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30 Cards in this Set

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