S6. liver function and pathology Flashcards
functions of liver
storage
(glycogen, vitamins,iron,copper)
synthesis of
glucose, lipids,cholesterol,bile,clotting. factors, albumin
metabolic
>generates energy and detoxifying harmful substances like (bilirubin, ammonia, drugs, alcohol, carbohydrates,lipids)
non specific symptoms of liver disease
- nausea
- vomiting
- loss of appetite
- abdominal pain
specific symptoms of liver disease
+ relate this to impairments in function
- jaundice (bilirubin build up. metabolic function)
- oedema/ ascites (fluid. within peritoneal cavity)
> less albumin synthesis. reduced oncotic pressure. can’t draw water in
-bleeding
> less clotting factor synthesis
-confusion
>impaired metabolic function NH4 build up
what’s the difference between acute liver failure and decompensated liver failure?
ALF= happens acutely with no underlying background of liver disease
>e.g. excessive acute alcohol intake/ paracetamol overdose/ viral infections e.g. EBV/ acute hepatitis/ some medications ASPRIN IN CHILDREN!
DL= symptoms seen suddenly
what is cirrhosis?
permanent, irreversible damage to liver that results in impairment of liver function and distortion of shape of liver itself.
> response to chronic inflammation of liver
cirrhosis can cause
fibrosis and hepatocyte necrosis
> healthy liver tissue pops out between the bands of fibrous tissue > appearance of NODULES on liver
broad causes of cirrhosis
categories
- drugs/alc
- infection
- deposition
- autoimmune
hepatomegaly seen when?
alcoholic liver disease
> fatty change over weeks
and
alcoholic hepatitis
example drug related causes of cirrhosis
- iatrogenic (e.g. from prescribed drugs)
- alcoholic liver disease (weeks)
- alcoholic hepatitis (worsening symptoms seen - years)
infection related causes of cirrhosis
- hep B> vaccine no cure. symptoms.
- heb C> cure but no vaccine. asymptomatic.
- can cause malignancy due to the chronic inflammation
deposition related causes of cirrhosis
fat!! non alcoholic fatty liver disease. > deposition of fat then inflammation of liver itself > link to insulin resistance >accumulation of triglycerides.
‘NASH’ = specifically if inflammation is present.
(non alcoholic steatohepatitis)
explain hereditary haemochromatosis
- autosomal recessive
- inc absorption of iron
- excessive iron deposition in liver
- inc ferritin
> treated through venesection. take blood from patient to reduce amount of iron in circulation
explain Wilson’s disease
abnormal copper matabolism
- reduced secretion of copper into circulation to be removed
> accumulation of copper in tissues and liver
> presents in children and young people
- can also affect CNS causing seizures and memory problems
autoimmune related causes of cirrhosis
- autoimmune hepatitis
> affect hepatocytes - primary biliary sclerosis
- primary biliary cholangitis (can have association with ulcerative colitis)
> affect bile duct
difference between portal and systemic circulation
portal= anything that drains to liver before IVC
systemic= venous network that DOES NOT go thru liver
which veins merge to form portal vein
Inferior MesentericV
splenic
Superior Mesenteric V
what is portal hypertension?
build up of blood within the portal venous system
complications with portal hypertension?
ascites (inc hydrostatic pressure. fluid in peritoneal cavity)
slenomegaly (enlarged spleen)
varices (distension of veins) > shunt of blood from systemic circulation to portal. points of anastomoses.
> oesophageal. (emergency as can bleed. haememesis)
> anorectal (typically painless as above pectinate line and rarely bleed)
> umbilical
umbilicus remnant remains as
ligamentum teres
what is hepatorenal syndrome
presence of rapid deteriorating kidney function due to underlying liver cirrhosis causing portal hypertension
what happens with hepatorenal syndrome?
leads to arterial (splanchnic) vasodilation
> perceived as decreased circulating volume
> RAAS activated
> renal artery vasoconstriction
> reduced perfusion to kidney so reduced kidney function
which ducts join at the ampulla of Vater?
common hepatic duct (formed from L and R) and pancreatic duct
rate at which duct substances get released into duodenum is controlled by?
sphincter of oddi
gallstones formed from?
cholesterol
bile pigments
