medical conditions of the liver Flashcards
three main histological patterns
- hepatitis - inflammation
- steatosis - fatty liver
- cholestasis - retention of bile
there can be overlap
acute liver inflammation
<6 months is acute hepatitis
symptoms not always present
- fatigue, anorexia, nausea, jaundice, tenderness
typically lasts 2-4 weeks
minority progress to acute liver failure
- multiple disparate causes
chronic liver inflammation
- greater than 6 months
- symptoms not always present
- weakness, tiredness and malaise
- often identified on screening blood tests
- aetiology dictates progression rate of damage and development of cirrhosis and carcinoma
causes of acute hepatitis
hep A, E, B, C, D
immunosuppressed/transplant - CMV, EBV, HSV
other infections - toxoplasma, Q fever, leptospirosis, brucellosis
alcohol
drugs - parecetomol
toxins - mushrooms, carbon tetrachloride
ischaemia
pregnancy
autoimmune conditions
metabolic
causes of chronic hepatitis
- hep B, C alcohol drugs autoimmune hepatitis biliary metabolic NAFLD - non-alcohol fatty liver disease
biliary causes of chronic hepatitis
- primary biliary cholangitis
primary sclerosis cholangitis
metabolic cause of chronic hepatitis
alpha -1 - antitrypsin deficiency
hereditary haemochromatosis
Wilson’s disease
aetiologies of steatosis
alcohol
NAFLD/NASH - non alcoholic stet-hepatitis
drugs - methotrexate, amiodarone
hep C
causes of cholestasis
primary biliary cholangitis
primary sclerosisg cholangitis
extra hepatic biliary obstruction
drugs
hepatitis and liver inflammation
a necro-infalmmatory process comparing inflammation, hepatocyte necoris and repair, involving the portal and lobular regions
histological features of liver inflammation
portal tract inflammation
limiting plate - interface hepatitis
lobular inflammation and hepaocyte necrosis - apoptosis of coagulative necrosis
repair - macrophages, hepatocyte regeneration and fibrosis which may progress to cirrhosis
macro vesicular steatosis
one vacuole is filling the cytoplasm, variable in size but often large
microvesicular steatosis
multiple small vacuoles filling the cytoplasm of a hepatocyte
uncommon
causes of microvessicular steatosis
Reye’s syndrome
acute faty liver of pregnancy
drugs - tetracycline, valproic acid
congenital metabolic disorders - urea cycle disorders, Jamaican vomtiting disease
causes of macrovessicular steatosis
alcohol
- acute hepatitis - hepatocyte necrosis with a neutrophil infiltrate. Mallory’s hyaline steatosis
- chronic stages - portal tract chronic inflammation and fibrosis, central vein sclerosis, often mild increase in iron
NASH - non alcohol steatohepatitis
- associated with obesity diabetes, GI surgery, TPN, metabolise syndrome features - fat, mallory’s hyaline, inflammation, fibrosis
- drugs - methotrexate, amiodarone
- hep C virus
NASH
non alcohol steatohepattitis
NASH causes of macrovessicular hepatitis
- obesity
- drugs
- hep C
cholestasis
incomplete excretion of bile
histology of cholestasis
- feathery degeneration of hepatocytes bile plugs cell death with inflmaammtion bile ductile proliferation at the edge of portal tracts fibrosis - cirrhosis
pre haptic cholestasis
excess production of bilirubin (RBC breakdown)
intrahepatic causes of cholestisis
inform errors
drugs - flucloxicillin - destroys bile ducts
primary biliary cholangitis
primary sclerosing cholangitis
primary biliary cholangitis
4 stages
- duct lesion - duct damage, portal inflammation, granulomata
- ductular proliferation - expanded portal tracts, interface hepatitis
- scarring - fibrosis, loss of bile ducts
- cirrhosis
primary sclerosis cholangitis
large duct vs small duct
inflammation and concentric fibrosis around ducts resulting in epithelial necrosis and duct loss
post hepatic cause of cholestasis
extra-hepatic biliary obstruction (gall stones, tumours in the head of the pancreas
- bile plug in ducts - may rupture to form bile likes +/- ascending cholangitis (neutrophils in bile ducts), abscesses
biopsy diagnosis
asses whether hepatitis, steaotic, cholestatic, fibrotic, overlap or other
rarely make a diagnosis in isolation
always a combination of serological, clinical and/or radiological
not frequently a non-specific pattern
- however, some etiologists can produce characteristic patterns that may be highly suggestive of a particular cause
ground glass hepatocytes
hepatocytes with ground glass inclusions
hep B surface antigen
auto-immune hepatitis
florid lobular and portal inflammation, interface hepatitis, hepatocyte rosettes, plasma cells
mallory bodies
occur in alcoholic hepatitis
biliary diseases
- primary biliary cholangitis - cirrhosis
- primary sclerosis cholangitiss
- extra hepatic biliary obstruction
histopathology of biliary diseases
inflammation/dmaaaage around the bile ducts cholestasis bile ductile proliferation hepatocyte damage fibrosis
PBC histology
jigsaw pattern of fibrosis
PSC histology
inflammation and fibrposis
sclerosing fibrosis
inborn errors
congenital - hereditary haemochromatosis - iron overload - alpha -1 anti-trypsin Wilson's copper storage disease cystic fibrosis
hereditary haemochromatosis
iron granules present in liver cells
investigations
- LFTs
- infective agents
- serology - autoimmune Ab, iron studies
- tumour markers, alpha-feto protein
- imaging for mass lesions
- liver biopsy
cirrhosis
diffuse alteration of the normal architecture by fibrous septa separating nodules of regenerating hepatocytes
the end point of many disease processes where there are cycles of necrosis/infalmmation and repair/fibrosis
aetiologies of cirrhosis
alcohol/drugs viral hepatitis auto immune hepatitis metabolic diseases genetic haemochomatosis alpha-1-antitrypsin deficiency Wilson's disease biliary tract disease non-alcoholic steatohepatitis idiopathic
clinical symptoms and signs of cirrhosis
- no symptoms, abnormal liver function tests
- non specific symptoms and signs - malaise, abdominal pain, hepatomegaly
- liver failure signs and symptoms
- multi organ failure/death
treatment of liver cirrhosis
remove/treat aetiology
- anti virals
- stop drinking
- Immunosuppressor
- cease medication
- remove iron -venesection
support and await repair
transplant
acute liver failure
rapid deterioration of liver function in a previously healthy individual
- coagulopathy - impaired protein synthesis - as measured by the prothrombin time in the blood
- hepatic encephalopathy - alteration of mental status
hyper acute is within 1 week - acute is 1-4 weeks and subacute is 4-12 weeks
aetiologies of acute liver failure
drugs/alcohol hep, EBV, CMV auto immune hepatitis metabolic diseases - Wilson's disease (copper overload) idiopathic
paracetamol overdose
characteristic appearance
nutmeg liver
zones of necrosis
liver transplantation
the replacement of a disease liver with some or all of a healthy liver from another person
usually the native liver is removes and replaced by the donor organ in some anatomic location
needs a blood group matched donor
multiple anastomoses
indications of transplantation
- end stage chronic liver disease
- acute liver failure
- hepatic neoplasms
