertain
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Hepatitis C:Prevention
Screening of donor blood
 Use of disposable equipment
 Sterilization of non-disposable equipment
 Abstinence/condom use
 No vaccine or use of IG at this time
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Chronic Hepatitis
Responsible for most cases of cirrhosis, liver
CA
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HCV responsible for 80% cases
Smolders over years…silently destroying liver
cells
Most asymptomatic but then develop…
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Malaise
Easy fatigability
Jaundice
Hepatomegaly
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Hepatitis-Cirrhosis: Laboratory
Assessment
AST-Aspartate aminotransferase
 ALT-Alanine aminotransferase
 ALP-Alkaline Phosphatase
 Total bilirubin
 Albumin
 Ammonia
 INR-Prothrombin time (PT)
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Hepatitis-Cirrhosis: Early Clinical
Manifestations
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Fatigue
Significant change in weight
Gastrointestinal symptoms
Abdominal pain and liver tenderness
Pruritus
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Hepatitis-Cirrhosis: Late Clinical
Manifestations
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Jaundice and icterus
Dry skin
Rashes
Petechiae, or ecchymoses (lesions)
Peripheral dependent edema of the
extremities and sacrum
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Hepatitis: Endstage Complications
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Mortality 1%
Higher w/elderly & other underlying
debilitating disease
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Hepatic failure
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Ascites
Chronic hepatitis
Cirrhosis
Hepatic cancer
Liver transplant
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Hepatitis: Care Planning Priorities
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Fatigue
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Physical rest
Nutritional intake
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Nausea
Knowledge deficit
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Sm. Frequent meals
High carb-low fat
Avoid Tylenol, ETOH
Diet
Drug therapy
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Interferon: SQ and po
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Cirrhosis
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Patho
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Inflammation
Causes
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ETOH
Hepatitis C
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Cirrhosis: Physical Assessment
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Massive ascites
Hepatomegaly (liver enlargement)
Assess nasogastric drainage, vomitus, and
stool for presence of blood
Bruising, petechiae, enlarged spleen
Neurologic changes
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Complications: Cirrhosis
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Portal hypertension
Ascites
Bleeding esophageal
varices
Coagulation defects
• Vitamin K not
absorbed
Jaundice
• Primary liver disease
• Intra-hepatic
obstruction
Portal-systemic
encephalopathy with
hepatic coma
• Ammonia levels
 lactulose
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Cirrhosis: Care Planning Priorities
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Excess fluid volume
 Diuretics
 Low
sodium diet
 Paracentesis
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Risk for imbalanced nutrition
Chronic pain
Risk for impaired skin integrity
Potential for hemorrhage
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Cirrhosis: Nursing Priorities
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Fluid-electrolyte management
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Bleeding precautions
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Na+, K+, BUN,
I&O
Assess INR-PT-platelet-Hgb
Monitor ortho’s
Assess sx bleeding
Neurologic assessment/monitoring
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Assess ammonia levels
Monitor LOC/orientation
Fall risk
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Liver Case Study
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67yr male
PMH: DMII, ETOH abuse, high cholesterol, PAF, CRI,
Kidney CA 2001, cardiomyopathy
CC: painless jaundice that started appx 4 weeks ago
when wife noted eyes becoming yellow…did not seek
medical care right away
Became visibly jaundiced, developed dark urine, stools
light in color, weak but no N-V-D or abd pain
MD office: Bili of 25. Amiodorone and Lipitor DC’d. US
abd done
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Hepatic duct dilation w/further testing found to have pancreatic
mass
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Acute Cholecystitis-Cholelithiasis
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Incidence/Prevalence
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Risk Factors
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20% US population impacted
Sedentary lifestyle
Obesity
Middle aged Caucasian women
High cholesterol
Estrogen-BCP
Patho
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Inflammation
Gallstones
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Cholesterol/bile salts
Cystic duct obstruction or may lie dormant in GB
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Acute Cholecystitis-Cholelithiasis:
Clinical Manifestations (chart 63-1 p.1398)
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Upper abd. pain
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RUQ or epigastric
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Rebound tenderness
Episodic or vague
Radiation to right shoulder
Triggered by high fat/large meal
Anorexia
N&V
Fever
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Acute Cholecystitis-Cholelithiasis
Diagnostic & Interventions
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Laboratory Findings
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Diagnosis
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WBC
CT or US
Interventions
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Nonsurgical
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Diet
Pharmocological
Surgical
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laparoscopic
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Acute Cholecystitis-Cholelithiasis:
Nursing Priorities
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Acute pain
Impaired skin integrity
Risk of infection
Knowledge deficit
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Pain management
Diet therapy
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Wound/incision care
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Low-fat
Smaller, more frequent meals
Signs of infection
Activity restrictions
Follow-up care
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Acute Pancreatitis
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Pancreas
• Functions as both exocrine/endocrine gland
Patho
• Lipolysis
• Proteolysis
• Necrosis of blood vessels
• Inflammation
Theories of enzyme activation
• ETOH
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Pancreatitis: Etiology
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Biliary obstruction
Cholecystectomy-postop
Trauma
Familial/genetic
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Incidence/Prevalence
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ETOH-holidays
Women-after cholelithiasis
Mortality
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10%
Higher w/elderly & postop
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Pancreatitis:Physical Assessment
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Abdominal pain-LUQ/epigastric
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Radiation to back, left
flank/shoulder
Nursing Assessment
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Abdomen
Respiratory
Neuro
VS
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Pancreatitis:Laboratory/Diagnostic
Assessment
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Lab
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Amylase
Lipase
Glucose
Bilirubin
WBC
Radiographic
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CT
MRI
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Complications of Acute Pancreatitis
p.1404 Table 63-2
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Pancreatic infection
Hemorrhage
Hypovolemic or septic shock
Respiratory
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Pleural effusion
Pneumonia
Acute Resp. Distress Syndrome (ARDS)
Multisystem organ failure
Disseminated intravascular coagulation
Diabetes mellitus
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Pancreatitis: Nursing Priorities
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Acute Pain
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Imbalanced nutrition
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PCA
Nothing by mouth in early stages-7-10 days
Antiemetics for nausea and vomiting
Total parenteral nutrition
Small, frequent, moderate to high-carbohydrate, highprotein, low-fat meals
Knowledge deficit
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ETOH avoidance
Recurrent abd pain
Jaundice-clay colored stools-darkened urine
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Pancreatic Carcinoma
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Etiology
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Smoking
Elderly 60-80 years
Genetic
Patho
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Primary vs. metastatic
Aggressive mets
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