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Lecture 1

PATH 310 Lecture Notes - Lecture 1: Vascular Smooth Muscle, Thrombomodulin, Endothelium

Pathology and Molecular Medicine
Course Code
PATH 310
Christine Hough

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HEMOSTASIS is the normal process that stops bleeding after vessel injury
with the formation of a hemostatic plug
- It is rapid, controlled, site specific, and removed
Components of Blood Erythrocytes, leukocytes, platelets, and plasma
Blood Vessels Endothelial Lining, Smooth muscle cells, Fibroblasts, Vessel walls
To keep blood in a fluid state you need…
1. An intact vascular endothelium
** Separates blood from prothrombic components
- Regulates vascular tone, vascular smooth muscle cell proliferation, and trans-
endothelial leukocyte migration
- Also plays a role in thrombosis and thrombolysis (through prothrombic
components TF, VWF, and collagen)
- There are molecules on resting endothelial cells
2. Platelets in a quiescent state
Prostacyclin and NO inhibit platelet aggregation
CD39/ADPase is a platelet antagonist
3. Regulation of coagulation
- Activators of Coagulation: coagulation activation, endothelial damage, platelet
- Inhibitors of Coagulation: anticoagulant factors, endothelium, fibrinolytic factors
Thrombomodulin inhibits thrombin. It also produces a protein C/S complex that
limits coagulation factors FV and FVIIa
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4. Regulation of fibrinolysis
t-PA and UK converts plasminogen to plasmin in order to break down fibrin
1. Primary hemostasis
Overall: Vasoconstriction to decrease blood loss and platelet plug formation
Damage causes exposure of subendothelium VWF and collagen
A. Platelet receptor gp1b95 interact with VWF and collagen. This causes platelet to
roll along the surface to slow it down
B. Platelet adhesion activates the release of alpha granules (ADP, and TXA2) in order
to recruit more platelets
C. Two other receptors gp6 and integrin a2b1 interact with collagen to create a firm
attachment to the injured area and cause activation
* Activated platelets have long protrusions while resting have none
D. Platelets are cross-linked through a 4th receptor with fibrinogen and VWF to
create a hemostatic plug
2. Secondary hemostasis
* Clot formation
* Clotting factors circulate as zymogens and are activated by limited proteolysis
_ First step in the coagulation cascade is the extrinsic pathway
- Upon vessel wall injury, tissue factor (TF) is exposed to blood and finds and
activates FVII (Factor 7)
** The extrinsic tenase complex: FX, TF, and FVIIa
- TF-FVIIa complex activates small amounts of FIX and FX
- FX then binds with FV to form the prothrombinase complex to generate a small
amount of thrombin from prothrombin
** There is positive feedback of thrombin
- The initiation phase is followed by the amplification phase
- Thrombin activates cell-surface bound FV and FVIII and platelet-bound FIX
** The intrinsic tenase complex: FIXa, FVIIIa, and FX with Ca
- Thrombin catalyzes fibrinogen to fibrin and activates procoagulant factors (V, VIII<
- The final reaction turns soluble fibrinogen to insoluble fibrin
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