Thrombosis Flashcards
A patient has no history of bleeding problems but family members have received
treatment for thrombosis. Explain why this patient may have an increased APTT
XII deficiency or Inhibitor
Heparins effects can be reversed by administration of what substance
protamine sulfate
Bill and Joe are playing with some venomous snakes they stole from the zoo. Not being
the smartest lads, Bill was bitten when Joe thought it would be funny to hide the snakes
in Bill’s boots. Knowing his own limitations in the healing arts, Joe calls you and asks
which medicine to administer to reduce thrombosis in his ailing friend. What do you tell
him?
Administer heparin, direct Xa inhibitor, or direct thrombin inhibitor. Aspirin will
only affect platelets – and not immediately, Warfarin’s affect is also not immediate. (A
large bottle of whiskey – won’t help… but probably wouldn’t hurt the situation
Why are some patients predisposed to recurrent thrombosis after heparin therapy
Heparin therapy causes a decrease in the patient’s own Anti-thrombin levels. This is
why patients must be slowly weaned off heparin
A young woman has developed swelling in her legs but otherwise seems healthy. Her PT
and APTT are normal. Her D-dimer is positive. What medication could be causing her
symptoms?
oral contreceptives
How does a Prothrombin mutation (G20210A) cause thrombosis
causes increased production of prothrombin
How does a Lupus Inhibitor (lupus anticoagulant) cause thrombosis
Inhibits
prostacyclin that is produced by endothelial cells to inhibit platelet adhesion
Name a drug that can be given to break down a clot
tpa, urokinase, streptokinase
How do the “clot-busting” drugs work to facilitate fibrinolysis
They convert
plasminogen to plasmin and the plasmin then breaks down the clot (or fibrinogen
What is the defect present in patients with Activated Protein C (APC) resistance that
causes thrombosis
Mutant Factor V – Factor V Leiden is resistant to being broken
down by Protein C
What is the effect of heparin in vivo
Heparin makes a conformational change in Anti-
thrombin which increases its function. AT inactivates thrombin (IIa), Xa, IXa, Xia, XIIa
and plasmin.
What is an emboli
A thrombus that has broken free from the original clot site and
becomes lodged in capillaries of an organ
How can protein C and protein S deficiencies cause thrombosis
Factor Va and VIIIa are
not inactivated (resulting in more clot formation) and TPA is not released from
endothelial cells (thus plasminogen is not converted to plasmin and clots are not broken
down)
Theoretically, what is the mechanism of thrombosis for defects in homocysteine
metabolism (increased homocysteine)
Increased levels cause damage to
endothelial cells
Differentiate between primary and secondary fibrinolysis
Primary – breakdown of fibrinogen
Secondary – breakdown of fibrin
