Liver Falure blood tests

#KYJ - Transaminitis

Pesky liver enzymes.  You’ve had patients who have had blood tests looking at liver function.

When running biochemistry on patients suspected of being in liver failure, a number of enzymes and other proteins are measured.  In this knowing your jargon blog post I’ll take you through the basics in a way you’ll understand, and be able to share with your patients.

There are many, but the rock stars are:

ALT and AST

Albumin

Prothrombin Time or PT.

Let’s start with the Acute /current liver injury ones.

Alanine Transaminase (ALT) and Aspartate transaminase (AST).  These enzymes are in your liver cells.  Locked up like a prisoner in a cell.   There roles are complex and outside the scope of this post, and frankly unimportant for the purpose of measuring  acute liver disease.  

Let’s just say that they are inside liver cells and during acute damage, trauma, infections or cancer of liver tissue, they leak out like myoglobin from damaged muscle cells, or troponin from damaged heart cells.

It stands to reason that when you injure your liver with one too many Yager bombs or a wild night of Beer-pong, you can expect to have released some ALT/AST into your blood stream where it can be measured on biochem blood tests.

ALT/AST is a sensitive marker for acute damage where a big number of liver cells died.  In chronic liver failure, cells die off slowly, so these enzymes leak or leach slowly into the blood.  For this reason, ALT/AST is aun reliable in Chronic disease like cirrhosis or cancer.

An acute injury and subsequent inflammation is termed transaminitis rather than hepatitis which is usually associated with infective inflammation.  Both cause ALT/AST rise.

PT

Prothrombin time or PT is a measure of function of the liver’s role in coagulation.

You know that your liver makes proteins for coagulation. These are called Factors.  Factors 2,7,8,9,10 (and 1&5), all undergo manufacture and activation using Vitamin K .

In acute and chronic liver failure, these proteins (factors) are not made efficiently or in big enough quantities, so the TIME it takes for blood to coagulate is slower.

Measuring Prothrombin Time (PT) allows a measure of hepatic function on coagulation.  

If it normally takes 10 sec for a blood sample to convert Prothrombin into Thrombin, it may take 20seconds in someone in liver failure.

PT is also measured as a blood test called an INR.  It means International Normalised Ratio.

A way of standardising the measure of PT all over the world.

A PT of 10sec roughly equals an INR of 1.0.  PT of 20sec = INR of 2.0 and so on. 

Adequate vit K in the diet allows the liver the ingredients to make those coagulation factors .  Not enough VitK and coagulation (PT/INR) will get longer.  This is why warfarin (a VitK antagonist) makes it longer for people to coagulate.  So... in liver disease, coagulation suffers, and bleeding / bruising can complicate patient symptom sets.

Finally Albumin.

A hugely important protein called Albumin is made in a functioning liver and released into the blood.   It acts as a water magnet and carrier protein of many drugs and other substances in the blood.  After being secreted into the blood by the liver, it has a half life of about 20days. 

If you went into acute liver failure today, we wouldn’t really notice a change in your serum Albumin for a few weeks.  So Albumin reduction is a marker for chronic liver damage.

Well that is it.  A wordy but simplified overview of the stuff they are looking for in liver function tests. 

Raised ALT/AST = acute liver damage

Slowed PT = acute and chronic damage

Reduced Albumin= chronic damage.

More?? Consider coming to one of our fun nurseing/paramedic seminars.   We love our Jargon.

Courses:

Www.Ect4Health.Com.Au/whats 

#KnowingYourJargon

Urobilinogen in Urine

#KYJ - Urobilinogen.

Ward test urine is such a common nursing assessment.

Occasionally I go through some of the urine values seen in abnormal urine tests, but one often poorly understood urine value is urobilinogen.

To understand this substance in urine we need to go back to the origin.

Red blood cells are born in bone marrow, and after 120 days, they are killed off by your immune system.  Components of the dead RBC are recycled, and processed by the liver.

RBC bodies become unconjugated bilirubin, which is processed into bilirubin and further into Bile. There,  bile is secreted to the Gall bladder to be concentrated and stored, waiting for your next fatty meal.

Once fat in your meal is detected by your gut, bile is secreted into your duodenum to mix with food, assisting lipase enzymes to break the fat down into triglycerides for absorption.

The reminant bile passes with undigested food into the large bowel and is acted on by intestinal flora .

This bile is converted into stercobilin, a dark brown pigment that gives faeces it’s colour, and urobilinogen a water soluble waste that is reabsorbed from the faeces.

Now stay with me:

All gut reabsorption of urobilinogen passes into your liver where it is converted into urobilin, and released into the blood stream so the kidneys can excrete it.

It is a light yellow colour and gives the urine it’s hue.  The more urobilinogen and subsequent urobilin you have the yellower your pee.

So it’s in there and it’s normal.

But...

There is a limit! If urobilin on dip stick is reactive (too high) it can represent one of two things.

More bilirubin than the liver can metabolise or hepatic failure.

1- RBC destruction

Haemolysis is the break down of RBCs.  In gut bleeds, haematomas or haemolytic anaemia ; even after a blood transfusion (massive), the sheer numbers of RBCs that are being broken down, and producing bilirubin overwhelms the liver’s capacity to convert to bile, so the liver converts it directly to urobilinogen where kidneys excrete what it can.

2- Liver failure. 

In hepatitis, liver disease like cirrhosis or liver Cancer, or any other liver disease; the conversion of bilirubin fails.  It therefore fails to be utilised adequately, and must be renally excreted.

Symptoms to check your patient for, when there is positive urobilinogen in their WTU, include 

Jaundice or skin yellowing 

Itch, or pruritus. 

Yellowing of the sclera.

Pale/ fatty /offensive faeces

Altered Liver Function Tests.

Coagulation issues leading to bleeding/bruising.

It is not too often that we get a chance to review the little physiology tips and pearls .  So our KYJ (#knowingyourjargon) blogs are one small way I contribute to Free open access medical-education. (#FOAM).

Check them all out on our website. WWE.ect4health.com.au