Hemostasis: Clinical and Laboratory Data Interpretation

Study Notes

Hemostasis is a physiological process that arrests bleeding at an injury site through a series of steps.

Vasoconstriction occurs when a blood vessel is damaged, reducing blood flow to the site of injury and minimizing blood loss.
Platelet plug formation occurs when platelets adhere to exposed collagen fibers at the site of injury, facilitated by molecules like von Willebrand factor (vWF).
Activated platelets release granules containing substances like ADP and thromboxane A2, recruiting more platelets to the site and forming a temporary platelet plug.

Firm fibrin clot formation and stabilization involve the coagulation cascade, a series of enzymatic reactions that convert soluble fibrinogen into insoluble fibrin strands.
The coagulation cascade can be divided into intrinsic and extrinsic pathways, which converge to activate factor X.
Activated factor X converts prothrombin to thrombin, which converts fibrinogen to fibrin, forming a stable blood clot.

Fibrinolysis is the process by which the blood clot is broken down once the injury has healed.
Plasmin, an enzyme, cleaves fibrin strands, leading to the dissolution of the clot.
Plasmin is generated from its precursor, plasminogen, through activation by tissue plasminogen activator (tPA) or urokinase-type plasminogen activator (uPA).

Factor I (Fibrinogen): forms fibrin, the structural framework of blood clots.
Factor II (Prothrombin): converts into thrombin, essential for fibrin formation.
Factor III (Tissue Factor): initiates clotting cascade via the extrinsic pathway.
Factor IV (Calcium): cofactor for several clotting factors.
Factor V (Proaccelerin): enhances thrombin's ability to convert fibrinogen to fibrin.
Factor VII (Proconvertin): activated by tissue factor, initiates clotting cascade.
Factor VIII (Antihemophilic Factor A): cofactor for factor IX, crucial in activating factor X.
Factor IX (Christmas Factor): activated by factor XIa, activates factor X with factor VIIIa.
Factor X (Stuart-Prower Factor): converts prothrombin into thrombin, final step in clotting.
Factor XI (Plasma Thromboplastin Antecedent): activates factor IX in the intrinsic pathway.
Factor XII (Hageman Factor): initiates intrinsic pathway upon collagen contact.
Factor XIII (Fibrin-Stabilizing Factor): cross-links fibrin strands, stabilizing clots.

Liver is the source of clotting factors (except VWF).
VWF is produced from endothelial cells and megakaryocytes.
Factor VIII is produced in the liver and endothelium.
Vitamin K is necessary for the production of clotting factors.
The half-life of coagulation factors varies, e.g., factor II 100 hours, dependent clotting factors 2, 7, 9, 10, and VII 5 hours, protein C 6 hours.

PT (Prothrombin Time): tests function of common and extrinsic pathways (factors I, II, V, VII, X).
APTT (Activated Partial Prothrombin Time): tests function of common and intrinsic pathways (all factors except VII, XIII).
Increased PT may indicate liver disease, vitamin K malabsorption, or vitamin K antagonists (Warfarin).
Increased APTT may indicate heparin, vitamin K antagonists, fibrin/fibrinogen, lupus anticoagulant, or deficiency of coagulation factors.