Hepatitis  Virus excretion may continue for up to 3
weeks after onset of symptoms.
Hepat: liver Itis: inflammation
Hepatitis = liver inflammation
What is it?
 Liver inflammation can occur for many
reasons:
Drugs, excessive alcohol usage, medications,
and viruses (most common and referred to as
viral hepatitis): this is where a virus attacks the
cells of the liver causing them to malfunction.
 found in the upper right quadrant just under
the diaphragm.
Functions of the
Liver
 The liver is a vital organ that plays a crucial
role in maintaining the body's balance by
filtering, protecting, breaking down, and
storing substances. Its failure can lead to the
failure of other body parts, making it a vital
organ.
 It produces bile that will help digest fats.
 It plays a role with the coagulation process.
 Provides immune system protection by
producing immune factor proteins and
eliminates dangerous bacteria from the blood.
 It helps regulate the blood glucose levels by
storing and creating glucose based on the
body’s needs.
 It turns ammonia into urea. Ammonia is
created with the breakdown of proteins. It is
highly toxic to the brain if it accumulates in
the blood, which is why the liver turns it into
urea and lets the kidneys dispose of it through
the urine.
 It breaks down red blood cells. When this
occurs it will create bilirubin. Bilirubin is
a brownish yellow substance, which is placed
in the bile and excreted in the stool. This is
why stool is normally brown.
Hepatitis A
 Picornavirus (RNA)
 Humans are only natural host
 Stable at low pH
 Inactivated by temperature of 185°F or higher,
formalin, chlorine
PATHOGENESIS
 Fecal-oral transmission
 Viral replication in the liver
 Virus present in blood and feces 10 to 12 days
after infection
Transmission
 Hepatitis A virus is primarily transmitted
through fecal-oral routes, such as ingesting
contaminated food or water, and waterborne
outbreaks are infrequent due to sewage-
contaminated or inadequately treated water.
 Close physical contact with an infectious
person, such as oral-anal sex, can also spread
the virus, although casual contact is not
considered spread.
SIGNS & SYMPTOMS
 Incubation period: 28 days (average)
 GI symptoms: nausea, vomiting, stomach
pain, loss of appetite
 Fever
 Very tired
 Arthralgia (joint pain)
Signs
 Dark urine (bilirubin)
 Clay-colored stool (no bilirubin in stool)
 Jaundice
 pruritus
 With Hepatitis A, the patient can be contagious 2
weeks BEFORE the signs and symptoms appear
and 1-3 weeks from when the symptoms
appeared.
RISK FACTORS
 Poor sanitation;
 Lack of safe water;
 Living in a household with an infected
person;
 Being a sexual partner of someone with
acute hepatitis a infection;
 Use of recreational drugs;
 Sex between men; and
 Travelling to areas of high endemicity
without being immunized.
DIAGNOSIS
 Diagnosed: anti-HAV (antibodies of the
hepatitis A virus) presence with IgM and
IgG in the blood
 anti-HAV IgM = active infection (in
icteric phase)
 anti-HAV IgG = past infection and
recovered and has immunity.
 IgM (think mean virus is present in the body) and
IgG (think the virus is gone)
TREATMENT
 It is important to avoid unnecessary
medications that can adversely affect the
liver, e.g. acetaminophen, paracetamol.
Prevention:
 Hepatitis A vaccination
 Hepatitis A Immune globin (IG)
immunization (need to receive within 2
weeks of exposure)
infection control practices:
 Handwashing
 Adequate supplies of safe drinking
water;
 Proper disposal of sewage within
communities; and
 Personal hygiene practices such as
regular handwashing before meals
and after going to the bathroom.
Hepatitis B
PATHOGENESIS
 Infection of the liver caused by hepatitis B
virus (HBV).
 DNA virus from the hepadna group.
 Incubation: 1-6 months, long term carrie
state established after, transmitted through
blood or semen.
 Immune system attacks infected
hepatocytes.
Transmission:
 blood and other body fluids like semen,
salvia, ammonitic or vaginal fluid etc.
 transmission route is sexual intercourse
and intravenous drug use. It can also be
spread via the birthing process if mother is
Hepatitis B positive. Can be spread via the
percutaneous (via a puncture in the skin…
example: needle) or mucosal routes.
 Acute and chronic infections can
occur. Infants and young children at most
risk for chronic infections.
 Chronic infections can lead to major
complications like: cirrhosis, liver failure,
and liver cancer
SIGNS & SYMPTOMS
 General Infection : Low grade fever,
malaise,
lethargy, and anorexia.
 Liver related: fatty stool, dark urine,
jaundice, hepatomegaly, scleral
icterus, pruritus, RUQ tenderness.
RISK FACTORS
 Intravenous drug user
 Unprotected sexual intercourse
 Blood transfusions
 Hemodialysis
DIAGNOSIS
 HBsAg (Hepatitis B surface antigen):
show infectious (educate: avoid sexual
intercourse and intimacy like kissing until
it is negative)
 Anti-HBs (Hepatitis b surface
antibody): means patient is recovered
(had a previous infection) and immune
(example: effective Hepatitis B vaccine)
TREATMENT
Medications:
 Interferon alpha, Nucleoside Reverse
Transcriptase Inhibitors (NRTI).
Prevention:
 Handwashing
 vaccine for all infants (3-4 doses over 6-
18 months) and
 people at risk for Hepatitis B. example:
healthcare workers (3 doses over 6
months),
 all pregnant women should be tested due
to transmission at birth, post-exposure
Hepatitis B immune globulin within 24
hours of exposure (12 hours after birth) to
provide temporary passive immunity.
Hepatitis C
 Hepatitis C is a viral infection that affects
the liver. It can cause both acute (short
term) and chronic (long term) illness. It
can be life-threatening.
PATHOGENESIS
 Viral hepatitis caused by hepatitis C virus
(HCV).
  From class of Flaviviridae.  Handwashing,
 Incubation: 6-7 weeks.  No vaccine currently or immune globulin
 Virus mutates often to bypass the host for post-exposure
immune system.  Strict blood and organ donation screening
Transmission:
 Blood and body fluids spread via Hepatitis D
percutaneous (via the skin through a
puncture) or in body fluids with mucosal
route PATHOPHYSIOLOGY
 Most common transmission  HDV infection only occurs in the presence
route intravenous drugs. of HBV.
 Other ways but not as common: sexual  In individuals who are susceptible to HBV,
contact, sharp injuries (needle or co-infection with both viruses results in an
instruments), long-term dialysis increases acute hepatitis B and D infection.
risk of exposure.  More severe cases than acute HBV mono-
infection may be seen in some cases with
SIGNS & SYMPTOMS an increased risk for liver failure.
 In individuals who are chronic carriers of
HBsAg, a full-blown superinfection can
 General Infection : Low grade fever, occur which may present as severe acute
malaise, hepatitis or exacerbation of preexisting
lethargy, and anorexia. chronic hepatitis B. In patients with
 Liver related: fatty stool, dark urine, chronic HBV infection, acute HDV
jaundice, hepatomegaly, scleral infection may be mistaken for a hepatitis B
icterus, pruritus, RUQ tenderness. virus flare.
 Acute and chronic infections can occur.  In those with hitherto undiagnosed
A high percentage of Hepatitis C becomes hepatitis B infection, clinical presentation
chronic, which increases the risk for liver and initial investigations may be mistaken
disease. for acute HBV infection if HDV
 Chronic infections can lead to major superinfection is not entertained as a
complications like: cirrhosis, liver failure, diagnostic possibility.
and liver cancer  Incubation: 6-24 weeks
Transmission:
 Only infects a person when they
RISK FACTORS have Hepatitis B.
 Blood and body fluids spread via
 Intravenous drug use percutaneous
 Sexual contact  Parenteral, sexual, perinatal
 From mother to child neonatal period
(Vertical transmission)
 Chronic hemodialysis SIGNS & SYMPTOMS

 Systemic Symptoms: fever, malaise, nausea,

and vomiting
 pale stool, dark colored urine, jaundice,
hepatomegaly, and RUQ tenderness.
DIAGNOSIS
RISK FACTORS
 presence of anti-HCV (antibodies to HCV)
for chronic infection.  Intravenous drug use
 Enzyme-linked immunosorbent assay.  Sexual contact
 HBV presence
TREATMENT
DIAGNOSIS
Medication:  presence of HDAg (hepatitis D antigen) and
 antiviral medication like direct acting anti-HDV
antivirals (DAAs).
 Interferon alfa, ribavirin
Prevention: TREATMENT
Medications:  avoiding consumption of water and ice of
 antiviral medications or pegylated interferon unknown purity.
alpha
Prevention: Hepatitis A and E
 handwashing  Both transmitted fecal-oral
 Hepatitis B vaccine  Both ONLY cause acute infections
 NO vaccine for Hepatitis D or post-exposure  Both treatment: supportive and rest
immune globulin.  Hepatitis A has a vaccine and immune
Surgery: globulin, while Hepatitis E does NOT have a
 Liver transplantation for chronic hepa D. vaccine.
Hepatitis B, C, D
Hepatitis E  All transmitted via blood/body fluids
 All cause either acute and chronic infections
 All treatment can include antivirals and
 Hepatitis E is an inflammation of the liver
interferon
caused by infection with the hepatitis E
 Only Hepatitis B has a vaccine and post-
virus (HEV).
exposure immune globulin.
 Class of hepeviridae
Transmission:
 Fecal-oral: from consuming contaminated Nursing Education to Provide to Patients
water or food (can also be transmitted in with Hepatitis
undercooked meat like pork or wild game)  Handwashing
 Acute infection only: can cause major  Eat low fat and high carb meals
complications in pregnant women in the  Personal hygiene products NOT to be shared
3rd trimester Activity conservation, patient needs to REST to
 Tends to be more prevalent in developing help the liver heal
countries and in people who globally travel.  Toxic substances AVOID over-the-counter
products that are liver toxic: alcohol, sedative,
SIGNS & SYMPTOMS aspirin, acetaminophen etc.
 Individual bathrooms, don’t share bathroom
 General infection: Low grade fever, malaise, with family members
lethargy, and anorexia.  Test results:
 Liver related: Fatty stool, dark urine (iron),  Hepatitis A: anti-HAV IgM (active) and anti-
Jaundice, hepatomegaly, icterus, and HAV IgG (recovered/immune)
pruritus.  Hepatitis B: HBsAG (infectious) and anti-
 Diarrhea, arthralgia, urticarial rash. HBV (recovered/immune)
 Interferon (Peginterferon alfa-2a given subq) and
RISK FACTORS Immune globulin for Hepatitis A (within 2 weeks
of exposure) and Hepatitis B Immune globulin
 Consuming contaminated food & water. (within 24 hours of exposure)
 Blood transfusions  Small but frequent meals.
 Mother to child Phases of Viral Hepatitis
DIAGNOSIS Preicteric (prodromal) Phase:
 body symptoms: joint pain, fatigue, nausea
 detection of specific anti-HEV vomiting, abdominal pain change in taste, liver
immunoglobulin M (IgM) antibodies enzymes and bilirubin increasing.
Icteric Phase:
TREATMENT  DECREASE in body symptoms but will have
jaundice and dark urine (from build-up of
bilirubin), clay-colored stool (bilirubin not going
Medication: to stool to give it’s normal brown color) enlarged
 Ribavirin used in immunosuppressed liver and pain in this area.
individuals Posticteric (convalescent) Phase:
Prevention:  jaundice and dark urine start to subside and stool
 Handwashing returns to normal brown color, liver enzymes and
 maintaining quality standards for public bilirubin decrease to normal
water supplies
 establishing proper disposal systems for
human faeces.
 maintaining hygienic practices