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imed3004 COPY > Hepatobiliary Infections > Flashcards

Hepatobiliary Infections Flashcards

1
Q

How is hepatitis diagnosed?

A

Clinically: jaundice (not always), fever, nausea, malaise, vomiting

Biochemistry: Bilirubin may or may not be raised. Hepatitic (ALT rise) vs cholestatic picture (ALP, GGT rise)

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2
Q

Which hepatitis viral strains are known to cause ciinical disease in humans?

A

Hep A to E; B, C and D cause chronic infections for longer than 6 months in the immunocompetent.

Hep E can cause hepatitis as part of a systemic infection.

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3
Q

What viruses other than hepatitis viruses can cause hepatitis as part of the systemic infection?

A

EBV

CMV

Yellow fever virus

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4
Q

What is the most common hepatitis virus?

A

Hep C virus

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5
Q

How is hepatitis A spread?

A

Faecal-oral route (oysters, water contaminated by sewage, berries)

World wide illness

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6
Q

What is used to diagnose hepatitis A?

A

Detection of IgM antibody for acute disease (lasts 6 - 9 months)

PCR of blood and stool

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7
Q

What happens after the body is able to clear hepatitis A infection?

A

Lifelong immunity is built

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8
Q

What is the incubation period of hep A?

A

About 1 month they typical hepatitis in adults

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9
Q

What kind of illness to children get when infected with HepA?

A

Asymptomatic or mild illness

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10
Q

What kind of vaccine is HepA?

A

Inactivated whole virus

Single dose protects for at least 1 year, 2 doses at least 10 years

Used for post exposure prophylaxis within 2 weeks of exposure.

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11
Q

What kind of virus is hep E?

A

RNA virus related to rubella virus

Found worldwide, especially SEA, India, Middle East, Africa, and Mexico

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12
Q

How is hep E diagnosed?

A

By serology and PCR; IgG in people that have gotten rid of hep E and IgM in people with ongoing disease.

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13
Q

How is hep E treated?

A

Therapy usually not required but can use interferon or ribavirin in chronic hepE infections in the immunosuppressed.

No vaccine

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14
Q

How is hep E transmitted?

A

Faecal oral route like hep A

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15
Q

What are the symptoms of hep E infections?

A

5% develop jaundice

Mortality up to 20% in pregnancy

Chronic hepatitis in immunosuppressed

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16
Q

What kind of virus is hep B?

A

Lipid coated DNA virus.

Has DNA polymerase.

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17
Q

Where is hep B most common?

A

Asia South African countries and Northern Canada.

Australian indigenous

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18
Q

How does hepB replicate?

A

HepB gets internalized

Capsid moves to nucleus and replicates

Forms a surface antigen

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19
Q

How is HBV infection different in neonates compared to adults?

A

In 95% of neonates it becomes chronic. In 5% of adults.

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20
Q

What does surface antibody, surface antigen, IgM anti HBC, anti HBe, and HBeAg tell us about state of infection?

A

Surface antibody is a marker of past infection

Surface antigen is a marker of current infection

IgM is a marker of recent infection

Over time you lose your e antigen and develop e antibody.

Someone with infection will be positive for HBV DNA

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21
Q

What happens in neonatal HBV infection that goes chronic?

A

Immune tolerance for the first 15 years (tolerant phase)

Immune clearance (formation of antibodies to HBV start to form)

Immune control where most HBV carriers sit. (No liver inflammation and minimal viral load)

Immune escape where viral load starts to rise as well as anti-HBe antibodies.

The immune escape stage is where liver damage can be severe.

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22
Q

What are the clinical consequences in HBV carriers?

A

Liver fibrosis: More likely in high HBV viral load, HBeAg +ve, raised ALT, older, other liver toxins combined. If fibrosis is severe it can become cirrhotic (Childs-Pugh score) Can lead to portal hypertension

Can also possibly develop hepatocellular carcinoma whether cirrhotic or not.

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23
Q

What are the types of cirrhosis?

A

Compensated (lots of scar tissue but still functional) vs decompensated (Lots of scar tissue and not functional)

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24
Q

How is HBV treated?

A

Used to use interferon but now antiviral tablets are used. HBV rarely gets cured completely so antiviral tablets are taken for entire life.

These antivirals include:

Nucleosides such as lamivudine and entecavir (more potent, less resistance)

Nucleotides such as tenofovir (More potent, less resistance)

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25
Q

What are the markers of successful suppression of HBV?

A

HBeAg seroconversion to antiHBeAb

HBV DNA negative

Settling of liver inflammation.(raised ALT)

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26
Q

What do nucleotides do?

A

They block DNA polymerase in virally infected cells preventing HBV replication.

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27
Q

What does the HBV vaccine consist of?

A

Subunit vaccine (HBsAg only)

Immunity indicated by HBsAb level >10mlU/ml

28
Q

How are infants of carrier mothers with HBV treated?

A

They are treated with a vaccine and Hep B ImmunoGlobulins (HBIG)

29
Q

What kind of virus is Hep D?

A

A defective satellite RNA virus. HDV super-infection of HBV have accelerated disease with more rapid progression to cirrhosis

30
Q

How is HDV detected?

A

Serology (IgG) and PCR

31
Q

Is there a vaccine for HDV?

A

No vaccine

32
Q

How is HDV co-infection with HBV treated?

A

Interferon therapy to control HBsAg

33
Q

What are the main genotypes of HCV?

A

6 common genotypes numbered 1 - 6.

Most common: 1 and 3

Newly emergent strains: 4 from middle eastern people and 2 from parts of Asia

34
Q

What kind of infection does HCV result in?

A

Unstable virus, many mutants called quasispecies.

This results in many different viruses causing the infection.

35
Q

What kind of infection does HCV result in?

A

Unstable virus, many mutants called quasispecies.

36
Q

How does HCV evade the host immune system and what percentage of cases are successful at evading host immune system?

A

Due to formation of so many quasispecies; many different viruses cause the infection.

This feature of forming quasispecies allows them to evade immune system in 75% of cases.

25% of cases are eliminated completely.

37
Q

How is HCV transmitted most often?

A

Parenteral (blood exposure)

Developed countries: IVDU, tattoos, transfusion.

Developing countries: Medical practices, traditional practices.

Vertical (Mother to child): 3 - 5% risk overall for HCV RNA positive mothers.

Sexual transmission is very low with increased risk as a result of genital ulceration or anal intercourse.

38
Q

What are the potential outcomes of HCV infection?

A

From 1000 infected with HCV

250 clear infection

750 get chronic infection

Of the 750 70 develop cirrhosis at 20 years (200 at 40 years)

of the 70 with cirrhosis 2 - 10 develop hepatocellular carcinoma (over 5 - 10 years) and 10 develop liver failure (over 5 - 10 years)

39
Q

What are the clinical symptoms of HCV infection?

A

Non-specific symptoms:

Tiredness (43%), RUQ discomfort (18%)

Depression is common

Symptoms of cirrhosis and hepatocellular carcinoma

Extrahepatic manifestations such as essential mixed cryoglobulinaemia (neuropathy and a rash), porphyria cutanea tarda, lichen planus, and membranoproliferative Glomerulonephritis

40
Q

How is HCV diagnosed?

A

HCV antibodies indicate infection with HCV at some time. (False negative results can occur in immunosuppressed)

PCR (Defines active infection and becomes +ve before antibody test in acute infection)

Genotype and viral load

41
Q

How is HCV treated?

A

Previously interferon and then in 2016 and 2017

Combination of 2 agents:

Polymerase inhibitors: sofosbuvir

Assembly (NS5A) inhibitors: daclatasvir, ledipasvir, velpatasvir

Protease inhibitors: Grazoprevir

42
Q

How effective is HCV treatment?

A

Doesn’t always clear the virus but when it does it is gone completely (Cured)

Some regimens are pangenotypic such as epclusa (sofosbuvir + velpatasvir)

Antiviral resistance is a problem only in a few people (genotype 3 cirrhotics for example)

43
Q

What are the types of biliary system sepsis?

A

Acute cholecystitis (gallstone obstruction of gallbladder neck)

Ascending cholangitis (CBD obstruction)

44
Q

What causes acute cholecystitis?

A

Enteric GNBs cause most infections

45
Q

What causes Ascending cholangitis?

A

Enteric GNBs cause most infections (more severe disease as liver is involved and associated with bacteraemia)

46
Q

How are acute cholecystitis and ascending cholangitis treated?

A

Both are treated exactly the same way:

Amoxycillin + gentamicin/ceftriaxone/tazocin

47
Q

What causes acute pancreatitis?

A

80% due to obstruction (bile duct stones) or heavy alcohol use.

Other causes include high triglycerides, direct infections, alcohol and 10 - 15% are idiopathic.

48
Q

How does acute pancreatitis occur?

A

Autodigestion of pancreatic enzymes (If severe necrotizing pancreatitis with pseudocysts)

49
Q

What do antibiotics do for acute pancreatitis?

A

Limited to secondary bacterial infection of pseudocysts (pancreatic abscess)

50
Q

Which antibiotics are used to treat acute pacreatitis?

A

It is most commonly caused by GNBs so tazocin/ceftriaxone + metronidazole

51
Q

What is done to pseudocysts in acute pancreatitis?

A

They are drained.

52
Q

What are the 3 major forms of liver abscesses?

A

Bacterial (80% of cases)

Amoebic (10% in travellers)

Fungal (candida) in lymphoma and leukaemia (10%)

53
Q

How does bacteria infect the liver?

A

Biliary sepsis from ascending cholangitis 60%

Portal blood flow from abdominal sources 24%

Haematogenous (kelbsiella pneumoniae) 15%

54
Q

What is the prognosis of bacterial abscesses?

A

5 - 30% mortality with treatment and 100% mortality without treatment

55
Q

How do liver abscesses present?

A

Fever, malaise, RUQ pain

56
Q

How is a liver abscess diagnosed?

A

Blood cultures positive (50% cases)

Amoebic serology if there is history of travel.

Abscess aspirate is definitive for aetiology

CT scan is 95+% sensitive, U/S is 80 - 90% sensitive

57
Q

How is a liver abscess treated?

A

Antimicrobials depending on aetiology:

Bacterial: Amoxyil + gent/ceftriaxone and metronidazole for 4 - 6 weeks

Amoebic: 7 days metronidazole

Fungal: Amphotericine, fluconazole

DRAINAGE NECESSARY

58
Q

When should liver abscess not be drained?

A

If CT scan/US scan suggests hydatid cyst

59
Q

How is a hydatid cyst diagnosed?

A

Serology

Imaging

60
Q

How is a hydatid cyst treated?

A

PAIR (puncture-aspirate-inject-re-aspirate) procedure or surgery

Albendazole

61
Q

What parasitic infections other than hydatid cysts cause parasitic liver infections?

A

Schistosomiasis

Fasciola

62
Q

How is schistosomiasis diagnosed and treated?

A

Dx: Serology + eggs in stool

Rx: Praziquantel

63
Q

How is fasciola diagnosed and treated?

A

Dx: Eggs in stool, serology

Rx: Triclabendazole

64
Q

Where is schistosomiasis located and how does it cause disease?

A

Found in Africa, Middle East, and Asia

Chronic inflammatory reaction to eggs cause periportal fibrosis

65
Q

Where is fasciola located and how does it cause disease?

A

Worldwide, especially Asia where sheep and cattle are.

It is caused by consumption of aquatic plants.

causes biliary obstruction and inflammation from adults.

imed3004 COPY (50 decks)

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