Hepatobiliary disease Flashcards
Function of the liver
- Performs 500+ chemical processes
- Produces 160+ different proteins
- Makes clotting factors for the blood
- Stores & releases sugar from glycogen
- Metabolism, detoxification, synthesis
6 Types of liver disease
- Autoimmune hepatitis
- Cirrhosis due to alcoholism, hepatitis, obstruction
- Genetic
- Hepatitis
- Infections
- Obstruction of bile ducts
markers for hepatocellular damage (liver damage)
ALT, AST, ALP, gammaGT
markers for determining liver excretory function
Bilirubin
markers for determining liver synthesis function
Albumin, PTT
What is de-ritis ratio & purpose? & significance of results
a) AST ÷ ALT ratio
> differentiate between causes of hepatocellular damage or hepatotoxicity (e.g. alcoholic)
b) >2.0 (& inc GGT) = alcoholic liver disease
which is more specific indicator for inflammation in liver? AST or ALT? How does this affect ALT/AST
ALT.
AST follows ALT (i.e. it will inc./dec. w/ it)
Define cholestasis. & marker for cholestasis
decrease in bile duct/f;low due to obstruction
marker inc. GGT, ALP (normal AST & ALT)
ALP is mainly high in the (organ)
placenta in pregnancy
An ALT result of >2 or 3:1 means
alcoholic liver disease
marker for cholestasis is __ as it [inc. / dec.] with _ or _ _
a. liver ALP
b. increases with obstruction or infiltrative disease (stones/tumour)
cholestasis is a condition where….
there is a dec. in bile flow (blocked fully/partially) from liver to duodenum
substrate, product, activator, pH for testing ALP (alkaline phosphatase)
Substrate: p-nitrophenyl phosphate
Product: p-nitrophenol
Activator: Magnesium sulfate
pH: ~10
Reason for rise GGT & ALP
cholestasis
Reason for rise GGT, ALT, AST (& normal ALP)
hepatodisease
Reason for rise GGT (& normal ALP, AST, ALT)
alcoholism/drug
Reason for rise ALP (& normal GGT)
skeletal bone disease
5’ nucleotidase (5’NTD) is a test that can substitute _ , to determine if inc ALP is due to biliary / extra-biliary origin
GGT (if not available in clinical settings)
people w/ cirrhotic liver can end up being _ because liver cells are dead ≠ can’t store _
a. hyoglycemic b/w meals
b. glycogen
_ is broken down to _ which is [water in/soluble] & converted by _ into _ which is [water in/soluble]
a. Haem (from RBC)
b. indrirect/uncojugated bilirubin - insoluble
c. UDP-glucuronosyl-transferase
d. direct/conjugate bilirubin - soluble
Gilbert’s syndrome cause _ due to reduced activity of (enzyme)
a. Unconjugated hyperbilirubinemia
b. UDP-glucuronosyl-transferase
describe the normal excretion of biliruben * (look back on slide 16)
- RBC broken down in spleen & bone haem => indirect biliruben
- indirect biliruben travel in blood w/ Alb to liver
- indirect converted to direct biliruben
- direct goes to kidney & intestine to be excreted => normal colour pee & poo
Reasons that you may get hyperbilirubinaemia = jaundice
- Increased haemolysis
- Gilbert’s syndrome due to lack of gulcuronyltransferase, which conjugates bilirubin
- Cholestasis
- Obstruction of bile duct
Describe the process of retention jaundice? slide 19
- excess haemolysis of RBC => heme => excess unconj./indirect bilirubin
- liver work @ full capacity to convert indirect bilirubin to direct, but still indirect > direct = jaundice
- Hi [ ] of direct bilirubin -> intestine & converted by a bacteria => stercobilinogen
- excess stercobilinogen
=> dark poo bc stercocilin
=> dark urine bc stercobilinogen
