Thread by @rabihmgeha

Teaching Rounds Day 8/15

Cellular lysis...

Not all cells are equal.

Join us, #medtwitter & #medstudenttwitter

"Why you do always start your talks with a vague statement and not actual learning objectives, Rabih?" - a dear friend

🤣🤣
I think it's more fun this way AND
75% of teaching is making sure everyone is having fun.

When it comes to learning

Climate > Content

OK.
Back to Cellular Lysis!

Each organ, and it's associated cells, are very different from each other.

But there is a common denominator.

Most cells have
1.K
2.Phos
3.LDH

in abundance...

If a large number of a cells from an organ underwent simultaneous necrosis, the blood

1.K
2.Phos
3.LDH

levels would rise significantly.

But, with this data alone, we'd have no idea which cells were suffering this injury.

Some organs have unique markers that allow us to readily identify them:

1. Troponin - heart
2. CK - skeletal muscle
3. Hemoglobin - red blood cells

What about AST/ALT for the liver?
Unfortunately, not super specific...

Can you think of some others, #medtwitter?

Ok.

Enough of this hypothetical construct.

How does this information help us clinically?

There are 3 clinical circumstances where large amounts of intracellular necrosis results in a clinical picture of

HyperK, HyperPhos and elevated LDH
(FYI - @CPSolvers schema for LDH here - bit.ly/31E5uWs)

Why only 3 clinical scenarios..?

Only a few organs have enough cellular reserve such that:

1. Accumulation of their toxic intracellular products, and 2. NOT loss of function of that organ

dominates the clinical picture.

Wow...what a vague statement.

Some examples...

The heart.

Acutely lose 50% of heart cells?
Cardiogenic shock will probably dominate the clinical picture well before enough toxic accumulation occurs.

Samsies with the brain, liver, kidney, etc.

1. Muscle
and
2. Red blood cells

have enough cellular reserve that toxic accumulation of their intracellular products can be a prominent part of their clinical picture.

A curious twist...

Both release a nephrotoxic Globin

1. Myoglobin - muscle
and
2. Hemoglobin - red blood cells

So...

Acute kidney injury is also a prominent part of the clinical picture

This is the key final step in this story:

HyperK
HyperPhos
Elevated LDH

and...

AKI

If kidney dysfunction did NOT occur in the setting of rhabdomyolysis or intravascular hemolysis, the incredible kidneys might have been able to handle all K and Phos coming their way.

Who knows...
I certainly don't.

If anyone does, #medtwitter, let us know!

To summarize:

[1] All cells have K, Phos, and LDH.

[2] Massive cellular necrosis resulting in the accumulation of these toxic products dominates the clinical picture when the organ involved

1.Has a lot of cellular reserve AND

2.Releases a nephrotoxic product

Wait. Wait.

We said there were 3 clinical scenarios where this occurred, and we've only mentioned 2 organs so far -

Muscle and
RBCs.

Yeah...
The final scenario results from cells that are not supposed to be there...

Tumor lysis syndrome...

With this cellular lysis story as a foundation, we'll talk more about TLS soon.

Thanks for joining us!