Function of blood
1. Transport:
o
O2 – CO2 – Nutrients– waste products and hormones
2. Homoeostasis:
o
o
Regulation of body temperature
Regulation of ECF (pH, nutrients, ions……..etc)
3. Protection against infections by:
White Blood Cells
o Antibodies (Immunoglobulins).
o
4. Haemostasis:
o
prevents blood loss by blood clotting
Composition of blood
1. Plasma
•
•
•
Water 91%
Ions
Plasma proteins
(Albumin , globulins, Fibrinogen)
2. Cellular
components
• Red Blood Cells
• White Blood Cells.
• Platelets
The Plasma
 Composition
 91% water
 9% solids :
of plasma:
o 7% plasma proteins,
o 2% inorganic salt; Na, HCO3,Cl)
 Types of plasma proteins:
 Albumin (4-4.5 gm/dl )
 Globulins (2.5 gm/dl )
 Fibrinogen (0.4 gm/dl)
 Prothrombin.
•
Total plasma proteins = 7.4 gm/dl.
Functions of Plasma Proteins
1-Production of an effective osmotic pressure:
Albumin causes the colloidal osmotic pressure which is
about 25 mmHg.
2.Blood Viscosity: Caused by fibrinogen mainly. It helps
in maintaining peripheral resistance.
3.Clotting of blood: by fibrinogen, prothrombin and
other clotting factors.
4.Defensive function: Gamma globulins are
immunoglobulins.
5.Act as carriers : for some hormones, drugs, metal
ions and other molecules and prevent their rapid loss in
urine (especially albumin).
Formed Elements - Cells

Erythrocytes (RBCs)
(4.5-5.5 million/mm3).

Platelets
(200,000 - 400,000/mm3).

Leucocytes (WBCs)
(4,000-10,000/mm3).
Erythrocytes (RBCs)
 Functions:
 Carry Hemoglobin
 Transport of O2 and CO2
 Counts:
 In males 4.5-5.5 million
/mm3
 In females 4.0 -5.0
millions /mm3
 Life
span 120 days
Types & causes of anemia
1. Normocytic normochromic anemia:
The size of RBC’s & their Hb content are normal but
their count is less than normal.
 Acute blood loss anemia: It results from rapid loss of
an excessive amount of blood e.g. during severe
hemorrhage.
 Aplastic anemia: It results from destruction or
inhibition of B.M. due to:
o Excessive exposure to X-ray or –radiation.
o Chemical toxins e.g. cancer therapy, chloramphenicol
or insecticides.
 Hemolytic
anemia: It results from excessive
destruction of RBC’s.

2.Microcytic hypochromic anaemia:
The size of the RBC’s & their Hb content are decreased.
It is caused by:

o
o
o
o


Iron deficiency anemia: causes:
intake: as in malnutrition.
iron requirements: as in pregnancy & lactation.
absorption: as in gastrectomy & malabsorption.
Chronic blood loss due to: peptic ulcer, bleeding
piles, bilharziasis, excessive menstruation.
Thalassemia.
Hypothyroidism (some cases are macrocytic).
3. Macrocytic (megloblastic) anemia
(maturation failure anemia)



o
o
o

o
o
o
o
The red volume & its Hb content (MCH) are increased but
the MCHC is normal.
It is caused by:
Folic acid deficiency anemia: Results from:
 intake in diet.
 requirements e.g. during pregnancy.
Failure of absorption.
Vitamin B12 deficiency anaemia: (Pernicious
anaemia) Results from:
 intake in diet (rare).
 absorption of vitamin B12 due to:
Absence of gastric intrinsic factor: Atrophy of gastric
mucosa, Partial or total gastrectomy, Cancer stomach.
Distal small intestine diseases.
Polycythemia
3.
Definition: number
of
RBC’s
above
6
million/mm
Polycythemia
 Types & causes:
Primary polycythemia (polycythemia vera):
 Caused by a tumor like condition of B.M.  excessive
production of RBC’s.
Secondary polycythemia (physiological polycythemia)
 It is 2ry to prolonged tissue hypoxia  overproduction of
erythropoietin. e.g.:- High altitude & Newly born infants.
 Effects:
o blood volume.
o blood viscosity   peripheral resistance   diastolic
blood pressure.
o Stagnant hypoxia due to slow blood flow.

Leucocytes (White Blood Cells)
White cell count : 4.000 – 11.000 / mm3.
1 - Granulocytes:

Neutrophils : (50 -70 % ) Phagocytosis of bacteria & some fungi.
Eosinophils : (1 - 4 % ) Destroy parasitic worms & immune
complexes.

Basophils : (0 - 1 % ) Causes vasodilation by the release of

histamine.
2 - Monocytes : (2 - 8 %) Differentiate into macrophages in
tissues.
3 - Lymphocytes : ( 20 - 40 % ) two types:

B-lymphocytes - Humoral Immunity (antibodies).

T-lymphocytes - Cellular Immunity.
Basophil
Lymphocyte
Eosinophil
Neutrophil
Monocyte
Hemostasis
It is the stoppage of blood loss from injured vessel
There are three major steps:
1-Vasoconstriction:
 When a large artery or vein is severed, smooth muscle in
its wall contracts.
 Platelets release serotonin which brings about
vasoconstriction.
2-Platelet plug formation :
 When capillaries rupture, the damage is too slight to
initiate the formation of a clot. The rough shape causes
the platelets to change shape (swollen) and become
sticky. They stick to each other and aggregate trying to
close the whole in the injured vessel.
o
o
Vascular
Spasm
Platelet plug
formation
Blood
Coagulation
3- Blood Coagulation (Clotting):
o It stops bleeding by occluding the opening in
damaged vessels.
o Clot is formed by conversion of soluble
plasma fibrinogen into insoluble fibrin
network with blood cells in its meshes.
o The clot begins to develop in 15 – 20
seconds & within 3 – 6 min.  clot is
completely formed in the injured vessel.
Intrinsic & extrinsic mechanism
17
Hemostasis process
Hemophilia
 Definition:
o It is a hereditary hemorrhagic disease transmitted by females (who
are usually not affected but act as carriers) to males (who are
affected) so, it is sex linked.
o The injured vessel causes severe hemorrhage for long time.
 Types & causes:
1) haemophilia A (classic Haemophilia): 83 %: Caused by deficiency of
factor VIII.
2) Haemophilia B (Christmas disease): 15 %: Caused by deficiency of
factor IX.
3) Haemophilia C: 2 %: Caused by deficiency of factor XI
Characters
1- Normal bleeding time.
2- Prolonged clotting time.
3-  clotting factors VIII, IX & XI .
19
Hemophilia pictures
Purpura
Definition: It is a disease characterized by spontaneous small
hemorrhages in skin & mucous membranes.
Causes & types:
A) Thrombocytopenic purpura:  number of platelets (below 40, 000/
mm3).
o Causes:
1) Idiopathic thrombocytopenia.
2)  Platelet production.
3)  Platelet destruction: As in case of hypersplenism.
B) Non-thrombocytopenic purpura: Platelet count is normal but
bleeding time is prolonged due to platelet or vascular abnormalities.
Characters:
o Normal clotting time.
o Prolonged bleeding time
o  number of platelets (in thrombocytopenic purpura).
21
Purpura pictures
ABO blood groups
Blood group
Agglutinogen
on RBC’s
Agglutinin
in plasma
% of
population.
A
A
Anti- B
42 %
B
B
Anti- A
9%
AB
A,B
––––
3%
O
––––
Anti-A
& Anti-B
46 %
Blood type
Group A
Group B
Group AB
Group O
Anti A
Anti B
Rh Factor
 People whose RBCs have the Rh
antigen (D antigen) are Rh+
 People who lack the Rh antigen
are Rh-.
 Normally, blood plasma does
not contain anti-RH antibodies.
 Hemolytic disease of the
newborn (HDN): if blood from
Rh+ fetus contacts Rh-mother
during birth, anti-Rh antibodies
are formed.
 Affect is on second Rh+ baby.
Significance of Rh:
1) Blood transfusion:
 If an Rh –ve person receives Rh +ve blood 
the body starts to make anti Rh agglutinins
that will remain in the blood. These
agglutinins develop slowly & reach maximum
after 2- 4 months.
 If 2nd transfusion of an Rh +ve blood is given
later  blood agglutination & hemolysis of
the donor’s RBC’s occurs.
2) Erythroblastosis fetalis
(hemolytic disease of the new born)
 If
an Rh –ve mother becomes pregnant from an Rh
+ve husband  the fetus will most probably be Rh
+ve like his father.
 Small amount of fetal blood leak into maternal
circulation at the time of delivery & mother
develops significant anti Rh agglutinins after
delivery.
 During the 2nd pregnancy  the mother’s
agglutinins cross the placenta (IgG) to the fetus
causing hemolysis of his RBC’s.
 The
fetus is usually born dead & if he live he will
have severe anemia & jaundice (due to excessive
bilirubin formation). & as a compensation, the B.M.
rapidly adds immature RBC’s (=Erythroblasts) to
the blood (hence the name).
 Bilirubin may precipitate in the brain cells causing
their damage (a condition called Kernicterus in
which the infant suffers from mental retardation &
motor disturbance).
 The hemolytic disease of the new born can be seen
in the 1st pregnancy if the mother has previously
received incompatible Rh +ve blood or has previous
abortion of an Rh +ve fetus.