jaundice Flashcards
various colours in a bruise
the result of the synthesis of various compounds that are produced when the heme group gets broken down
bilirubin
- the end product of heme degradation.
- most of which will originate from the spleen.
- yellow in colour
properties of bilirubin
-in its free form is highly toxic
- water-insoluble, binds to albumin (a transporting protein)
- metabolises in the liver
direct bilirubin
bilirubin conjugated with one or two glucuronic acid molecules
urobilinogen
found in the duodenum, deconjugated direct bilirubin
enterohepatic circulation
the process of bilirubin transformed into direct and UGB forms into the liver to be deconjugated again. creating a cycle
urobilin
oxidized urobilinogen, producing a yellow colour
jaundice
hyperbilirubinemia. Accumulation of indirect and direct bilirubin systematically.
unconjugated (indirect reacting) bilirubin
- water insoluble
- bound to plasma albumin
- physiologically present in plasma
- does not get filtered
conjugated (direct-reacting) bilirubin
- water soluble
- does not bind to plasma albumin
- should not be present in plasma
- if it is, it is filtered and present in urine
kernicterus
when indirect bilirubin levels are pathologically high in newborns, the unbound fraction of unconjugated bilirubin passes through the blood brain barrier and causes irreversible neuronal damage
prehepatic jaundice
increased haemolysis
stercobilin
oxidized bilirubin present in stool, giving it its brown colour
post hepatic jaundice
biliary obstruction
hepatic jaundice
hepatocellular damage
neonatal prehepatic jaundice
- higher heme degradation occurs in babies, increasing bilirubin production.
- due to a babies immature liver, they have a decreased capacity to conjugate bilirubin
- blue light therapy is used to increase conjugation of bilirubin
biliary obstruction jaundice
obstruction of the common bile duct. increased pressure onto the bile ducts as bile continues to get produced but not released as it cant enter the duodenum.
- this leads to the bile ducts bursting, due to the pressure and bile enters the blood
complications of obstruction jaundice (after ducts burst)
- both indirect and direct bilirubin found in urine
- no UBG can be produced and thus non in urine
- stercobilin cannot be produced, leading to a clay-coloured stool
- bile enters the BV, lipid digestion and absorption are impaired
alcoholic liver disease (post hepatic jaundice due to hepatocellular damage)
exposure to alcohol causes hepatocyte steatosis ( a fatty change of the liver) dysfunction of mitochondrial and cellular membranes, hypoxia and oxidative stress
- both types of bilirubin and UBG in the urine
factors contributing to the pathenogenesis of cirrhosis
- sex, females are more suseptible
- ethnic and genetic differences, asians typically have an intolerance as they are unable to oxidize acetaldehyde
- comorbid conditions, UP of iron, infections etc..
Hepatocellular steatosis
- impaired assembly and secretion of lipoproteins
acetaldehyde
the major intermediate metabolite of alcohol
Reactive Oxygen Species
they react with cellular proteins, damage membranes and alter hepatocellular function
endothelins
a 21-amino acid long peptide that is a vasoconstrictor produced from endothelial cells, impair hepatic blood flow
aspartate transaminase (AST)
an enzyme that is found mostly in the liver
Alanine transaminase (ALT)
an enzyme that’s mainly found in your liver
most likely causes of death in end-stage alcoholics
- hepatic coma
- gastrointestinal haemorrhage
- infection
- hepatocellular carcinoma
[ALT] > [AST]
most chronic liver diseases serum
[AST] > [ALT] 2:1 ratio
alcoholic liver disease serum
