Clotting and Bleeding Flashcards
Primary Hemostasis
- arterial vasoconstriction, to reduce blood flow to the injury site. 2. VWF released, the wall becomes “sticky” 3. Platelet adhesion- initial platelet is friable and can be washed away one vasorelaxation occurs.
Secondary Hemostasis
involves and intrinsic and extrinsic pathway
Intrinsic pathway
this is contact activation. when blood hits exposed collagen, it activates factor XII
Extrinsic Pathway
the damaged tissue itself releases tissue factors, which complex with factor VII
The work horse of the coag cascade
Thrombin Activates 5, 7, 8, 11, 13
Vitamin K dependent clotting factors
II VII IX X
Factor I
Fibrinogen
Factor II
Prothrombin
Factor III
Tissue factor, or thromboplastin
Factor VIII
Anti-hemophillic factor
Factor IX
Christmas factor
Bleeding disorders and genetics
30-40% of patients with Hemophilia A or B do not have a family history!
Signs indicating it is a platelet defect
Mucocutaneous bleeding of oral cavity, nasal, GI, GU Increased bleeding after cuts Small areas of superficial bleeding Variable amounts of bleeding after major surgery immediate
Signs indicating it is a clotting defect
Deep tissue bleeding (joint and muscle) Large hematomas Can be delayed bleeding post-surgery
Platelet disorders
Von Willebrand disease (most common) Immune thrombocytopenia
Clotting deficiencies
Factor VIII (Hemophilia A) Factor IX (Hemophilia B) Factor XI (Hemophilia C)
Inherited coagulation disorders
Increased propensity for forming blood clots. Not all patients with a venous or arterial blood clot will have a coagulation disorder, but can be a factor in 50% of patients presenting before age 40. Risk for clots can also be increased in pregnancy, cancer and estrogen therapy.
Antithrombin
alpha-2 globulin made in the liver functions as a negative feedback moderator- is an anticoagulant. Works on Thrombin and factor Xa. Deficiency increases coagulation (if this goes unchecked, can deplete all clotting factors and eventually will result in uncontrollable bleeding).
decreased antithrombin manifestations
DVT Pulmonary embolism Phlebitis Heparin resistance getting clots early in age
Protein C
Anticoagulant, synthesized in the liver
•inhibits factor Va and factor VIIIa
Vitamin K dependent
Test with Protein S
Protein S
anticoagulant, made in the liver
•co-factor to protein C and enhances the function of Protein C
vitamin K dependent
Protein C/S defeciency manifestation
- Venous thromboembolism (VTE) → increased risk 7 fold!
- Disseminated Intravascular Coagulation
- Neonatal purpura fulminans
Factor V Leiden
inherited, mutated form of factor V
Doesnt allow protein C to cleave at normal site, so it stays in circulation longer, increasing coagulation
Test indicated in pts who have had a thrombotic event without any other predisposing factors, if pt has a strong family hx of thrombosis, DVT when pregnant or on OCP
Fibrinogen
clotting factor, produced in the liver
is converted to fibrin via Thrombin
Is an acute phase reactant