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40 Cards in this Set

  • Front
  • Back
Platelets are formed in a process called
Platelets are regulated by a circulating growth factor called
thrombopoietin (TPO)
The large, precursor cell to platelets in the bone marrow. They have no nucleus, just a little cytoplasmic RNA, and virtually no ability to synthesize proteins. They do display active metabolism.
How do megakaryocytes react to injury or inflammation?
they change shape, release contents, and form a platelet plug
Function of open canalicular system of platelets
increase surface area by 50%
has receptors for IgG and fibrinogen
platelet membrane contains what?

why is this important?
and how does it stay this way? what if it doesn't stay this way?
phosphatidylserine and phosphatidylethanolamine

stays on interior leaflet because of atp translocase

atp pump shuts during release reaction, and scramblase causes PS to relocate to exterior
What does glycocalix do?
causes net negative charge causing repulsion of platelets from eachother
release of platelet granules caused by:
profilin relinquishes hold on g actin under influence of DAG, and F actin becomes prominent in filopodia following calcium influx
what maintains discoid shape of platelet?

what allows for shape change?
tubulin and MAP (microtubule associated protein)
- when calcium influx, these depolymerize allowing platelets to change shape
What do dense bodies contain?
(called dense because of electron density from Ca++ and MG++)
serotonin, ADP, ATP
what do alpha granules hold?
large molecules like proteins
IgG and fibrinogen are taken up by
PF4 and beta thromboglobulin are taken up by
energy dependent concentrations
thrombospondin and platelet derived growth factor are included through
What is Adhesion?
sticking and spreading of discrete platelets on damaged endothelium via binding to collagen in the subendothelial, intimal and medial layers
what holds platelets to subendothelial collagen?

how is this done?

what happens at high shear rates?

this is accomplished by receptor complex GPIb/IX/V

vWF becomes sticky and hypercoagulable or thrombotic
What causes Bernard-Soulier syndrome?
inherited defects in any of the subunits of GPIb/IX/V
that affect their ability to interact and bind with vWF
What is Aggregation?

What is it dependent on?
the sticking of activated platelets to one another in a clump. Dependent on fibrinogen.
receptor for fibrinogen is GPIIb/IIIa
What causes Glanzmann's Thrombasthenia?
damage to GPIIb/IIIa (receptor for fibrinogen)
what activates GPIIb/IIIa?
agonist of injury like ADP, collagen, thrombin, serotonin, TxA2
response to injury agonist:
a)influx of free calcium into cytoplasm
b)shape change into spiny sphere
c)phosphorylation via calcium dependent and independent kinases
d)breakdown of PIP2 to IP3 and DAG
e)liberation of arachidonic acid to TxA2
f)aggregation via fibrinogen to GPIIb/IIIa
g)scrambling of PS to outer leaflet
h)release of alpha granule contents and fusion with outer membrane
i)release of dense granule contents and fusion with outer membrane
What is thrombin?
Thrombin is an agonist that acts on platelets and other cells by binding to and then proteolytically cleaving its own receptors
production of arachidonic acid:
hydrolysis of phospholipids , converted by cyclooxygenase to prostaglandin PGH2 which is converted to TxA2 by thromboxane synthetase

NSAIDS target the synthesis of TxA2

NSAIDS do not block thrombin because it can independently relase vWf and phospholipase A2
Weak and strong agonists
ADP (but can potentiate other agonists)
Epinephrine (inhibits adenylyl cyclase and cAMP, increasing platelet aggregation)

Collage is a strong agonisht and acts via GPVI to trigger Ca++
Von Willebrand Factor vWf
is made in megakaryocytes and endothelial cells

is processed in Weibel-Palade body

platelet vWf is stickier than other forms becasue not proteolytically processed

binds to collagen

binds to GPIb/IX/V (resting and active)
binds to GPIIb/IIIa on activated
What is plasma?

What is Serum?
the fluid, non cellular part of blood with its clotting mechanisms intact. clotting tests are always done on plasma.
Serum is clotted plasma
what do Zymogen factors do?
are activated to form protease factor a
clotting enzymes:
clotting proteases:
serine proteases
trypsin-like enzymes
contact activation
factor XIIa + Tissue Factor cofactor, prekallikrein, and HMW-kininogen = activated XI, which activates IX

see chart
fibrin formation
fibrinogen has A alpha and B Beta chains cleaved to form fibrin. *starts with A alpha removal, strengthened by loss of B primer
Vitamin K is required for?
factor VII
factor IX
factor X
Protein C
Protein S
coumadin and warfarin are antagonists of vitamin K

advantage over heparin because they can be taken orally for years
Inhibitors of clotting cascade:

antithrombin III
inhibits factor Xa and thrombin. a partial deficiency of ATIII causes problem because rate of inhibition is decreased in proportion to the concentration.

heparin accelerates rate of action of ATIII
Tissue Factor Pathway Inhibitor
**formed in negative feedback

TFPI:Xa inhibits TF:VIIa complex
Protein C
works with protein S to inactivate cofactors VIIIa and Va

need thrombomodulin (TM) for Protein C activation)
clotting tests:
Prothrombin Time
initiated with preparation of TF

extrinsic pathway (VII)
Partial Thromboplastin Time (PTT)
involves contact system: (intrinsic pathway)
factor XI which activates IX, which activates X
Thrombin TIme
involves adding exogenous thrombin to plasma and timing clot formation
Fibrin degradation products (FDPs)
products of fibrinolysis used to measure a thrombotic state
part of the repair and restitution of vessel function that follows either normal clotting or deep vein thrombosis.
closely linked to both clotting and inflammation pathways

requires plasmin (which recognizes both lysine and arginine)