1 Blood22
1 Blood22
1 Blood22
● Substance distribution
- Oxygen from the lungs and nutrients from the digestive tract
elimination
● Regulation
● Protection
3. Fibrinogen, it
functions in blood clotting
Formed Elements(cells)
Blood loss
<10% nothing
10 ~30 % clinic symptom
>30% danger
Calculating haematocrit Important
Higher Lower
concentration concentration
Semi-permeable
Membrane
高 低
Hypertonic solution Isotonic solutiion Hypotonic solution
Animal
cell
vertebrae Vertebrae
ilium
sternum
Life Span Erythrocytes (RBCs)
Erythrocytes lack a nucleus and mitochondria
Because of these deficiencies, erythrocytes have a circulating life span
of only about 120 days before they are destroyed in the liver, spleen
and bone marrow.
Reticulocytes. Immature young RBCs appear (reticular) when stained.
They contain a few ribosomes & can be seen in bone marrow.
? mm
Normal range
Male : 3--7 mm
Female: 5 – 10 mm
● Rouleaux formation
- more erythrocytes adhibit with concavity one another
□ cause ( RBC ? plasma ?)
RBC from patient with high ESR RBC from the health
RBC
Rouleaux
inhibit promote
Rouleaux formation
down up
ESR
Both folic acid & vitamin B12 are necessary co-factors for DNA
synthesis, which is essential for maturation of the red cells.
folic acid
Absorption of Vit.B12 requires
vitamin B12
a protein called intrinsic
tetrahydrofolic acid factor secreted by stomach
(THFA)
erythroblast
Leukocytes ( white blood cells )
Our bodies have special system to defend against infecant agents,
including leukocytes and tissue cells from leukocytes
granulocyte
Lymphocytes function in
connection with the immune
system
Granular Leukocytes
Neutrophils. 60 % - 70%.
Function: Cellular immunity by phagocytosis.
Eosinophils. 2-4%.
Function: Limit the action of
basophils in the rapid allergic
reactions, participate in the
immune response to parasites
urticaria asthma
Agranular Leukocytes
Monocytes. 3% - 8%.
Function: fixed tissue macrophages.
● Vascular constriction
● Formation of a platelet plug
● Formation of a blood clot as a result of blood coagulation
● Growth of fibrous tissue into the blood clot to close the
hole
in vessel permanently
1 2 3
Vasoconstriction
Tissue Factor
2. Formation of the Platelet Plug
Platelets Adhere to the damaged vascular wall, such as
the collagen fibers and damaged endothelium.
3. Blood Coagulation
The third stage for hemostasis is formation of the blood clot, which
is the production of a web of fibrin proteins that penetrates and
surrounds the platelet. Blood clots therefore contain platelets and
fibrin, trapped red blood cells. Finally, contraction of the
platelet mass in the process of clot retraction forms a more
compact and effective plug. Fluid squeezed from the clot as it
retracts is called serum, which is plasma without fibrinogen, the
soluble precursor of fibrin.
Vessel injured
collagen in
subendothe-
lium exposed to blood
fibrin
Temporary platelet Plug platelet plug formation
formation
Hemostasis progress
● General Mechanism of blood coagulation
i. In response to rupture of the vessel , a complex cascade of
chemical reactions is initiated. The net result is formation of a
complex of activated substance collectively called prothrombin
activator
ii. The prothrombin activator catalyzes the conversion of
prothrombin into thrombin
iii. The thrombin acts as an enzyme to convert fibrinogen into
fibrin fibers that enmesh platelets, blood cells, and plasma to
form the clot
iv. The conversion of fibrinogen into fibrin may occur via
either of two pathways. (1) intrinsic pathway that begin
in the blood itself and (2) extrinsic pathway that begins
with trauma of the vascular wall and surrounding tissues
Coagulation cascade
Intrinsic system (surface contact) Extrinsic system (tissue damage)
XI XIa
VIII VIIIa
X Xa
V Va
II IIa (Thrombin)
Fibrinogen Fibrin
Plasminogen Activator
Plasminogen Plasmin
Inhibitor
Plasmin
t-PA
FDPs
PG PL
Fibrin