Liver disease Flashcards
=These 4 things suggest chronic stable liver disease (not alcohol or cirrhosis or decompensated-as nothing end stage about this, they are functioning perfectly well.
If examined liver they would have hepatomegaly and liver would be infiltrated with fat. These patients often come in final year as they are stable
Liver enzymes
After Mi, will also get rise in AST!
ALT-what does it do?
This enzyme is part of gluconeogenesis
Liver function tests:
Leak out in different amounts depending on where damage is.
Important to also measure waste products (bilirubin) and things liver makes are albumin and fibrinogen so need to measure these.
Measure PT and PTTK (APTT)
=obstructive jaundice or post hepatic obstruction (as ALP is the highest, suggesting liver is okay but biliary tree is blocked.
Could be due to obstruction by stone or pancreatic cancer.
If patient comes up jaundice and has no abdominal pain, probs not gallstones, on other hand painless jaundice suggests pancreatic cancer and it unfortunately it has just blocked the duct.
-High ALT
Suggests inflamed hepatocytes are damaged and this is hepatitis. Probs since ALT is higher we are thinking the cause is viral (a,b,c,d,e all need to be thought about).
Random: If AST is higher-think alcoholic liver disease since ST for STella beer.
Role of bile salts are to emulsify fats. Fat becomes water soluble and can be absorbed. Ten resorb bile salts with fat which goes into portal vein which goes back to liver and is recycled, so they don’t get into peripheral circulation.
Bilirubin is dark yellow and is waste product. Also some of bilirubin is broken down by bacteria into sterco and uro bilinogen (same thing just in poo and urine). The only way this can happen is if the bilirubin comes into contact with bacteria. So if no bacteria this will disappear
Urobilinogen is present in normal urine. T/F
=True
If bile duct exposes bilirubin to bacteria then you will have urobilinogen in urine.
If obstructive jaundice then bilirubin can’t meet bacteria so pale stools and dark urine with bilirubin in it but it is negative for urobiliogen, so this is another clinical clue the patient has obstructive jaundice before you have blood tests (which will show high ALP). Also bilirubin leaks into blood and so do bile salts. These are very irritant to the skin and so will make you itch. If itching a lot, then probably something obstructing the bile duct.
Urine dipstick for urobilinogen
Pruritis-there is only itching in obstructive jaundice because bile salts should end up in portal vein then they get into systemic circulation. If liver damaged then no bile salts made so they never get into systemic circulation.
Bacteria are only in gut to convert bilirubin to urobilinogen
Bile salts=bile acids
Obstructive jaundice
Learn to draw this
Ask patient if they have pale stools
Bilirubin in blood makes you yellow
Difference between yellow patient with hepatitis and obstructive jaundice
Signs of chronic stable liver disease
Gynecomastia and palmar erythema is that they break down estrogen less aggressively
=Heart failure
In corner there is a nutmeg as this liver looks like it has nutmegs on autopsy.
This is called nutmeg liver because appearance of liver in lines is thought to be like a nutmeg, Liver is arranged into hexagons and they each have a central vein which collect together.
When patient has heart failure and it cannot pump. If get bit of ischaemia the BP will fall a bit which is picked up by kidneys and RAS will activate so renin will pick up and angiotensin 2 will increase and so will aldosterone, kidneys will retain some sodium and therefore water and JVP will raise +1 JVP and BP then gets back to normal so you can continue to live and fight etc. Heart is still a bit weak though, iscahemia gets worse and the cycle continue. As JVP goes up and up (to about +18, suddenly the jvp is higher than the oncotic pressure so get flash pulmonary oedema and suddenly gasping and drowning. The central venous pressure will also go up.
High JVP, crackles everywhere and essentially have pulmonary oedema secondary to HF.
Treat using IV furosemide (40mg one dose)-Like magic will dilate veins and pressure will drop below 18 and so this causes a drop in hydrostatic pressure and oncotic pressure is now higher and albumin sucks water in. BP stays low so have to break cycle and so give ACE inhibitor- ramipril to inhibit renin production and break cycle. So patient goes home on furosemide and ramipril.
LH fails first as power house, this puts pressure on lungs and then RH fails. So ischaemia causes R and L heart failure.
If have alcoholic hepatitis and destroy hepatocytes you get regeneration but instead of nice hexagon anatomy you get nodular hepatocytes and if keep doing it you get nodular cirrhosis.
Over years the pressure around the portal vein goes up and you get portal hypertension.
Alcohol destroys hepatocytes and some cells regenerate and grow around forming nodules. This is micronodular and it happens because you drink again and again and you end up with nodular cirrhotic disease.
