1. What is the treatment for acute hep B?
    • Conservative, OP
    • Liver function, PT, HBV status (HbsAg, eAg, anti-Hbe and anti HBs) monitored
    • Advice: do not drink alcohol and avoid hepatotoxic drugs until hepatitis resolved.
  2. Who needs to be tested for HBV? And what needs else to be done to them
    • Sexual and close household contacts: tested for evidence of current of past HBV infection
    • Give first dose of hep B vaccine to all sexual partners whilst awaiting results.
    • If NO evidence of either give active immunisation with hep B vaccine
    • If infected or already immune to HBV discontinue immunisation.
    • Give HBIG to recent susceptible sexual contacts. Close household contacts do not need HBIG, just the vaccine.
  3. What does the patient with HBV infection need to be warned about infectivity?
    Warn patient: infectivity of his blood: sharing razors, toothbrushes, needles. Do not donate blood for at least 2 years. Condom until no longer infectious and blood no longer contains HbsAg.
  4. What are the indications for hepatitis B vaccine?
    • 1. injecting drug users
    • 2. multiple sexual partners – prostitutes, homosexual and bisexual men
    • 3. household and sexual contacts of HBV infected persion
    • 4. baby born to HBV infected mother
    • 5. patients receiving lots of blood transfusion eg thalassaemic or blood products eg haemophiliacs
    • 6. relatives responsible for administration of blood products to eg haemophiliacs
    • 7. health care and lab workers who have contact with blood or blood contaminated body fluids
    • 8. chronic renal failure: need double dose of vaccine
    • 9. staff and patients in residential accommodation for mentally handicapped
  5. what is the HBV vaccine used in this country?
    • Recombinant HbsAg
    • Expressed in yeast cells
  6. If anti-HCV antibodies are absent, does that exclude an acute HCV infection?
    No because anti-HCV seroconversion may be delayed up to 1 month after an acute HCV infection.
  7. How is diagnosis of HCV made?
    Detection of serum HCV RNA or HCV Ag
  8. What are the ways HCV can be transmitted?
    • Needle stick
    • Blood products
    • Sexual
    • Mother to child
  9. What are the pathological features of Hepatitis?
    • Liver cell necrosis
    • Inflammatory cell infiltrate
  10. What are clinical features of viral hepatitis?
    • Liver enlarged and tender
    • Jaundice
    • AST:ALT ratio <1 (compared to alcoholic where it is >1)
  11. Which drugs can cause hepatitis?
    • Anti TB eg isoniazid
    • Paracetamol OD
    • Halothane
    • NSAIDs
  12. Acute heptatitis pathology
    • Ballooning degeneration
    • Councilman bodies (acidophils)
    • Inflam lymphocytes
  13. Which drugs can cause chronic active hepatitis?
    • Methyldopa
    • nitrofurantoin
  14. what are the symptoms of acute hepatitis?
    • Non-specific, pro-dromal symptoms eg fever, malaise, N+V, anorexia, diarrhoea, abdo pain, headache, myalgia, arthlagia
    • Jaundice follows a few days-2weeks later
  15. What examination findings of acute hepatitis?
    • Tender hepatomegaly
    • Splenomegaly
    • Cervical lymphadenopathy
    • Skin rash
  16. What is the most common type of acute hepatitis?
    Hep A
  17. How is hep A spread, who?
    • Travellers tropics
    • Faeco-oral
    • Raw or poorly cooked shellfish
  18. What is the incubation time for hep A? and what type of virus?
    • 2-6 weeks
    • ssRNA
  19. when is the virus present in the infected person’s faeces?
    • 2 weeks before onset of jaundice
    • But only a few days after symptoms! So spread before you know you've got it!
  20. How is hep A diagnosed?
    showing IgM anti-HAV in the patient's blood. This antibody is present within 10 days of onset of viraemia and therefore detectable at presentation in almost all cases.
  21. What is the treatment of hep A?
    • Supportive, no alcohol
    • If fulminant then give interferon alpha
  22. Who needs hep A prophylaxis?
    • 1. pre-exposure: active immunisation eg Havrix monodose, an inactivated protein derived from HAV
    • a. traveller
    • b. severe CLD
    • c. job risk
    • d. haemophiliac
    • e. homosexual
  23. 2. post exposure
    a. passive immunisation HNIG (human normal Ig) to contacts and household, remember faeco-oral!
  24. What is the natural progression of hepatitis A?
    • Usually self-limiting
    • Over in 3-6 weeks
  25. Which kind of people are at risk of hep A?
    • 1. travellers
    • 2. vagrants
    • 3. sanitation workers
    • 4. workers in child care centres and institutions for the destitute
    • 5. homosexual men
    • 6. recipients of clotting factors
    • 7. community wide outbreaks
  26. what type of virus is hep B?
    dsDNA virus
  27. what is the incubation period for hep B?
    2-6 months
  28. What are the modes of transmisison of hep B?
    • Vertical: mother to infant
    • Needle stick injury
    • Needle sharing IVDU
    • Tattoos
    • Piercings
    • Sexual
    • Blood and blood products
  29. Where can expression of HbcAg be seen in the cell?
    Hepatocyte nuclei
  30. Where can expression of HbsAg and HbeAg be seen in the cell?
  31. When is the eAg made and what does high levels indicate?
    • Made in active viral replication
    • High levels indicates high degree of infectivity
  32. What do the cells look like in acute hep b?
    Ground glass hepatocytes
  33. What is the mortality assocaietd with acute hep b infection?
    Less than 1%
  34. What % of adults will become HBV carriers?
  35. Which age group/type of people are most likely to become HBV carriers?
    HBV infections in neonates and immunosuppressed
  36. What may HBV carriers develop?
    • CLD
    • Cirrhosis
    • HCC
    • Extra-hepatic disease: GN in childern, PAN, cryoglobulinaemia
    • Cholestasis
  37. What makes a carrier have high infectivity and what are they referred to and why?
    • When their serum contains lots of sAg and eAg
    • Referred to as supercarriers as are principal reservoir of infection
  38. How do carriers become less infective? Describe blood results and what are these people referred to as?
    • After time the infection becomes partially suppressed
    • The sAg remains in serum but eAg is replaced by anti-HBe and virions disappear from circulation
    • These carriers are less infectious and referred to as SIMPLE carriers
  39. What defines chronic hep B?
    Presence of surface antigen for over 6 months = carrier status: chronic
  40. If a patient had anti-HbsAg alone, what would that indicate?
  41. In HBV, what is the method of monitoring the response to treatment?
    HBC PCR – see the viral load
  42. What is the prognosis of an acute HBV infection which presents with jaundice?
    Virtually NEVER leads to CHRONIC carriage
  43. What is the treatment of acute hep B?
    • Conservative
    • Supportive
    • No alcohol
  44. What is the treatment of chronic hep B, which group of patients are treated and why?
    • Treat supercarriers (eAg+) in order to seroconvert them to simple carriers who have anti-HBe
    • Use interferon-a and lamivudine (nucleoside analogue. Nucleoside reverse transcriptase inhibitor (NRTI)
  45. What needs to be given to non-immune contacts after high risk exposure? Give example of who
    • Passive immunisation with HBIG
    • Eg newborn baby of HBsAG positive mother
  46. Which staff cannot do EPPs?
    If HBeAg carriers
  47. Which parts of the world is HBV common in?
  48. How do you know if an acute hep B infection has recovered completely?
    Disappearance of HBsAg frin serum (and will have anti-HBs)
  49. What are the SE of lamivudine?
    • Lactic acidosis
    • Loss of subcut fat
    • Nausea, dyspnoea
  50. What are SE of pegINF?
    • Neutropenia
    • Insomnia
    • Flu like symptoms
  51. What are the adv of pegINF over normal INF?
    • Increased half life
    • Reduced clearance
    • Only need once weekly dosing
    • Better response rates with peg
  52. What are the complications of HBV infection?
    • Chronic hepatitis
    • CLD
    • Cirrhosis
    • HCC
    • Cholestasis
    • GN
    • Cryoglobulinaemia
    • Fulminant hep failure
  53. Where has a national HBV vaccine been introduced and what has this led to?
    reduction in incidence of HCC particularly in countries such as Taiwan, which has high prevalence of hepatitis B
  54. What type of virus is HCV?
  55. what is the incubation period of HCV?
    2-3 months
  56. Before screening of blood donoation, what was the most important cause of post-transfusion NANB hep?
  57. What is the MAIN mode of transmission of HCV?
    • IVDU and needlestick
    • Mother to child and sexually is seen but not as much
  58. How many different genotypes of HCV are there?
  59. What are the clinical features of most acute infecitons?
    Subclinical! If there are symptoms they are usually MILD. Jaundice is uncommon, only in about 10%
  60. What proportions of acute infections develop into chronic?
    Majority! 70%
  61. What can chronic HCV infection act as a trigger factor for developing…?
    • GN
    • Mixed essential cryoglobulinaemia
    • Porphyria cutanea tarda
    • GN
    • Autoimmune liver disease
  62. What is Porphyria cutanea tarda?
    • Blistering of the skin in areas receiving high levels of sunlight exposure. Heals with scars
    • It is due to enzyme deficiency is the last step of haem synthesis
  63. How is ACUTE HCV infection diagnosed?
    • Detection of HCV RNA by RT-PCR
    • Serology cannot be used for HCV infection as seroconversion may be delayed for several months
  64. How is chronic HCV infection diagnosed?
    Serology: antibody detection (as takes several months for antibodies to form after acute infection)
  65. What is the treatment of HCV? And how many get viral eradication?
    Infereon and ribavirin. 40% eradication
  66. How does the treatment of HCV depend on its genotype?
    • Genotype 1, 4: treat for 1 year (40% sustained response)
    • Genotype: 2, 3: treat for 6 months (80% sustained response)
  67. How is HCV treatment monitored?
    Quanititative real time RT PCR to measure viral load
  68. What is the prophylaxis for HCV infection?
    There is none at the moment! No vaccine yet
  69. What type of virus is hep D? what does it need to replicate?
    • Delta virus
    • Defective RNA virus
    • Dependent on Hep B for its own replication
  70. What are the 2 patterns of replication of Hep D? which is more likely to become chronic?
    • Co-infection: HDV simultaneously with HBV infection
    • Superinfection: infection of HDV into a person with acute or chronic HBV. Superinfection usually develops into chronic HDV infection and high risk of CLD, cirrhosis, hepatoma
  71. What happens to the total anti-HDV levels in co-infection? Also what happens to ALT?
    • Become undetectable fast, even though it’s a severe infection, it is ACUTE
    • ALT goes high first then low quickly
  72. What happens to the total anti-HDV levels and ALT in superinfection?
    Total anti-HDV remains high and ALT remains high
  73. What is the MAIN mode of transmission of HDV?
    Parenteral – IVDU (can sexually)
  74. How is prophylaxis of HDV achieved?
    By preventing HBV infection
  75. What type of virus is Hep E?
  76. how is Hep E transmitted? And what is it assoc with?
    • Faeco-oral route
    • Assoc with large water-borne outbreaks eg sewage overflow into water reservoirs
  77. What is the spread of HEV like in household contacts
    LOW as its not spread by close contact
  78. What is the natural progression of HEV and what makes its prognosis bad?
    • Usually self-limiting, like HAV.
    • In pregnancy: very high mortality of 20%
  79. How is the diagnosis of HEV made?
    • Serology: anti-HEV antibodies
    • Can use HEV RT-PCR to confirm infection
  80. What is the treatment of HEV?
    Supportive with complete resolution in most cases.
  81. What is the prophylaxis for HEV?
    None but ENSURE CLEAN WATER SUPPLY (no uncooked or shellfish)
  82. What are the features of Hep GBV-c?
  83. What is spread of Hep GBV and who gets it?
    • Spread: parenteral
    • post-transfusion hepatitis
  84. what is the progression of HGV?
    • Infections resolve spontaneously
    • But persistent infections are common with a prevalence of 2% in UK
  85. When there is jaundice, what level of bilirubin is likely to be in the blood?
    Over 50umol/l
  86. When you think a patient has Gilberts but want to clarify, which simple blood test can be done?
    Split bilirubin and the unconjugated will be higher than the conjugated
  87. Which clotting factor does the liver NOT make?
    Factor 8
  88. Give 2 situations when there is a raised unconjugated bilirubin?
    • Haemolysis: acquired/inherited…
    • Failure of conjugation: Gilberts, neonate
  89. If there is a raised conjugated bilirubin, what does that indicate?
    Haemolysis or failure of conjugation
  90. Give 2 reasons why urinary urobilinogen would be absent?
    • Obstruction
    • No gut flora
  91. When would you see a raised urobilinogen?
    • Haemolysis
    • Hepatocellular dysfunction
  92. Which protein is an important marker of acute liver damage and why not another one?
    • Clotting factors as short half life.
    • Not albumin as long half life of 20 days
  93. What is the deficiency in Wilsons?
  94. What are the values for iron, ferritin and TIBC in haemochromatosis?
    Iron up, ferritin up, TIBC down or normal (as transferrin is fully saturated)
  95. Which Ig is raised in PBC?
  96. Which Ig is raised in micronodule cirrhosis?
  97. If there is a raised ALP, which simple test can you do to confirm the ALP is coming from liver?
    GGT as it follows ALP pattern
  98. What type of liver disease do you see a raise in GGT?
    Alcoholic liver disease
  99. What are the causes of pre-hepatic jaundice?
    • Ineffective erythropoeisis: pernicious anaemia
    • Excess RBC destruction: immune anaemia, sickle cell
    • Breast feeding
    • Novobiocin
    • Gilbert’s
    • Crigler Najjar
    • prematurity
  100. what are the causes of intrahepatic jaundice?
    • Drugs: chlorpromazine
    • Hepatitis
    • CLD
    • Infiltration: tumour, sarcoid,
    • Rotor syndrome
    • Dubin Johnson
  101. What are causes of extrahepatic jaundice?
    • Head of pancreas ca
    • Stones in CBD
    • PSC
    • Biliary atresia
    • Cholangiocarcinoma
  102. Why do you get excess urobilinogen in hepatic jaundice?
    Failure of liver to take it up after gut absorption therefore more excreted via kidneys
  103. If you suspect tumour and detect noradrenaline which tumour is it?
    in phaeochromocytoma
  104. If you suspect tumour and detect 5HIAA which tumour is it?
    in carcinoid tumours
  105. If you suspect tumour and detect Calcitonin which tumour is it?
    in Medullary Ca Thyroid
  106. If you suspect tumour and detect HCG which tumour is it?
    in Choriocarcinoma / Teratoma
  107. If you suspect tumour and detect Prolactin which tumour is it?
    in prolactinoma
  108. If you suspect tumour and detect paraprotein which tumour is it?
    in myeloma
  109. If you suspect tumour and detect PSA which tumour is it?
    in prostate
  110. If you suspect tumour and detect AFP which tumour is it?
    in hepatoma / testicular teratoma
  111. If you suspect tumour and detect CEA which tumour is it?
    in colorectal carcinoma
  112. If you suspect tumour and detect CA125 which tumour is it?
    in ovarian carcinoma
  113. If you suspect tumour and detect CA15-3 which tumour is it?
    in carcinoma of breast
  114. If you suspect tumour and detect CA19-9 which tumour is it?
    in adenocarcinoma of pancreas
  115. if you suspect ca pancreas, which Ix would u do?
  116. If you suspect cholangitis which Ix would u do and what are u looking for?
    Ultrasound to look for GS and thickened GB wall
  117. What is the most likely cause of a swinging temperature and a cystic liver mass in an international aid worker?
    Amoebic liver abscess
  118. What type of liver damage does paracetamol do?
    Acute hepatitis
  119. What type of liver damage does methotrexate do?
  120. What type of liver damage does octreotide do?
    Gallstones as it alters fat absorption and reduces GB motility
  121. What type of liver damage does chlorpromazine do?
    Acute cholestatic
  122. By eating mouldy food, what is the potential liver damage?
    Neoplasm – aflatoxins made by fungi increase risk of HCC
  123. What is Dubin-Johnson syndrome? symptoms
    • Autosomal recessive cause of intrahepatic cholestatic jaundice
    • Defective hepatocyte excretion of conjugated bilirubin
    • Intermittent jaundice and pain in R hypochondrium
  124. What is Rotor syndrome?
    Defective excretion of conjugated bilirubin producing cholestatic jaundice
  125. If a lady of age 44 had high ALT and AST and was feeling malaise and fatigue, what liver problem is it and what further test?
    • Autoimmune hepatitis
    • Do antiSMA (not LKM1 as children get type 2)
Card Set
hepatitic etc