Hemostasis and Blood Coagulation

Hemostasis

• Hemostasis is the process of stopping bleeding.
• It involves three main stages:
  • Blood vessel spasm
  • Platelet plug formation
  • Blood coagulation

Blood Vessel Spasm

• Triggered by pain receptors, local myogenic spasms, and release of chemicals like thromboxane A2, 5-hydroxytryptamine (serotonin).
• Results in vasoconstriction to minimize blood flow from the injured site.

Platelet Plug Formation

• Triggered by exposure of platelets to collagen.
• Steps of platelet plug formation include:
  • Platelet adhesion (using von Willebrand factor)
  • Platelet activation (secretion of chemicals, including ADP and thromboxane A2)
  • Platelet aggregation (platelets clump together)

Blood Coagulation

• Triggered by cellular damage and contact with foreign surfaces.
• Result is the formation of a blood clot.
• This is a cascade of reactions; two pathways:
  • Extrinsic pathway (tissue factor pathway): tissue damage initiates the process.
  • Intrinsic pathway (contact activation pathway): exposed collagen and other factors initiate the process.
• Both pathways converge to activate factor X, leading to the following:
  • Conversion of prothrombin to thrombin
  • Conversion of fibrinogen to fibrin
  • Formation of a blood clot.

Fate of Blood Clots

• Plasmin digests the blood clots.
  • Plasminogen is converted to plasmin
  • Plasmin breaks down fibrin.

Prevention of Blood Clotting

• The smooth lining of blood vessels prevents the accumulation of platelets and clotting factors.
• Fibrin absorbs thrombin, preventing the clotting reaction from spreading.
• Cells like basophils and mast cells release heparin, an anticoagulant.
• The dynamic blood flow helps prevent clotting.

Defects in Hemostatic Mechanisms

• Thrombus: abnormal intravascular clot attached to a vessel wall.
• Emboli: freely floating clots; factors include: roughened vessel surfaces, imbalances in clotting and anticlotting systems, slow-moving blood.

Defects in Hemostatic Mechanisms (Continued)

• Vitamin C deficiency (lack of stable collagen), hepatic failure (reduced clotting factors), vitamin k deficiency (reduced clotting factors II, VII, IX, X).
• Fat malabsorption, hemophilia (deficiencies in clotting factors VIII or IX), thrombocytopenia (bleeding in small vessels / capillaries).

Antihemostatic Drugs

• Heparin: potentiates antithrombin III.
• Aspirin: inhibits cyclooxygenase (COX) and thromboxane A2.
• Clopidogrel: inhibits ADP receptors on platelets.
• Warfarin: blocks vitamin K epoxide reductase.
• Streptokinase: activates plasminogen.

Tests for Hemostasis

• Platelet disorders: bleeding time (2-6 minutes).
• Coagulation disorders: clotting time, partial thromboplastin time (PTT), prothrombin time (PT).

Additional Information

• Objectives for Hemostasis Lecture
  • Definition and mechanisms of hemostasis
  • Steps of coagulation, prevention, and abnormalities
  • Tests for evaluation of hemostasis
• A 60-year-old diabetic man's myocardial infarction: tissue plasminogen activator is used to lyse the fibrin of the clot.
• Patient with reddish-purple spots: thrombocytopenia (a platelet disorder) affects the platelet plug formation phase of hemostasis.