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GI, liver, kidney > Acute Hepatitis + chronic hep B > Flashcards

Acute Hepatitis + chronic hep B Flashcards

1
Q

What is hepatitis A

A

self-limiting viral illness spread through the faecal-oral route that primarily causes inflammation of the liver.

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2
Q

How does hepatitis A present

A

Flu like symptoms
Right upper abdominal pain
Nausea, diarrhoea, vomitting
Jaundice can develop

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3
Q

Incubation period hep A

A

Incubation - 28 days/4 weeks

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4
Q

First line test for heatitis A

A

PCR test for hep A RNA

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5
Q

Second line test for hep adn when repeat

A

IgM HAV + IgG HAV blood tests
Repeat in 1-2 weeks if within 10 days of symptom onset

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6
Q

What does + IgM HAV antibodies mean

A

Acute hep A infection

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7
Q

Negative IgM and + IgG HAV antibodies suggests

A

Past hep A infeciton or immunity (vaccination)

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8
Q

Investigations for hep A

A

PCR/IgG/M HAV antibodies
LFTs

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9
Q

LFTs in hep A

A

Significant raise ALT and AST (>1000)
Bilirubin and PT may be elevated
ALP may be elevated, less thna 2 x upper limit
Check INR <1.5 /albumin

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10
Q

Diagnosis of hep A probabale

A

Acute illness + onset of suggestive features + jaundice OR raised ALT and confirmed contact with hep A case OR HAV IgM antibodies

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11
Q

Confirmed case of hep A

A

Acute illness + suggestve features + raised ALT OR jaundice +
Hep A RNA etected
Asymptomatc but anti-HAVIgM and contact with confirmed case

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12
Q

General management hep A

A

Manage at home unless severely unwell
Rest and hydrate
Pain relief as required
Anti emetics - metoclopramide/cyclizine
Itch - loose clothing, avoid hot baths + showers, use chlorphenamine
Avid alcohol
AVOID FOOD PREP AND SEX 7 days after onset
Off school or work 7 dyas after onset

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13
Q

Monitoring f hep A

A

LFTs every 1-2 weeks and general follow up, repeat until ALT and AST in normal ranges

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14
Q

Why is it important to identify hep A

A

Notifiable disease

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15
Q

Rare complications of hep A

A

Relapsing course of illness over several months
Fulminant liver failure, acalculous choleccystitis, pancreatitis, aplastic anaemia, post viral encephalitis, reactive artheritis, AI haemolysus, TP, G6PD def, GBS, transverese myelitis, renal failure, cryoglubinaemia, mononeurtis multiples

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16
Q

Routes of transmission of hep B

A

Vertical - transplacental, childbirth
Sexual
Percutaneous transmission - IVDU, tattoos, piercing etc
Blood transfusion or organ donation - v rare

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17
Q

Hep B pathophysiology

A

cyctotoxic T cells target hepatocytes -> liver damage by inflammation, fibrosis
Cytotoxic direct damage in fibrosing cholestatic hepatitis

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18
Q

4 phases of HBV

A

Immune tolerance
Immune clearance - symptoms and damage occur
Immune control - biochem tests normalise
Immune escape - HBV escapes and replicates again

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19
Q

Problems with hep B presentation

A

Non specific - similar to many other causes of liver damage
Risk factors help differentiate
Massive clinical variation between individuals

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20
Q

Acute hep B infection presentation

A

Majority asymptomatic - >90% asymptomatic in children, 70% in adults
Prodrome - N+V, anorexia, fever, abdo pain (Flu like = serum sickness like syndrome - malaise,chills, lethargy, arthralgia )
Acute hep - Jaundice,
Hepatomegaly, RUQ pain, dark uirne pale stools
Fulminatn acute liver failures

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21
Q

Fulminnat acute liver failure presentation

A

Jaundice
Altered mental state (e.g. confusion, lethargy, drowsiness, stupor comatose)
Asterixis
Symptoms of raised intracranial pressure from cerebral oedema (e.g. headache, sluggish pupillary response, systemic hypertension and bradycardia, seizures)

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22
Q

Chronic heo B presentation

A

Asymptomatic until complications often
Non specific symptoms eg fatigue, anorexia, wight loss, weakness, malaise
Symptoms of chronic liver disease
Cirrhosis and portal HPTN
Extra hepatic manifestations - serum sickness like syndrome
Polyarteritis nososa, membranous nephropathy

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23
Q

Symptoms of chronic liver disease

A

Palmar erythema
Spider angiomas (the number and size of spider angiomata correlate with increasing severity of liver disease)
Asterixis
Easy bruising (reduced production of clotting factors in liver)

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24
Q

Symptoms of cirrhosis and portal HPTN

A

Ascites
Hepatmogealy
Splenomegaly
Peripheral oedema
Caput medusae

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25
Q

Investigations for hep B

A

LFTs
Hepatitis serlogy - HBsAg (surface antigen), anti-HBs (surface antibody), anti-HBc (core antibou)
Serum HBV DNA
FBC, U+Es, creatinine, coag screen, albumin
Liver US

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26
Q

ALT+AST in hep B acute infection

A

> 25 x upper limit of ALT+AST

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27
Q

ALT+AST in chronic HBV

A

Mildly raised - 2 x upper limit of normal

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28
Q

Active flares/exacerbations of chronic HBV AST/ALT

A

> 10 x upper limit normal

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29
Q

AST/ALT in chronic HBV carriers

A

Usually normal

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30
Q

ALP+GGT in hep B

A

AST/ALT will be raised much further in hep B infection

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31
Q

What happens to AST:ALT ratio in cirrhosis from viral hepatitis

A

AST>ALT - ratio doesnt normally exceed 2

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32
Q

When will HBsAg be positive? acute vs chronic?

A

ONLY in current infection - acute or chronic
Acute - appears 1-10 weeks after exposure
Chronic - persistent raised over 6 months

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33
Q

When are anti-HBs positive

A

For life after infection, aslo after vaccination, confirms immunity

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34
Q

When are anti-HBc antibodies present

A

Only present in prev or current infective state, not post vaccination
IgM - acute infectin, IgG - chronic infection

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35
Q

What antibodies would you see in previously infected patient hep B

A

HBsAg - Negative
Anti-HBc - Positive
Anti-HBs - Positive

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36
Q

Acute HBV antibodies on serology

A

HBsAg - positive
AntiHBc - IgM postiive
Negative antiHBs

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37
Q

Chronic HBV antibodies on serology

A

Postiive HBsAg
IgG positive Antib-HBc
Negative AntiHBs

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38
Q

Prev vaccination antibodies

A

ONLY anti-HBs

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39
Q

What clinical use does serum HBV DNA testing have

A

Identify if patient -> antiviral therapy

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40
Q

Who is a candidiate for antiviral therapy hep B

A

Active liver disease, high HBV DNA titre

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41
Q

What can cause abnormal FBC in HBV?

A

Complications
Reduced Hb and microcytic aneamia- GIT bleed from portal HPTN
Normocytic anaemia - chronic disease
Reduced platelets - portla HPTN

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42
Q

What can cause U+e DISTURBANCE IN HBV

A

Hyponatremia - ascites dilutational
Hepatorenal syndrome from cirrhosis increases urea and creatinine

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43
Q

Synthetic liver function effect complications HBV

A

Reduced albumin
Elevated PT and INR

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44
Q

When use US in HBV

A

Chronic hepatitis B - evaluate fibrosis, cirrhosis and monitor for HCC

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45
Q

Monitoring in HBV

A

LFTs every 3-6 months when in crhonic state, more frequent if exacerbations
US every 6 monhts if chronic infection+/- cirrhosis or if high risk

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46
Q

Transmission of hep A

A

Faeco-oral route - contaminated food or water
Travel to places where virus ighly endemic

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47
Q

Risk factors for hep A transmission

A

Travel to endemi areas
Clotting factor disorders - factor VIII and IX concentrates can be sourecs
mEN WHO HAVE SEX WITH MEN/RISKY SECUAL BEHAVIOURS
IVDUs
Ocupational risk

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48
Q

High risk for hepatitis B

A

Exposue to virus
Sexually assaulted
Needle stick
HIV psotive
Babies of mothers with HBV
Risky sexual behaviour
Close family contacts with hep B

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49
Q

How is hep B prophylaxis given

A

Rapid immunisation schedule - 0,1 and 2 months or over 21 days
Can give immunoglobulins IM within 48 hrs of exposure alongside first vaccine
otherwise 0,1 and 6 months

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50
Q

Acute HBV management

A

Supportive - low risk of progression
Screen for other BBVs - HIV, hep C
Screen for hep D co-infection

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51
Q

What criteria need to be met before give active treatment for HBV acute infection

A

Sever coagulopathy (INR>1.5)
Persistent symptoms >4 weeks
Marked jaundice - bilirubin >3mg/dL
Presence of ascites or encephalopathy (acute liver failure)

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52
Q

What use in acute HBV infection

A

Entecavir
Tenofovir
Until HbSaG CONFIRMED ON SEROLOGY
Liver transplant for fulminnat hepatic failure - continue with drugs indeficitely

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53
Q

Chronic HBV indications for anti-viral therapy clincal criteria

A

Acute liver failure
Decompensated cirrhosis
Compensated cirrhosis + HBV DNA >2000IU/ml
Concurrent immunosupressive therapy
HCC

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54
Q

First line treatments anti viral therapy chronic HBV infection

A

Nucleotide analogues - Entecavir, tenofocir, Pegylated IFN-a

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55
Q

Nucleoside analogues vs nucloetide analogues

A

Nuceloside - entecavir, lamivudine
Nucleotide - tenofovir, adefovi

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56
Q

Goal of antiviral treatemtent

A

Reduce hepatic dysfunction and serocoversion HBsAg +-> negative , keep HBV DNA non detecetable in serum
Improved long term outcomes eg crrhosis/HCC developments
Reduce transmission HBV

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57
Q

Monitoring of treatment in chronic HBV

A

3 monthly HBV DNA until undetectable
LFTs 3 monthly
HBsAg yearly

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58
Q

High risk patietns foor HCC development

A

Cirrhosis
ASian men >40
asian Women 50 years old
FH HCC
Super infection hep D

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59
Q

Lifestyle with HBV

A

Avoid alcohol and hepatotoxc drugs eg paracetemo, amoxicllin-clavunate
Vaccinations- hep A + flu annually

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60
Q

3 main omplications of HBV

A

Fulminant liver failure
Liver irrhosis
HCC

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61
Q

What serum test direcely relates to risk of HCC from HBV infection

A

HBV DNA in serum

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62
Q

What is hep C

A

Slow progressive disease of liver caused by infection with hep C virus

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63
Q

What are most genotypes of hep C in england

A

1 + 3

64
Q

How is hep C transmitted

A

Contact with infected blood or blood derived products

65
Q

Those at risk of HCV

A

IVDUs most common (1/4)
Transufion of infected blood products before 1991
Re-use of medical equipment
Needelsticks and sharps injuries
Sharing razors, tattoo, piercings etc
Sexual trasnmission can occur in more risky behviours
Vertical trasmission mother lower risk than hepB, more if have HIV

66
Q

What increases risk of fulminant liver failure in hep C

A

Co-infection with hep A

67
Q

What increases risk of cirrhosis and HCC with HCV

A

Alcohol intake
Coinfection with hep B or HIV
IMmunosupression

68
Q

What is the significance of HCV in pregnancy

A

Adverse foetal outcomes - FGR, low BW. Most chilren - chronic infection and liver damage

69
Q

Most common comorbidities with HCV

A

Most to least common
Depression
DM
CKD
Sjrogens
Chronic renal disease
Symptomatic cryoglibulinaemia
Lichen planus
RA

70
Q

What HCV genotupes are more responsive to anitbirals

A

2+3 -
1,4,5,6 less

71
Q

Who do yuo offer HCV screening to

A

High risks:
IVDUs
Blood transfusion before 1991
Origin in country of med or high prevalence
Babies - HCV mothers
Prisoners
Cared for children
Hostels, homeless HIV+ men who have sex with men
Close contacts of known chronic infection with HCV
Also increased risk + clinical features, abnormal LFTs (ALT>10x upper limit)

71
Q

What risks worsen prognosis of HCV

A

Infection at older age .40 decrease resonse to treatment as age
Genotype
Men more likely -> cirrhosis
Black african american and hispanic people lower susteained viral reponse rates to antivirals
Co infection hep A or B or HIV
BMI >25
Smoking
Alochol intake
Immunosupression

72
Q

Clincial features of HCV

A

Non specific fatigue, myalgia, anxiety, depression, poor memory and conentration
N+V
RUQ abdo pain
Jaundice - cholestasis
Chronic liver disease if advanced
Majority asymptomatic in early stages of infection

72
Q

Routine screening for HCV

A

People who intend to donate blood or organs/tissue.
People with end-stage chronic kidney disease requiring renal replacement therapy.
Healthcare workers who perform invasive or exposure-prone procedures (for example surgeons).
Mothers at higher risk of HV

73
Q

Diagnosis of HCV

A

HCV RNA PCR/genotyping
for acute infection
antiHCV antibodies (if ever had, cat differentiate current)

74
Q

Assessment before initiating treatment for Hep C

A

Confirm diagnosis - HCV RNA
Genotype
Liver disease stage - biopsy, elastography, erum markers
Co-infections - HIV, hepB, hepA
LFTs - ALT, AST, bilirubin, albumin
FBC, U+Es, clotting screen, HbA1c, TFTs, ferritin level
Assess for CIs to DAAs + drug interactions

75
Q

What is sponteanous resolution of HCV defined as

A

Loss of serum HCV RNA in blood < 6 months

76
Q

What is a DAA

A

Direct acting antivirals

77
Q

What does regimen and treatment duratio =n of HCV depend on

A

HCV genotype
Whetehr cirrhotic
Treatment history
Renal unction

78
Q

First line for HCV

A

8-12 weeks of once daily DAA eg daclatasvir + sofosbuvir or sofosbuvir+simeprevir with o without ribavirin

79
Q

Monitoring of DAAs in HCV

A

HCV RNA LEVELS - assess response to therapy
adverse effects - rare
LFTs - ALT, AST, bilirubin

80
Q

Post treatment monitoring of HCV

A

Sustained virological response - undetectable HCV RNA 12 weeks post treatment
SVR12 = cure
Liver disease - HCC and cirrhotic complications if already cirrhotic/fibrotic

81
Q

How often monitor ALT in immune tolerant and clearnace phases of hep B Ag +

A

every 24 weeks
every 12 weeks at least 3 consecutive occassions if increase in ALT levels

82
Q

How often monitor inactive chronic he B

A

every 48 weeks - ALT and HBV DNA levels

83
Q

When can contract hep D

A

Only super infection if already have hep B

84
Q

Which hepatitis especially accelerates alcohol related liver disease

A

hep C

85
Q

When is hepatitis acute

A

<6 month duration of inflammation

86
Q

Complications of acute hepatitis

A

Acute liver failure
Progression to chonic hepatitis

87
Q

Causes of acute hepatitis

A

Drugs eg paracetamol
Infections esp viral hep
Autoimmune
Pregnancy related
Toxins
Ischaemia
Malignancy
Budd-chiari syndrome
Wilsons disease

88
Q

What can cause acute hepatitis in immunocomp - rare/travel ass

A

immunocomp - VZV, HSV, adenovirus, invasive fungal eg candidiasis
Rare/travel - hep D, yellow fever, leptospira, typhoid, TB, Q fever (coxiella), malaria, liver flukes, schistosomiasis

89
Q

Prodrome hep A how long and what causes

A

3-10 dyas - flu like, GI, low grade fever

90
Q

Icteric period hep A (acute hepatitis)

A

Acute hep caused by own immune response After 10 dyas infection
Jaunduce, fatigue, anorexia, vomitting, RUQ pain, HEPATO/SPLENOMEGALY
Improve - 1-3 weeks, up to 12.

91
Q

Convalescent phase - hep A

A

recovey 6 up to 6 months - muscle weakness, malasie, anorexia, heptaic tenderness

92
Q

Different presentations of hep A

A

ASymtpomatic - younger children
Acute liver failure - rare - old/pre-exist liver disease
Death

93
Q

How long is hep A infectious for

A

Approx 1 week after onset of jaundice - need to be in side room w own toilet in hospital
Dont handle food if at home

94
Q

What give hep A close contacts

A

Hep A vaccine
Human normal immunoglobulin if immunosupressed

95
Q

Prevention of hep A

A

Improved sanitation and hygeine
Education eg travellers
Hep A vaccination - purified, ina tivated

96
Q

Hep A vaccination who give to

A

Travellers to endemic areas
Men who have sex w men
IVDU
Chronic liver disease
Haem
Haemophilia
Occupational risk eg lab workers, sewage workers
Following exposure to infected

> 2 weeks before required, booster needed after 6-12 months

97
Q

What are the two types of hep E infection

A

Classical - 1/2
Sporaduc - 3/4

98
Q

Endemic countrie classical vs sporadic

A

Classic = resource limited countries
Sporadic - Resource ricj

99
Q

Hep E routes of transmission calssical

A

faeco-oral, like hpe A, mainly enedemic country travel

100
Q

Hep E routes of transmission sporadic

A

Zoonosis - undercooked meat esp pork
Faexo oral - contaminated water, shellfish
Blood transfusion

101
Q

At risk groups for classical hep E

A

Travellers
Usually young adults 15-40 - asymptomatic in children
Pregnant women

102
Q

At risk frous hep E sporadic

A

Increasing age
M>F
No increased mortality in pregnancy

103
Q

Incubation period in hep E

A

40 dyas - 2-9 weeks

104
Q

How does symptomatic hep E present

A

Prodrome - N+V, anorexia, fever, abdo pain
After 1 week -> acute hep - jaundice, dark urine pale stools, RUQ pain, hepatomegaly

105
Q

What are possible outcomes of hep E

A

Acute liver failure
Extraheaptic manifestations eg neuro
Full clinical recovery <2/3 months
Chronic hep E

106
Q

Who gets chronic hep E

A

Immunocompromised patients with genotype 3/4 - sporadic hep E

107
Q

Death in hep E - who

A

Classical - 1/2 genotype
25% fatality in pregnancy

108
Q

LFTs in hep E

A

Raised serum aminotransferases - ALT + AST >1000
Raised bilirubin + ALP

109
Q

How differentiate hep A + E

A

Hep E serology

110
Q

IgM vs IgG hep E serology - how test for chronic infection

A

IgM = acute
IgG = past infection
PCR + = current (confirm or test for chronic infection)

111
Q

Management for hep E

A

Supportive care
Infection control
Prevention of secondary cases

112
Q

What do for infection controlk hep E

A

Infectious for 3 weeks after jaundice onset
Side room, no handling food etc

113
Q

Mortality in hep B

A

Higher than in hep A/E

114
Q

Prognosis of hep B

A

Majority of adults clear hep B spontaneously without complication

115
Q

Chronic hep B who does it progress into this in

A

> 90% those infected perinatally
20-50% children
5% adults

116
Q

Prognosis of chronic hep B

A

Majority still clear on own
May progress to chronic iver sdisease

117
Q

Hep B incubation period

A

Incubation 60-90 days

118
Q

What markers are present when patients are symptomatic with acute hep B

A

HBsAg
IgM Anti-HBc
HBeAg
ALT increase, jaundice

119
Q

What markers are present after acute infection

A

Anti-HBe
IgG anti-HBc
Anti-HBs

120
Q

Why need to contact sexual partners in hep B quickly

A

Can give hep B vaccine +/- HBIG to prevent infection within certain window

121
Q

What test for to check hep B clearnance

A

Loss og HBsAg
antiHBs antibodies present

122
Q

Prevention of hep B transmission

A

Education re modes of transmission - safe sex, needle exchange
Increased testing - antenatal screening, blood products
HepB immunoglobulin
HepB vaccines

123
Q

Hep B immunoglobulins when give them

A

Neonates w highly infectious mothers, unvaccinated who have definitive exposure eg needlesitck/sexual to HBV positive source, HBV vaccine non responders who recieve possible exposure

124
Q

What is hepB vaccine

A

Recombinant hepatitis B surface antigen
Safe and highly effective
Pre and post exposure to preevnt infection

125
Q

Who is vaccinated against hep B

A

All neonates
Anyone at increased risk exposure to HBV - close contacts, travellers, risky sexual behaviour, IVDU, regular blood products, renal failure haemodialysis, residential accom learning difficulties, inmates, occupational risk

High risk complications disease eg HIV, chronic liver disease

Post exposure vaccination - needlesticj, sex, neonates Hb +

126
Q

Hep B vaccination how give

A

Usually at least 3 doses
Neonates -8,12,16 weeks of age
0,1,6 months - healthcaer
0,1,2,12 months - rapid course

127
Q

EBV + CMV hepatitis

A

Ass w glandualr fever/mononucleosis syndrome (fever, sore throat, lymphadenopathy, fatigue etc)
Mild hepatitis 90%, rest have clinical jaundice
Risk increased hepatitis

128
Q

Pathogenesis of Hep B chronic infection

A

Host immune response to virus -> liver inflammation and heptitis
Persistent -> liver fibrosis and damage
Doesnt happen to everyone w hep B

129
Q

Investigating chronic hep B

A

Lab markers LFT - ALT
HBsAg, HBeAg, Anti-HBe, HBV DNA, Anti-HBs
Liver imaging, biopsy, non invasive methods eg transient elastography

130
Q

What is the E antigen

A

HBV specific protein secreted from virus infected cells
Supresses immune system
E antibodies reduces viral replication - reduces severity and infectivity
Seroconversion from E antigen to antibody does not equate to disease history

131
Q

When does seroconversion from E antigen to E antibody occur in chronic hep B

A

End of stage 2 - after immune system triggered

132
Q

Stages of chronic hep B

A

Stage 1 - infection - viral load high, liver function normal
Stage 2 - Immune system triggered after months - years, high ALT, decreased E antigen
Stage 3 - months/years, normal ALT, low HBV DNA levels
Stage 4 - HBeAg negative, mod to sev fibrosis, moderate raised ALT, can clear virus from blood
Stgae 5 - functional cure - past infection

133
Q

What can persist in cells after clearnace of hep B infection

A

cccDNA
Can reactivate if then become immunosupressed, therefore screen before start drugs

134
Q

General management of hep B

A

Referr to specialist for full assess
Prevent scondary cases - transmission, testing etc
Prevent further liver damage - other BBVs, vaccinate for hep A, reduce alcohol
Treatment w antiHBV durgs if needed

135
Q

Function of treatment for hep B

A

Supresses hep B, doesnt clear - therefore long term

136
Q

End points of treatment for hep B

A

Ideally loss of HBsAg but RARE
Loss of HBeAG/anti-HBe seroconversion
Supression of HBV DNA
ALT normalisation

137
Q

Nucelotide analogues how work in chronic hep B

A

Inhibit viral DNA polymerase
Oral tablets long term

138
Q

When is pegylated IFN-a used in chronic hep B, how is it iven and what does it do

A

If no cirrhosis
Long term immunological control
Finite duration of treatment
Injected

139
Q

INdications for chronic hep B treatment

A

Prevent disease progression and development of cirrhosis/HCC
-cirrhosis, HIV, FH HCC or corrhosis, hepatitis, high HBV DNA or ALT or HBeAg + >30yrs
Reduce transmission
Pregnancy w high HBV DNA levels
HBV + health care workers >200

140
Q

Co-infection vs super infection hep D

A

Co-infection = contracted at same time as hep B
Super infection = after hep B infection

141
Q

Clinical presentation of hep D

A

Acute infection - suspect if fulminant acute HBV, acute hepatitis in HBV patient
Chronic HBV + HDV - more rapid prgression to corrhosis and HCC

142
Q

Screen for hep D

A

Anti-HDV antibodies
HDV RNA for current infection

143
Q

Treatment hep D

A

Treat hep B and its cleared

144
Q

Why are genotypes of hep C important

A

Some are treatment specific
Can be co-infected with multiple genotypes or re-infected

145
Q

Hep B vs Hep C acute -> chronic infection

A

Hep C much less likely acute spmtomatic (20%)
Hep C much more likely to c=cause chronic (55-85%), hep B (5%)

146
Q

Development of cirrhosis in hep B

A

slow development - 20-30% over 20-30 years

147
Q

What is beneficial about hep C and immunosupression

A

Cure is possible - CANNOT reactivate once immunosupressed

148
Q

Wy is anti-HCV not that helpful in HCV diagnosis

A

Cant differentiate past and current infection
False negatives in immunocompromised patinets eg HIV
Negative in acute HCV infections

149
Q

When use HCV RNA PCR

A

Immunocomp patients
Acute hepatitis

150
Q

End goal of DAA treatmet of hep C

A

Clearance of hep C RNA from blood

151
Q

WHO elimination of viral hep 2030

A

INcrease hep B vaccination
Prevent vertical trasnmission
Blood and injection safety
Screening
Haem rediction
Diagnosis improved

152
Q

When can hep E be cause of chronic hepatitis

A

Immunosupressed paitents
Genotypes 3/4

153
Q

What test need to do diagnose hep E in immunocomp cases

A

HEV PCR
other tests may be falsely negative

154
Q

WHO elimination target for hepB and hepC

A

2030

GI, liver, kidney (50 decks)

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