Thursday, February 19, 2015

Study group discussion: Multiple myeloma and tumor lysis syndrome

Alright! Let's do review questions!

Patient has a high serum protein, normal albumin, rouleax formation on blood smear and monoclonal IgG spike. Urine analysis shows proteinuria. What do you think the patient has?

Multiple myeloma.

Correct!

What are the proteins on urinalysis called?

Bence jones proteins.

Patient develops bone pain. Why?

Lytic lesions!

Which factor causes the lesions?

Interleukin 2?
Umm. IL 2 causes proliferation of T cells.

It's IL 1 aka osteoclast activating factor

Oh.. OAF is right!

What is the characteristic appearance of plasma cell nucleus?

Cart wheel. Due to clumped chromatin.

Correct! Also a perinuclear halo!

What will you see on the xray skull in the patient?

Punched out lesions.

Will you do a bone scan to detect lytic lesions?

Nope.

Why no?

Ummm because the lesions will be visible right on X-ray so why use any more complex technique!

Not exactly but you're right!

Bone scan misses lytic lesions so you do a skeletal survey instead.

O woahhh!

Okay, so our patient now develops tingling numbness in the palm thumb, index and middle finger. What happened?

Hypocalcemia.. But in multiple myeloma hypercalcemia happens!

It's not related to calcium. That's why it's a trick question!

Seems like carpal tunnel due to some protein deposition!!??

On the right thinking process. Which protein?

Think, think, think! It's a basic pathology concept. Which protein will accumulate over time?

Amyloid!

Correct!

Patient developed amyloidosis due to light chains.

Patient now develops renal failure. Although there are a number of mechanisms for it which would be the two most likely cause of renal failure?

Amyloid
Hypercalcemia
And?

Amyloid isn't that common.

Why hypercalcemia will lead to renal failure?

Hint: Think more basic. What is going into the Kidneys?

Calcium :P

I gave you the labs of the patient in the question.

It's the proteins, guys! They'll block the tubules and cause RF.

Weren't we discussing the hypercalcemia leading to renal condition?

Oh that! Nephrocalcinosis.. Due to calcium!

Yeah that's why I was worried about sending calcium to kidney! :P

What will you do about the calcium? So that the patient won't go into renal failure? He has high calcium and is not responding to chemo. Calcium is 12 mg/dL

Fluids!

It won't bring the calcium levels down. Patient is still having calcium deposition in his kidneys!

We can use the bisphosphonates! Dronates?
Yes!

You'd give fluid and diuretics if he was having a hypercalcemic crisis

Yeah this is a chronic condition.

Why did our patient have rouleax formation on his blood smear?

Hyperviscosity?

Nope. That ain't the reason why the RBC's are sticking to each other!

ESR? That would lead to hyperviscosity syndrome.
Something to do with the changing shapes of RBC?

Nope.

Think more basic. What is in the blood of this patient?

Monoclonal antibodies!

Yes! Immunoglobulins coat the RBC and neutralize the ionic charge than normally repells em.

Nice!!

Is the rouleaux formation confined to these ig's only?...i mean what about any other ig?(if present, say)

Any immunoglobulins would cause rouleax formation! Usually it's IgG or IgA.

oes that mean rouleaux formation occurs whenever there are Ab's in blood?

I think only when they are present in excess such as in this state!!

Yes! In multiple myeloma, there are so many that it is effecting the RBC charge.

Ooh! Thanks guyz !

No but infections and inflammatory conditions also cause rouleax formation.. So I think it's reasonable to think that way!

Our patient now develops pneumococcal pneumonia. Why?

Although proteins are in excess they are not functional.

Exactly. They don't have clonality required to fight off infections!

This one has no thinking associated with it - what, if present in the patient, will be associated with a poor prognosis?

It's IL 6

Ohh!! So IL6 is associated with poor prognosis?

Yup. I donno why though. It's just a fact you should remember!

Patient is just diagnosed and is started on chemo, responding well and suddenly his creatinine levels start to spike. Calcium normal. No proteins in urine. What could be the cause?

Bence Jones protein not detected by dip stick?

Nope. No proteins in urine.

Tumour lysis.

Correct!

Wouldn't uric acid be detected in urine?

It would. Pathologist comes back to you and says he switched reports. Uric acid crystals were present in urine of your patient :P

How come creatinine is up? Creatinine would increase either due to excess muscle breakdown or renal failure!

That's because he went into renal failure due to urate nephrolithiasis. As in uric acid crystals caused obstructive nephropathy!

Which drug could've prevented this?

Allopurinol. Fluids.

Mechanism of action of Allopurinol.

Xanthine oxidase inhibitor.

What other ______ oxidase inhibitor do you know of?

Rasburicase.

Mechanism?

Urate oxidase inhibitor!

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