Hepatobiliary disease Flashcards
Liver synthesise
- Albumin
- prothrombin
- AST & ALT & gamma GT
Function of liver
- Performs 500+ chemical processes
- Synthesise: fat, CHO, protein, clotting factors
- Stores: gly., Vit, minerals, nutrients
- Excrete: bile & bilirubin
- detoxify: toxins & drugs
Describe the blood flow in & out of the liver via hepatic vein, Hepatic artery, portal vein
- HV: deox. blood & nutrients out of liver to <3
- HA: ox. blood from <3
- PV: deox. blood, nutrients & toxins from most organs to liver
List the liver function tests
- Enzymes: ALP, ALT, AST, gamma GT
- Proteins: Alb, PT
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, 5’ nucleotidase (instead of GGT), ammonia, LDH, glucose
Ehrlich rxn measures _ by
D. bilirubin by reacting w/ Diazo agent => red/blue
How are In.d bilirubin detected in the lab?
Ind. bilirubin + Diazo agent + ACCELERATOR => red/blue
Types of hyperbilirubinemia (3)
- Pre/intrahepatic: inc. breakdown of Hb = inc Ind. bilirubin
- Extra/Hepatic: obstruction = partial cholestasis = damage to hepatocytes = inc. Ind + D. bilirubin
- Complete obstructive jaundice / Posthepatic: Complete biliary obstruction = inc D. bilirubin
bilirubin metabolism from formation of bilirubin (haemolytic jaundice)
- excess haemolysis of RBC => heme => excess unconj./indirect bilirubin
- Ind. bilirubin in blood -> liver via Alb
- liver converts Ind. bilirubin to D w/ UDP-glucuronosyl-transferase
- Hi [ ] of direct bilirubin -> intestine & converted by a bacteria => stercobilinogen
- excess stercobilinogen
=> dark poo bc stercocilin
=> dark urine bc stercobilinogen
Expected lab results of Hemolytic jaundice*
- AST, ALT, ALP, PT & Alb normal
- Hb dec
- inc Ind. bilirubin
- Dark colour poo & pee
What happens when you have cholestasis (obstructive bilirubin)
- excess haemolysis of RBC => heme => excess unconj./indirect bilirubin
- Ind. bilirubin in blood -> liver via Alb
- liver converts Ind. bilirubin to D w/ UDP-glucuronosyl-transferase
- obstruction/cholestasis ≠> intestine = low stercobilinogen formed = pale poo
- direct bilirubin reabsorbed back in blood excreted via urine (water-soluble) = v. yellow urine
Expected lab results of intrahemolytic/hepatocellular jaundice (diagnosis)*
- inc AST & AST
- inc D. & Ind. bilirubin in blood
- pale poo
- urine dark brown (bc only exit for bilirubin)
posthepatic/ obstructive jaundice*
- inc D. bilirubin
- ALP >3
- ALT & AST not inc. ~normal
diagnose a patient w/ High GGT & High ALP
cholestasis
ALP 3x higher than the upper limit =
(complete) obstructive jaundice
diagnose a patient w/ High GGT (& normal ALP, AST, ALT)
Alcoholism & drugs
diagnose a patient w/ High GGT, Hi ALT & Hi AST (& normal ALP)
Hepatocellular disease
diagnose a patient w/ High ALP (& normal GGT)
Skeletal bone disease (occur in pregnant females)
State where in&direct biliruben can appear whther in plasma or urine
In: plasma (bc insoluble in water)
Direct: plasma & urine (bc water soluble)
Where can you find ALT, AST, ALP & GGT
- ALT: hepatocyte
- AST: hepatocyte, RBC, skeletal muscles
- ALP: bone, liver, placenta, kidney, intestines
- GGT: liver
Define cholestasis. & marker for cholestasis
decrease in bile duct/f;low due to obstruction
marker inc. GGT, ALP (normal AST & ALT)
Total Bilrubin (TBIL) RRange
0.2–1.2 mg/dL
Direct Bilirubin (Conj. Bilirubin): RRange
0–0.4 mg/dL
—–jaundice is very common in babies and neonates and may cause —– damage (Kernicterus).
If conc. ~200 µmol/L, then use —-
If conc. ~300 µmol/L, then use ——-
a. haemolytic
b. brain
c. PHOTOTHERAPY to breakdown the molecules in the skin.
d. blood exchange TRANSFUSION
The marker that can differentiate b/w acute & chronic liver disease
- Alb
- Acute: normal Alb lvls
- Chronic: dec. Alb lvls
Alpha Fetoprotein (AFP) is a tumor marker, which is synthesized by __ liver. However, it can be increased in —— giving false positive.
embryonic liver
pregnant women
An increased —— is more sensitive and earlier indicator of reduced hepatic synthesis than __ (in hepatocellular disease).
PT than Alb
—–is a more specific indicator of liverinflammationthan —-, and, —-often follows —-.
ALT more specific than AST
AST follows ALT
a) An AST:ALT result of >2:1 or >3:1 means
b) an AST:ALT result of > 1 or >2
a) alcoholic liver disease
b) acute hepatocellular disorders (viral hepatitis)
Acute liver disease occurs due to one of the following
- Poisoning (e.g. w/ paracetamol)
- Infection (e.g. Hepatitis A, B & C)
- Inadequate perfusion / shock
The stages of Hepatitis and liver damage are:
Fat accumulation – Fibrosis – Cirrhosis (chronic liver failure)
Among the rare causes of cirrhosis are:
Jaundice in (a)
Wilson disease in (b)
Hemochromatosis in (c)
a) Neonates
b) Children
c) Adults
Clinical features of cirrhosis (chronic liver failure)
- Developing jaundice.
- Encepholopathy (high ammonia are not removed from the plasma).
- Ascites (low albumin).
- Bleeding tendencies (low coagulation factors, PT).
Patient with cirrhosis may suffer from a bad itch due to accumulation of ———-.
bile acids
liver diagnosis usally done w/
liver biopsy
If AST & ALT are —-, liver damage is more likely to be due to hepatocellular injury.
> 1000 U/L (*Note: 300 U/L non-specific)
and the AST:ALT ratio is >1 bu not >2
—— enzyme is 10x-100x normal in acute hepatitis and it is ˂10x normal in obstructive jaundice .
ALT
In case of obstructive jaundice, ALP is usually very high due to injury in the ———attached to the liver.
Bile canaliculi
