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30 Cards in this Set
- Front
- Back
Four "steps" for how blood clots:
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1) Primary Hemostasis
2) Secondary Hemostasis 3) Hemostasis 4) Fibrinolysis All happen at the same time, not sequentially. |
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Primary hemostasis
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platelet activation, platelet plug forms, and sets up the phospholipid surface of platelets
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Secondary hemostasis
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coag factors generate thrombin, fibrin mesh forms, and hold plug in place
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Hemostasis Stops
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regulatory proteins stop thrombin generation which controls the size of the clot
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Fibrinolysis
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Clot dissolves when injury healed
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Clotting Cascade Crucial Step
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Generating thrombin (factor IIa) from prothrombin (factor II).
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Two Ways to Activate Factor X which converts prothrombin
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Tissue factor pathway (VIIa) with Ca and Phospholipids, and Contact Activation pathway (factor IXa) with assistance from VIIIa, Ca, and Phospholipids.
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Factors which accelerate reactions in the clotting cascade
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VIIIa and Va
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Initial vs. Big Burst of Thrombin
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- Daily generate small amount of thrombin to keep from bleeding into vessels and brusing (Initial).
- Big Burst is initiated by a tightly regulated system which takes over when needed releasing large amounts of thrombin |
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Describe Protein C and S
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Proteins which stop hemostasis or the clotting cascade.
- Protein C - works on thrombin Protein S - works on factor VIIIa and Va |
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Heparin mechanism
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Heparin accellerated inactivation of several factors in casacade acting as anti-thrombin
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A bleeding history with one symptom of significant bleeding is enough to suggest the etiology of a bleeding disorder. (T or F)
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F - a constellation of symptoms is needed. More than one like brusing, melena, hemarthroses, soft tissue hemorrhages
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Features of Primary Hemostatic Defect
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- Issue with platelets
- Relatively common congenital - very commonly acquired from drugs |
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Features of Secondary Hemostatic Defect
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- Problem with clotting factor
- Congential: uncommon transmission - Very rare to acquire the disorder from outside sources |
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Clinical Features of Primary Hemostasis
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- Prolonged bleeding, petechiae, mucosal bleeding, and bruising
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Clinical Features of Secondary (Factor Issues)
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late re-bleeding, hemarthroses, ecchymoses, and soft-tissue bleeding
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Lab testing for Primary Hemostasis Issue
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CBC with platelet count, platelet function testing, and von Willebrand panel
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Lab testing for Secondary Hemostasis Issue
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PT/INR, aPPT, fibrinogen; mixed studies, and clotting factor levels.
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Most common inherited bleeding disorder
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von Willebrand disease
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Functions of von Willenbrand factor
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Platelet adhesion to enothelial injury (platelet plug) and plasma carrier of factor VII (factor VIII would have short half-life without von Willenbrand).
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Types of von Willenbrand Disease
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Type I: most common (quantitative deficiency), Type II: qualitative abn with several types, Type III: very rare - complete def of von Willenbrand factor
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Lab findings for von Willenbrand patient
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Normal: INR, platelet count
Normal to mildly prolonged: aPTT Abnormal PFA-100 Low: von Willenbran antigen, factor VIII, and ristocetin cofactor activity - looks at how vW factor is functionally working |
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Treatment options for von Willenbrand Disease
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- Avoid platelet inhibiting drugs
- Desmopressin - releases stored vW factor, nasal spray or IV - Amicar - oral antifibrinolytic - plasma derived factor VIII concentrate |
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Hemophilia General
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Congenital bleeding disorder due to loss of factor VIII or IX, gene for both is located on the X chromosome which means females are carriers and males are affected
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Hemohpilia A
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Def of factor VIII, classic hemo,, more common with one in 5,000
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Hemophilia B
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Def of factor IX, called Christmas Disease, 1 in 30,000.
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Lab Diagnosis of Hemophilia
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Normal INR, LONG PTT, normal platelet count and function, measure specific factor levels
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Treatment of Hemophilia
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Complicate and expensive! Tx with factor VIII and IX concentrates, treat on demand and prophylactic factor replacement
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Virchow's Triad
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- Vessel wall injury
- stasis - changes in the composition of blood |
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Most preventable cause of hospital death
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PE
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