Uremic platelet dysfunction

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EazyE1907

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got a world question on uremic platelet dysfunction but the explanation doesn't give any insight to the pathophysio behind the disease. It just says that there might be some platelet inhibiting factors in patients on dialysis. is this it? or does anyone have a better understanding of why these pts have platelet dysfunction. thanks

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There are lot of factors contributing to the platelet dysfunction, and really it's WAY beyond the scope of STEP1.

I have a funny way of remembering that there is platelet dysfunction in renal failure, maybe this'll help:
1) Ca2+ is needed for platelet adhesion, I kind of think of Ca2+ as a sticky positively charged "double-sided tape" for all the negatively charged molecules so that they can bind. e.g. GPIIb/IIIa, vWF, cadherins, etc etc etc.

2) In renal failure, one of the complications is renal osteodystrophy - you can't dump phosphate or synthesize calcitriol, so you get DECREASED serum Ca2+ with increased serum phosphate and blah blah blah. Point is, serum Ca2+ is decreased.

3) Without Ca2+, you don't have the double sided tape anymore, now all those negatively charged molecules are going to repel each other rather than stick to each other - i.e. you no longer have platelet aggregation/adhesion/things sticking to the negatively charged vWF, glycoproteins, phospholipids and collagen.

4) Dialysis would correct for the electrolyte imbalance and "fix" the problem.

Again, it's actually way more complicated than that (since you can have platelet dysfunction without electrolyte imbalance), and I can't even begin to understand the whole picture, but for the purposes of STEP1 this is enough to help me remember that there are going to be problems with platelet functions in renal failure.

EDIT:
Did some digging and it does seem like there is a GIANT laundry list of reasons for platelets to not work in renal failure, but I really wouldn't worry about remembering all of these:
Factors related to the vessel wall
Decreased production of the largest multimers of von Willebrand’s factor
Enhanced nitric oxide production
Enhanced prostacyclin production

Factors related to platelets
Abnormal mobilization of calcium ions in platelets
Defective activation of glycoprotein IIb -IIIa receptors
Defective cyclooxygenase activity (reduced ability to generate thromboxane A2)
High levels of cyclic adenosine monophosphate
Low levels of serotonin and adenosine diphosphate

Factors related to the blood
Anemia
Altered blood rheology (ie, deranged radial transport of platelets)
Altered transfer of adenosine diphosphate from erythrocytes to platelets
Uremic toxins (eg, guanidinosuccinic acid, phenol, phenolic acid, urea)
 
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Hard to follow up teotuf's post but for uremia itself, one of the main reasons touted is dysfunction in platelet degranulation, preventing platelet aggregation and adhesion.
 
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