Transcript Slide 1
Nursing Care and
Interventions with Diseases
of the Liver, Gallbladder
& Pancreas
Keith Rischer RN, MA, CEN
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Today’s Objectives…
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?
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
Fever/chills
•
Benefits
Increased
killing of microorganisms
Increased phagocytosis by neutrophils
Increased activity of interferon
Leukocytosis
Plasma Proteins
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Patho Review
Liver
• Produces bile…elimination of bilirubin
• Drug/hormone metabolism
• CHO-fat-protein metabolism
• Clotting factor synthesis
• Storage of vitamins & minerals
Gallbladder
• Store & concentrate bile
Pancreas
• Endocrine
• Exocrine
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Hepatitis
Definition:
Inflammation of the
Liver
Causes:
•
Viral (most common)
•
Toxic
•
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
•
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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•
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Good hygiene
Water treatment
Hepatitis A vaccine
booster
•
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
•
•
Incubation period: 48-180 days (mean 56-96)
Chronic & carrier status
Transmission
•
Exposure to infected blood, blood products or body
fluids
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Perinatal: mother to baby (10-85% liklihood)
•
•
90% become chronic carrier…25% mortality as adults
Percutaneously (IV drug use, needle sticks)
•
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
•
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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•
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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
•
•
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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•
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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
Mortality 1%
Higher w/elderly & other underlying
debilitating disease
•
Hepatic failure
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Ascites
Chronic hepatitis
Cirrhosis
Hepatic cancer
Liver transplant
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Hepatitis: Care Planning Priorities
Fatigue
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•
Physical rest
Nutritional intake
Nausea
Knowledge deficit
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•
Sm. Frequent meals
High carb-low fat
Avoid Tylenol, ETOH
Diet
Drug therapy
•
Interferon: SQ and po
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Cirrhosis
Patho
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•
Inflammation
Causes
ETOH
Hepatitis C
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Cirrhosis: Physical Assessment
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
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
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
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
•
Hepatic duct dilation w/further testing found to have pancreatic
mass
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Acute Cholecystitis-Cholelithiasis
Incidence/Prevalence
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Risk Factors
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•
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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
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)
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
Laboratory Findings
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Diagnosis
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WBC
CT or US
Interventions
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Nonsurgical
•
Diet
Pharmocological
Surgical
laparoscopic
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Acute Cholecystitis-Cholelithiasis:
Nursing Priorities
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
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
Biliary obstruction
Cholecystectomy-postop
Trauma
Familial/genetic
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
Abdominal pain-LUQ/epigastric
•
Radiation to back, left
flank/shoulder
Nursing Assessment
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•
•
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Abdomen
Respiratory
Neuro
VS
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Pancreatitis:Laboratory/Diagnostic
Assessment
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
Pancreatic infection
Hemorrhage
Hypovolemic or septic shock
Respiratory
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•
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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
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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•
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ETOH avoidance
Recurrent abd pain
Jaundice-clay colored stools-darkened urine
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Pancreatic Carcinoma
Etiology
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•
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Smoking
Elderly 60-80 years
Genetic
Patho
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Primary vs. metastatic
Aggressive mets
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