Primary + Secondary Hemostasis

Front 1

Endothelium

Back 1

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)

Front 2

Platelet production

Back 2

Produced in bone marrow. Megakaryocyte is precursor cell. Platelets are fragments of cytoplasm of megakaryocyte. Anuclear

Front 3

Platelet release

Back 3

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)

Front 4

Platelet function

Back 4

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)

Front 5

Platelet adhesion

Back 5

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

Front 6

Platelet activation

Back 6

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

Front 7

Thrombopoietin

Back 7

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.

Front 8

Platelet structure

Back 8

4 zones: peripheral, sol gel or structural, organelle, and membrane system

Front 9

Peripheral zone

Back 9

Component: glycocalyx (surface coat) and membrane
Function: adhesion and aggregation

Front 10

Glycoprotein Ib

Back 10

Receptor for vonWillebrand factor

Front 11

Glycoprotein IIb and IIIa

Back 11

Receptor for fibronectin, vWF, fibrinogen, and factors V and VIII

Front 12

Sol gel or structural zone

Back 12

Component: microtubules, actin
Function: structure and support

Front 13

Organelle zone

Back 13

Component: mitochondria, glycogen particles, granules
Function: secretion and storage

Front 14

Granules

Back 14

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

Front 15

Membrane system

Back 15

Components: dense tubular system
Function: secretion and storage (secretion of granule contents and calcium storage site)

Front 16

Platelet aggregation

Back 16

After plts are activated by contact with agonists ADP and TXA2, they aggregate (attach to one another) in two phases.

Front 17

Primary phase of aggregation

Back 17

Platelets adhere loosely to one another

Front 18

Secondary phase of aggregation

Back 18

Platelets release their own ADP and other granule contents

Front 19

Platelet secretion (release)

Back 19

After adhesion and shape change, platelets begin to discharge granule contents. Requires ATP. Secretion occurs before or concurrently with secondary aggregation.

Front 20

Platelet role in hemostasis

Back 20

Formation of primary hemostatic plug, surface for coagulation factors to make secondary hemostatic plug, and aid in healing of injured tissue

Front 21

Aggregating agents

Back 21

Epinephrine, ADP, collagen, and arachidonic acid

Front 22

Primary hemostasis summary

Back 22

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

Front 23

Aspirin

Back 23

Alters platelet function, inhibits enzyme cyclooxygenase and inhibits platelet aggregation for the life-time of the platelet

Front 24

Activated platelets

Back 24

Initiate arachidonic acid pathway to produce TXA2. Activates other platelets. TXA2 inhibited by aspirin.

Front 25

Secondary hemostasis

Back 25

Results in production of an insoluble fibrin clot and occurs on plt surface

Front 26

Coagulation cascade components

Back 26

Enzymes (zymogens and active [E] forms - protease), cofactors (accelerate [E] activity), substrates (substance on which [E] acts on, and inhibitors (keeps system in balance)

Front 27

Zymogens

Back 27

Inactive coagulation factors

Front 28

Coagulation factors

Back 28

Plasma proteins produced primarily in the liver

Front 29

Prothrombin group

Back 29

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.

Front 30

Vitamin K dependent prothrombin coagulation proteins

Back 30

Vitamin K: fat soluble vitamin, necessary for binding the factor to CA bridges
Warfarin: coumadamin; antagonistic drug; inhibits Vit-K dependent factors

Front 31

Fibrinogen group

Back 31

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

Front 32

Contact group

Back 32

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

Front 33

Coagulation cascade

Back 33

"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"

Front 34

Intrinsic pathway

Back 34

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)