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34 Cards in this Set

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Normal: smooth, continuous surface w/ anticoagulant properties

Injury: vasoconstriction, exposed collagen binds vWF and plts, damaged endothelial cells secrete vWF, tissue plasminogen activator (TPA), and plasminogen activator inhibitor-1 (PAI-1)
Platelet production
Produced in bone marrow. Megakaryocyte is precursor cell. Platelets are fragments of cytoplasm of megakaryocyte. Anuclear
Platelet release
Platelets shed from megakaryocyte into sinuses and are released in groups called proplatelets. It takes 5 days for a megakaryoblast to produce platelets (platelet lifespan = 9.5 days)
Platelet function
Adhere (cling to endothelium; reversible process that needs vWF), aggregation (stick to one another; irreversible; plt plug), and secretion (irreversible; plts discharge contents of their granules and is necessary for coagulation; leads way for secondary hemostasis)
Platelet adhesion
Attach to collagen fibers in subendothelium, shape change, and requires presence of vWF and GPIb receptor of the plt membrane; reversible process; triggers platelet activation
Platelet activation
Changes in metabolic biochemistry, platelet shape, surface receptors, and membrane phospholipid orientation. Key outcome: activation of GPIIb/IIIa receptors for fibrinogen and the ability of plts to secrete their granules
aka TPO (from liver). Hormone that regulates platelet development. Bound to circulating platelets.
Increased plt count: more TPO is bound and stimulation of BM production of megakaryocytes is decreased.
Decreased platelet count: more free TPO is available to bind to megakaryocyte progenitor cells in the BM to stimulate megakaryocyte production, so plt production is increased.
Platelet structure
4 zones: peripheral, sol gel or structural, organelle, and membrane system
Peripheral zone
Component: glycocalyx (surface coat) and membrane
Function: adhesion and aggregation
Glycoprotein Ib
Receptor for vonWillebrand factor
Glycoprotein IIb and IIIa
Receptor for fibronectin, vWF, fibrinogen, and factors V and VIII
Sol gel or structural zone
Component: microtubules, actin
Function: structure and support
Organelle zone
Component: mitochondria, glycogen particles, granules
Function: secretion and storage
Stimulate membrane receptors on additional platelets and release ADP and thromboxane A1 (plt plug).
Dense granules: ADP, ATP, and serotonin
Alpha granules: coagulation factors (fibrinogen, vWF, V, VIII, and PDGF)
Lysosomes: enzymes
Membrane system
Components: dense tubular system
Function: secretion and storage (secretion of granule contents and calcium storage site)
Platelet aggregation
After plts are activated by contact with agonists ADP and TXA2, they aggregate (attach to one another) in two phases.
Primary phase of aggregation
Platelets adhere loosely to one another
Secondary phase of aggregation
Platelets release their own ADP and other granule contents
Platelet secretion (release)
After adhesion and shape change, platelets begin to discharge granule contents. Requires ATP. Secretion occurs before or concurrently with secondary aggregation.
Platelet role in hemostasis
Formation of primary hemostatic plug, surface for coagulation factors to make secondary hemostatic plug, and aid in healing of injured tissue
Aggregating agents
Epinephrine, ADP, collagen, and arachidonic acid
Primary hemostasis summary
Injured blood vessel, vascular constriction, platelet adhesion (circulating vWF attaches to subendothelium; glycoproteins on plt surfce adhere to "sticky" vWF), platelet activation-shape change, platelet aggregation/secretion, and primary hemostasis plug
Alters platelet function, inhibits enzyme cyclooxygenase and inhibits platelet aggregation for the life-time of the platelet
Activated platelets
Initiate arachidonic acid pathway to produce TXA2. Activates other platelets. TXA2 inhibited by aspirin.
Secondary hemostasis
Results in production of an insoluble fibrin clot and occurs on plt surface
Coagulation cascade components
Enzymes (zymogens and active [E] forms - protease), cofactors (accelerate [E] activity), substrates (substance on which [E] acts on, and inhibitors (keeps system in balance)
Inactive coagulation factors
Coagulation factors
Plasma proteins produced primarily in the liver
Prothrombin group
Factors: II, VII, IX, and X
Protein regulators: C, S, and Z
Produced in liver. Vit K dependent. Binding site for CA. Inhibited by warfarin. Stable and well preserved in stored plasma.
Vitamin K dependent prothrombin coagulation proteins
Vitamin K: fat soluble vitamin, necessary for binding the factor to CA bridges
Warfarin: coumadamin; antagonistic drug; inhibits Vit-K dependent factors
Fibrinogen group
Factors: I, V, VIII, and XIII
Consumed during coagulation
Factor V and VIII are labile; increase during pregnancy, during use of oral contraceptives, and inflammation. Not found in serum
Contact group
Factors: XI, XII, prekallikrein, and HMWK.
Involved in the initial activation of intrinsic pathway. Requires contact w/ negatively charged surface for activation. Not consumed during coagulation. Found in serum
Coagulation cascade
"Clotting begins with activation of 2 enzymatic pathways that lead to fibrin formation. It occurs on platelet surface membranes. Clotting factors bind to phospholipid membrane surface and rearrange until a complex (enzyme, substrate, and cofactor) is formed"
Intrinsic pathway
Initiated/activated by trauma within the blood vessel. Contact factors: XII, XI, PK, and HMWK. Exposed collagen in a damaged vascular wall.
I, II, V, X (common pathway)