Flashcards in Liver Deck (31):
What are the 7 key functions of the liver?
-Glucose homeostasis - gluconeogenesis & glycogen storage
-Synthesis of clotting factors
-Drug & toxin metabolism
-Bilirubin conjugation & clearance
If ALT > AST in an acute presentation, what 3 aetiologies should you be most suspicious of?
-Acute viral hepatitis
-Acute drug toxicity
If LFTs show AST > ALP, what 3 aetiologies does it raise the suspicion of?
What 3 parameters of the LFTs are mostly greatly affected in cholestasis?
Bilirubin, GGT, ALP
What are some of the definitions of acute liver failure?
-Rapid deterioration of liver function in a previously normal liver
-INR >1.5 or any encephalopathy that develops in under 26 weeks
-'Jaundice to encephalopathy in
Name the 4 broad causes of acute liver failure.
-Acute viral hepatitis
-Other drug reaction
What intervention can improve the outcome of acute liver failure from paracetamol toxicity?
What intervention can improve the outcome of acute liver failure from hepatitis B?
What intervention can improve the outcome of acute liver failure from Wilson's disease?
What intervention can improve the outcome of acute liver failure from Budd-Chiari syndrome?
Shunt insertion (TIPS - transjugular intrahepatic portosystemic shunt)
What intervention can improve the outcome of acute liver failure from acute fatty liver of pregnancy?
What intervention can improve the outcome of acute liver failure from autoimmune hepatitis?
What abnormalities would you expect on liver biopsy following paracetamol overdose?
-Relative preservation of portal tracts
-No early inflammatory response
Outline the pathogenesis of acute liver failure in paracetamol toxicity.
-Paracetamol is normally metabolized by hepatic glutathione, which conjugates it to glucuronide & excretes it in bile
-When this path is saturated, paracetamol is metabolized via the CYP450 pathway, and becomes a toxic metabolite - NAPQI
-Glutathione normally conjugates NAPQI to make it non-toxic
-When glutathione stores are depleted, the NAPQI accumulates & becomes hepatotoxic
What is considered a toxic dose of paracetamol?
200mg/kg or 10g, whichever is less
How does N-acetylcysteine work & how soon after paracetamol OD does it need to be given?
NAC works by acting as a glutathione donor (so paracetamol can be excreted even when hepatic glutathione stores are depleted)
-it needs to be given within 8 hours of OD to be 100% effective
Name 4 steps in the management of acute paracetamol overdose.
-Reduce absorption: give activated charcoal
-Symptomatic care: anti-emetics
-Risk assessment: dose based/plasma paracetamol concentration
-Specific treatment: NAC
Name the causes of chronic liver disease under the following headings - Big 3, Metabolic 3, Autoimmune 3, Other 3:
Big 3: alcohol, hepatitis B, hepatitis C
Metabolic 3: Wilson's disease, A1AT deficiency, haemochromatosis
Autoimmune 3: Autoimmune hepatitis, Primary sclerosing cholangitis, Primary biliary cirrhosis
Other 3: fatty liver disease, Budd-Chiari, chronic biliary obstruction
What are 5 symptoms of chronic liver disease?
-Weight loss or gain
What are 9 signs of chronic liver disease?
-Parotidomegaly (only alcohol)
Outline the stages of liver fibrosis from F0 to F4.
F0 = no fibrosis
F1 = periportal fibrosis, no septa
F2 = periportal fibrosis, some periportal septa
F3 = numerous septa, no architectural distortion
F4 = architectural distorsion & nodule formation
Name 5 major complications of CLD and how they should be managed.
1. Oesophageal varices - beta-blockade, band ligation, endoscopic banding
2. Fluid retention - fluid & salt restriction, diuresis
3. Jaundice - no specific treatment
4. Osteoporosis - vitamin D supplementation, regular surveillance of BMD
5. Encephalopathy - supportive care, withdraw potential precipitants
What are 5 findings to suggest decompensated liver disease?
Jaundice, coagulopathy, ascites, variceal bleeding, hepatorenal syndrome
What is the difference between type 1 and type 2 hepatorenal syndrome?
Type 1 is acute & a more severe renal failure
Type 2 is a more insidious renal failure that is less severe
Name a pre-hepatic, a hepatic & a post-hepatic cause of portal hypertension.
Pre-hepatic: portal vein thrombosis, stenosis or compression of the hepatic blood supply
Hepatic: cirrhosis, schistosomiasis, severe steatosis, sarcoidosis
Post-hepatic: hepatic vein obstruction, severe RHF, constrictive pericarditis
Outline the biopsy findings in hepatocellular carcinoma.
-Abnormal bile canalicular architecture
-Thickened trabeculae >3 cells
-Pseudo-bile duct spaces
What serum marker is usually elevated in HCC?
What 2 autoantibodies are present in type 1 autoimmune hepatitis?
Anti-smooth muscle antibodies
What is primary biliary cirrhosis? Name 2 biopsy findings.
Primary biliary cirrhosis is an autoimmune disease causing non-suppurative cholangitis.
-Florid bile duct lesions
-Loss of small bile ducts
-Variable periportal hepatitis
What is the mainstay of treatment of primary biliary cirrhosis?
Ursodeoxycholic acid (responds poorly to steroids, unlike autoimmune hepatitis)