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40 Cards in this Set

  • Front
  • Back
Primary vs. secondary hemostasis
pri: platelet plug formation, seconds

sec: plasma coag. system, minutes
platelets: char
from megakaryocytes in marrow
some in spleen, most in plasma
no nuclei
platelet action
1. adhesion
2. aggregation
3. granule release
adhesion: char
mediated by memb. receptor proteins = glycoproteins (integrins)
adhesion receptors on platelets
GP IaIIa: for collagen

GP Ib-IX: for for VWF
aggregation receptors
GP IIbIIIa: for fibrinogen

to stick platelets to each other
platelet activation
release of granules

adhesion->activates (P)lipase A2 enzyme

serotonin: vasoconstr
ADP: activates more platelets
adhesion cascade
adhesion->(P)lipase A2->cleaves (P)lipids-> releases Arachidonic acid-> (COX-1)-> prostaglandin H2-> (T-boxane synthase)-> Thromboxane A2 (TxA2)-> positive feedback @ (P)lipase A2
TxA2 char
feedback amplification
vasoconstrictor: promotes thrombux formation
inhibits platelets

blocks COX-1 and COX-2 irreversibly

reduces TxA2 form. and platelet activ.-> bad for ulcers
Endothelial cells: adhesion cascade
Arach. acid-> (COX-2)-> P-glandin G2-> (PGI synthase)-> PGI2
PGI2 and TxA2 char
PGI2: vasodilator, causes inflammation
TxA2: vasoconstr., activates platelets, causes clotting

PGI2 inhibits positive feedback action of TxA2
selective COX inhibitors
takes brakes off platelet activation-> innapropriate clotting in heart, etc
thrombosis: treatment/inhibition
drugs against platelet receptors

ex. GP IIbIIIa blockers inhibit aggregation
platelet defects

membrane receptor defects: Bernard Soulier and Glanzmann's

treatment: platelet xfusions
Bernard Soulier syndromE
mut. in VWF receptor

measure adhesion of platelets to endoth. tissue to diagnose
v platelet count

-> petachiae (sub-cutan. hemorrhages)
Glanzmann's disease
mut in fibrinogen receptor IIbIIIa

affects aggregation
platelet storage
only active if kept @ room temp-> bacterial contam. risk

UDP galactose glycosylation prevents recognition & clearance-> allows refrig.
thrombin points of regulation
fibrinogen-> fibrin

feedback amplif: XI, V & VII activation

stimulates cross-linking: XIII activation
type B hemophilia

Factor IX problem: Christmas Factor
type A hemophilia

Cofactor VIII problem:
Factor XIII

cross links fibrin polymers
extrinsic pathway
more common

involves Tissue Factor: receptor in memb of epithelial cells
intrinsic pathway
HMWK complex act. by neg charged surfaces
Factor V
enhances Xa activity
Factor VIII
essential for IXa activity, critical for clotting

deficiency-> Hemophilia A
calcium role in clotting
mediates binding of factors to (P)lipids

to concentrate clotting factors @ region
Vitamin K role in clotting
necessary to activate coag. factors

bile acid problems-> can't absorb lipid sol. vitamins (like Vit K)
stimulates antithrombin/ thrombin interaction
thrombin receptor on intact endothelial surfaces

binds and inhibits thrombin

-> therefore, only damaged tissues will not be able to inhibit thrombin
Protein C
activated by thrombin/ thrombomodulin complex

cleaves Va and VIIIa-> tones down cascade
Factor V Leiden
no cleavable by APC (activated Protein C)

-> ^clotting (inhibits inhibition)

30-40% of famillial thrombosis
Protein S
binds Protein C, enhances activity
clot lysis
plasmin: protease, hydrolyzes fibrin in clots

TPA: Tissue plasminogen activator makes it (TPA secreted by endothelial cells)
Hemophilia treatment
missing factor (VIII or IX prep'n)

can get AIDS and HepB

use recomb. Factor VIII
Von Willebrand's Disease
less activity of VWF

more common (pseudohemophilia)

less platelet adhesion
APC resistance
Factor V Leiden most common risk factor for thrombosis

resistant to protein C cleavage
Acquired bleeding disorders

Vitamin K dependent: malabsorbtion, newborns
Rapid: Calcium chelators: citrate, oxalate, heparin (not main activity)

Long Term: Vit K Antagonists (analogs): Warfarin, Dicoumarol