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;
33 Cards in this Set
- Front
- Back
|
Pathway associated with tissue injury and release of thromboplastin
|
Extrinsic
|
|
|
Pathway associated with vascular injury and release of collagen
|
Intrinsic
|
|
|
Plt's are activated by ___
|
Exposure to collagen secondary to bv injury
|
|
|
How long does vascular spasm tend to be maintained
|
20-30 minutes until Plt's can respond
|
|
|
Which system is fast
-Exstrinsic or intrinsic |
Extrinsic
|
|
|
Most powerful enzyme in clotting cascade
|
Trombin which converts fibrinogen to firbin
|
|
|
Essential component of clot
|
Fibrin
|
|
|
Enzyme required to breakdown clot
|
Plasminogen which converts to plasmin that is then able to dissolve fibrin clot (which will then produce FDP's/FSP's
|
|
|
increased consumption of Plt's
-ITP, TTP, DIC |
TTP and DIC
|
|
|
More rapid destruction of Plt's
-ITP, TTP, DIC |
ITP via antibodies
|
|
|
Dx in which Plt membrane is coated with autoantibody (IgG) and sensitized Plt are destroyed by RES in spleen/liver.
|
ITP
|
|
|
Main clinical feature of ITP
|
Bleeding (may be gradual or abrupt)
|
|
|
Initial therpay for ITP
|
Steroids/prednisone
Block binding receptors of macrophages Usually enough to induce remission (some still ahve long term probs) |
|
|
Prednisone works short term for ITP pt but is not controlling long term.
What next? |
Spleenectomy possibly.
|
|
|
ITP pt at high risk for bleeding may require what tx
|
IVIG
Plt transfusion not used prohylactically but may be indic in acute bleed |
|
|
When would plasmapharesis be indic in ITP pt
|
Refractory to all interventions
-Prednisone -Spleenectomy -IVIG |
|
|
Plt's b/c snesitized and clump in blood producing occlusions
|
TTP
|
|
|
Caused by defieciency of von Willebrand cleaving protease
|
TTP
|
|
|
How is thrombocytopenia induced in ITP
|
RES/macrophages secondary to immune mediation
|
|
|
How is thrombocytopenia induced in TTP
|
Increased consumption of Plt's
|
|
|
lab finding that is hallmark of TTP
|
Shistocytes
|
|
|
Why is simple plasma transfucion potentially adequate in TTP
|
Based on knowledge that pt's are deficient of von Willebrand protease
|
|
|
TOC in acutely ill TTP pt
|
Plasmapharesis ASAP
Prednisone (prevents further damage to endothelium) |
|
|
Why is a Plt transfusion C/I in TTP
|
It's a Dx of thrombosis thus Plt's will only exacerbate the problem
|
|
|
Dx of bleeding
-ITP or TTP |
ITP
|
|
|
Dx of thrombosis
-ITP or TTP |
TTP
|
|
|
Plasmapharesis (but not Plt transfusion) indic in
|
Acute TTP pt
FFP may be inidic otherwise ITP=postentially Plt transfusion in life thrreatening bleed along with IVIG |
|
|
Why is PTT time longer the PT
|
It measure the intrinsic pathway which is slower in clot formation
|
|
|
Lab test that measures local fibrinolysis
|
D-Dimer
|
|
|
Normal lab value or FDP
|
<10
|
|
|
Procoagulants
|
Thromboplastin/Prothrombin/Thrombin
Fibrinogen/Fibrin |
|
|
Anticoagulants
|
Plasminogen/Plasmin
|
|
|
Describe two (2) common complications associated with plasmapheresis.
|
Hypotension
Citrate tox |
