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year 4 CDM 2 > Case 13: Hepatitis > Flashcards

Case 13: Hepatitis Flashcards

1
Q

How is sporadic Hep E transmitted

A
  • consumption of undercooked meat esp pork
  • faeco oral route: water, shellfish
  • blood transfusion
  • Zoonosis: direct contact
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2
Q

How does acute Hep E present: timeline

A
  • prodrome: N/V, anorexia, fever, abdo pain, fatigue
  • hepatitis after 1 week: jaundice, pale stools, dark urine, RUQ pain, hepatomegaly
  • may be asymptomatic esp in young children
  • Takes 2-3 months for full recovery
  • Incubation period: 40 days
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3
Q

Complications of acute Hep E

A
  • ALF (rare)
  • Death: up to 25% die with genotypes 1/2 in pregnancy
  • Extrahepatic manifestations: more common than hepatitis A i.e. neurological
  • Chronic hep E: Occurs in immunocompromised patients and sporadic (genotype 3/4- not travel associated)
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4
Q

Chronic Hep E

A
  • If a patient with acute hepatitis E is immunocompromised, they should be followed up to ensure clearance.
  • Occasionally treatment may be required (Ribavirin).
  • Hepatitis E serology may be falsely negative in immunocompromised patients – diagnosis needs HEV RNA PCR.
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5
Q

Investigations for Hep E

A
  • LFT’s: raised ALT/AST (in the 1000’s), raised bilirubin, raised ALP
  • Hep E serology of serum (IgG or IgM). IgM is acute and IgG is chronic
  • Hepatitis E PCR: confirming current or chronic infection
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6
Q

Management of Hep E

A
  • Supportive care
  • Infection control: infectious during incubation period and 3 weeks after jaundice onset. I.e. side room, no food handling
  • Notify PHE and contact tracing
  • No vaccine
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7
Q

Hepatitis B transmission

A
  • Vertical transmission, blood born transmission i.e. sexually or needles.
  • Small risk of transmission in houshold contacts
  • Type of DNA (all other viral hepatitis are RNA)
  • Vertical transmission is the most common cause worldwide
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8
Q

Hepatitis B risk factors

A
  • Risk factors: MSM, unprotected sex, sex workers, IV drug use
  • Globally biggest cause of chronic hepatitis especially Sub-Saharan Africa, Asia and Pacific islands
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9
Q

Hepatitis B timeline

A
  • Incubation period: 60-90 days
  • Acute hepatitis B: Majority of people are asymptomatic especially children. Tends to be spontaneously cleared
  • Chronic hepatitis B: can occur from asymptomatic and symptomatic acute hepatitis B. Higher risk of developing in infants, children and immunosuppressed.
  • NOT all patients with chronic hepatitis B infection have active inflammation and hepatitis
  • NOT all patients with hepatitis B develop cirrhosis
  • Liver damage is mainly immune-mediated
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10
Q

Acute hepatitis B: clinical features

A
  • Asymptomatic: majority
  • Jaundice, RUQ pain, N+V, Hepatomegaly, fever/chills, Malaise, Lethargy, Arthralgia
  • Fulminant acute liver failure (extremely rare): altered mental state and raised ICP
  • Hepatitis forms 1 week after prodrome
  • Can develop ALF and death
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11
Q

Chronic Hep B: clinical features

A
  • Asymptomatic: majority, may have no previous history of acute hepatitis. Will remain asymptomatic till complications develop (hepatocellular carcinoma, cirrhosis)
  • Non specific: fatigue, malaise, weight loss
  • Chronic liver disease symptoms: palmar erythema, spider angioma, asterixis, easy bruising
  • Cirrhosis: Ascites, Hepatomegaly, Splenomegaly, Caput medusae
  • <5% of acute progresses to chronic
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12
Q

Hep B antibodies and antigens

A
  • HBsAg: current infections either acute or chronic
  • Anti-HBs (Hepatitis B surface antibody): past infection or vaccination
  • Anti-HBc Ab: previous or current infections (IgM in acute, IgG in chronic)
  • Serum HBV DNA (by PCR): help identify if a patient is a candidate for anti-viral therapy, detects viral load. Shows current infection (acute or chronic)
  • Anti Hbe IgG: detected when there’s past, cleared infections
  • In vaccination you inject HBsAg and Anti-HBs forms
  • HbeAg: correlates with activity of virus and how infectious it is. Present in acute and chronic
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13
Q

5 stages of Hepatitis B infection (1-2)

A
  • HBeAg positive chronic infection: lots of viral replication, no inflammation/fibrosis. High levels of HBV DNA and HBsAg.
  • HBeAg positive chronic hepatitis: active inflammation and increase ALT, reduced HBV DNA. Seroconversion to anti-Hbe IgG. Variable degree of fibrosis (progressing). Active hepatitis
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14
Q

5 stages of hepatitis B infection (3-5)

A
  • HBeAg negative chronic infection: minimal hepatitis. Last months- years. Normal ALT but low levels of Hepatitis B replication and HBV DNA. Variable degree of fibrosis (progressing). Not active
  • HbeAg negative chronic hepatitis: moderate inflammation and raised ALT. Fluctuating HBV DNA levels. Seroconversion of HBsAg to Anti-HbS and clearance of the virus from the blood. Moderate to severe fibrosis (resolving). Active hepatitis
  • Functional cure: cleared the virus so no active replication. cccDNA from Heb B stays in the cell lifelong, normally causes no issues but can reactivate if immunosuppressed.
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15
Q

Hep B investigations

A
  • LFT: ALT and AST rise the most
  • Hepatitis serology: HBsAg, HBeAg, Anti-HBe, HBV DNA, Anti-HBs
  • FBC, U&E
  • Liver US: if chronic hep B
  • Assessment for fibrosis/Cirrhosis: Liver biopsy, transient elastography
  • Monitor: LFT’s every 3-6 months when chronic. Liver US every 6 months if chronic infection +/- cirrhosis
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16
Q

Management of Hepatitis B

A
  • Referral to Hepatology or infectious disease for specialist management
  • Supportive treatment in majority
  • Only adults who are HBsAg-positive, have compensated liver disease, are pregnant or of young age may be referred for treatment
  • Nucleotide analogues i.e. Entecavir or Tenofovir monotherapy taken long term PO (first line).
  • Pegylated IFN-a injected used for less time, rarely used
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17
Q

Goals of Hepatitis B treatment and endpoint

A
  • Goals: prevent disease progression and reduce transmission
  • Endpoints of treatment: Ideally loss of HBsAg +/- anti-HBs seroconversion but rare. Loss of HBeAg/anti-HBe seroconversion. Suppression of HBV DNA. ALT normalisation
  • Medications: tends to be long term, suppresses infection but rarely causes clearance
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18
Q

Criteria for Hepatitis B treatment

A
  • Severe acute hepatitis (active hepatitis) i.e. INR >1.5, protracted course (persistent symptoms/ marked jaundice >4 weeks), signs of acute liver failure
  • Pregnant women with high HBV DNA start at 24-28 weeks gestation and continue till 12 weeks after delivery
  • Health care works performing exposure prone procedure
  • All patients with Cirrhosis, HIV, family history of HCC or Cirrhosis
  • Patients age >30 who are e-Ag positive, high HBV DNA, persistently normal ALT
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19
Q

Complications of chronic Hep B

A
  • Periods of active hepatitis which may eventually cause liver fibrosis and cirrhosis
  • Fibrosis: virus replication in hepatocyte causes immune response which helps clear the virus but causes liver inflammation and fibrosis
  • Extrahepatic manifestations
  • From cirrhosis can form HCC or decompensated liver disease
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20
Q

Risk factors for development of Cirrhosis from chronic Hep B

A
  • Active inflammation
  • Co-infection with other hepatitis viruses (C/D) or HIV
  • Other liver damage i.e. alcohol consumptions
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21
Q

Conservative management of Hep B

A
  • Education about reducing transmission
  • Contact tracing and informing potential at-risk contacts
  • Notify PHE
  • Screen for Hep D co-infection and other blood born viruses
  • Prevent further liver damage: vaccination against hepatitis A, avoid alcohol
  • Follow up blood tests to demonstrate clearance
22
Q

What is given to close contacts of patients with Hep B

A
  • hep B vaccine
  • Hep B immunoglobulin (HBIG): i.e. neonates to infectious mothers, unvaccinated and definite exposure
23
Q

How can clearance of Hep B infection be demonstrates

A
  • loss of hep B surface antigen
  • hep B surface antibody seroconversion
24
Q

Prevention of Hep B

A
  • education on modes of transmission i.e. needle exchange
  • Increased testing: antennal testing, testing of blood products and increased testing of high risk groups
  • hep B vaccination and immunoglobulin: Hep B vaccine should be given to high risk groups or with high risk of complications. Can be given pre or post exposure.
25
Q

Hep B vaccine: who gets it

A
  • All new-borns: part of childhood immunisation
  • Anyone at increased risk: close contacts with HBV, Travelling to high prevalence areas, lots of sexual contacts, IVDU, health workers, in prison, Have HIV
  • Post exposure: after sexual contact, Neonate of HBV positive women, post needle stick injury
  • 3 doses of vaccine required
26
Q

End goal of Hep B infection based on lab results

A
  • loss of surface antigens
  • loss of e antigens/ presence of antibodies against e antigens
  • suppression of hep B DNA
  • ALT normalisation
27
Q

Hepatitis C

A
  • RNA flavavirus
  • Transmitted through blood and bodily fluids: main risk is parenteral through shared needles and blood products. Sexual and vertical transmission but lower risk than HBV
  • Breast feeding is contraindicated in Hep C
  • Incubation period of 6-9 weeks
  • Increased prevalence in Africa, Russia and Eastern Europe
28
Q

Different genotypes of Hep C and where are they most commonly found

A
  • 1,2 and 3: Northern hemisphere
  • 4: Middle East
  • 5: South Africa
  • 6: South Asia
  • Most common genotypes in the UK: genotype 1 and 3
29
Q

Acute and chronic Hep C

A
  • Acute → Chronic → Cirrhosis → HCC
  • Most acute infections are asymptomatic (only 20% symptomatic)
  • 75% go on to develop chronic infection
  • Patients with chronic infection have persistently high LFTs, and cirrhosis develops in 20-30%. Cirrhosis develops slowly over 20-30 years
  • 1-4% of patients with cirrhosis develop hepatocellular carcinoma, and 2-5% develop liver failure.
30
Q

Hepatitis C: Investigations

A
  • Anti-HCV serology - 90% are positive 3 months after infection
  • HCV RNA - if positive for more than two months then need to be treated. (gold standard for diagnosis). PCR- positive in current infection, used when immunocompromised or acute infection.
  • Hep C antibody: screening (cant distinguish current vs past). May have false negatives if immunocompromised i.e. HIV or in acute infection.
  • Hepatitis C genotyping: differentiate different strains
  • At end of treatment test Hep C RNA (PCR)
31
Q

Management of Hepatitis C

A
  • Symptomatic treatment in the early stages of the disease
  • Drug therapy should be given to all patients and depends on the genotype of the virus.
  • Nucleoside analogues are preferred (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir). Examples of DAA’s
  • Older drugs are Ribaviron and Pega-interferon
  • Direct Acting Anti-virals (DAAs). Given for 8-12 weeks: for example- sofosbuvir, a combination of ledipasvir and sofosbuvir
32
Q

Choice of which DAA to use

A
  • DAA’s: Cause regression of fibrosis and cirrhosis
  • HCV genotype
  • Drug interactions
  • Treatment history
  • Prescence of cirrhosis
  • Cost
  • National/local guidelines
33
Q

Why do we carry out Hep C genotyping

A
  • no cross protection
  • can be co-infected by more than one genotype
  • some treatments are genotype specific
  • different genotypes respond differently to treatment
34
Q

Chronic hepatitis

A
  • Liver inflammation for more than 6 months
  • Causes: Hep B, Hep C, Hep D, Hep E
35
Q

Important differences between Hep B and C

A
  • acute hep C is often asymptomatic whereas acute hep B is often symptomatic
  • most hep C cases progress to chronic infection whereas only a small % of hep B cases progress
  • there is no reactivation of hep C (cure is possible)
  • there are multiple genotypes of hep C (reinfection is possible)
  • there is no vaccine for hep C but there is a vaccine for hep B
36
Q

Ways to eliminate viral hepatitis

A
  • Aim to eliminate Hep B and C by 2030
  • Increased screening and testing
  • Reduced stigma
  • Increased education and awareness around modes of transmission
  • Public health: needle exchange, safer sexual practises, sterile medical equipment
  • Screening blood products
  • Increased HBV vaccination
  • Obstetric services
  • Increased access to treatment i.e. reduce cost of DAA’s
37
Q

Hepatitis D

A

A single stranded RNA virus transmitted parenterally. Needs hepatitis B surface antigens for replication and transmission. Transmitted in same way as Hep B (exchange of body fluids)

38
Q

How is Hep D transmitted

A
  • Co-infection: Hepatitis B and Hepatitis D infection at the same time.
  • Superinfection: A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection.
39
Q

Diagnosis and treatment of Hepatitis D

A
  • Diagnosis: via PCR
  • Screen for anti hep D antibodies and confirm diagnosis with Hep D RNA
  • Treatment: Interferon and treating Hep B
40
Q

Presentation and treatment for Hepatitis D

A
  • Acute infection: suspect if acute hepatitis in HBV patient or fulminant acute HBV (rapid progression of liver failure)
  • Diagnosis: Anti-HDV antibodies (screening), HDV RNA through PCR (current infection)
41
Q

Complications of chronic Hep B and D co-infection

A

Results in more rapid progression to cirrhosis and HCC

42
Q

Lyme disease: how its spread and where is it prevalent

A
  • Causes by the Spirochete bacterium Borrelia burgdorferi through Ixodes ticks
  • Prevalent in North America, Europe and Asia in heavily wooded and grassy area i.e. Highlands. Tends to be late Spring/early summer
  • Transmission occurs 36-48hrs after tic attachment
43
Q

Lyme disease species

A
  • B.burgdorferi sensu lato: US
  • B.garninii, B.afzelii (Europe)
44
Q

Early clinical features of Lyme disease (within 30 days)

A
  • Erythema migrans: bulls eye rash, develop 1-4 weeks after initial bite. Painless and >5cm in diameter, slowly increases in size. Lasts several weeks. Not itchy, painful or hot
  • Systemic: headache, lethargy, fever, arthralgia
45
Q

Non specific symptoms of Lyme disease

A
  • fever and sweats
  • swollen glands
  • malaise, fatigue
  • neck pain or stiffness
  • migratory joint or muscle aches and pain
  • cognitive impairment i.e. memory problems and difficulty concentrating (sometimes described as ‘brain fog’)
  • headache
  • paraesthesia
  • Can occur at any stage of disease
46
Q

Less common features of early Lyme disease

A
  • Cardiovascular: heart block (1st but can progress to 3rd), peri/myocarditis
  • Neurological- weeks to months after exposure: facial nerve palsy (can be bilateral), other cranial nerve palsies, radicular pain (Mononeuritis multiplex), lymphocytic meningitis
  • Neurological issues are rare but classical of Lyme and so should be suspicious
47
Q

Late clinical features of Lyme disease (after 30 days)

A
  • Lyme arthritis (more common with US strains): inflammatory arthritis affecting 1 or more joints, fluctuating and migratory. Knee always affected
  • late cutaneous features (more common with European strains): Acrodermatitis chronica atrophicans, Lymphocytoma
  • non specific symptoms such as fever, lymphadenopathy, fatigue etc
48
Q

What are the late cutaneous features of Lyme disease

A
  • acrodermatitis chronica atrophicans (rash with skin thickening on extremities)
  • lymphocytoma (flesh coloured nodular lesion esp near earlobe)
49
Q

How to remove a tick bite

A

fine tipped tweezers, grasping tick as close to the skin as possible and pulling upwards

50
Q

Management of Lyme disease

A
  • Doxycycline in early disease i.e. ECM rash for 21 days (Amoxicillin if contraindicated i.e. pregnancy)
  • IV Ceftriaxone if disseminated disease for 21 days (meningitis, radiculopathy or CN palsy)
51
Q

Lyme disease investigations

A
  • If erythema migrans is present its a clinical diagnosis
  • ELISA test for IgG and IgM antibodies (takes 6 weeks to be positive)
  • If ELISA positive confirm with Immunoblot test
  • If ELISA negative but symptoms persist for >12 weeks then Immunoblot test
  • Can only do PCR in joint disease
52
Q

Lyme treatment outcomes

A
  • Successful treatment- resolution of symptoms after 12 months. Symptoms can persist for a couple months
  • There is no test for ‘active infection’
  • Re-treatment: can give another antibiotic for 7 days
  • No role for long term antibiotics

year 4 CDM 2 (39 decks)

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