Term
| What causes the initial vasoconstriction and what produces it? |
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Definition
| -Serotonin and thromboxane A2 released by damaged endothelial cells |
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Term
| What stimulates platelet release? |
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Definition
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Term
| What 2 major granules are in the platelets and what do they contain? |
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Definition
ELECTRON DENSE GRANULES
-Ca2+, ADP, serotonin, and histamine
α-GRANULE
-heparin antagonist, PDGF, fibronectin, fibrinogen, von Williebrand factor, platelet factor 4 |
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Term
| What does the released ADP do? |
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Definition
| -Promotes swelling and aggregation of activated platelets. |
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Term
| What two things cause platelet degranulation? |
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Definition
| -Their aggregation, or also platelet activating factor (PAF) from neutrophils |
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Term
| Idiopathic thrombocytopenic purpura (ITP)? |
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Definition
-Caused by autoimmune attack on platelets, usually directed at GPIIb/IIIa
-caused a petechial rash (purpora) which are tiny red spots that do not go white when pressed
-Lowers the platelet count and increases bleeding time, but does not affect PTT & PT |
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Term
| Glanzman's thrombasthemia? |
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Definition
-GPIIb/IIIa is defective or absent
-Increased bleeding time with normal platelet count |
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Term
| Von Willebrand disease and three types? |
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Definition
Type 1 - low vWF
Type 2 - defective vWF
Type 3 - missing vWF
-This is the most common congenital bleeding disorder with type 1 being the most common
-Essentially, platelets will have trouble adhering and aggregating
-Normal platelet count with prolonged bleeding |
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Term
| Bernard-Soulier Syndrome? |
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Definition
| -Defective GPIb (binds vWF) |
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Term
| Which are the vitamin K dependent factors? Why do they need it? |
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Definition
-2, 7, 9, & 10
-because they have glutamate residues that need to be carboxylated forming γ-carboxyglutamates (γGLA)
-γ-glutamate carboxylase needs vit K as a cofactor
-This improves Ca2+ binding (these are the factors that use Ca2+) |
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Term
| Where are the factors made? |
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Definition
-7 by endothelial cells (in extrinsic pathway)
-13 by platelets (fibrin stabilizing factor)
-The rest are made by the liver |
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Term
| Which factor doesn't need activated? |
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Definition
-Tissue factor (factor 3)
-It spills out and activates 7 |
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Term
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Definition
-Heparan; increases activity of antithrombin III (ATIII)
-Warfarin; inhibits vitamin K |
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Term
| What all factors can thrombin activate? |
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Definition
| - 1, 5, 8, 11, 13, and protein C |
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Term
| Which factors are serine proteases, what does that mean, and why is that important? |
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Definition
-2, 7, & 9-12
-Means they have Asp, His, & Ser in the active site
-They will be inhibited by organophosphorus compounds such as DIFP
-Also, antithrombin III (AT-III) inhibits all of the serine proteases |
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Term
| What is the extrinsic path? |
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Definition
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Term
| What is the intrinsic path? |
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Definition
| 12, 11, 9 & 8(activated by thrombin), 10 |
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Term
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Definition
-10 + 5(activated by thrombin) -> thrombin -> fibrin & 13
-13 links fibrin |
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Term
| How does protein C fit in? |
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Definition
-It is activated by thrombin and works together with protein S (the cofactor) to deactivate factor 5 in a feedback inhibition situation
-Prevents additional thrombin from being made |
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Term
| What is plasmin and how is it activated? |
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Definition
-Plasmin breaks down the fibrin of the clot
-It is activated by t-PA and also streptokinase (from bac) |
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Term
| What is PAI-1? What inhibits it? |
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Definition
-It inhibits t-PA
-It is inhibited by protein C |
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Term
| PT vs PTT vs Thrombin time |
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Definition
-Prothrombin time; tests integrity of extrinsic and common
-Partial thromboplastin time; tests intrinsic and common
-Thrombin time; tests fibrinogen levels |
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Term
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Definition
-Def. factor VIII
-PTT goes up and PT stays the same |
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