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Viral Hepatitis (Hepatitis E Virus (Usually spread by contaminated water,…
Viral Hepatitis
Hepatitis E Virus
Usually spread by contaminated water, rodents, dogs and pigs
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Serology is similar to Hepatitis A (HEV IgM, IgG)
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Hepatitis A Virus
Pathophysiology - Replicates in the liver, is excreted in bile and then excreted in the faces for about 2 weeks before onset of clinical illness
Clinical Presentation
As the jaundice deepens, the urine becomes dark and the stools pale due to intrahepatic cholestasis
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Viraemia causes patient to feel unwell, with non-specific symptoms that include nausea, fever, malaise
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Epidemiology
- Most COMMON acute viral hepatitis in the world, often in epidemics
- Endemic in Africa and South America
- Most commonly seen in Autumn and affects children and young adults
- Arises from the ingestion of contaminated food or water e.g. shellfish
- Overcrowding and poor sanitation facilitate spread
- NOTIFIABLE DISEASE
- Spread via the face-oral route
Diagnosis
Blood tests
- Leucopenia - reduced white cells
- Raised ESR
Viral markers
- Hepatitis A virus (HAV) antibodies
- Anti-HAV IgM means acute infection
Liver biochemistry
Prodromal stage - between initial symptoms and jaundice
- Serum bilirubin normal
- Bilurubinuria and raised urinary urobilinogen
- Raised serum AST or ALT
Icteric stage - once jaundice has presented
- Serum bilirubin reflects the level of jaundice
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Treatment
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Manage close contacts by giving human normal immunoglobulin for Hep A to contacts within 14 days as well as vaccination
Prognosis is excellent, with most patients making a complete recovery
Prevention
- Good hygiene
- Resistant to chlorination but not boiling water
- Active immunisation
Hepatitis D Virus
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Pathophysiology
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Co-infection
- Infection of HBV + HBD
- Clinically indistinguishable from acute icteric (jaundice) HBV infection
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Superinfection
- When person who has chronic HBV gets HBD
- Results in secondary acute hepatitis and increased rate of liver fibrosis progression
- Increase risk of fulminant hepatitis - VERY BAD
- Rise in serum AST or ALT may be only indication of super-infection
- Since it can result in chronic hepatitis can result in HEPATOCELLULAR CARCINOMA
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Chronic Hepatitis
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If scarring is too severe then decompensated function - jaundice, ascites, low albumin, coagulopathy and encephalopathy
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+/- signs of chronic liver disease - clubbing, palmar erythema, Dupuytren's contracture, spider naevi
Causes
Infection - Hepatitis B (+/- D), Hepatitis C
Non-infective - alcohol, drugs, autoimmune, hereditary metabolic
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Hepatitis B Virus
Pathophysiology
Following infection, around 1-10% of patients will not clear the virus and will develop chronic Hep B
Around 1-5% will develop chronic infection which can lead to cirrhosis and then decompensated liver failure
After penetration into hepatocyte the virus looses its coat and the virus core is transported to the nucleus without processing
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HBsAg is produced in excess by the infected hepatocytes and can exist separately from the whole vision in serum and body fluid
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Clinical Presentation
Also there may be rashes e.g. urticaria and poylarthritis (rare in children) and symptoms often improve
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Viraemia causes patient to feel unwell, with non-specific symptoms that include nausea, fever, malaise, anorexia and arthralgia (joint pain)
As the jaundice deepens, the urine becomes dark and the stools pale due to intrahepatic cholestasis
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In chronic HBV can result in cirrhosis, liver failure and hepatocellular carcinoma - very bad
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Risk Factors
- Healthcare personnel
- Emergency and rescue teams
- CKD/dialysis patients
- Travellers
- Homosexual men
- IVDU
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Epidemiology
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Blood borne transmission (sexual, IVDU, blood products)
Endemic in Far East, Africa and Mediterranean
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Treatment
Acute
- Supportive
- Avoid alcohol
- Monitor liver function
- Manage close contacts by giving human norma immunoglobulin for Hep B and vaccination
- Monitor HBsAg at 6 months to ensure there is full clearance and no progression
- Primary prevention is vaccination
- Majority will get spontaneous resolution and will not progress to chronic infection
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Hepatitis C Virus
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Clinical Presentation
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Most patients present years later with evidence of abnormal transferase values at regular health checks or with chronic liver disease
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In chronic HBV can result with cirrhosis, liver failure and hepatocellular carcinoma - very bad
Risk Factors
Men, HIV, high viral load, alcohol - more severe infection
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Diagnosis
HCV antibody
- Present within 4-6 weeks
- False negative in immunosuppressed and in acute infection
HCV RNA
- Indicates current infection
- Diagnoses acute infection
Epidemiology
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Transmitted by blood and blood products and was common in people with haemophilia treated before screening of blood products was introduced
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Treatment
Interferon based drugs have many mental side effects so direct acting antiviral treatment that is interferon free is better
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Acute Hepatitis
Raised AST, ALP +/- bilirubin
Causes
Infection
Viral - hepatitis A & E, herpes viruses e.g. EBV, CMV, VZV
Non-viral - leptospirosis, toxoplasmosis, coxiella
Non-infective
Alcohol, drugs, toxins/poioning, pregnancy, autoimmune, hereditary metabolic
Can be symptomatic
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With/without cholestatic jaundice (pale stools, dark urine)
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