Viral Hepatitis Flashcards
Clinical manifestations of Acute viral hepatitis
- Fever
- Malaise
- Anorexia
- Nausea
- Vomiting
- Jaundice
- Abdominal/RUQ pain
- Hepatomegaly
Understand Hep A virus serology
refer to image
When do you have symptoms with Hep A virus?
Where do you see virus in body?
Symptoms peak at 1 month post exposure with high ALT
fecal HAV high
What lab is ordered if pt is suspected of HAV infeciton?
Order Hep A IgG test~ if comes back +, run for IgM to tell if it’s acute or old infection of over 6 months
When does IgM anti HAV peak?
IgG anti-HAV?
peaks at 3 months, then goes down
IgG starts to rise as 1 month and stays elevated= IMMUNITY
How do you prevent HAV
- Hygiene (e.g., hand washing)
- Sanitation (e.g., clean water sources)
- Immune globulin (pre- and post-exposure)
- Hepatitis A vaccine (pre-exposure)
Who do we recommend to recieve the Hep A vaccine?
Recommended for:
– Infants
– People working in or traveling to areas with high incidence of HAV
– People with chronic liver disease
– People working with HAV
Hep A:
____virus
____transmission
infection and serotypes:
Incubation period:
Hep A
RNA virus
fecal-oral transmission
inucbates for about 4 weeks
A patient of yours is going to an HAV infected area, what do you do for your pt?
Give patient the hepatitis A immunoglobulin; better then vaccine and you would need booster in 6 months
A pt of yours works at a daycare and just found out several of her kids have Hep A
What do you recommend?
Give pt the Hep A immunoglobulin if it’s w/in 14 days
recommend all her contants get it too
Area of HAV prevealance
is it chronic?
is it symptomatic?
Prevelant in S. America, Africa, Asia
not chonic
more sypmtomatic in adults (70%) and only 10% in children
What body fluids is HepA concentrated in?
Feces
Serum
Saliva
NOT urine
Understand Serology of Hep E virus
Understand serology
Transmission of Hep E:
Incubation period:
Case-Fatality:
Transmission: fecal-oral, contaminated water, minimal person-person contact, recent travel to endemic area
Incubates 40 days
Case fatality: ovearll 1-3% pregnant women 15-45%
no chronicity
When do we see Symptoms in Hep E pts?
Symtpoms when ALT rises during 5 months post exposure
see virus in stool
When do we see increase in IgG and IgM in Hep E infection
IgG increases at 2 months and stays elevated
IgM rises and goes back down after 6 months and is present during acute infection
How do you diagnose Hep E?
• Hep E ab (there is no tx for Hep E)
• Hep E IgM = acute (<6 months)
• Hep E IgG = previous exposure (>6months) and now immune
***protective antibody
Acute Hep B:
describe HBeAg and anti-HBe
in acute; HBeAg elevated and then there is seroconversion to anti-HBe
this is spontaneous and generally occurs around week 12
In the pt that clears Hep B virus, when do we see the peak in HBsAg
peaks at week 12 then goes back down
In acute Hep B what does the total anti-HBc stand for?
its teh core antigen for IgM and IgG
what is the sign that you are immune to hep B?
At 32 weeks there is increase in anti-HBs which means you are immune
Hep B is a _____virus
who does it infect?
Incubation period?
Acute-fatality:
DNA virus
infects humans and some primates
incubation is 60-90 days
Hep B
- Acute case-fatality :
- Chronicity determined by :
- Premature mortality from chronic disease 15%-25%
- Leading cause of ________worldwide
0.5%-1%
age at exposure
hepatocellular carcinoma
Understand chronic Hep B
know figure
Why do we have chronic hep B?
there is no seroconversion from HBeAg to anti-HBe
the E antibody never develops and viral load never gets cleared
What is the window period in Hep B?
The HBsAg will increase at week 4 adn then goes back down at 24 weeks
the anti-HB IgG will start to rise at 32:
there is an 8 week window to detect Hep B core antigen
• Hep B Surface ag+ =
current hep B
(acute or chronic)
• Hep B surface ab+ =
immune
(recovered from natural infection, vaccine)
Hep B
• Core antibody = _______
IgM= recent exposure (
IgG= old exposure (> 6 months)
natural exposure
Candidates for HBV vaccine
• Routine immunization
• All infants and previously unvaccinated children by age 11
• Increased risk for HBV
People with multiple sexual partners
Sexual partners or household contacts of HBsAg-positive people
Homosexually active men
Users of illicit drugs
Travelers to regions of endemic disease ( > 6 months)
People occupationally exposed to blood or body fluids
Clients or staffs of institutions for developmentally disabled persons
Patients with chronic renal failure
Patients receiving clotting-factor concentrates
Chronic Hep B virus is more common in adults or children
children, adults that get Hep B usually have acute infection
Hep B infection is done via vertical transmission
You have pt with Hep B exposure in unvaccinated patients, what can you do for them?
• Give hepatitis B immune globulin (HBIG), within 24 hours or up to a week after
Second HBIG dose 1 month after first
-or-
• Hepatitis B vaccine, preferably within 24 hours but can be given up to a week after
Second dose of vaccine 1 month after first
Third dose of vaccine 6 months after first
• In Hepatitis B surface antigen positive mothers,
give newborn
both HBIG and vaccine
CHRONIC HEPATITIS B:
GOALS OF THERAPY
- Eliminate or significantly suppress HBV replication
- Prevent progression to cirrhosis and possibly hepatocellular carcinoma (HCC)
- ALT normalization
- Histological improvement
- Loss of HBeAg, development of HBeAb (seroconversion)
- Loss of HBsAg
What are modes of intervention in the treatement of chornic hepatits B infection
Antiviral therapy; works by smoking out virus or blocking DNA/RNA synthesis
Immune response targeted such as immunomodulatorys or antiviral therapy to rev up immune system; these are interfeurons.
How does chronic Hep B Interferon work?
• Interferon
proteins (cytokines)
released by host cells when infected by viruses
activate immune system.
Chronic Hep B therapy works with nucleotide/nucleoside analogues:
block reverse transcriptase thats necessary for HBV replication; this is enough to acocmpish seroconversion, if you don’t achieve seroconversion, need to stay on drugs
Two recommended Hep B treatments that are nucleotide/nucleoside analogues
Entecavir; nucleoside no resistance
Tenofovir; nucleotide, no resistance develops
These are both 1st line therapies
Peg-IFN has potential in specific population (low viral load, high ALT/AST) gives chance for eradication
Side effect of Peg-INF
flu-like symptoms
neuropsychiatric symptoms/depression
bone marrow depression
Goal of Hep B therapy:
- Eliminate or significantly suppress HBV replication:
- Prevent progression to :
approx. 30% after therapy discontinuation
cirrhosis and possibly HCC
Therapy: for HBV
• ALT normalization: approx. ___
• Histological improvement
• Loss of HBeAg, development of HBeAb
(seroconversion): approx. ___%
• Loss of HBsAg: approx. ___%
• ALT normalization: approx. 30%
• Histological improvement
• Loss of HBeAg, development of HBeAb
(seroconversion): approx. 30%
• Loss of HBsAg: approx. 5-7%
Understand serology of Hep B/D coeinfection
person exposed to both at the same time. Pt clears Hep B and will still have anti-HB but anti-HD goes down
Concentration of HBV in various body fluids
High in blood, serum, wound exudates
some in semen, vaginal fluid but low in urine, feces, sweat, tears
Hetero/homosexual men at high rish
What does a Hep B-D Superinfection look like on serology?
Pt will have chronic Hep B, later time will get Hep D and will have chroinc infection of both
Ig-M from Hep D will go back down but IgG for Hep D don’t decrease
Have chronic levels of HDV RNA and HBsAg
Diagnosis Hep D with antigens
• Hep D IgM = acute infection (< 6 months)
• Hep D IgG= previous exposure (> 6 months)
IgG is not protective antibody
Natural history of HBV infection: starting with acute
acute–> chronic in 90% children, 10% adults
Chronic–> cirrhosis 30% time
Chronic–> Liver cancer without going to cirrhosis 5-10%
Cirrhosis–> liver fail
Hep C is what kind of virus?
RNA, spherical
Half-life = 2.7 hours
Daily production= 10 to 12 virions
some in US, all over the world with wide genotype distribution
1a most common in US
Hep C antibody seen in all exposures and
remains present in all patients including those
who spontaneously clear the virus or undergo
successful treatment; what is present in only people that are viremic?
• Hepatitis C viral RNA is present only in those
who are viremic
Understand Hep C serology
know this diagram
When do we see anti-HCV in pts?
starts to rise at 2 months, peaks at 6 months and stays elevated
*have HCV RNA present in blood w/in two weeks
Pattern of Hep C from acute to chronic infection
HCV RNA levels persist
What antivirals are there for Hep C?
Sofosbuvir/Ledipasvir
Cuase of Hep C
IVdrug use
How does fibrosis progress in Hepatits pts?
variable progression of fibrosis over time
HBsAg: negative
anti-HBc : negative
anti-HBs: negative
Susceptible to Hep B
HBsAg : negative:
anti-HBc positive
anti-HBs positive
Immune due to natural infection
HBsAg negative
anti-HBc negative
anti-HBs positive
Immune due to hepatitis B vaccination
HBsAg positive
anti-HBc positive
IgM anti-HBc positive
anti-HBs negative
Acutely infected
HBsAg positive
anti-HBc positive
IgM anti-HBc negative
anti-HBs negative
Chronically infected
Hepatitis B surface
antibody (anti-HBs):
The presence of anti-HBs is generally interpreted as
indicating recovery and immunity from hepatitis B
virus infection. Anti-HBs also develops in a person
who has been successfully vaccinated against hepatitis B
IgM antibody to hepatitis B core antigen (IgM anti-HBc):
Positivity indicates recent
infection with hepatitis B
virus (<6 mos). Its presence
indicates acute infection.
Total hepatitis B core
antibody (anti-HBc):
Appears at the onset of symptoms in acute
hepatitis B and persists for life. The presence of anti-HBc indicates previous or ongoing infection with
hepatitis B virus in an undefi ned time frame
Hepatitis B surface
antigen (HBsAg):
A protein on the surface of hepatitis B virus; it can
be detected in high levels in serum during acute or
chronic hepatitis B virus infection. The presence of
HBsAg indicates that the person is infectious. The
body normally produces antibodies to HBsAg as
part of the normal immune response to infection.HBsAg is the antigen used to make hepatitis B vaccine.
Hep B window period
both serological markers HBsAg (Hepatitis B surface antigen) and Anti-HBs (antibodyagainst HBsAg) are negative (which is due to the fact that, although there are Anti-HBs antibodies present, they are actively bound to the HBsAg). Other serological markers, IgM (antibody) against HBc can be positive at this point but person wont be infective
