Unit IV: Hemostasis Flashcards
Hemostasis
Ability of the body to stop bleeding from a damaged blood vessel and repair its function
Serine Protease Coagulation Factors
Prekallikrein, Factors II, VII, IX, X, XI, XII
Related to Trypsin/ChymoTrypsin, cleave at arginyl residues
Cofactor Coagulation Factors
Tissue Factor, HMWK, Factors V, VIII
Intrinsic Tenase
Factor IX, Factor VIII, phospholipid, calcium
Extrinsic Tenase
TF, Factor VII, phospholipid + calcium
Prothrombinase Complex
Factor X, Factor V, Phospholipid, Calcium
Vitamin K Dependent
Factors II, VII, IX, X. Proteins C and S
Glutamic acid residues modifies to gamma-carboxyl glutamic acid so that they can bind calcium
Functions of von Williebrand Factor (2)
Stored in enodthelial cells and platelets
Binds Factor VIII (increased half life)
Platelet Adhesion and Aggregation
Thrombin Functions (5)
Cleaves Fibrinogen to Fibrin
Activates V and VIII for prothrombinase/intrinsic
Activates XI to create more IXa
Activates XIII to strengthen/stabilize clot
Platelet Activation (flip phosphatidylserine)
Primary Hemostasis
Adhesion, Aggregation, and Activation of Platelets
Secondary Hemostasis
Coagulation cascade to form fibrin clot at injury site
Three Mechanisms of Thrombocytopenia
Decreased platelet production (1’ or 2’ marrow disorder)
Increased Platelet Destruction (Acute or Chronic AB)
Increased Platelet Consumption (DIC, Sepsis, TTP, HUS)
How to treat ITP
IVIG to block RES macrophages, splenectomy, corticosteroids to reduce B cell responses
vWF Disease Treatment
Secondary hemostasis impaired in severe cases (increases half life of VIII)
DDAVP releases extra vWF from endothelials
3 Types of vWF disease
Type 1: Not enough made
Type 2: Non-functional
Type 3: Zero made