Platelet Problems

Question 1

where are platelets made?

Answer 1

megakaryocytes, made in the bone marrow.

Question 2

why does renal failure impact platelet function?

Answer 2

it makes them have decreased aggregation and adhesion because the kidney is what makes the Gp1b protein that does that

Question 3

what is the half life of a platelet?

Answer 3

8-12 days. hence you stop aspirin 7 days before surgery, thats the lifetime of a platelet

Question 4

what are the main categories to help think about thrombocytopenia

Answer 4

decreased production -
increased destruction
Consumption/ Sequestration

I would also add drugs - lots of things impact platelets levels, hence Heparin induct thrombocytopenia etc

Question 5

what temperature range impacts platelets?

Answer 5

under 30 degrees youre in trouble and spontaneous bleeds will occur

Question 6

what are the two types of Heparin Induced Thrombocytopenia

Answer 6

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

Question 7

what is the gold standard test for HIT

Answer 7

serotonin release assay -

Question 8

what are the sequelae of HIT?

Answer 8

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

Question 9

what do you put someone on if they have had HIT in the past?

Answer 9

they cant be on heparin, so you need to choose something like argatroban or lepirudin. Mostly there are direct thrombin inhibitors

Question 10

what is ITP and what is its pathophysiology

Answer 10

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

Question 11

what is the pathophys behind TTP

Answer 11

Thrombotic Thrombocytopenic Purpura = lot plts + neurologic symptoms.
Treatment is plasma exchange : get rid of the ADAMS13 that is sticking around and messing everything up

Question 12

what is the Pathophysiology of HUS

Answer 12

think of thrombocytopenia + renal failure.

treatment is supportive mgmt - DO NTO transfuse anything in!

Question 13

what is the pathophys of DIC?

Answer 13

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

Question 14

what labs do you expect to see in DIC

Answer 14

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

Question 15

How do you treat DIC?

Answer 15

essentially just replace everything even though it seems platlets would add fuel to the fire, try to maintain plts above 20

Question 16

if someone gets a huge venous thrombosis, what diagnosis should you think of?

Answer 16

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

Question 17

what is the most common cause of thrombosis??###

Answer 17

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

Question 18

explain to a patient what a diagnosis of lupus anticoagulant is

Answer 18

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

Question 19

most common cause of thrombosis

Answer 19

factor V Leiden - autosomal dominant condition discovered in “Leiden, Netherlands”

Question 20

what is the genetic change that causes factor 5 leiden

Answer 20

glutamine to arganine substitute in favtor 5 of the clotting cascade, makes you have increased incidence of both arterial and venous clots,

Question 21

do homozygotes with factor V leiden die?

Answer 21

no but they need to be considered for anticoagulation

Question 22

if someone has a PE, what is the most likely site for the original clot

Answer 22

iliofemoral vessels -90% of the time they harbour the stuff