This document summarizes hematopoiesis and hemostasis. It describes how (1) all blood cells originate from hemocytoblasts, which can become red blood cells, lymphocytes, or non-lymphocyte white blood cells. (2) Red blood cells develop by increasing hemoglobin and ejecting organelles to become biconcave and nucleus-free. (3) The kidneys release erythropoietin to stimulate bone marrow production of more red blood cells when counts are low. (4) Hemostasis, or blood clotting, occurs in three phases: vascular constriction, platelet adhesion, and coagulation through a fibrin mesh that seals the break.

1. ANATOMY
Unit 3 Notes:
Hematopoiesis
& Hemostasis

2. (1) Hematopoiesis
• The process of blood cell formation and
development.
• All blood cells originate from the stem cell the
Hemocytoblast.
• If it becomes a red blood cell:
– Hemocytoblast  Erythroid Stem Cell  RBC
• If it becomes a Lymphocyte white blood cell:
– Hemocytoblast  Lymphoid Stem Cell  Lymphocyte
• If it becomes a Non-Lymphocyte white blood cell:
– Hemocytoblast  Myeloid Stem Cell  Neutrophil,
Basophil, Monocyte, Eosinophil

4. (2) Red Blood Cell Development
• As red blood cells develop they increase
hemoglobin production.
• Once hemoglobin production reaches
maximum, ALL organelles are ejected.
– This gives red blood cells their biconcave
shape.
– This also means red blood cells contain no
nucleus or anything!

6. (3) Making More RBC’s
• Red Blood Cells are produced within your bone
marrow.
• Erythropoietin:
Protein released from the kidneys which stimulates
the production of RBC’s from the bone marrow.
• Cause for Release of Erythropoietin:
– Low RBC count
– Low oxygen levels
• Body stops producing / releasing erythropoietin when
RBC / oxygen numbers are back at homeostasis.

8. (4) Hemostasis
• The process of blood clotting.
• Occurs in 3 Phases:
– Vascular Phase
• Goal: Constrict the blood vessels as much as possible to
decrease blood flow.
– Platelet Phase:
• Goal: Stick platelets to sides of torn blood vessels to
patch up hole.
– Coagulation Phase:
• Goal: Form the final mesh-net that will full cover the hole
and seal up the blood vessels.

9. (5) The Vascular Phase
•
Blood vessel tears.
•
Serotonin is released from torn vessel cells.
•
Serotonin triggers vasoconstriction of blood
vessels.
•
Blood flow temporarily slowed or
constricted.

10. (6) The Platelet Phase
(This begins at the same time as the Vascular Phase.)
1. The same torn vessel cells release Von Willebrand
Factor.
2. Free-Floating platelets adhere to Von Willebrand
Factor.
3. Adhered platelets release Thromboplastin AND
Thromboxane.
4. Thromboxane causes further vasoconstriction of
blood vessels.

11. (7) The Coagulation Phase Pt 1
THE EXTRINSIC PATH
Thromboplastin binds
with Calcium and
Phospholipids.
THE INTRINSIC PATH
1. Thromboplastin binds
with Calcium and AntiHemolytic Cofactor.
2.
Thromboplastin +
Calcium + Phospholipid =
“Proconvertin Enzyme”
3.
Proconvertin binds with
Stuart Prower Enzyme
2. Thromboplastin +
Calcium + AntiHemolytic Cofactor =
“”Prothrombin”
4.
Proconvertin + Stuart
Prower = “Prothrombin”
1.

12. (8) The Coagulation Phase Pt 2
1. Prothrombin binds with Proaccerin Cofactor.
2. Prothrombin + Proaccerin Cofactor = “Thrombin”
3. Thrombin binds with Fibrinogen.
4. Thrombin + Fibrinogen = “Fibrin”.
*Fibrin is the mesh net that finally seals up the
wound.

13. (9) After Coagulation
1. Contractile proteins in platelets bring
edges of wound and tissue together to
help close up hole.
2. Plasmin Enzyme is slowly released from
platelets.
3. Plasmin will begin to degrade clot tissue to
help naturally remove scab from the body.