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;
34 Cards in this Set
- Front
- Back
Endothelium
|
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
|
|
Thrombopoietin
|
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 |
|
Granules
|
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
|
|
Aspirin
|
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)
|
|
Zymogens
|
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.
IX, VIII I, II, V, X (common pathway) |