Platelet Problems Flashcards
where are platelets made?
megakaryocytes, made in the bone marrow.
why does renal failure impact platelet function?
it makes them have decreased aggregation and adhesion because the kidney is what makes the Gp1b protein that does that
what is the half life of a platelet?
8-12 days. hence you stop aspirin 7 days before surgery, thats the lifetime of a platelet
what are the main categories to help think about thrombocytopenia
decreased production -
increased destruction
Consumption/ Sequestration
I would also add drugs - lots of things impact platelets levels, hence Heparin induct thrombocytopenia etc
what temperature range impacts platelets?
under 30 degrees youre in trouble and spontaneous bleeds will occur
what are the two types of Heparin Induced Thrombocytopenia
Hit 1 - transient drop in platelets that resolves with D/cing heparin
HIT II - way bigger problem, plts drop to 25-100, usually within 5-20 days of starting heparin
what is the gold standard test for HIT
serotonin release assay -
what are the sequelae of HIT?
1) Skin necrosis - little areas get blocked from blood flow by the clot
2) bleeding - the platlets that are around are dysfunctional
3) intravascular thrombosis - the platelets are dysregulated and clump any old place
what do you put someone on if they have had HIT in the past?
they cant be on heparin, so you need to choose something like argatroban or lepirudin. Mostly there are direct thrombin inhibitors
what is ITP and what is its pathophysiology
Idiopathic/autoimmune thrombocytopenic purpura is
- an isolated thrombocytopenia
- IgG antibodies coat the platelets so they get destroyed in the spleen
- treatment : steroids to calm down the immune system , can also plasma exchange to try and get rid of some of the rogue IgG
what is the pathophys behind TTP
Thrombotic Thrombocytopenic Purpura = lot plts + neurologic symptoms.
Treatment is plasma exchange : get rid of the ADAMS13 that is sticking around and messing everything up
what is the Pathophysiology of HUS
think of thrombocytopenia + renal failure.
treatment is supportive mgmt - DO NTO transfuse anything in!
what is the pathophys of DIC?
its a massive systemic activation of the coagulation system in a dysregulated way
- when you activate everything there is a depletion of factors causing global bleeding,. - you lose fibrinogen, and have high end-line degradation products like ddimer etc
what labs do you expect to see in DIC
low plts- the plts are in microvascular clumps high INR, PTT - all the factors are used low fibrinogen - its in the clumps high Ddimer fragmented RBCs on smear- schistos
How do you treat DIC?
essentially just replace everything even though it seems platlets would add fuel to the fire, try to maintain plts above 20
if someone gets a huge venous thrombosis, what diagnosis should you think of?
protein C and S deficiency - these are factors made by the liver.
If you see a big clot and they are low in C and S then they need anticoagulation with heparin for life
what is the most common cause of thrombosis??###
Factor V Leiden - a missense mutation that makes the platlet immune to protein C cleavage - so it makes you clot abnormally. it is the most common inherited hypercoaguable disorder
explain to a patient what a diagnosis of lupus anticoagulant is
this is a disorder that is essentially a misnomer. In the end it is a factor that makes you procoagulant - so you have a risk for clots. However in our in vitro lab tests it abnormally prolongs the PTT (intrinsic) so we initially called it an anticoagulant.
-The treatment is then to anticoagulate people
most common cause of thrombosis
factor V Leiden - autosomal dominant condition discovered in “Leiden, Netherlands”
what is the genetic change that causes factor 5 leiden
glutamine to arganine substitute in favtor 5 of the clotting cascade, makes you have increased incidence of both arterial and venous clots,
do homozygotes with factor V leiden die?
no but they need to be considered for anticoagulation
if someone has a PE, what is the most likely site for the original clot
iliofemoral vessels -90% of the time they harbour the stuff
