Reading...
Play button
Play button
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;
27 Cards in this Set
- Front
- Back
|
define primary, secondary, and tertiary hemostasis
|
Primary hemostasis: This is defined as the formation of the platelet plug.
Secondary hemostasis: This is defined as the formation of fibrin through the coagulation cascade. Tertiary hemostasis: This is defined as the formation of plasmin for breakdown of the clot |
|
|
what granules in the platelet play a role in forming a hemostatic plug?
|
Alpha
Hemostatic Proteins: fib, FV, vWf, PAI-1(inhibits fibrinolysis) & plasminogen (fibinolysis) |
|
|
what is platelet adhesion?
|
Attachment of platelets to something besides other platelets
Binding of plts to subendothelial collagen via plt GP Ib and vWf forming a bridge |
|
|
Adhesion triggers morphologic & functional changes known as ...?
what does this do? |
Activation
Changes in: Metabolic biochemistry Generation of thromboxane A2 and 2nd messangers Platelet shape change Disc shape to spheres with psuedopod via actin/myosin |
|
|
in primary hemostais, what is responsible for surface receptor exposure? what is this required for?
|
Activation
Required for plt binding to fibrinogen |
|
|
what is aggregation? what is need for this to occur? (2)
|
Aggregation is the attachment of platelets to one another.
Fibrinogen and Calcium are needed for aggregation to occur |
|
|
what is secretion?
|
after aggregation the plts discharge granule contents into the surrounding area stimulating other plts.
|
|
|
what is Template Bleeding Time?
|
Standardized incision made on forearm, length of time for bleeding to stop measured.
1 to 9 minutes normal A defect in platelet function will cause prolongation |
|
|
When do you do a platelet aggregation study?
|
Tests ability of platelets to aggregate with various agonist
Indicated with normal platelet count, but prolonged bleeding; (History & Physical) |
|
|
what test can discriminate between inherited platelet disorders (vWD, Glanzmann’s) and acquired drug related disorders (ASA)?
|
Platelet function Analyzer
|
|
|
Defined as the formation of fibrin through the coagulation cascade =
|
secondary hemostasis
|
|
|
what is the extrinsic secondary pathway?
|
Extrinsic: involves tissue factor and FVII, which activates FX
|
|
|
what is the intrinsic secondary pathway?
|
Intrinsic: cofactors, Ca plus phospholipid mediating activation of FX
|
|
|
what is the common secondary pathway?
|
the extrinsic. and intrinsic paths converge at aFX which mediates fibrin formation
|
|
|
what is the main pathway for for initiation of secondary hemostasis? which is used to amplify?
|
extrinsic pathway
the intrinsic is used to amplify the effect |
|
|
what initiates the extrinsic pathway of hemostasis?
|
Exposure of Tissue Factor, expressed by endothelial cells, subendothelial connective tissue & monocytes.
|
|
|
what activates the intrinsic pathway?
|
Thrombin generated from extrinsic path. Activates FXI & VIII directly
|
|
|
what activates protein C and S? What do they do?
|
Interestingly, thrombin activates them.
Activation of C and S then downregulates to coagulation pathway thus thrombin both activates and inactivates these pathways |
|
|
what are the vitamin K dependent factors?
**TEST |
Requires vitamin K for synthesis; needs Ca & phospholipid. (known as Vitamin K dependent factors)
II VII IX X 1972 |
|
|
why is Vitamin K so important?
***TEST |
Provides critical Ca receptor essential for binding the pro-coagulant factor to phospholipid
In absence of Vit K, factors (1972) still synthesized in liver, found in plasma, but are nonfunctional, so YOU CANNOT CLOT |
|
|
what screens for intrinsic and common pathway problems?
|
Activated Coagulation Time
|
|
|
What does a prolongation of PT mean?
|
defect in Extrinsic or Common pathways
Sensitive monitor of Vit K dependent FVII. |
|
|
So PT measures what?
and aPTT? |
PT: Extrinsic/Common
aPTTT: Intrinsic/Common |
|
|
PT is a good monitor for what therapy
|
comadin
|
|
|
aPTT is good to monitor what therapy?
|
heparin
|
|
|
What is the thrombin time? what does it allow you to detect?
|
Measures only conversion of fibrinogen to fibrin
can show: Deficiency in fibrinogen Dysfibrinogenemia Presence of inhibitors such as heparin, FDPs |
|
|
SUMMARY SLIDE
Thrombin time Common pathway Monitor for presence of heparin aPartial thrombopastin time Intrinsic pathway; common pathway Monitor heparin therapy Prothrombin time Extrinsic pathway; common pathway Monitor coumadin therapy |
That is the Take home slide
|
