Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

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?
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
destroys complement C1
What are the contact factors?
Factor XI
Factor XII
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?
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?
factor V
factor XI
factor XIII
where is factor V produced?
endothelial cells
where is factor V III produced?
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?
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?
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?
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).