Lecture 13: Blood + Hemostasis Flashcards
Plasma
Organic and inorganic substances dissolved in water (90% water). Most solutes by weight are plasma proteins
3 groups of plasma proteins
- Albumins
- Globulins
- Fibrinogen
Serum
Plasma w/ fibrinogen and other clotting proteins removed
RBC shape
High surface area:volume of isc shape enables fast diffusion and flexibility
RBC removal
Spleen and liver destroy old/damaged RBCs, producing bilirubin
Active red marrow
Children: most bones
Adults: only chest, skull base, vertebrae, pelvis, limb ends
Hemostasis
Stoppage of bleeding. Most effective in small vessel injuries
Hematoma
Accumulation of blood in tissues from bleeding
Hemostasis processes
2 interdependent processes
1. Formation of platelet plug
2. Blood coagulation (clotting)
Both involve platelets
Constriction of injured vessels
Immediate intrinsic response of injured/severed vessels is constriction due to local substance changes from endothelium/blood cells. Slows blood flow and presses opposed endothelia together to induce “stickiness”
Formation of platelet plug
- CT exposure
- Platelet-collagen binding + secretory vesicle release
- Platelet activation and aggregation
- Fibrinogen binding
- Clot retraction
CT exposure
Platelets must adhere to surface; vessel injury disrupts endothelium and exposes CT collagen
Platelet-collagen binding
Plasma von Willebrand factor (vWF) intermediates platelet-collagen adhesion
von Willebrand factor
vWF secreted by endothelial cells/platelets, binds+changes conformation of exposed collagen fibers as to bridge btwn damaged vessel wall and platelets
Platelet secretory vesicle release
Binding to collagen triggers vesicle release to induce further platelet activation (ADP, serotonin, etc.) and platelet aggregation (pos. feedback loop where new platelets adhere to old ones)
Platelet activation
Local factors induce changes in local platelet shape, metabolism, and surface protein to facilitate forming platelet plug. Platelet activity also induces local vasoconstriction.
Fibrinogen binding to platelets
Platelet activation exposes fibrinogen binding sites; fibrinogen fills gaps in between platelets to seal plug
Clot retraction
Platelets have high actin+myosin content; aggregation induces interaction to compress and strengthen clot.
Platelet plug regulation
Undamaged endothelial cells secrete prostacyclin and NO; strong inhibs. of platelet aggregation, adhesion, activation, and vasodilator
Prostacyclin
Aka prostaglandin I2 (PGI2). Acts to limit platelet plug formation to damaged area and prevent unnecessary plug formation
Blood coagulation (clot formation)
Transformation of blood to solid gel clot (thrombus); chemical cleavage cascade. Dominant hemostatic defense.
Thrombus
Primarily made of fibrin polymers, occurs locally around platelet plug. Traps RBCs/other cells
Key point of clot formation
Activation of prothrombin -> thrombin; thrombin catalyzes fibrinogen -> fibrin and XIII -> XIIIa (X-linking of fibrin in clot).
Clotting also requires Ca++ (never deficient)
Thrombin-platelet activation
Thrombin activated platelets bind several clotting factors and display platelet factor (PF); cofactor for clotting cascade