Gastroenterology (Liver 2/2) Flashcards
types of hepatitis
- Alcoholic
- Heptatitis A
- Hepatitis B
- Hepatitis C
- Hepatitis D and E
- Autoimmune
- Drug- induced
hepatitis A
Type: RNA
Incubation: 2 weeks
Route: faecal oral
Long term: not associated with chronic liver disease
Hep A symptoms
Patients tend to have a flu-like prodrome and may have:
- Fever
- Jaundice
- Malaise
- Nausea and vomiting
- Tender hepatomegaly
- Dark urine and pale stools
- Due to bilirubin excretion in the urine instead of the gastrointestinal tract, see Jaundice.
management of hepatitis A
1st-line: symptom management and analgesia + notify Public Health England
* All viral hepatitides are notifiable diseases
* Most cases of hepatitis A are mild and self-limiting
* Any severely unwell patient should be admitted to hospital
Hepatitis B
Type: double-stranded DNA
Incubation: 6-20 weeks
Route: infected blood or bodily fluids
Long term: can be self limiting but can result in chronic hep B - liver cirrhosis and hepatocellular carcinoma
Risk Factors for Hep B
- Visiting or being born in high-risk countries
- Close contact with people infected with HBV
- Injecting intravenous drugs
- High-risk sexual behaviours (e.g. unprotected sex with multiple partners)
- Family history
- Infants born to mothers with HBV
presentation of Hep B
Many patients are asymptomatic until liver cirrhosis, failure, or hepatocellular carcinoma develops. Features seen may include:
- Flu-like prodrome: fever, chills, malaise, joint pain
- Nausea and vomiting
- Right upper quadrant pain
- Jaundice
- Tender hepatomegaly
- Palmar erythema
- Spider naevi
- Ascites
- Asterixis
prevention of Hep B
Immunisation
investigations for Hep B
Liver function
Acute:
- Bilirubin – increased (usually >85 µmol/L)
- ALT, AST – increased (usually 500 – 10,000 IU/L) and ALT > AST
- ALP – may be raised to up to 2 times the upper limit of normal
Chronic
- AST and/or ALT may be slightly elevated or normal
Hepatitis serology
HBV DNA
- higher levels indicate greater infectivity and higher likelihood of developing complications
hepatitis serolgy
1) Hepatitis B surface antigen (HBsAg):
- Suggests the patient is infectious
- Chronic hepatitis B is likely if this is elevated for >6 months
2) Hepatitis B e antigen (HBeAg):
- Associated with viral replication and a higher infectivity
3) Antibody to HBe (anti-HBe):
- Indicates an immune response and control of viral replication
- 4) Antibody to HBcAg (anti-HBc):
- Indicates current or previous HBV infection and persists for life
IgM antibody to hepatitis core antigen (anti-HBc IgM):
- Indicates recent (within the last 6 months) HBV infection
- This is released first by the immune system and is gradually replaced by IgG
5) IgG antibody to hepatitis core antigen (anti-HBc IgG):
- Indicates past infection
6) Antibody to HBsAg (anti-HBs):
- Indicates recovery and immunity to HBV
- If there is no anti-HBc, the person has been vaccinated (as the core antigen is not given in the vaccine).
- If there is anti-HBc, the person has fought off a previous infection
management of Hep B
- 1st-line: referral to gastroenterology/hepatology and notify Public Health England
- Pegylated interferon is used for the treatment of HBV, although other antivirals such as entecavir may also be used.
Patients with Hep B should have screening for
- Cirrhosis
- Hepatocellular carcinoma
patient advice for Hep B
Patients should avoid drinking alcohol as this can increase the risk of cirrhosis and hepatocellular carcinoma
Patients should take steps to minimise transmission to other people:
- Avoid sharing items that may be contaminated with blood (e.g. toothbrushes and razors)
- Avoid unprotected sexual intercourse including oro-anal or oro-genital sex until they have become non-infectious or their partner has been immunised
- Avoid sharing needles
- Avoid donating blood, semen, or organs
Hepatitis C
Type: RNA
Incubation: 6-9 weeks
Route: infected blood or bodily fluids
Long term: can be self limiting but can result in chronic hep B - liver cirrhosis and hepatocellular carcinoma
RF for hepatitis C
- Close contact with people infected with HCV
- Injecting intravenous drugs
- High-risk sexual behaviours (e.g. unprotected sex with multiple partners)
- Family history
- Infants born to mothers with HCV
presentation of hep C
- Flu-like prodrome: fever, chills, malaise, joint pain
- Nausea and vomiting
- Right upper quadrant pain
- Jaundice
- Tender hepatomegaly
- Palmar erythema
- Spider naevi
- Ascites
- Asterixis
investigations for Hep C
Liver function tests:
In acute hepatitis C:
- Bilirubin – increased (usually >85 µmol/L)
- ALT, AST – increased (usually 500 – 10,000 IU/L) and ALT > AST
- ALP – may be raised to up to 2 times the upper limit of normal
In chronic hepatitis C
- AST and/or ALT may be slightly elevated or normal
Hepatitis C RNA testing:
- If positive, send a repeat test for confirmation of infection
- If negative, send a repeat test after 6 months. If still negative, then the person has cleared the infection but is not immune to reinfection.
hepatitis prevention
no immunisation
BUT CAN BE CURED NOW
management of hep C
- 1st-line: refer to gastroenterology/hepatology and notify Public Health England
- Antivirals are given depending on the HCV genotype which is tested before treatment.
Hepatitis D
Type: RNA
Route: infected blood or bodily fluids
CANNOT GET INFECTION WITHOUT BEING CO-INFECTED WITH HEP B
Type: RNA
Incubation period: 3-8 weeks.
It causes a similar pattern of disease to hepatitis A but has more severe effects and higher mortality in pregnant people.
Like hepatitis A, hepatitis E does not cause chronic disease or an increased risk of hepatocellular cancer.
Autoimmune hepatitis (AIH)
is a chronic autoimmune disease of unknown aetiology affecting the liver commonly seen in young women. It is associated with circulating autoantibodies, elevated serum IgG and increased serum transaminases.
AIH can be categorised into two main types based on the autoantibodies present:
Type 1 AIH – seen in adults and children and is associated with:
- Antinuclear antibodies (ANA)
- Anti-smooth muscle antibodies (SMA)
- Perinuclear anti-neutrophil cytoplasmic autoantibodies (pANCA)
- Anti-soluble liver antigen (SLA)
Type 2 AIH – seen in children only and is associated with:
- Anti-liver kidney microsomal-1 antibodies (LKM1)
presentation of autoimmune hepatitis
- Nausea
- Fatigue
- Myalgia
- Pruritus
- Abdominal discomfort
- Small joint arthralgia
- Signs of advanced chronic liver disease (such as ascites, splenomegaly, spider naevi, palmar erythema etc.)
investigations for autoimmune hepatitis
bLiver function tests
Serum-gamma globulin
AIH autoantibodies
Liver biopsy
management of autoimmune hepatitis
Management involves the use of corticosteroids and immunosuppressants such as azathioprine. Liver transplants may also be necessary.
drugs which can cause drug-induced hepatitis
Drugs that can cause hepatitis
- Paracetamol
- Statins
- Alcohol
- Amiodarone
- Methotrexate
- Isoniazid
- Nitrofurantoin
Drugs that can cause cirrhosis
- Alcohol
- Methotrexate
- Amiodarone
Drugs which can cause cholestasis with/without hepaitis
- oral oestrogen
- fibrate
- anabolic steroids
- tamoxifen
Budd-Chiari syndrome (BCS)
describes the blockage of the hepatic veins that drain from the liver into the inferior vena cava. It is commonly associated with underlying conditions leading to hypercoagulability.
RF for Budd-Chiari syndrome
- Myeloproliferative disorders, such as polycythaemia vera and essential thrombocytosis
- Thrombophilias: Factor V Leiden, protein C and S deficiency, antithrombin III deficiency
- Combined oral contraceptive pill use
- Pregnancy and the postpartum period
budd-chiari triad of
- Sudden-onset and severe abdominal pain, typically right upper quadrant pain
- Ascites
- Hepatomegaly that is usually tender
*
investigations for Budd-Chiari syndrome
FBC
- may show myeloproliferative disorder
LFT
- may be midly deranged
Thrombophilia screen
- to identify underlying hypercoagulable states
Dobbler US
- high sensitivity and specificity
complications of Budd-Chiari
- Liver failure
- Hepatic encephalopathy
- Portal hypertension
- Spontaneous bacterial peritonitis
- Hepatorenal syndrome
management of Budd-Chiari
anticoagulation
haemachromatosis
autosomal recessive condition characterised by a deficiency in hepcidin
hepcidin and pathophysiology of haemachromatosis
a hormone that usually reduces iron absorption and keeps iron trapped in macrophages and liver cells
-> therefore lack of hormone effect leads to iron accumulation
presentation of haemachromastosis
Early features may be vague and non-specific, including fatigue and joint pain, usually in the hands. Other features may be:
- Skin pigmentation – often described as bronzing, but can be grey or brown
- Erectile dysfunction and loss of libido due to hypogonadism
- Diabetes mellitus due to iron deposition in the pancreas
- Features of liver disease and cirrhosis
- Congestive cardiac failure due to dilated cardiomyopathy
investigations for haemachromatosis
FBC
- can rule out leukocytosis suggesting inflammation which increases ferritin
Iron study
- Transferrin saturation is elevated: iron has ‘taken up’ a lot of binding spots
- Total iron-binding capacity (TIBC) is low: fewer spots are available for iron to bind
- Serum ferritin is elevated, however, this is an acute phase reactant and may be elevated in other situations such as infection and inflammation
LFTs:
- AST and ALT are usually elevated up to 2 times as high as the upper limit
Liver biopsy:
- The diagnostic test
Genetic testing
management of haemachromatosis
- 1st-line: regular venesection (around 1-2 times a week)
Transferrin saturation is used to monitor treatment response - 2nd-line: desferrioxamine: iron-chelating agent
- Liver transplantation may be necessary if end-stage liver disease develops
complications of haemachromatosis
- Liver cirrhosis and hepatocellular carcinoma
- Diabetes mellitus
- Congestive heart failure
- Hypogonadism
Wilson’s disease (WD)
is an autosomal recessive disorder characterised by impaired Wilson disease protein (ATP7B protein) function. This protein normally moves excess copper into bile where it is incorporated into caeruloplasmin for excretion. If copper is not bound to caeruloplasmin using the WD protein, it quickly degrades.
presentation of wilsons
- Features of hepatitis or cirrhosis
- Parkinsonism – tremors, rigidity, bradykinesia, postural instability:
- This is because, in the brain, most copper is deposited in the basal ganglia
- Incoordination
- Cognitive impairment and dementia
- Psychiatric problems – depression, personality changes
- Kayser-Fleisher rings: Brown rings in the periphery of the iris due to copper deposition
LFTs:
- AST and ALT are elevated
Slit-lamp examination:
- Assesses Kayser-Fleisher rings
Serum caeruloplasmin:
- Reduced
- May be normal in inflammation as it is an acute-phase reactant
Serum copper:
Reduced
* This may seem unusual given that WD is a disease of copper excess. As mentioned above, the WD protein is non-functional, so copper is not incorporated in caeruloplasmin, therefore caeruloplasmin degrades quickly. Caeruloplasmin is needed to carry copper in the serum, but since it is low, serum copper is also low. The copper is instead deposited in tissues.
management of wilsons disease
- 1st-line: penicillamine: copper-chelating agent
- Liver transplantation may be necessary
complication of wilsons
liver failure and cirrhosis
