Q: Why is the term “liver function tests” misleading?
A: They do not directly test liver function; they are surrogate biochemical markers that suggest liver injury or dysfunction.
Q: What did Klatskin (1948) argue about LFTs?
A: They are confirmatory at best and only valuable when interpreted with clinical context.
Q: Give two limitations of LFTs.
A: Many markers are not liver-specific; abnormal results can occur without loss of liver function.
Q: When are LFTs most useful?
A: When interpreted as a panel alongside history, examination, and other investigations.
Q: Why must LFTs be interpreted as a panel?
A: Each test reflects a different liver function or pathology; no single test is diagnostic.
what are the 4 functonal roles of the lvier
- energy metabolism (of glucose, glycogen, lipids)
- protein synthesis
- detoxification
- bilirubin handling
What does serum albumin reflect in liver disease? What does low albumin mean and what is the function of albumin
______________________
Q: Why is albumin a poor marker of acute liver injury?
: Hepatic synthetic function.
Core idea
Albumin:
Maintains oncotic pressure
Binds cations, foreign compoints, fatty acds, steroids, other drugs, bilirubin, hormones
Made MAINLY ONLY in liver
Low albumin = chronic liver dysfunction
It has a long half-life and falls mainly in chronic disease.
SDS-PAGE, then to stain with a generic protein stain, say Coomassie Blue, the amount of ____ blasts out the image compared to the other proteins. Albumin is exclusively generated by the ____
Albumin, liver
What clotting fx does liver make
_______________________
Why is INR a sensitive marker of liver failure?
How do you distinguish vitamin K deficiency from liver failure using INR?
A: INR corrects with vitamin K in deficiency but not in liver failure.
Liver makes clotting factors II, V, VII, IX, X.
Vitamin K–dependent carboxylation occurs in liver.
_______________
: Clotting factors have short half-lives and reflect hepatic protein synthesis.
AMINOTRANSFERASES = AST and ALT are markers of __________ ______ not ___
which is most liver specific?
which is found in muscle, heart and rbs
———-
MARKERS OF HEPATOCTE INJURY NOT FUNCTION
ALT: more liver-specific
AST: found in muscle, heart, RBCs
What does an elevated ALT indicate?
Why is AST less specific than ALT?
Hepatocellular injury.
Q: Why is AST less specific than ALT?
A: It is present in many non-hepatic tissues.
important!!!!
ALT > AST → hepatitis
AST > ALT → alcohol or advanced fibrosis
AST:ALT > 2 → strongly suggests alcohol-related liver disease
Q: What does an AST:ALT ratio >2 suggest?
Q: What does an AST:ALT ratio >2 suggest?
A: Alcohol-related liver disease.
important!!!
Why does alcohol raise AST more than ALT?
A: Mitochondrial injury and pyridoxal phosphate deficiency in many tissues right, ALT is merely in liver while ast is in rbc’s, heart, muscle
- what are the liver markers for hepatitis
- what are the liver markers for advanced fibrosis or alcohol
- what are the liver markers for alcohol related liver disease
important
- ALT>AST
- AST>ALT
- AST:ALT > 2
ALP rises when ______ _____ is impaired. What does a raised ALP suggest?
Q: Why is ALP alone insufficient?
ALP rises when bile flow is impaired.
A: Cholestasis (intra- or extra-hepatic).
because it exists in bone intestine annd placenta a lil bit g
important
γ-GT GGT
High sensitivity for liver disease
Low specificity
Helps confirm hepatic source of raised ALP
Often raised in alcohol misuse
: Why is γ-GT used alongside ALP?
A: To confirm a hepatic source of raised ALP. - matlab ki dono bhi high honge then its much more likely that its a liver issue
.
AST & ALT very high (>10×) → acute hepatocellular injury
ALP & γGT predominant → cholestasis
Low albumin / high INR → synthetic failure
important
What LFT pattern suggests cholestasis?
What suggests acute hepatocellular injury?
Marked ALP and γGT rise with modest AST/ALT changes
What suggests acute hepatocellular injury?
A: AST and ALT >10× upper limit of normal.
Core idea
Bilirubin reflects:
Haem breakdown
Hepatic conjugation
Biliary excretion
LFTs + bilirubin = localise the problem.
: Why is bilirubin central to interpreting LFTs?
.
A: It reflects liver excretory function and helps localise pre-hepatic, hepatic, or post-hepatic pathology.
Q: Which LFTs rise most in obstructive jaundice?
A: ALP and γ-GT, with raised conjugated bilirubin
As resident hepatocytes, AST is ________
ALT is ______________
mitochondrial = AST
cytosolic = ALT
functional roles of liver - energy metabolism Longer term energy storage is facilitated in the liver, where the liver is the central organ for fatty acid metabolism. Fatty acids in the liver from uptake from the plasma or de novo lipogenesis are eliminated through beta-oxidation or secretion as very low density lipoproteins (VLDL) as esterified triglyceride. The liver is also the hub for cholesterol synthesis that likewise is packaged in VLDL for transport to periphery tissues. Cholesterol can only be converted to bile acids in the liver and excreted into the gut in what comprises the hepatobiliary circulation.
You can cross reference the glucose control lecture here, as the liver is a major site for glycogen synthesis and storage as stores of glycogen. It is also a major site of triglyceride synthesis and the centre for cholesterol synthesis and management. The image here is the protein glycogenin surrounded by the glucose chains that compose the glycogen. As you have learned the synthesis and catabolism of glycogen is highly controlled by insulin and glucagon signalling. The glycogen store of the liver is key in maintaining blood glucose homeostasis.
