The hematopoietic system, also known as the blood-forming system, is a complex network of organs, tissues, and cells responsible for the production and circulation of blood cells throughout the body. The primary function of the hematopoietic system is to maintain a constant supply of healthy blood cells, including red blood cells, white blood cells, and platelets.
3. Transportation
Blood transports oxygen from the lungs to the cells of the
body and carbon dioxide from the body cells to the lungs
for exhalation.
how blood transports oxygen and carbondioxide?
It carries nutrients from the gastrointestinal tract to body
cells.
How are nutrients absorbed from GIT into blood stream?
Hormones from endocrine glands to other body cells.
How blood transports hormones from endocrine glands?
Blood also transports heat and waste products to various
organs for elimination from the body.
Why blood transports heat to the skin?
4. Regulation
Circulating blood helps maintain homeostasis of all body fluids.
How blood maintains homeostasis of body fluids?
Blood helps regulate pH through the use of buffers.
How blood regulates the pH?
Also helps adjust body temperature through the heat-absorbing
and coolant properties of the water in blood plasma
How water in the blood plasma helps adjust body temperature?
In addition, blood osmotic pressure influences the water content of
cells, mainly through interactions of dissolved ions and proteins.
How blood osmotic pressure influences the water content of cells?
5. Protection
Blood can clot (become gel-like), which
protects against its excessive loss of blood
during any injury
White blood cells protect against disease by
carrying on phagocytosis.
Several types of blood proteins, including
antibodies, interferons, and complement,
help protect against disease in a variety of
ways.
8. Formed elements
Hematocrit: The percentage of total blood volume occupied by RBCs
Females: 38-46%
Males: 40-54%
A significant drop in hematocrit indicates anemia.
Polycythemia: Abnormally high percentage of RBCs (> 65%)
Causes: Tissue hypoxia, dehydration, blood doping.
11. Hemopoiesis
Process by which formed
elements of blood develop
Red bone marrow is the
primary site of hemopoiesis
About 0.05-1% of red bone
marrow cells are
pluripotent stem cells or
hemocytoblasts
Red bone marrow is present
chiefly in bones of the axial
skeleton, pectoral and
pelvic girdles, and the
proximal epiphyses of
humerus and femur.
As the person ages, the red
bone marrow is replaced by
yellow bone marrow.
Under certain conditions
such as severe bleeding,
yellow bone marrow can
revert to red bone marrow.
12. Hemopoiesis
• Stem cells: Stem cells are cells that can self-renew
and give rise to multiple cell types. They have not
yet taken on a specific function or form. They are
considered "blank slate" cells that can become any
type of cell in the body.
• Pluripotent stem cells: Pluripotent stem cells are
undifferentiated cells that can develop into any type
of cell in the body.
• Progenitor cells: Also known as committed stem
cells, because they are committed to giving rise to
more specific elements of the blood.
• Examples of progenitor cells include hematopoietic
progenitor cells, neural progenitor cells, and muscle
progenitor cells.
13. Hemopoiesis
• Myeloid stem cells: Myeloid stem cells are a type of
stem cell that give rise to the myeloid lineage of
blood cells, which includes red blood cells, white
blood cells, and platelets. They are found primarily
in the bone marrow and are responsible for the
continuous production of these cells throughout a
person's lifetime.
• Lymphoid stem cells: Lymphoid stem cells are a type
of stem cell that give rise B cells, T cells, and natural
killer cells. Lymphoid stem cells are found primarily in
the bone marrow and thymus and are responsible
for the continuous production of these cells throughout
a person's lifetime.
• Precursor cells: Precursor or blast cells are
immature cells that have the potential to
differentiate into specific types of mature cells.
They are typically found in the bone marrow and blood
and are an important part of the body's blood-forming
system.
14.
15. Hemopoietic growth factors
• Hold tremendous potential for medical uses when a person’s natural
ability to form new blood cells is diminished or defective.
• The artificial form of erythropoietin (epoetin alfa) is very effective in
treating the diminished red blood cell production that accompanies
end-stage kidney disease.
• Granulocyte–macrophage colony-stimulating factor and granulocyte
CSF are given to stimulate white blood cell formation in cancer
patients who are undergoing chemotherapy.
• Thrombopoietin shows great promise for preventing the depletion of
platelets, which are needed to help blood clot, during chemotherapy.
• Hemopoietic growth factors are also used to treat thrombocytopenia in
neonates, other clotting disorders, and various types of anemia.
16. Blood disorders
Iron deficiency Anemia
• Iron deficiency anemia is a
condition where there is a lack of
iron in the body, leading to a
decrease in the number of red
blood cells and a decrease in the
amount of hemoglobin.
• Iron is necessary for the formation
of hemoglobin. Iron is necessary to
produce red blood cells.
17. Blood disorders
Megaloblastic anemia
• Megaloblastic anemia is a
type of anemia
characterized by the
production of abnormally
large red blood cells,
known as megaloblasts.
• This type of anemia is
caused by a deficiency of
either vitamin B12 or
folic acid, which are both
necessary for the proper
maturation of red blood
cells.
18.
19. Blood
disorders
Pernicious anemia
• Pernicious anemia is a type of
megaloblastic anemia caused by a
deficiency of vitamin B12.
• In pernicious anemia, the body is
unable to absorb vitamin B12
properly due to a lack of a
substance called intrinsic factor,
which is produced by cells in the
stomach.
• This leads to a deficiency of vitamin
B12 in the body.
• Ovalocytes are a type of red blood
cell that are shaped like an oval or
flattened disc, rather than the
typical biconcave disk shape of
normal red blood cells.
20.
21. Blood
disorders
Hemolytic anemia
• Hemolytic anemia is a type of anemia
characterized by the destruction of red
blood cells at a faster rate than the
body can replace them.
• Certain drugs, such as penicillin, and
toxins, such as lead, can cause
hemolytic anemia.
• Certain infections, such as Lyme disease
and babesiosis, can cause hemolytic
anemia.
• In some cases, the body's immune
system may attack and destroy its own
red blood cells, leading to hemolytic
anemia.
• Some genetic conditions, such as sickle
cell anemia and thalassemia, can cause
hemolytic anemia.
22. Blood
disorders
Sickle cell anemia
Sickle cell anemia is a genetic
blood disorder that affects the
shape of red blood cells.
In normal red blood cells, the
hemoglobin (a protein that carries
oxygen) forms a soft, flexible,
biconcave disk shape.
However, in sickle cell anemia, the
hemoglobin forms a stiff, rigid,
crescent- or sickle-shaped
structure.
23.
24. Blood
disorders
Thalassemia
• Deficient synthesis of
hemoglobin occurs in
thalassemia (thal′-a-SE-- mē-a), a
group of hereditary hemolytic
anemias.
• The RBCs are small
(microcytic), pale
(hypochromic), and short-lived.
25.
26. Blood
disorders
Aplastic anemia
Aplastic anemia is a type of anemia
characterized by the failure of the
bone marrow to produce enough red
blood cells, white blood cells, and
platelets.
Hemophilia
Hemophilia is a genetic bleeding
disorder that affects the ability of the
blood to clot properly.
27. Blood
disorders
Leukemia
• The term leukemia (loo-KE--mē-a;
leuko- = white) refers to a group of red
bone marrow cancers in which
abnormal white blood cells multiply
uncontrollably.
• Lymphoblastic leukemia (lim-fō-BLAS-
tik) involves cells derived from
lymphoid stem cells (lymphoblasts)
and/ or lymphocytes.
• Myelogenous leukemia (mī-e-LOJ-e-
nus) involves cells derived from
myeloid stem cells (myeloblasts).
29. Blood
clotting
The process of gel formation, called clotting or
coagulation (kō-ag-u-LA- -shun), is a series of
chemical reactions that culminates in formation of
fibrin threads.
If blood clots too easily, the result can be
thrombosis-clotting in an undamaged blood vessel
If the blood takes too long to clot, hemorrhage can
occur.
Most clotting factors are identified by Roman
numerals that indicate the order of their
discovery.
30.
31. Clotting can be divided into three
stages
1)Two pathways, called the extrinsic pathway and
the intrinsic pathway
2)Prothrombinase converts prothrombin (a plasma
protein formed by the liver) into the enzyme
thrombin.
3)Thrombin converts soluble fibrinogen (another
plasma protein formed by the liver) into insoluble
fibrin. Fibrin forms the threads of the clot.
32.
33. The Extrinsic Pathway
• Occurs rapidly—within a matter of seconds if trauma is severe.
• A tissue protein called tissue factor (TF), also known as
thromboplastin, leaks into the blood from cells outside
(extrinsic to) blood vessels and initiates the formation of
prothrombinase.
• TF is released from the surfaces of damaged cells.
• In the presence of Ca2+, TF begins a sequence of reactions
that ultimately activates clotting factor X.
• Once factor X is activated, it combines with factor V in the
presence of Ca2+ to form the active enzyme
prothrombinase, completing the extrinsic pathway.
34.
35. The Intrinsic Pathway
• Occurs more slowly, usually requiring several minutes.
• The intrinsic pathway is so named because its activators are either
in direct contact with blood or contained within (intrinsic to) the
blood
• If endothelial cells become roughened or damaged, blood can
encounter collagen fibers in the connective tissue around the
endothelium of the blood vessel.
• In addition, trauma to endothelial cells causes damage to platelets,
resulting in the release of phospholipids by the platelets.
• Contact with collagen fibers activates clotting factor XII which begins
a sequence of reactions that eventually activates clotting factor X.
• Platelet phospholipids and Ca2+ can also participate in the activation
of factor X.
• Once factor X is activated, it combines with factor V to form the
active enzyme prothrombinase.
36. The Common Pathway
•The formation of prothrombinase marks the beginning
of the common pathway.
•Prothrombinase and Ca2+ catalyze the conversion of
prothrombin to thrombin.
•Thrombin, in the presence of Ca2+, converts
fibrinogen, which is soluble, to loose fibrin threads,
which are insoluble.
•Thrombin also activates factor XIII (fibrin
stabilizing factor), which strengthens and stabilizes
the fibrin threads into a sturdy clot.
37.
38. Platelets
Between 150,000 and 400,000 platelets are
present in each microliter of blood.
Each is irregularly disc-shaped, 2–4 μm in diameter,
and has many vesicles but no nucleus
Their granules contain chemicals that, once released,
promote blood clotting. Platelets help stop blood loss
from damaged blood vessels by forming a platelet plug.
Platelets have a short life span, normally
just 5 to 9 days.
Aged and dead platelets are removed by
fixed macrophages in the spleen and liver.
39. • Within many vesicles are clotting factors, ADP, ATP,
Ca2+, and serotonin.
• Also present are enzymes that produce thromboxane
A2, a prostaglandin;
• fibrin-stabilizing factor, which helps to strengthen a
blood clot;
• lysosomes;
• membrane systems that take up and store calcium and
provide channels for release of the contents of granules;
• and glycogen
• Also within platelets is platelet-derived growth factor
(PDGF), a hormone that can cause proliferation of
vascular endothelial cells, vascular smooth muscle
fibers, and fibroblasts to help repair damaged blood
vessel walls.
40. Coagulation
disorders
• Coagulation disorders are conditions that
affect the body's ability to control blood
clotting. Eg.: hemophilia, von Willebrand
disease, DVT.
• This can result in either excessive bleeding
(bleeding disorder) or abnormal blood
clots (thrombotic disorder) which can lead
to serious health problems such as stroke,
deep vein thrombosis, and heart attack.
• These disorders can be inherited or
acquired and are caused by a variety of
factors such as genetics, medications,
liver disease, and more.
• They can be diagnosed by blood tests and
treated with medication, lifestyle changes,
or in severe cases, surgery.
41. Hemostasis-
sequence of
responses to
stop bleeding
• Three mechanisms reduce blood loss:
• (1) vascular spasm,
• (2) platelet plug formation, and
• (3) blood clotting (coagulation).
• When successful, hemostasis prevents
hemorrhage, the loss of a large amount of
blood from the vessels.
• Hemostatic mechanisms can prevent
hemorrhage from smaller blood vessels, but
extensive hemorrhage from larger vessels
usually requires medical intervention
42. Vascular Spasm
•When arteries or arterioles are
damaged, the circularly arranged
smooth muscle in their wall's contracts
immediately, a reaction called vascular
spasm.
•This reduces blood loss for several
minutes to several hours, during which
time the other hemostatic mechanisms
go into operation.
43. Platelet Plug Formation
Initially, platelets
contact and stick to
parts of a damaged
blood vessel, such
as collagen fibers of
the connective
tissue underlying the
damaged
endothelial cells.
44. Platelet Plug
Formation
• Liberated ADP and
thromboxane A2 play a
major role by activating
nearby platelets.
• Serotonin and
thromboxane A2 function
as vasoconstrictors,
causing and sustaining
contraction of vascular
smooth muscle, which
decreases blood flow
through the injured
vessel.
45. Platelet Plug
Formation
• The release of ADP
makes other platelets in
the area sticky, and the
stickiness of the newly
recruited and activated
platelets causes them to
adhere to the originally
activated platelets
• Eventually, he
accumulation and
attachment of large
numbers of platelets form
a mass called a platelet
plug.
46. ABO Blood
Grouping
• The ABO blood group is
based on two glycolipid
antigens called A and B
• People whose RBCs display
only antigen A have type A
blood.
• Those who have only antigen B
are type B.
• Individuals who have both A
and B antigens are type AB;
• Those who have neither
antigen A nor B are type O.
47. • Blood plasma usually contains antibodies called
agglutinins that react with the A or B antigens if
the two are mixed.
• These are the anti-A antibody, which reacts with
antigen A, and the anti-B antibody, which reacts
with antigen B.
• You do not have antibodies that react with the
antigens of your own RBCs, but you do have
antibodies for any antigens that your RBCs lack.
• For example, if your blood type is B, you have B
antigens on your red blood cells, and you have
anti-A antibodies in your blood plasma.
48.
49. •Type AB- Universal recipient
•Type O- Universal donor
•In about 80% of the population,
soluble antigens of the ABO type
appear in saliva and other body fluids,
in which case blood type can be
identified from a sample of saliva.
50. Rh Blood Group
•Normally, blood plasma does not contain anti-Rh
antibodies.
•If an Rh− person receives an Rh+ blood transfusion,
however, the immune system starts to make anti- Rh
antibodies that will remain in the blood.
•If a second transfusion of Rh+ blood is given later,
the previously formed anti-Rh antibodies will cause
agglutination and hemolysis of the RBCs in the
donated blood, and a severe reaction may occur.
Tissue hypoxia leads to an increase in erythropoietin production by the kidneys. It stimulates bone marrow to produce more red blood cells and results in polycythemia.
Dehydration increases hematocrit, leading to relative polycythemia. This occurs because dehydration reduces the volume of plasma, leading to an increase in the concentration of red blood cells. However, this is not true polycythemia as the total red cell mass does not increase.
Blood doping refers to the practice of artificially increasing the number of red blood cells in circulation to enhance athletic performance. This can be done by erythropoietin (EPO) administration. The increase in red blood cells enhances oxygen transport, leading to improved endurance and performance. This results in true polycythemia as the total red cell mass increases.