Liver Disease Flashcards
Name the three zones of liver hepatocytes.
Periportal (outer), midacinar, pericentral (inner)
Why is the liver important?
Large functional reserve. No replacement
Describe how scar formation (fibrosis) occurs in hepatocytes.
Quiescent stellate cells activated by Kupffer cells (releasing PDGF, TNF, ET-1, TGF-B) into myofibroblasts, laying down collagen and destroying hepatocytes
Define acute liver failure.
80-90% functionality lost. No prior liver disease
Describe the cellular change seen in acute liver failure.
Massive hepatic necrosis
What are the two most common causes of liver failure?
Acute - acetaminophen/paracetamol
Chronic - alcohol
Describe the symptoms seen in acute liver failure.
Nausea, vomiting, jaundice, icterius
Encephalopathy and coagulopathy
Describe the cellular changes seen in cirrhosis.
Diffuse transformation into regenerative nodules, fibrous band formation, vascular shunts.
Which classification system is used for cirrhosis?
Child-Pugh (A-C)
Describe the main symptoms seen in chronic liver disease.
Anorexia, weight loss, weakness, pruritus, hyperoestrogenaemia
What is usually the cause of death in chronic liver disease?
Encephalopathy, variceal bleeds, and infection (if predisposed)
Describe the transmission, symptoms, and antibodies seen in hepatitis A.
Faecal-oral route, poor sanitation/hygiene, shellfish
Acute illness - fatigue, anorexia, jaundice
IgM initially, then anti-HAV IgG
Describe the causes and risks seen in hepatitis D.
Co-infection/Superinfection with HBV
IV Drug users and multiple blood transfusions
Broadly describe hepatitis E.
Zoonotic. Enteric and equatorial. Generally self limiting and acute. Chronic in immunosuppressed.
Describe the causes and overview of symptoms seen in different groups of patients suffering from HBV.
Blood, birthing, ‘bonking’
65% - asymptomatic, 25% constitutional, 10% chronic
Usually self-limiting
Describe the antigens seen in hepatitis B infection.
HBsAg, HBeAg, IgM, Total anti-HBc, anti-HBVs
First three appear in acute phase
Second two remain through life
What is the purpose of treatment in HBV?
Slow disease progression, prevent carcinoma
Describe the disease progression of hepatitis C.
75% are chronic (> 6 months). Infection to cirrhosis > 20 years, to HCC > 30 years
Why is there no vaccine for HCV?
Quasispecies cause genetic variablity and different genotypes 1-6.
Describe the four different types of progression in alcoholic liver disease.
Days - steatosis -> reversible
Weeks - hepatitis -> may be reversible
Months - fibrosis -> irreversible
Years - cirrhosis -> irreversible
Describe the LFTs and chemicals seen in alcoholic liver disease.
Acetylaldehyde (from alcohol metabolism) decreases glutathione, sensitising to injury.
P450 increases toxic metabolism
Increased bilirubin, alk phos
AST higher than ALT (unlike other disease)
Describe the two types of autoimmune hepatitis.
Name the two main triggers.
Type 1 - any age, commoner. ANA/SMA/anti-SLA/LP, AMA
Type 2 - mainly younger. Anti-LKM-1, ACL-1
Viruses and drugs/toxins
What are the two main treatments for autoimmune hepatitis?
Immunosuppression (80% survival), liver transplant
Describe the gender spread and histology of PBC and PSC.
PBC - female. florid duct lesions, Mallory-Denk bodies, hepatomegaly
PSC - male with UC. Obliterate fibrosis, ‘beading’
Which treatments are used for PBC and PSC?
PBC - ursodeoxycholic acid/transplant
PSC - cholestyramine, endoscopic dilatation/transplant
Name the two types of reaction by drugs to the liver.
Predictable (i.e. paracetamol)
Unpredictable (based on host response)
Name the main features of nonalcoholic fatty liver disease.
Steatosis with ethanol < 20g.
Metabolic syndrome: diabetes mellitus/insulin issues with hypertension, dyslipidaemia, central obesity, microalbuminuria.
How should NAFLD be treated?
Reverse underlying cardiovascular issues, exercise and diet
Describe haemochromatosis.
Iron buildup. Decreases liver size. Hepatomegaly, abdo pain, glucose issues, cardiac dysfunction, arthritis
Treated by regular venesection (phlebotomy)
Describe Wilsons disease.
Impaired copper secretion.
Diagnosed by ceruloplasmin.
Causes atrophy/cavitation of the brain, Kaiser-Fleischer rings
Copper cholation or zinc based treatment
Describe alpha1-antitrypsin deficiency.
Usually inhibits proteases. Causes emphysema and liver disease. Smoking cessation and liver transplant
Name the two types of nodular hyperplasia.
Focal -> single demarcated nodule
Regenerative -> whole liver, looks like cirrhosis
What is the main risk of benign adenomas? Name the three main types and the risk associated with them.
HNF1-a inactivated: almost no risk
B-caterin: very high
Inflammatory: medium
Almost all associated with oral contraceptive
Describe hepatoblastomas.
Children under 3. Common in FAP. Resection and chemotherapy
Describe the pathogenesis of hepatocellular carcinoma and the main risks.
Patients > 60 and after cirrhosis.
HBV, HCV, aflatoxin, alcohol
B-caterin activation/p53 inactivation
Name the main causes of death associated with HCC.
Cachexia, coma, variceal or tumour rupture
Name the main tumour of the biliary duct.
Cholangiocarcinoma
Are primary or secondary tumours more common?
Secondary
Describe the three main vessel components of the liver.
Hepatic artery (oxygen), portal vein (nutrients), portal vein drains to IVC
Name the main investigations for acute liver disease.
HISTORY AND EXAM!!
LFTs, prothrombin time, US, virology, biopsy
What are the main treatments for acute liver failure?
Rest, fluids (no alcohol) and nutrition.
Symptomatic relief from ursodeoxycholic acid with cholestyramine.
What are the main treatments for Hep B?
Peginterferons -> antiviral treatment (if not tolerated, tenofovir, entecavir)
Which factor most increases carcinoma risk from HBV?
Initial starting load
What treatment is used for PBC?
Ursodeoxy, obeticholic acid
What treatment is used for autoimmune hepatitis?
Corticosteroid (prednisone) and azathioprine
What is Budd-Chiari syndrome? What are the causes? What is the treatment?
Thrombosis, by webs or protein C/S deficiency
Treated by recanulation or TIPS
How is ascites treated?
Spironolactone, paracentesis or TIPS
How is encephalopathy treated?
Lactulose/rifaxalin, transplant
What is the prophylaxis of varices?
B-blockers, ligation
Describe the pathogenesis of hepatorenal syndrome.
Accumulation of toxic metabolites, causing the renin-aldosterone cascade. K is lost, Na/H2O retained
What are the treatment options for pain relief in liver disease? Which ones should be used?
Paracetamol, NSAIDs, opioids
Lowest dose paracetamol (<3g/day) with very low dose opioids if needed
Which four main drugs may cause liver disease?
Co-amoxiclav, aminoglycosides, quinolones, metronidazole
What are the alcohol guidelines in the UK for men and women?
14 or less units a week, ideally spread over 3 days
Not in pregnancy
What serum markers are seen in alcoholic liver disease?
Hypoalbuminaemia, raised prothrombin time, AST>ALT
Describe the FRAMES model of alcohol advice.
Feedback, Responsibility, Advice, Menu (of options), Empathy, Self-efficacy
