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16 Cards in this Set
- Front
- Back
How is platelet production stimulate?
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When Plates dec.=fewer MPL receptors for TPO (constituitively made and abs by adeq. platelet number) causeing free TPO to increase, stims Stem Cells and Megakaryocytes
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MPL, the binder of TPO (to keep free TPO level down when platelets are in plenty) works through which communication System
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Jak/STAT (Jak2, Stat5)
& MAP Kinases |
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Why do platelets have receptor for Collagen
--Which platelet Factors help with this |
When vessel damaged, the collagen is exposed and platelets can begin to work there
--think Thromboxane A2 & Serotonin---- |
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Describe Step 1 of Hemostasis
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Vascular Spasm (direct myogenic-NO neurons reqd.)
-Smooth MM. contracts indep. -P.Factors Serotonin and Thromboxane A2 help (serotonin may be impt for headache where vessels constrict) |
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Describe Step 2 of Hemostasis (2 steps)
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Formation of a Platelet Plug--collagen exposed
1-VonWF-binds BETWEEN Plate Rec and Collagen. 2-Bind of Platelet Integrin Rec. to diff part of Collagen =activation of platelet -swelling and podocyts |
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In Step 2, after platelets are activated, they contract (release Ca+ from ER) causing Granules to Leave and the Plates Stick to the Vessels and to Each other. What are two important factors in platelets for the stickiness
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Thromboxane A2 and ADP
--note, Thromboxane can be blocked by Aspirin (acetylminophen) |
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What are 3 essential steps of Step 3 of Homeostasis. The Blood Coagulation Step resulting in Clot Retraction
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1. Formation of Prothrombi Activator
2. Activation of Thrombin 3. Creation of Fibrin from Fibrinogen (constituitively produced by liver, like TPO) |
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Name & Describe Step 4 of hemostasis
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Repair of Damage
-PDGF--stims fibroblasts to grow in area -Fibroblasts diff into smooth muscle and contract to close hole (note, bleeding may have ceased as early as end of step 2) |
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Which Step do the following occur
-excess fluid in clot removed/clot solidified --new platelets reqd to contract fibrin polymer |
These occur during Step 3--Blood Coagulation
-this is the clot retraction phase |
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Which two factors are Required to get rid of the Clot
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1. Plasminogen --constituitively made by liver/floats inactively
2. tPA--Tissue Plasminogen Activator--released by damaged tissue. note, circulating plasminogen stays inactive by inhibitio of tPA inhibitor in the blood) |
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Fibrin form Fibrinogen is made via what
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Thrombin
--initially makes Fibrin, Later, it chews up Fibrin clot indirectly via Plasmin |
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How does Thrombin indirectly chew up Fibrin Cloat (which it initially helped form)?
What intermediate Pr/Factor is required |
Thrombin activates Protein C
Protein C INactivates tPA inhibitor (tissue plasminogen inhibitor) activated tPA turns Plasminogen to Plasmin, which lyses Fibrin |
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In un-injured Blood Vessel, name 3 features of membrane that prevent unwanted clot formation
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1. Smooth Surface prevents rupture of plates
2. Glycocalyx is neg, repels plates 3. Thrombomodulin |
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List 4 Chemicals that limit clotting
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1. Fibrin, binds Thrombin, prevents it from working
2. Prostacyclin (PGI2)--vasodilates, limits Plate aggreg 3. Antithrombin III -- works as anticoagulant when thrombin binds to it 4. Heparin --from mast cells, inc. antithrombin efficacy. |
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Most important part of hemostasis for stopping bleeding in small breaks
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Platelet Plug
(NOt the clot,which forms next) |
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How can Fibrin, the stuff that makes clots, limit blood clotting?
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Fibrin binds thrombin. Thrombin cannot work then and will not further activate fibrinogen to form fibrin. This is the fate of 80+% of Thrombin once clot is formed
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