iii.

Increased erythrocytes cause an increase in

BLOOD kineso! blood O2 levels.
Functions of Blood:

1. Transport of gases, nutrients and waste products

2. Transport of processed molecules

3. Transport of regulatory molecules

4. Regulation of pH and osmosis

5. Maintenance of body temperature

6. Protection against foreign substances

7. Clot formation

Composition of Blood:

1. Plasma - 55% of total blood. Pale, yellow liquid that surrounds

cells. 91% water, 7% proteins, and 2% other. Plasma proteins:

a. Albumin - 58% of plasma proteins. Helps maintain

water balance
- Fate of Old Erythrocytes and Hemoglobin:
b. Globulins - 38% of plasma proteins. Helps immune
system i. Old red blood cells are removed from blood by
macrophages in spleen and liver
c. Fibrinogen - 4% of plasma proteins. Aids in clot formation
ii. Hemoglobin is broken down

iii. Globin is broken down into amino acids

iv. Hemoglobin’s iron is recycled

v. Heme is converted to bilirubin

vi. Bilirubin is taken up by liver and released into

small intestine as part of bile

2. Formed Elements - 45% of total blood. Cells and cell

fragments:

a. Erythrocytes (Red blood cells/ RBC) - Disk-shaped with thick

edges. Nucleus is lost during development. Live for 120
days. Transport O2 to tissues.

 Hemoglobin - Main component of erythrocytes.

Transports O2. Each globin protein is attached to a
heme molecule. Each heme contains one iron atom. O2
binds to iron.

 Oxyhemoglobin - hemoglobin with an O2

attached

- Production of Erethrocytes:

i. Decreased blood O2 levels cause kidneys to

increase production of erythropoietin.

ii. Erythropoietin - stimulates red bone marrow to

produce more erythrocytes.
 b. Leukocytes (White blood cells/WBC) - Lack hemoglobin. chemicals released by cells of the damaged blood
Larger than erythrocytes. Contain a nucleus. Fight vessel wall and by platelets.
infections, remove dead cells and debris by phagocytosis.
Types of Leukocytes: ii. Platelet plugs - can seal up small breaks in blood
vessels. A platelet plug is very important in
i. Granulocytes - contain specific granules, include: maintaining the integrity of the damaged blood
vessels.
 Neutrophils - most common. Remain in blood for
10 to 12 hours then move to tissues. Phagocytes - The formation of a platelet plug can be described
as a series of steps, but in actuality many of these
 Eosinophils - reduce inflammation, destroy parasites steps occur at the same time.

 Basophils - least common. Release histamine and  Platelet adhesion - occurs first, when platelets stick
heparin to the exposed collagen in the damaged blood
vessel wall. After platelets adhere to collagen, they
ii. Agranulocytes: no specific granules: become activated, change shape, and release
chemicals.
 Monocytes - largest sized white blood cells. Produce
macrophages  Platelet aggregation - fibrinogen forms bridges
between the fibrinogen receptors of numerous
 Lymphocytes - immune response. Several different types
platelets, resulting in a platelet plug.
(T cells and B cells). Lead to production of antibodies
- Ex: Vessel Injury -> exposure of collagen ->
Platelets bind with collagen using Von
Willebrand Factor (a protein secreted by Blood
vessel endothelial cells that serves as mediator
between collagen & platelets) -> PPF

iii. Blood clotting (coagulation) - Blood can be

First line of defense: Macrophage
transformed from a liquid to a gel
2nd line of defense: Neutrophils (circulation), margination,
 Clot - network of thread-like proteins called fibrin
diapedesis
that trap blood cells and fluid. It depends on
3rd line of defense: 2nd wave of macrophage clotting factors

4th line of defense: Bone marrow will produce more  Clotting factors - proteins in plasma. Only
macrophage and neutrophils activated following injury. Made in liver. Require
vitamin K. Types:
c. Thrombocytes (Platelets) - minute fragments of cells, each
1. Fibrinogen
consisting of a small amount of cytoplasm surrounded by
a cell membrane. Platelets play an important role in 2. Prothrombin
preventing blood loss
3. Thromboplastin (Tissue Factor)
- They are produced in the red bone marrow from large
cells called megakaryocytes. Small fragments break off 4. Ca2+ Ions
from the megakaryocytes and enter the blood as
platelets. 5. Labile Factor

 Blood loss - When blood vessels are damaged, blood 6. Stable Factor
can leak into other tissues and disrupt normal function.
Blood that is lost must be replaced by production of new 7. Anti-Hemophilic Factor A
blood or by a transfusion.
8. Anti-Hemophilic Factor B (Christmas
- Preventing blood loss: Disease)

i. Vascular spasm - temporary constriction of blood 9. Stuart Factor

vessel. An immediate but temporary constriction of a
10. Anti-Hemophilic Factor C
blood vessel that results when smooth muscle within
the wall of the vessel contracts. 11. Anti-Hemophilic Factor D (Hageman)
- This constriction can close small vessels 12. Fibrin Stabilizing Factor
completely and stop the flow of blood through them.
Vascular spasm is stimulated by
 - Clotting factors: A antigen and type B antigen. The types of antigens found on the
surface of the red blood cells are genetically determined.
1. Injury to a blood vessel causes inactive
clotting factors to become activated due to 1. Type A blood - has type A antigens. Plasma from type A blood
exposed conn. tissue or release of contains anti-B antibodies, which act against type B
thromboplastin antigens.

2. Prothrombinase (clotting factor) is formed 2. Type B blood - has type B antigens. Plasma from type B blood
and acts upon prothrombin contains anti-A antibodies, which act against type A
antigens.
3. Prothrombin is switched to its active form
thrombin 3. Type AB blood - has both types of antigens. Type AB blood
plasma has neither type of antibody
4. Thrombin activates fibrinogen into its
active form fibrin 4. Type O blood - has neither A nor B antigens. Type O blood
plasma has both anti-A and anti-B antibodies.
5. Fibrin forms a network that traps blood
(clots) - In Caucasians in the United States, the distribution is type O,
47%; type A, 41%; type B, 9%; and type AB, 3%.

- Among African-Americans, the distribution is type O, 46%; type

A, 27%; type B, 20%; and type AB, 7%.

Clot Formation Control - Clots need to be controlled so they

don’t spread throughout the body

 Anticoagulants - prevent clots from forming. Example -

heparin and antithrombin

- Injury causes enough clotting factors to be activated that

anticoagulants can’t work in that particular area of the body

Clot retraction - condensing of clot. Serum in plasma is squeezed

out of clot. Helps enhance healing

Fibrinolysis - process of dissolving clot.

 Plasminogen (plasma protein) - breaks down clot (fibrin)

Blood Donor and Recipient According to ABO Blood Types:

1. O are universal donors because they have no antigens

2. Type A can receive A and O blood

3. Type B can receive B and O blood

4. Type AB can receive A, B, AB blood

5. Type O can only receive O blood

Rh positive - means you have Rh antigens. 95 to 85% of the

population is Rh+

Rh negative - means you don’t have Rh antigens

Injury or surgery - can lead to a blood transfusion Antibodies only develop if an Rh- person is exposed to Rh+ blood
by transfusion or from mother to fetus.
Transfusion reactions/Agglutination - clumping of blood cells
(bad) Rh Incompatibility in Pregnancy - If mother is Rh- and fetus is Rh+
the mother can be exposed to Rh+ blood if fetal blood leaks
Antigens - molecules on surface of erythrocytes
through placenta and mixes with mother’s blood.
Antibodies - proteins in plasma. Antibodies against the antigens
- First time this occurs mother’s blood produces antibodies against
are usually present in the plasma of blood.
antigens. Any repeated mixing of blood causes a reaction.
Blood groups - named according to antigen (ABO). In the ABO
blood group system, there are two types of antigens that may
appear on the surface of the red blood cells; type
Hemolytic Disease of Newborn - This condition occurs when White Blood Cell Disorders:
mother produces anti-Rh antibodies that cross placenta and
agglutination and hemolysis of fetal erythrocytes occurs. Can be 1. Leukopenia - low white blood cell count. Caused by
fatal to fetus. Prevented if mother is treated with RhoGAM. radiation, chemotherapy drugs, tumors, viral infections

 RhoGAM - contains antibodies against Rh antigens. 2. Leukocytosis - high white blood cell count. Caused by
infections and leukemia

Hematopoiesis - the process that produces formed elements. In

the fetus, hematopoiesis occurs in several tissues, including the
liver, thymus, spleen, lymph nodes, and red bone marrow.

- After birth, hematopoiesis is confined primarily to red bone

marrow, but some white blood cells are produced in lymphatic
tissues.

- All the formed elements of blood are derived from a single

population of cells called stem cells, or hemocytoblasts.

 Hematocytoblasts - stem cells that differentiate to give rise to

different cell lines, each of which ends with the formation of a
particular type of formed element.

Diagnostic Blood Tests:

1. Complete blood count - provides information such as RBC

count, hemoglobin, hematocrit, and WBC count

2. Hematocrit - % of total blood volume composed of RBC

3. Hemoglobin - determines amount of hemoglobin.

Indicate anemia

4. Prothrombin time - time it takes for blood to begin clotting (9 to

12 sec.)

5. White blood cell count - total number of white blood cells

6. White blood cell differential count - Determines the % of

each 5 kinds of leukocytes

a. Neutrophils: 60 to 70%

b. Lymphocytes: 20 to 25%

c. Monocytes: 3 to 8%

d. Eosinophils: 2 to 4%

e. Basophils: 0.5 to 1%