Download Etiology Hepatitis B virus

Focus on
Hepatitis
(Relates to Chapter 44,
“Nursing Management:
Liver, Pancreas, and Biliary Tract Problems”
in the textbook)
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Hepatitis
• Inflammation of the liver
• Viral hepatitis
 Most common cause
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Hepatitis
• Types of infectious viral hepatitis
A
B
C
D
E
G
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Hepatitis
• Other possible causes
 Drugs (alcohol)
 Chemicals
 Autoimmune liver disease
 Bacteria (rarely)
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Hepatitis
• 3000 new cases of hepatitis A occur
annually in the United States.
• 1.4 million new cases of hepatitis A
occur worldwide.
 Nearly universal during childhood in
developing countries
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Hepatitis
• Nearly 2 billion people infected with
hepatitis B
 350 million have chronic infection.
• 43,000 new cases of hepatitis B
annually in United States
 Incidence decreased because of HBV
vaccine
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Hepatitis
• Approximately 170 million people
are infected with the hepatitis C
virus (HCV) worldwide.
• Estimated 3 to 4 million new cases
are diagnosed annually.
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Hepatitis
• 8000 to 10,000 people in the
United States die each year from
complications of end-stage liver
disease secondary to HCV.
• Approximately 30% to 40% of
HIV-infected patients also have
HCV.
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Etiology
• Causes
 Viral hepatitis (A, B, C, D, E, and G)
 Cytomegalovirus
 Epstein-Barr virus
 Herpes virus
 Coxsackievirus
 Rubella virus
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Etiology
• Hepatitis A virus (HAV)
 RNA virus
 Transmitted fecal-oral route,
parenteral (rarely)
 Frequently occurs in small outbreaks
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Etiology
• Hepatitis A virus (HAV)
 Found in feces 2 or more weeks before
the onset of symptoms and up to 1
week after the onset of jaundice
 Present in blood briefly
 No chronic carrier state
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Serologic Events in HAV
Infection
Fig. 44-2. Course of infection with hepatitis A virus (HAV). ALT, Alanine
aminotransferase; IgG, immunoglobulin G; IgM, immunoglobulin M.
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Etiology
• Hepatitis A virus (HAV)
 Anti-HAV immune globulin M (IgM)
• Appears in the serum as the stool
becomes negative for the virus
• Detection of IgM anti-HAV indicates
acute hepatitis.
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Etiology
• Hepatitis A virus (HAV)
 Anti-HAV immune globulin G (IgG)
• IgG anti-HAV: Indicator of past infection
• Presence of IgG antibody provides
lifelong immunity.
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Etiology
• Hepatitis B virus (HBV)
 DNA virus
 Transmission of HBV
• Perinatally by mothers infected
• Percutaneously (IV drug use)
• Horizontally by mucosal exposure to
infectious blood, blood products, or other
body fluids
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Etiology
• Hepatitis B virus (HBV)
 Transmission occurs when infected
blood or other body fluids enter the
body of a person who is not immune to
the virus.
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Etiology
• Hepatitis B virus (HBV)
 Sexually transmitted disease
 Can live on a dry surface for 7 days
 Kissing/sharing food items may spread
the virus via saliva.
 More infectious than HIV
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Serologic Events in HBV
Infection
Fig. 44-3. Course of infection with hepatitis B virus (HBV). ALT, Alanine aminotransferase; anti-HBc, antibody
To hepatitis B core antigen; anti-HBe, antibody to HBeAg; anti-HBs, antibody to HBsAg; DNA,
Deoxyribonucleic acid; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; IgG, immunoglobulin
G; IgM, immunoglobulin M.
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Etiology
• Hepatitis B virus (HBV)
 Complex structure with three antigens
• Surface antigen (HBsAg)
• Core antigen (HBcAg)
• E antigen (HBeAg)
 Each antigen—corresponding antibody
may develop in response to acute viral
hepatitis B
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Etiology
• Hepatitis B virus
 Presence of hepatitis B surface
antibodies
• Indicates immunity from HBV vaccine
• Past HBV infection
 With chronic infection, liver enzyme
values may be normal or ↑.
 15% to 25% of chronically infected
persons die from chronic liver disease.
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Etiology
• Hepatitis C virus (HCV)
 RNA virus
 Transmitted percutaneously
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Etiology
• Hepatitis C virus (HCV)
 Risk factors
• IV drug use
• Most common mode of transmission in
United States and Canada
• Blood transfusions
• Transmission <1 per 1 million blood
transfusions
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Etiology
• Hepatitis C virus (HCV)
 Risk factors (cont’d)
• High-risk sexual behavior
• Hemodialysis
• Occupational exposure
• Perinatal transmission
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Etiology
• Hepatitis C virus (HCV)
 Up to 10% of patients with HCV cannot
identify a source.
 Additional data needed regarding risk
of body piercings, tattooing, and
intranasal drug use in transmission of
HCV
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Etiology
• Hepatitis D virus (HDV)
 Also called delta virus
 Defective single-stranded RNA virus
 Cannot survive on its own
 Requires the helper function of HBV to
replicate
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Etiology
• Hepatitis D virus (HDV) (cont’d)
 Transmitted percutaneously
 HBV-HDV co-infection
• ↑ risk of fulminant hepatitis
• More severe acute disease
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Etiology
• Hepatitis E virus (HEV)
 RNA virus
 Transmitted fecal-oral route
 Most common mode of transmission is
drinking contaminated water.
 Occurs primarily in developing
countries
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Etiology
• Hepatitis G virus (HGV)
 RNA virus
 Poorly characterized parenterally and
sexually transmitted virus
 Found in some blood donors
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Etiology
• Hepatitis G virus (HGV) (cont’d)
 Coexists with other hepatitis viruses
and HIV
 Does not appear to cause liver damage
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Pathophysiology
• Acute infection
 Liver damage mediated by
• Cytotoxic cytokines
• Natural killer cells
 Liver cell damage results in hepatic cell
necrosis.
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Pathophysiology
• Acute infection (cont’d)
 Proliferation and enlargement of
Kupffer cells
 Inflammation of the periportal areas
may interrupt bile flow.
 Cholestasis may occur.
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Pathophysiology
• Widespread inflammation of the
liver tissue
• Pathophysiologic changes in the
various types of viral hepatitis are
similar.
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Pathophysiology
• Liver cells can regenerate over time
and, if no complications occur, can
resume their normal appearance and
function.
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Pathophysiology
• Antigen-antibody complexes
• Systemic effects of this activation
include
• Rash
• Angioedema
• Arthritis
• Fever
• Malaise
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Pathophysiology
 Systemic effects (cont’d)
• Cryoglobulinemia
• Abnormal proteins in blood
• Glomerulonephritis
• Vasculitis
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Clinical Manifestations
• 30% of patients with HBV are
asymptomatic.
• 80% of patients with acute HCV will
be asymptomatic.
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Clinical Manifestations
• Acute phase
 Lasts from 1 to 4 months
 May be icteric (symptomatic) or
anicteric
 During incubation, symptoms include
• Malaise
• Anorexia
• Fatigue
• Nausea
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Clinical Manifestations
• Acute phase (cont’d)
 Symptoms (cont’d)
• Occasional vomiting
• Abdominal discomfort
• Headache
• Low-grade fever
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Clinical Manifestations
• Acute phase (cont’d)
 Symptoms (cont’d)
• Arthralgias
• Skin rashes
 Physical exam may reveal
hepatomegaly, lymphadenopathy,
and splenomegaly.
 Maximal infectivity period
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Clinical Manifestations
• Jaundice
 Results when bilirubin diffuses into
tissues
• Urine darkens because excess
bilirubin is excreted.
• If bilirubin cannot flow out of liver,
stool will be light or clay-colored.
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Clinical Manifestations
• Pruritus can accompany jaundice.
 Accumulation of bile salts beneath the
skin
• When jaundice occurs, fever
subsides.
• Liver is usually enlarged and tender.
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Clinical Manifestations
• Convalescent phase
 Begins as jaundice is disappearing
 Lasts weeks to months
 Major complaints
• Malaise
• Easy fatigability
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Clinical Manifestations
• Almost all cases of hepatitis A are
resolved.
• Absence of jaundice does not mean
recovery.
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Clinical Manifestations
• General considerations
 Not all patients with hepatitis virus
have jaundice.
• Termed anicteric hepatitis
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Clinical Manifestations
• General considerations
 Hepatitis A virus
• Acute onset
• Mild, flulike manifestations
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Clinical Manifestations
• General considerations
 Hepatitis B virus
• Insidious onset
• Symptoms more severe
• Fewer GI symptoms
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Clinical Manifestations
• General considerations
 Hepatitis C virus
• Majority of cases are asymptomatic or
mild.
• High rate of persistence
• Leads to chronic liver disease
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Complications
• Most patients with acute viral
hepatitis recover completely with no
complications.
• Overall mortality rate <1%
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Complications
•
•
•
•
Fulminant hepatic failure
Chronic hepatitis
Cirrhosis
Hepatocellular carcinoma
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Complications
• Fulminant hepatitis
 Results in severe impairment or
necrosis of liver cells and potential liver
failure
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Complications
• Fulminant hepatitis
 Develops in small percentage of
patients
 Occurs because of
• Complications of hepatitis B
• Toxic reactions to drugs and congenital
metabolic disorders
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Diagnostic Studies
• Hepatitis C
 Several tests available
 Antibodies to HCV are not protective.
 May be indicator of chronic disease
 Anti-HCV antibody test by
immunoassay
• If positive, confirmatory testing must be
done.
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Diagnostic Studies
• Hepatitis C (cont’d)
 HCV recombinant immunoblot assay
may be used if false-positive HCV
antibody test
 HCV RNA polymerase chain reaction
performed
• Documents viremia if antibody positive
• To detect active disease
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Diagnostic Studies
• Hepatitis C (cont’d)
 Six genotypes and 50 subtypes of HCV
 Genotyping: Important role in
managing infection
• One of the strongest predictors of
response to therapy and influences
duration of treatment
• Should be determined before drug
therapy is started
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Diagnostic Studies
• History
• Physical assessment findings
 Hepatic tenderness
 Hepatomegaly
 Splenomegaly
 Palpable liver
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Diagnostic Studies
•
•
•
•
Aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)
-glutamyl transpeptidase (GGT)
Alkaline phosphatase
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Diagnostic Studies
•
•
•
•
•
Serum proteins
Serum bilirubin
Urinary bilirubin
Urinary urobilinogen
Prothrombin time
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Collaborative Care
• No specific treatment or therapy for
acute viral hepatitis
• Most patients can be managed at
home.
• Emphasis on resting the body and
receiving adequate nutrients
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Collaborative Care
• Drug therapy
 No specific drug therapies
 Support therapy
• Antiemetics
• Dimenhydrinate (Dramamine)
• Trimethobenzamide (Tigan)
• Phenothiazines should not be used.
• If sedative or hypnotic is required,
diphenhydramine (Benadryl) may be
used.
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Collaborative Care
• Drug therapy for chronic hepatitis B
 Focused on
• ↓ viral load
• ↓ liver enzyme levels
• ↓ rate of disease progression
• ↓ rate of drug-resistant HBV
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Collaborative Care
 Long-term goals
• Prevention of cirrhosis and hepatocellular
cancer
 Not all patients respond to current
therapeutic regimens.
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Collaborative Care
• Drug therapy for chronic hepatitis B
 α-interferon
• Multiple effects on viral replication cycle
• Must be administered subcutaneously
• Side effects
• Flulike symptoms, depression, hair thinning,
diarrhea, insomnia
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Collaborative Care
• Drug therapy for chronic hepatitis B
(cont’d)
 Nucleoside analogs
• When active viral replication exists
• Inhibit viral DNA synthesis
• Lamivudine (Epivir)
• Taken for 1 year
• Adefovir (Hepsera)
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Collaborative Care
• Drug therapy for chronic hepatitis C
 Directed at eradicating virus
 Reducing viral load
 Decreasing progression of disease
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Collaborative Care
• Drug therapy for chronic hepatitis C
(cont’d)
 Treatment
• Pegylated α-interferon with ribavirin
(Rebetol, Copegus)
• Ribavirin side effects:
• Anemia, anorexia, cough, rash, pruritus,
dyspnea, insomnia, teratogenicity
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Collaborative Care
Prevention
• Hepatitis A
 Hepatitis A vaccine
• Preexposure prophylaxis
• IM in deltoid
 Immune globulin (IG)
• Pre/post exposure
• Temporary passive immunity
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Collaborative Care
Prevention
• Hepatitis B
 Immunization
• Most effective method
• Part of routine vaccination schedules for
newborns, adolescents, and adults in
major risk groups
• Recombivax HB, Engerix-B
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Collaborative Care
• Hepatitis B
 Immunization (cont’d)
• Recombinant DNA using HBsAg
• Promotes synthesis of specific antibodies
against hepatitis B
• Series of three IM injections given at 0, 1-,
and 6-month intervals
• More than 95% effective
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Collaborative Care
Prevention
• Hepatitis B
 Hepatitis B immune globulin (HBIG)
• Used post exposure with vaccine
• Contains antibodies to HBV
• Should be given within 24 hours of
exposure
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Collaborative Care
Prevention
• Hepatitis C
 No vaccine to prevent HCV
 CDC does not recommend IG or
antiviral agents for postexposure
prophylaxis
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Nursing Management
Nursing Assessment
• Past health history
 Hemophilia
 Exposure to infected persons
 Ingestion of contaminated food or
water
 Past blood transfusion (before 1992)
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Nursing Management
Nursing Assessment
• Medications (uses and misuses)
 Acetaminophen
 Phenytoin
 Halothane
 Methyldopa
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Nursing Management
Nursing Assessment
• IV drug and alcohol abuse
• Weight loss
• Dark urine
• Fatigue
• Right upper quadrant pain
• Pruritus
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Nursing Management
Nursing Assessment
• Low-grade fever
• Jaundice
• Abnormal laboratory values
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Nursing Management
Nursing Diagnoses
• Imbalanced nutrition: Less than
body requirements
• Activity intolerance
• Ineffective self-health management
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Nursing Management
• Overall goals: Planning
 Relief of discomfort
 Resumption of normal activities
 Return to normal liver function without
complications
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Nursing Management
Nursing Implementation
• Health promotion
 Hepatitis A and B
• Education
• Vaccination
• Good hygiene practices
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Nursing Management
Nursing Implementation
• Health promotion
 Hepatitis C
• Education
• Infection control precautions
• Modification of high-risk behavior
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Nursing Management
Nursing Implementation
• Acute intervention
 Rest
 Jaundice
• Assessment of degree of jaundice
• Small, frequent meals
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Nursing Management
Nursing Implementation
• Ambulatory and home care
 Dietary teaching
 Assessment for complications
 Regular follow-up for at least 1 year
after diagnosis
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Nursing Management
Nursing Implementation
• Ambulatory and home care
 Avoidance of alcohol
 Medication education
• Α-interferon administered
subcutaneously
• Side effects
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Nursing Management
Evaluation
• Expected outcomes
 Adequate nutritional intake
 Increased tolerance for activity
 Verbalization of understanding of
follow-up care
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Nursing Management
Evaluation
• Expected outcomes
 Able to explain to others methods of
transmission and methods of
preventing transmission
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Case Study
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Case Study
• 30-year-old man admitted to the
hospital with general fatigue, lack of
appetite, headaches, and yellowish
complexion
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Case Study
• Symptoms became progressive
during the past few days.
• One month ago, he was in
Guadalajara, Mexico, where he ate a
lot of seafood and Mexican food.
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Case Study
• Physical examination indicates an
enlarged tender liver and icterus.
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Case Study
• Laboratory results show
 Hemoglobin 12 g/dL
 Bilirubin (direct) 5.6 mg/dL
 Bilirubin (indirect) 3.4 mg/dL
 Alkaline phosphatase 600 U/mL
 AST 1200 U/mL
 ALT 1510 U/mL
• Urine positive for bilirubin
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Discussion Questions
1. What type of hepatitis does he
probably have?
2. How did he get infected?
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Discussion Questions
3. What is the treatment for the type
of hepatitis he has?
4. What is the priority for his care?
5. What teaching topics are
important to discuss with him?
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