BLOOD A LIVING TISSUE

HEMOSTASIS 2

**Red Blood Cell Life and death

The red blood cell does not possess the structures required for DNA synthesis nor, for transcription and translation of proteins.
Cellular life depends on the cell’s ability to generate ATP through the utilization of glucose. Without the pathway for ATP generation, the cell would not be able to maintain its membrane integrity, and ionic gradients.
The ability to maintain hemoglobin in its reduced form for the transport and delivery of oxygen would also be limited.
Glucose is the primary fuel of the erythrocyte. It enters the cell through diffusion from the plasma, and through glycolysis ultimately is converted to lactate and pyruvate.
This process uses 2 moles of ATP and produces 4 moles of ATP, for a net gain of 2 ATP molecules.
The rate limiting step is controlled by the activity of phosphofructokinase, which converts fructose 6-phosphate to fructose 1,6 phosphate. This enzyme is inhibited by high concentrations of ATP, which signal the “fed” state.
Conversely, high concentrations of AMP signal an “energy starved” state favouring continued glycolysis.
The energy generated by glycolysis is utilized by the Na+ -K+ ATPase pump to regulate cell membrance potentials.
Maintenance of the appropriate redox potential is essential for the red blood cell to complete its function of oxygen delivery.
The red cell ultimately dies as its enzyme systema burn out.
The inability to continue glycolysis to maintain membrane gradients leads to changes in membrane permability and ultimately to cell destruction.
More than 90% of red cells with altered membrane are destroyed by the macrophages of the reticuloendothelial system (spleen, liver and marrow).
As the cells are destroyed, the hemoglobin molecule is further degraded. The iron is largely conserved, redistributed to the marrow, and incorporated into new hemoglobin**

1. Coagulation

1.1 Intrinsic
In all injuries, there is injury to blood vessels with the
resulting exposure of blood to tissue factors and collagen in the
injured wall of the blood vessels factors V and VIII are
available in the endothelium.
There follows as a result platelet aggregation and adherence with formation of a plug at the injury
site.

Hemostasis(control of bleeding) is achieved within the body by four events occurring in
sequence:

* Vessel wall smooth muscle constriction at the site of injury
Vasoconstriction limits the blood loss. This occurs in
response to release of Thromboxane A and Serotonin from the
platelets. Endothalin is also responsible and is released
from the endothelial cells.
* Platelet function. The platelets adhere to one another and
also to the vessel wall at the site of injury to form a plug
* Coagulation wherein prothrombin is converted to thrombin and
their product in turn converts fibrinogen to fibrin
improves the platelet plug
* Fibrinolysis. This process causes the lysis of the fibrin
to restore the patency of the blood vessel.
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