Ow: Hepatitis, ALD, NAFLD + CASE 1 -cirrhosis Flashcards
LFT:
- GGT up alone
- GGT and ALP up
- AST and ALT up
LFT:
- GGT up alone = Usually indicates steatosis (fat deposit into liver cells)
- GGT and ALP up = Think cholestasis (obst. to biliary drainage)
- AST and ALT up = Hepatitic (hepatocellular damage)
Causes of steatosis?
- Alcohol
- NAFLD
- metabolic syndrome
- diabetes, dyslipidaemia, hypertension, increased BMI
Causes of hepatits?
- Viral hepatitis
- Alcohol hepatitis
- Non-alcoholic hepatitis
- Autoimmune
- Ischaemic
- Haemochromatosis
- drugs/herbal and natural supplements - (can give cholestasis and or hepatits and only way to really know is stop the drug)
Liver tumours can present with? Can be? risk factors?
Present with:
- Cholestasis
- Muixed pattern
- Primary/hepatocellular carcinoma
- secondary/metastatic
Risk Factors:
- HCC is rare outside of HepB with/without underlying liver cirrhosis
- Liver mets arise from other known cancer
Differentiation between alcoholic and NAFLD?
Compare results after abstaining from alcohol or you can get the patient to loose weight however, changes as a result of reversal of metabolic syndrome can take some time so not overly easy in many patients.
Presentation of ALD?
- Alcohol exposure causes fatty change and periventricular fibrosis
- Severe exposure can lead to hepatitis
- Repeated attacks of both of these leads to cirrhosis - fibrosis and hyperplastic nodules
NAFLD?
- Metabolic syndrome drives steatosis
- Intermittently causes hepatitis
- Drives fibrosis through recurrent attacks
ALD and NAFLD common pathophysiology?
- BOTH are related to excessive fat and inflammation
- BOTH are diagnosed using clinical parameters with history and LFTs and don’t use biopsy as diagnostic due to unnecessary risk
Viral Hepatits? - Transmission, Can give chronic?
A = Faecal-oral, No -(mostly subclinical)
B = Parenteral, Yes -(mostly spontaneously resolved)
C = Parenteral, Yes -(mostly chronic)
D = Parenteral, Yes (must be co-infected with B)
E = faecal-oral, No
EBV and CMV - All resolved causing infection mononucleosis - characteristic atypical nucleocytes on blood film.
Autoimmune Hepatitis?
- Chronic autoimmune disease
- Unknown aetiology
- Episodic, recurrent (look at history!)
- More common in females than males
- Biomodal age distribution
- Diagnosis: autoimmune screen or liver biopsy
Ischaemic hepatitis is? Caused by?
Results from severe haemodynamic compromise (ie. shock)
- Cardiogenic
- Severe dehydration/blood loss
- Severe sepsis
- Blood clot to hepatic artery
What is haemochromotosis? Diagnosis?
Hereditary, autosomal recessive mutation of the HFE gene
- Elevated ferratin (with high saturation - will be low or normal in inflammation)
- Gene analysis looking for mutation of genes - C282Y is most common
Seconday haemochromotosis:
- Blood disorders that require repeated blood transfusion
Drugs causing hepatitis?
- Paracetamol overdsose
- Many others: present with cholestasis, mixed but predomionantly hepatitis
- Causes of AST and ALT in the 1000s?
- AST and ALT in the 100s?
- AST > 2x ALT?
- Viral, ischaemic or paracetamol
- Can be anything….
- Usually suggests alcoholic hepatitis (AST/ALT ratio reversal)
What can we assess from the Bilirubin, Albumin, PR and CBC?
If bilirubin is elevated/ patient is jaundice it suggests they have severe inflammation or decompensated cirrhosis (rise in Bilirubin with only slight hepatitis is indicative of liver impairment)
Albumin looks at the synthetic function of the liver, low albumin suggests possible cirrhosis - normal PR suggests NO acute liver failure
Low platelet count in the context in CLD indicates portal hypertension leading to splenomegaly caused by cirrhosis