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73 Cards in this Set

  • Front
  • Back
which hep?

source of virus: feces
Hep A

Hep E
source of virus: blood/blood-derived body fluids
Hep B

Hep C

Hep D
route of transmission: fecal-oral
Hep A

Hep E
route of transmission percutaneous permucosal
Hep B

Hep C

Hep D
chronic infection:
Hep B

Hep C

Hep D
t/f

hep A and E are chronic infections
f
prevention:

ensure safe drinking water
Hep E
prevention: pre/post exposure immunization:
Hep A

Hep B

Hep D (risk behavior modification)
prevention :

blood donor screening

risk behavior modification
Hep C
hep A can be received via --- contact
person to person via oral fecal contact

oral-anal contact
what's is hep a inactivated by
high temp

formalin

chlorine
infectious time of hep a
2 weeks prior to illness to 1 week after onset of symptoms
who's usu asymptomatic
kids < 6 yrs

usu carriers
t/f

hep a usu self limiting
t

and conferes lifelong immunity upon recovery
s/s of hep a
flu like symptoms (n, anorexia, fatigue, fever, ha)

acute illness (worsening of symptoms)

icteric hepatitis

mild wieght loss

ruq pain
icteric hepatitis s/s
dark urine

light stools

icteric sclera, secretions, skin
why ruq pain w/ hep a
due to hepatomegaly
in hep a what comes first IgM or IgG
1st: IgM . . . acute infection

if you see IgG. .. past infection
hep A

--- if n/v present
hydration
what do you limit in hep a
meds that may cause liver damage

APAP 2 g/day
prevention of transmission:
proper hygiene

vaccinations ~ 2-4 weeks prior to exposure

IgG w/in 2 weeks of exposure (protects for 4-5 months)
hep a: routine vaccination for kids -- yr old
1 year old
routine hep A vaccination for kids > 2 yres of age in -- areas
endemic
routine hep A vaccine for men:
who have sex w/ men
routine hep A vaccination for:
illegal drug use

occupational risk

have chronic liver disease

receive bl products for clotting

adopt kids from endemic areas

travel to endemic areas
symptoms of hep E similar to
hep A
hep E can be fatal in:
pregnant women

greatest in 2nd and 3rd trimester
t/f

there's a vaccine for hep E
f
modes of transmission of hep E
parenterally

sexually

perinatally

rarely bl transfusion
highest conc of hep B
blood

serum

wound exudates
mod conc of hep B
semen

vag fluid

saliva
low/not detectable conc of hep b
urine

feces

sweat

tears

breast milk
the --- --- to the hep b virus is cytotoxic hepatocytes. . .esp over long periods
immune response
risk factors for disease progression:

hbv dna levels:
> 10^3 to 10^4 virions/mL
risk factors for disease progression

genotype:
C infection
risk factors for disease progression

HBeAg neg ----
mutants. .. change virus. .. . toxic to liver
risk factors for disease progression

co----

--- age

--- sex
coinfections

older

male
risk factors for disease progression

severity of --- ---
liver disease at diagnosis
risk factors for disease progression

frequency of --- ---/ ab --- ---
hepatic flare

liver function
risk factors for disease progression

--- use and ---
etoh

smoking
if positive active viral infection:
HBsAg

(acute or chronic)
w/ chronic hep b virus what's not present
no antiHBs
if positive: immunity is present (via vaccination or infection)
HBsAb
if present it indicates exposure to HBV (not vaccine)

core antigen cannot be detected
HBcAb

only seen in infection
derived from HBV pre-core and serves as a marker of HBV replication and infectivity
HBeAg
if ABsAg - and antiIIBs-

what do u do
give vaccine
if ABsAg - and anti-IIBs +

what do you give
nothing

immune
HBeAg +

alt < 1 uln?
monitor

q 3-6 months ALT

q 6-12 month HBeAg
HBeAg +

ALT 1-2 x ULN
Q 3 mo ALT

q 6 mo HBeAg

bx persistent or more than 40 yrs

treat
HBeAG +

ALT > 2 x ULN
q 1-3 mo ALT, HBeAg

Bx optional

Treat! (jaundice, decompensated or persistent)
HBeAg-

ALT > 2 x ULN

HBV DNA 2000 IU/L
bx optional

treat if persistent
HBeAg-

ALT 1-2 x ULN

HBV DNA 2000-20,000
q 3 mo ALT

consider Bx

treat prn
HBeAg-

ALT < 1 x ULN

HBV DNA < 2,000 U/mL
Q 3 mo ALT x 3

then

6-12 mo if stable

monitor
goasl of tx:

reduction in ---- ---


limit --- disease

improve or control the extent of -----
HBV replication

progressive disease

damage
surrogate endpoints of tx:

--- reduction

biochemical ------

---- improvements

---- loss or seroconversion
virological reduction ( dna undetectable or suppression)

biochemical normalization (ALT)

histological improvements (dec inflammation and stage of fibrosis)

HBeAG adn HBsAg loss or seroconversion
interferon/pegylated interferon
has better responses in genotype:
A and B
interferon/pegylated interferon

not recommened for
decompensated cirrhosis
interferon/pegylated interferon

HBeAg+: increased -------

lower level -----

give to -- and ---- if inc in ALT's
ALT's

DNA

asians

kids
interferon/pegylated interferon

does not respond well to high --- ---
viral loads > 200, 000
frequency of interferon
3 x week
how long should you give interferon HBeAg +
4-6 months
how long should you give interfereon HBeAg-
1 yr
benefits of interferon
no drug resistance and set duration
ae of interferon
flu like symptoms

leukopenia

thrombocytopenia

depression

anxiety

irritability

hair thinning

hypo/hyper thyroidism

visual disturbances
interferon should not be used w/
cirrhosis . . .due to flares
the least potent nucleoside/nucleotide analogs
adefovir

~30% resistance at 4 yrs
what are not cross resistant
adefovir

tenofovir
what's x resistant
lamivudine

telbivudine

entecavir
nucleoside/nucleotide analogs

which do you monitor for nephrotoxicity
tenofovir

adefovir
telbivudine increases --- and --- ---
CK

peripheral neuropathy
nucleoside/nucleotide analogs

prob w/ hiv pos patients
increase risk of HIV drug resistance w/ monotx
duration of nucleoside/nucleotide analogs tx
> 1 yr

additional 6 mo after eAg conversion
benefits of nucleoside/nucleotide analogs
oral meds can be used in decompensated disease or thos waiting transplant