exam 1 Flashcards
what is the major regulatory enzyme for thrombopoiesis?
thrombopoietin (TPO)
where does TPO come from and how does it work?
continually produced by the liver, BM, endothelium etc.
it binds to Receptors of PLTs…if there is a decrease in PLT then increased free TPO will go back to BM and will increase megaK production to push out more PLTl
why do we get increased PLT is IMHA?
beacuse EPO will cross stimulate to megaK
what role do platelets have in hemostasis?
increased metabolic activity, primary hemostasis (inital clot cover), support secondary hemostasis (serve as increased surface area), clot retraction (contract, facilitate wound closure)
how is primary hemostatic plug formed?
adhesion, activation, secretion, aggregation
what lab tests are used to access platelet concentration?
blood smear and hematology analyzer
when does spontaneous hemorrhage occur?
<20,000/uL
when do you get falsely decreased platelet concentrations on the analyzer?
analyzer does not measure platelets because
- too big (macrothrombocytes)
- clumped
what lab test are used to access platelet morphology?
blood smear and hematology analyzer
what does an increased MPV mean?`
thrombopoeisis
what does the presence of macrothrombocytes suggest?
increased PLT production
what test are used to access platelet production?
BM aspirate
in a thrombocytopenic patient, how should healthy bone marrow respond?
should increase and see megaK and immature ones, if not then you should suspect a disease such as immune mediated thrombocytopenia
what are you major mechanisms for thrombocytopenia?
production, destruction, sequestration, loss, consumption
thrombocytopenia-production
decreased: bone marrow hypoplasia, neoplasia, myleonecrosis, degree depends one extent of bone marrow disease
thrombocytopenia-destruction
IMMUNE MEDIATED THROMBOCYTOPENIA. primary or secondary: get a little ab that attach to platelets get ID by spleen and get phagocytized. get severe thrombocytopenis**
- alloimmune thrombocyto in piglets/foals
- MLV
thrombocytopenia- sequestration
in large vascular beds: splenomegally, splenic torsion, neoplasia, hepatomegally, portal hypertension
thrombocytopenia-loss
hemorrhage (alone does not cause signif thrombocto, except severe)
thrombocytopenia- consumption
utlization of PLT during coagulation, especially DIC, vasculitis (ricketsial, FIP) ,viral infection,,,usually mild to moderate, hemorrhage if other coagulation defects and vasculitis
signs of platelet bleeding
- mucosal bleeding
- petechiation
- ecchymosis
- spontaneous hemorrhae <20,000
what are you two ddx for sevocyto
1) evans- immune mediated
2) DIC
2 major mechs for thrombocytosis
increased production
increased distribution
3 dz’s that may cause a reactive thrombocytosis
- chronic inflamm dz*
- iron def anemia
- IMHA
- some neoplasm
3 situations of thrombocytosis
- rebound from thrombocytopenia
- post-splenectomy
- response to some drugs (vincristine)
- excitement and exercise (epi)
aquired qualitative disorder
uremia, drugs, fibrin degradation, paraproties
inherited qualitative disorder
absence of glycoprtoein R, absence or reduction in PLT granuled, signal transduction defects, vW dz
what changed see in wVF dz
- normal PLT
- buccal mucosal bleeding time prolong
- if suspect then analyze plasma
- PTT/ACT usually normal, but can prolong if VII is def
expression of what cofactor iniated coagul?
tissue factor III aka thromboplastin
what factor drive amplificatin?
thrombin (IIa)
what are the 4 vit K dep factor
II, VII, IX, X
what coag factor has shortest half life?
VII
what are 3 components contribute to coag efficiency
Ca 2+, platelet membrane, nonenzymation factors
antithrombin inhibits?
Xa, thrombin and fibrin
what cofactor is required for antithrombin to inactivate thrombin?
heparain
what are two major end produce of fibrinolysis?
FDP, and D-Dimer(more specific)
Intrinsic
12,11,9,8
extrinsic
7
common
10,5,2,1
what are two test that do intrinsic pathway?
aPTT, ACT
what test is extrinsic?
PT
what two test access fibrinolytic activity?
FDP and D-dimers
how does CBC of warfarin look?
- PT prolong
- aPTT, ACT prolong
- PIVKA pos
- platelet count is normal
- not forming FDP beacuse no clots happening
how does CBC for DIC look?
- thrombocytopenia
- prlong PT, aPTT
- decreased fibrinogen concentration
- increased FDP and D-dimer
two phases of DIC
1) hypercoagulable phase
2) consumptive phase
what two tests do you run before liver biopsy?
PT & aPTT
why might you get a coagulopathy in liver dz?
- decreased synthesis of coag factors
- production of dysfunctional factor
