Chapter 14 - Alterations In Homeostatsis & Blood Coagulation Flashcards
How do the factors released from platelets contribute to hemostasis?
Factors released from platelets contribute to hemostasis by enhancing vasoconstriction, platelet aggregation, and vessel repair.
How is a fibrin clot formation initiated and what is the ultimate result?
By both the intrinsic and extrinsic pathway. Each pathway requires the sequential activation of specific clotting factors, ultimately resulting in enzymatic cleavage of fibrinogen to form an insoluble fibrin clot.
When does the initiation of fibrinolysis occur?
Fibrinolysis occurs simultaneously with clot formation to prevent excessive clotting and vessel occlusion.
How does one obtain bleeding tendencies?
Bleeding tendencies may be inherited or acquired.
What are important risk factors for bleeding tendencies?
Abnormal bleeding, liver disease, and anticoagulant drug use may be important risk factors.
What physical findings are indicative of bleeding tendencies?
Petechiae, purpura, ecchymoses, telangiectasia, and occult or frank bleeding are indicative.
What are usual laboratory tests included in the evaluation of hemostasis and coagulation?
Platelet count, bleeding time, PT/INR (extrinsic pathway), and activated partial thrombophlebitis time (intrinsic pathway).
Disorders of the vasculature that result in altered hemostasis include:
Inflammation (allergic purpura)
Structural abnormalities (collagen diseases)
Weakened vessel walls (telangiectasia)
What number indicates an insufficient quantity of platelets?
Fewer than 50,000/mm3
What are the important causes of thrombocytopenia?
Autoimmune destruction (ITP) DIC Mechanical destruction (artificial valves).
What does an insufficient quantity of platelets result from?
Decreased production, sequestration, increased destruction, or dilution.
What does an excessive quantity of platelets result from?
Excessive production (proliferation of bone marrow cells).
What is considered an excessive quantity of platelets?
More than 400,000/mm3
What may thrombocythemia result in?
Excessive coagulation with thrombosis or Excessive bleeding (???)
A normal platelet count does not ensure adequate platelet function, so what else can cause prolonged bleeding time?
What is the usual cause prolonged bleeding time?
Platelet adhesion, aggregation, and degranulation
The usual cause is drug related (e.g. Aspirin), but rarely, the platelet defect is inherited (e.g. Von Willebrand disease).
What can coagulation disorders result from?
Defects in the clotting cascade or fibrinolytic process.
Is hemophilia an inherited or acquired bleeding disorder? Which is the most common and which factor is associated with it?
Hemophilia is an inherited disorder that results from deficient clotting production.
Hemophilia A (factor VIII) and hemophilia B (factor IX) are the most common.
Is von Willebrand disease inherited or acquired and what clotting factor is associated with it?
Von Willebrand disease is inherited and is caused by abnormal factor VIII carrier protein production. The disease results in a deficiency of factor VIII in the circulation and decreased platelet function.
What coagulation disorder is vitamin K deficiency associated with?
Vitamin K deficiency is associated with hemorrhagic disease of the newborn and bleeding related to malnutrition and liver disease.
Vitamin K is a necessary cofactor for liver production of which factors?
II
VII
IX
X
Is DIC acquired or inherited and how is it caused?
DIC is an acquired bleeding syndrome associated with trauma, malignancy, burns, shock, and abruptio placental.
How is DIC characterized?
DIC is characterized by widespread clot formation in small vessels. Clotting factors and platelets are consumed, leaving the patient with deficient resources for the appropriate clot formation. The platelet count and fibrinogen levels are typically decreased, and values for PT, aPTT, thrombin time, bleeding time, and fibrin split products are elevated.
What are the critical steps involved in hemostasis?
Vasospasm, formation of a platelet plug, and activation of the clotting cascade to form a fibrin clot
