Hemostasis 2 Flashcards
What is heparin-induced thrombocytopenia?
Platelet destruction and thrombocytopenia arises secondary to heparin therapy.
The idea here is that the heparin can form a complex with a molecule on the surface of the platelets (Platelet Factor 4), against which auto-antibodies develop (IgG). This results in consumption of the platelets by the spleen.
Feared complication of heparin-induced thrombocytopenia?
Thrombosis
we need to continue give the patient another anti-coagulant because of the continued risk of thrombosis. **You do not want to give these patients coumadin, because these patients are at an increased risk of coumadin skin necrosis
When would you want to look at Factor 1 levels?
Factor 1 is fibrinogen. This is generally tested to help diagnose disseminated intravascular coagulation
What lab study is most likely to show the anticoagulant effects of heparin?
the activated partial thromboplastin time (aPTT). The PTT measures the intrinsic and common pathway of the coagulation cascade.
How does heparin work?
It stimulates/accelerates the activity of antithrombin III, which inactivates thrombin.
*It does not lyse existing clots
Tissue factor
Protein released from injured tissues that works together with vactor VII to initiate the extrinsic pathway of the coagulation cascade.
Tissue factor + FVII cleave FX to Xa
What is DIC?
Disseminated Intravascular Coagulation
Widespread activation of clotting leads to widespread microthrombi and consumption of platelets and clotting factors, which creates a bleeding state, especially from IV sites and mucosal surfaces (bleeding from body orifices)
What are the causes of DIC
STOP Making New Thrombi
Sepsis (gram-negative) Trauma Obstetric complications acute Pancreatitis Malignancy (adenocarcinoma, acute promyelocytic leuk) Nephrotic syndrome Transfusion
Rattle snake bite–venom activates coagulation
What lab values would we see for DIC?
The most effective tests to evaluate DIC are: platelet counts, fibrinogen levels, and fibrin degradation products
- -increase in fibrin split products (D-dimers)
- -decrease in fibrinogen
- -decrease in factors V and VIII
- -decrease platelet count
- -increased PT/PTT
- -Microangiopathic hemolytic anemia
What are D-dimers?
D-dimer is a fibrin split product, derived from the splitting of cross-linked fibrin.
**D-dimer is not produced from splitting of fibrinogen. The presence of D-dimer indicates that we are successfully making clots; its elevation indicates we are making (and subsequently degrading) lots of clots.
What is the last step in clot formation?
Fibrinolysis. We now was to remove the clot we made after the vessel is healed. This is achieved via the molecule plasmin.
How is plasmin made?
tPA (tissue plasminogen activator) converts plasminogen to plasmin
What does plasmin do?
(1) cleaves fibrin and serum fibrinogen
(2) destroys coagulation factors
(3) cleaves vWF (blocks platelet aggregation)
*It lyses clots, as well as reduces the ability to form new ones (by degrading clotting factors, and inhibiting platelet aggregation)
What inactivates plasmin?
alpha2-antiplasmin
If a patient has symptoms that resemble DIC, but labs show no elevated D-dimer, what should we think about?
A disorder of fibrinolysis.
The patient’s plasmin is being activated outside the coagulation cascade…this is leading to increased bleeding. However, because there are no clots to actually lyse, there will be no fibrin to cleave, and therefore the D-dimer will not be elevated.
