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
|
white thrombus
|
predominately a platelet thrombus. can obstruct flow to the coronary arteries, brain, etc.
|
|
|
red thrombus
|
few platelets, mostly fibrin-RBC networks. can form pulmonary emboli
|
|
|
vWF disease
|
most common inherited bleeding disorder, dominant inheritance. platelets can't bind to the damaged endothelium
|
|
|
Bernard-Soulier Disease
|
Rare. recessive. defect in vWF-R, or Gp Ib
|
|
|
Glanzmann's Thrombasthenia Disease
|
Rare, recessive. Defect in platelet fibrinogen-R which is GpIIb/IIIa.
|
|
|
Desmopressin
|
Short term treatment - leads to releasing stores of vWF into blood, thus increases F VIII. oral or IV
|
|
|
Aspirin
|
blocks TXA2 synthesis
|
|
|
Ticlopidine, Clopidogrel
|
block platelet's ADP-R, thus inhibit ADP induced platelet aggregation
|
|
|
Abciximab, eptifibatide, tirofiban
|
binds GpIIb/IIIa, blocking fibrinogen binding
|
|
|
Epoprostenol
|
PGI2, prostacyclin derivative, vasodilator
|
|
|
Dipyridamole, cilostazol
|
inhibit phosphodiesterase
oral, thus long-term use |
|
|
NO
|
vasodilation
|
|
|
PT assay:
uses: |
Prothrombin Time, tests extrinsic pathway. Plasma + TF + Ca + (-)phospholipids.
used to monitor Warfarin therapy, assay liver dysfunction |
|
|
aPTT assay:
uses |
activated partial thromboplastin time, tests intrinsic pathway. Plasma + Ca + (-)phospholipids + Kaolin.
used to assay Hemophilia A&B and to monitor pt's before heparin |
|
|
Hemophilia A
PT, aPTT? |
defective Factor VIII
-x linked most common of Hemophilias assays:normal PT, long aPTT |
|
|
Hemophilia B
PT, aPTT? |
defective Factor IX
assays: normal PT, long aPTT |
|
|
Hemophilia C
|
defective Factor XI
seen in ashkenazi jews |
|
|
how does thrombin regulate clotting?
|
thrombin binds thrombomodulin on healthy endothelium. this activated thrombin can activate Protein C; Protein C (w/ prot S) inactivates F VIII and F V.
|
|
|
what is factor V Leiden?
|
a mutated F V that is resistant to inactivation by Protein C. same phenotype with defective Protein C.
|
|
|
how is TF regulated?
|
TFPI - TF pathway inhibitor - binds and inhibits F X, eventually leading to inhibition of TF--F VII complex.
|
|
|
fibrinolysis activation
|
tPA, from endothelium, activates Plasminogen to Plasmin
|
|
|
what are d-dimers?
|
d-dimers are breakdown products of fibrin clots, done by Plasmin.
|
|
|
how is fibrinolysis regulated?
|
PAI-1 and alpha2-antiplasmin
|
|
|
anti-platelet drugs - long vs short term uses
|
long term: prevent MI, TIA, stroke in pt's with Hx or atherosclerosis
short term:pt's suffering MI, DVT therapy |
|
|
uses of low-dose aspirin:
how long is the effect? |
suspected MI
prophylaxis of MI inhibits platelet COX-1 for life of platelet, 10 days |
|
|
aspirin should be avoided in pt's:
|
w/ peptic ulcers, liver/kidney problems
|
|
|
Ticlopidine/Clopidogrel: MOA, similarities and diffs b/w aspirin?
|
Blocks ADP-R on platelets. Orally. =like aspirin
diffs=1-2 day lag in effect (vs aspirin, which is why only aspirin is indicated for an acute MI) |
|
|
Ticlopidine side effects:
|
bone marrow toxicity:
neutropenia. also TTP - thrombotic thrombocytopenic purpura w/ pentad Sx |
|
|
Benefits to Clopidogrel over Ticlopidine?
|
fewer side effects, long term use seems okay.
|
|
|
List three Fibrinogen-R antagonists. how are they administered? use is limited or not?
|
abciximab, eptifibatide, tirofiban
all given IV, thus use is limited to short-term use. given with aspirin and heparin. inhibitors of GpIIb/IIIa -think Glanzmann's thrombasthenia |
|
|
list two PDE inhibitors, how are they administered?
|
dipyridamole, cilostazol. orally = long term.
|
|
|
prostacyclin primary uses:
|
pulmonary HTN. IV. very-short 1/2 life.
|
|
|
what is the role of gamma-carboxyglutamate residues in some of the clotting factors?
|
these residues bind Ca2+, which then allows them to bind (-)phospholipids
|
