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Lecture

PSL201Y1 Lecture Notes - Vasospasm, Von Willebrand Factor, Extracellular Fluid


Department
Physiology
Course Code
PSL201Y1
Professor
Christopher Perumalla

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Lecture 31
Hemostasis
For bleeding to occur from a blood vessel, two things need to happen.
Firstly, there needs to be damage done to the blood vessel. The second
thing that needs to happen is that the pressure in the blood vessel (in the
lumen) must be greater then the pressure outside the blood vessel (the
pressure in the interstitial fluid). When the blood vessel is damaged, a
number of physical and physiological mechanisms are activated that
promote hemostasis. Smaller blood vessels are frequently ruptured by minor
traumas of everyday life. Hemostasis seals these defects and stops loss of
blood so we are not even aware of the damage to these small blood vessels.
When there is damage to the blood vessel, the endothelial lining is disrupted
and the underlining collagen protein from the subendothelium tissue is
exposed. This initiates two separate but overlapping hemostatic
mechanisms. These hemostatic mechanisms include vascular spasm, platelet
plug formation and blood coagulation (clotting).

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1. Vascular spasm
Vascular spasm is a physical response resulting from the constriction of the
blood vessel. This constriction minimizes blood loss. The vascular spasm is
an intrinsic vascular response and is sympathetically mediated. Vascular
spasm reduces blood loss but does not stop the bleeding completely.
2. Platelet plug
The formation of the plug is a physical response. The plug forms around the
site of vessel damage and thereby decreases blood loss. Platelets are chief
players in the formation of the platelet plug. They are the fragments of large
cells called megakaryocytes that are released from the stem cell in the bone
marrow. Platelets have granules that contain certain secretory products.
Both the formation of the platelet plug and the subsequent blood clot require
the presence of platelet and a fairly large set of specific proteins. These
platelet proteins and other clogging proteins are floating around the plasma
inside the blood vessel.

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In platelet plug formation, the key protein is von Willebrand factor (vWf).
This factor is secreted by megakaryocytes, platelets as well as endothelial
cell lining in the blood vessel. The vWf is present in the plasma at all times
but only accumulates at the site of vessel damage when the vessel is
damaged.
When the tissue is damaged and the blood comes into contact with the
subendothelium tissue, vWF binds to collagen fibers in the subendothelial
layer, thereby triggering the binding of platelets that are flowing in the blood
vessel to the vWf. This anchors platelets in the area of damaged blood
vessel. Contact between the platelets and the vWf changes the metabolism
and the surface properties of platelets, making them sticky and at the same
time stimulating secretion of certain chemicals. These secretory products
include ADP that stimulates morphological changes in the platelets, causing
them to adhere to each other and to form a mass at the site of the injured
vessel. This mass of platelets secrete more ADP which stimulates further
adhesion of platelets, thereby providing a positive feedback loop that
increases the rate of platelet plug formation. Furthermore, the adhered
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