viral hepatitis Flashcards

(27 cards)

1
Q

hep A:
— virus enterivrus ( — )
hep B:
— virus infects hepatocytes
Express viral — on surface and
triggers the – immune response
Hepatitis D:
—- viral particle
Defective—- virus
Uses hepatitis — surface — for propagation
Hepatitis C:
— virus (—-)
At least – distinct genotypes (—)
No cross— (ie can get reinfected with another —)
Hepatitis E
— virus
— genotypes

A

rna
picornavirus
dna
viral proteins
cellular immune
incomplete
rna
hep b
surface antigen
rna
flavivirus
6 (1-6)
cross protection
genotype
rna
4

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2
Q

Hepatitis B
3 virus forms : — particle, — form &—-
Filaments & Spheres:
Consist of — virus envelope
(contain — ) but lack —

A

dane ( its infectious )
spherical and filament
surplus
HBsAg
dna

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3
Q

Hepatitis A
* — only - virus shed in —
* Transmission
– Primarily — via — route
– Also - contaminated food and water
* Incubation period (time from infection to symptoms): 30 days (range 15-50)
* Period of Infectiousness — before
- — after onset of symptoms
* Worldwide
– Highest levels: — countries (almost all — have antibodies indicating prior infection)
– Developed countries most commonly seen in
* travellers to — countries
* Household or — contacts of known cases
* —
* Occasional foodborne outbreaks

A

humans
feaces
person to person
faecal oral
2 weeks
1 weeks
developing
children
endemic
sexual
gbMSM

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4
Q

epidemiology:
1- High HAV endemicity:
≥ — % seropositive by — yrs
Widespread — immunity
2- Intermediate HAV endemicity
≥ — % seropositive by — y, <—%
seropositive –y
3-Low HAV endemicity
≥ — % seropositive by — y, <— %
seropositive by — y
Increased — susceptibility
Higher risk of severe disease
4-Very low HAV endemicity
< – % seropositive by — y

A

90
10
natural
50
15
90
10
50
30
50
15
adult
50
30

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5
Q

Hepatitis E
* Infects both— and —
- —- genotypes = different — distribution + —
* 1 and 2: — , transmitted via —-contaminated water in developing countries
* 3 (dominant in — ) and 4: humans, pigs and other mammals.
Transmission to humans
1. Via food: undercooked/raw pig and game meat, processed pork and
shellfish (genotype —)
2. Spread —- through handling animals, particularly pigs
3. Contaminated water (when poor sanitation, outbreaks post flooding –
monsoons/storms)
Incubation period: 30-40 days post exposure (ie similar to hepatitis A and
shorter than hepatitis B or C)

A

animals and humans
4
geographic and epidemiology
humans
faecally
europe
3
directly

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6
Q

— is vaccine preventable and incubation period is 1-6 months
— has no vaccines and incubation period is 8 weeks
transmission to humans ( in both) :
1. Perinatally
2. Sexually
3. Parenterally (‘blood-borne virus’)
▪Sharing equipment used by injecting drug users
▪Haemodialysis, non-sterile glucometer equipment
▪Sharing personal care items (toothbrushes, razors)
▪Needle-stick injuries
▪Ear-piercing, tattooing, acupuncture

A

hep b
hep c

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7
Q

hep b :
Low prevalence areas:
Acute infection – / –
Spread = – / —
High prevalence areas
Acute infection in – & —
Spread = — /Close — contact

A

sporadic adult
sex / parentally
infants and young children
intrapartum / household
info :
Patients don’t present with a hepatitis virus
https://surewash.com/products/surewash-pocket/
They present with symptoms/signs of hepatitis or
complications of that viral infection

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8
Q

clinical presentation of viral hepatitis :
1- Signs/Symptoms
* Asymptomatic
* Symptomatic
– Often preceded by
prodromal symptoms (fever,
appetite loss, nausea,
fatigue, RUQ abdominal
pain)
– — urine
* bilirubin —
– pale greasy stools
* need bile to absorb fats
– jaundice
* build up of bilirubin
Abnormal Liver Function Tests (LFTs)
* Aspartate Aminotransferase
(AST) —
* Alanine Aminotransferase (ALT) —
* Bilirubin —

A

dark
increase
increase
increase
increase

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9
Q

hep a clinical course:
Acute Infection
* Asymptomatic in —
* Risk of symptomatic infection increases with — and — (e.g.,hepatitis B)
–prodromal symptoms X 1-2 weeks
* Fulminant disease (acute hepatitis failure) unusual <1%
NO — liver disease or — state
* Protective antibodies develop – infection

A

children
age and co-infection
chronic or carrier
after

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10
Q

Hepatitis E: Clinical Course
Acute infection
* 90% —
* Can be associated with— mortality
–fulminant hepatitis in — women (20%) Genotype —
= life-threatening to — and —
Chronic hepatitis:
* Reported in — patients (solid-organ
transplants, HIV)
* Can be associated with high mortality
– liver transplant recipients
– Genotype —

A

asymptomatic
high
preggo
1
mom and fetus
immunocomrpomseod
3

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11
Q

acute infection clinical course of hep b:
1- — infection
2- — infection
3- — hepatic failure 80% mortality without OLT

A

resolve
chronic
fulminant

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12
Q

Occurrence of symptoms during acute infection + outcome (resolved vs chronic infection) depend on the — at infection
* Occurrence of symptoms:
– 10% of children will have symptoms of acute infection
– 30-50% adults will be symptomatic with acute infection
* Outcome: Chronic infection or not
* Infected as an infant = — % will develop chronic infection
* Infected as an adult = < — % will develop chronic infection

A

age
90
<5%

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13
Q

Chronic Hepatitis B Infection
Infections persisting for more than —with
detection of — (surface antigen)
* Most patients = — carriers
* Symptoms may be — and patients may not present until very —- stages
* Cirrhosis, stigmata of chronic liver disease (25%of cases)
* Extrahepatic manifestations (10–20% of cases)
complication :
* —
* — cancer
* Reactivation of hepatitis B infection if —

A

6 months
HBsAg
inactive
non specific
late
cirrhosis
hepatocellualr
immunocomprosed

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14
Q

Hepatitis D
* Epidemiology: 5% of patients with chronic
hepatitis B infection are carriers
* Transmission: same as hepatitis B
* Course
– Co-infection with Hep B: more — acute
hepatitis, but 90% rate of convalescence
– Superinfection of a chronic HBsAg carrier: ↑ risk of
cirrhosis
– In rare cases, fulminant hepatitis

A

severe

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15
Q

hep c clinical course :
* Acute infection
– Most asymptomatic - rarely acute hepatitis
– Most develop chronic infection
* Chronic infection
– Cirrhosis, hepatocellular carcinoma
– Patients can be
* Asymptomatic
* Fatigue, nausea, anorexia, myalgia, arthralgia
* Present with signs of chronic liver disease
* Risk for progression: Alcohol++ / co-infection with hepatitis B or HIV
* Extrahepatic features (common):
– Haematological
– Endocrine: — , —
– —
– Dermatological

A

diabetes and thyroid’s
rheumatological

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16
Q

Hepatitis E
▪ RNA (stool & blood) during prodrome and up to 3 months
after onset of symptoms
▪ Antibodies (HEV – / —)
Hepatitis B: What can the
laboratory detect?
* Parts of the virus
– Hepatitis B surface Antigen (HBsAg)
– Hepatitis B e Antigen (HBeAg)
– Hepatitis B DNA (HBV DNA)
* The body’s response to the virus i.e antibodies
– Antibodies to HBsAg (Anti-HBs)
– Antibodies to Hepatitis B e Antigen (Anti-HBe)
– Antibodies to Hepatitis B core antigens (Anti HBc IgM &
Anti HBc IgG)

17
Q

Are you currently infectious?
HBsAg– Hepatitis — surface antigen
* —- serological marker
*Present >6 months = chronic
infection
Positive = current
hepatitis B infection
(acute or chronic)

18
Q

Are you “very” infectious?
Hepatitis B e antigen (HBeAg)
* Detectable when the virus is
actively —- (i.e. the person is infectious)
* Present in acute and chronic
infection
Also - Hepatitis B DNA
* Indicates presence of —
virus
* Used to — and —
treatment

A

reproducing
replicating

monitor and guide

19
Q

Has your immune system
recognised there is a problem?
* Hepatitis B core
antibody HBcAb
* First detectable
antibody to appear —- infection
* HBcAb ( — ) = acute
infection then…
* HBcAb ( – ) = usually
positive for life

A

after
IgM
IgG

20
Q

Has the infection resolved
(or have you been vaccinated)?
Anti Hepatitis B surface antibody (Anti-HBs)
* Usually the — hepatitis B antibody to
appear
* Positive = usually indicator that initial
infection —
(if Anti-HBs is the only positive HBV marker then the person
has been vaccinated)

A

last
resolved

21
Q

Hepatitis C Laboratory Diagnosis
* Hepatitis C antibody (Anti-HCV) – positive — months⃰ after
exposure to hepatitis C, will remain positive even if patient has
cleared the infection
* Hepatitis C antigen (HCV ag) – positive in acute and chronic
infection
* Hepatitis C virus (HCV) RNA – positive in acute and chronic
infection

22
Q

hep a :
treatment is —
prevention : hygien , sanitation , vaccination , travellers advice
1. Vaccination
Inactivated (not live) vaccine
Post-exposure: Management of
contacts of cases and for
outbreak control
Pre-exposure:
1. Travellers to endemic
countries
2. At risk individuals:
– Chronic liver disease
– Injecting drug users
– gbMSM
– Workers exposed to raw
untreated sewage
2. Passive Immunisation
( —- )= Post-exposure prophylaxis
In addition to or instead of the
vaccine
Needs to be given within 2 weeks
of exposure to be effective
Persons aged over 60 years
Immunosuppressed patients
> 12 months of age and at risk of
severe complications
* (those with chronic liver
disease, including chronic
hepatitis B or C infection)

A

supportive care
immunoglobin

23
Q

Hepatitis E
* Acute infection usually —- = symptomatic treatment
* Chronic infection in
transplant patients
– Reduce
immunosuppression
– —
* Vaccine developed but only
licensed in China

A

self limiting
anti virals

24
Q

hep b:
Acute infection = —- therapy
Chronic infection
1. Patient education
2. Vaccination
3. —- therapy
- Aim = prevent progression to — / liver
failure/cancer but can’t eradicate the virus
- Goal = reduce Hepatitis B DNA below detectable levels +
seroconversion of e antigen to e antibody
4. Monitor for Liver Cancer (Ultrasound, Alpha Feta Protein)
5. Transplant (Fulminant hepatitis, End Stage Chronic
Hepatitis)
Strategy varies with high & low prevalence areas
1. Standard precautions & avoidance of risk factors
2. Passive Immunisation (Immunoglobulin) = Post-exposure prophylaxis
– safe sex
– screen blood products
– clean needles / disposable
– good practice (standard
precautions)
* hand hygiene
* gloves , goggles, aprons etc
* safe disposal of sharps
Immunoglobulin (asap)
▪neonates
▪needle stick if no vaccine or inadequate
antibodies
▪after high risk sexual exposure
Vaccine - Given along with above

A

supportive
anti viral
cirrhosis

25
3. Pre-exposure prophylaxis = vaccination Cloned surface antigen(HBsAg) – Therefore you develop antibodies to HBsAg only i.e. Anti-HBs – There is no Hep B core antigen so WILL NOT have detectable Anti Hep B core Course of 3 Titres >10 IU/ml – ideally >100 IU/ml of Anti-HBs Who gets vaccinated? * High risk groups ( e.g. healthcare staff) * Part of national immunisation program
26
Hepatitis C Management Acute infection * No post-exposure prophylaxis Chronic infection – aim to ‘cure’ * Goal = ‘cure’ = sustained virological response (no detectable RNA at end of therapy and beyond 12 weeks after therapy is stopped) * Treatment regimens: – Depends on genotype, other co-infections (e.g., HIV), past history of antiviral treatment and degree of fibrosis – Directly-acting antivirals – cure rate >95% (previously cure was rare) – Also give hepatitis A + B vaccine
27
Prevention Standard Precautions Avoidance of risk factors – safe sex – screen blood products – clean needles / disposable – good practice (standard precautions) * hand hygiene * gloves , goggles, aprons etc * safe disposal of sharps No vaccine / immunoglobulin available