Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
|
TPA and urokinase are both finbrinolytics but act in different locations. Where do they act?
|
TPA: within clot
Urokinase: extrinsically |
|
|
How does urokinase work?
|
It activates matrix metalloproteinases (MMP) which degrade adhesion proteins (eg fibronectin)
|
|
|
How does TPA work?
|
TPA primarily activates plasminogen
|
|
|
What is the screening test for fibrinolysis?
|
short ELT
|
|
|
What does TAFI (thrombin activatable fibrinolysis inhibitor) do?
|
cleaves lysine from fibrin
prevents plasminogen from binding to fibrin |
|
|
What are ATIII, protein C, protein S and plasminogen levels in newborns compared to older individuals?
|
Decreased
therefore increased tendency to clot |
|
|
Which clotting factors do Protein C/S and ATIII inactivate?
|
Protein C/S: factor V, VIII
ATIII: vitamin k dependent factors (2,7,9,10) |
|
|
Which is vitamin k dependent: Proteins C/S or AT III?
|
Protein C/S
|
|
|
Which is the most common contact factor deficiency?
|
factor XII
|
|
|
Does having a Factor XII deficiency increase your risk for thrombosis?
|
probably not
|
|
|
What are the effects of kallikrein?
|
liberates kinin
releases renin activates plasminogen (urokinase) destroys complement C1 |
|
|
What are the contact factors?
|
Factor XI
Factor XII Prekallikrein High Molecular Weight Kininogen |
|
|
What happens to the PTT in a mixing study when the prolongation is due to a contact factor deficiency?
|
It corrects (you give back the deficient factors by mixing with normal plasma)
|
|
|
How prolonged is the PTT when there are heterozygous contact factor deficiencies?
|
slightly prolonged for Factor XII heterozygous deficiency. Normal for prekallikrein and high molecular weight kiniogen deficiencies.
|
|
|
how do you confirm the presence of lupus anticoagulant?
|
neutralization by phospholipid
|
|
|
how do you confirm that the presence of heparin is what is causing a prolonged PTT?
|
reptilase time is normal
|
|
|
what does a prolonged reptilase time indicate?
|
fibrinogen deficiency
|
|
|
What are three possible diagnoses in the setting of "platelet- vessel" bleeding symptoms (immediate, superficial, mucosal bleeding) but normal screening tests?
|
VWD
plasminogen activator deficiency (PAI-I) platelet dysfunction |
|
|
What are three possible diagnoses in the setting of "factor deficiency " bleeding symptoms (delayed, deep, joint/muscle) but normal screening tests?
|
Factor XIII deficiency
antiplasmin deficiency mild hemophilia (FVIII, FIX, FXI) |
|
|
what is the lab abnormality with factor VII deficiency?
|
prolonged PT.
|
|
|
which factors are made in the liver AND in megakaryocytes?
|
fibrinogen
factor V factor XI factor XIII VWf |
|
|
where is factor V produced?
|
liver
megakaryocytes endothelial cells |
|
|
where is factor V III produced?
|
liver
RE system |
|
|
what ethnic group gets factor XI deficiency?
|
ashkenazi jews
|
|
|
what syndrome is factor XI deficiency associated with?
|
Noonan's syndrome
|
|
|
what is the screeing test for Factor XIII deficiency?
|
5M urea clot dissolution test
(urea solubility test) |
|
|
which type of leukemia is particularly associated with DIC?
|
AML
|
|
|
what are the associated coagulation factor abnormalities in nephrotic syndrome?
|
decreased FIX, FXII, ATIII, plasminogen
increased fibrinogen, FVIII prolonged bleeding time platelet dysfunction (uremia) |
|
|
describe the three main components of the clotting system
|
propagation of the clot
inhibition of the clotting process (limits and localizes formation of the clot at the site of injury) breakdown of the existing clot |
|
|
what inhibits the plasminogen activators: TPA and urokinase
|
PAI-1: plasminogen activator inhibitor
|
|
|
what inhibits plasmin
|
alpha-2 antiplasmin
|
|
|
which clotting factors are acute phase reactants?
|
F VIII
fibrinogen VWF |
|
|
when is the thrombin time prolonged?
|
in hypofibrinogenemia and dysfibrinogenemia as well as in the presence of heparin or FDPs (fibrin degredation products)
|
|
|
which phase of the coagulation system is thrombomodulin a part of?
|
the anticoagulant or inhibitor pathway
|
|
|
how is activated protein c formed?
|
thrombin binds to thrombomodulin
|
|
|
what does the protein c system do?
|
it inactivates FVa and FVIIIa
|
|
|
which factors are normal in the newborn?
|
FV
FVIII fibrinogen |
|
|
which is the last coagulation component to reach adult levels
|
protein C
adult levels are not reached until adolescence |
|
|
what factor deficiency classically presents with prolonged bleeding from the umbilical cord?
|
homozygous FXIII deficiency
|
|
|
what is the cause of early HDN (hemorrhagic disease of the newborn)?
|
maternal ingestion of medications that pass through the placental circulation: warfarin, carbamazepine, barbituates, phenytoin, rifampin, isoniazid, certain cephalosporins
|
|
|
When does early hemorrhagic disease of the newborn occur?
|
within the first 24 hours
|
|
|
what is FV Leiden?
|
point mutation of FV protein, makes FV resistent to degredation by activated protein C.
|
|
|
how do you screen for FV leiden?
|
APTT-based assay for activated protein C resistance. (or directly by DNA analysis).
|
