2. Presentation Out line
1.
Objectives
2.
Introduction
3.
Blood volume and constituent
4.
Plasma constituents
5.
Erythrocytes and blood grouping
6.
Leukocytes and immune responses
7.
Platelets and Hemostasis
2

3. 1.Objectives

At the end of this session, students will able to:

List the functions of blood

Appreciate blood composition

Understand the structure and functions of RBCs,
WBCsand platelets.
3

4. 2. Introduction

The Only Fluid tissue in the body.

Specialized type of connective tissue in which formed
elements are suspended in non living fluid matrix called
plasma.
4

5. 3. Blood volume and constituent


Physical Characteristics of Blood
viscosity: sticky opaque fluid, due to the presence of
RBCs(sticky and thick), Viscosity (thickness) = 4 – 5.

color :
o
Scarlet red-high oxygen
o
Dark red-poor oxygen
5

6. 
PH: 7.35-7.45

Temperature: Blood temperature is slightly higher than
body temperature.

Blood volume: 5–6 L for males; 4–5 L for females. Blood
accounts for approximately 8% of body weight.
6

7. 
The amount of blood varies with body size, changes in
fluid concentration, changes in electrolyte concentration,
and amount of adipose tissue.

Density ( specific gravity): Refers to the weight of blood
compared to water.

Specific gravity of H20 is taken as 1(i.e.,1 ml of H2O
weighing 1 gm at 4 oc).
7

8. 
Male:1.052-1.063

female:1.050-1.058 ( i.e.,1 ml of whole blood
weighing 1.060gm).

Osmolarity = 300 mOsm or 0.3 Osm, reflects the
concentration of solutes in the plasma.

Salinity = 0.85%, Reflects the concentration of NaCl in the
blood.
8

9. 
Functions of blood

Blood performs a number of functions dealing with:
1.
Substance distribution (Transportation )
2.
Regulation of blood levels of particular substances
3.
Body protection
9

10. Cont’d……
1.Distribution (Transports )
o
Oxygen from the lungs and nutrients from the
digestive tract to the tissues .
o
Metabolic wastes from cells to the lungs and kidneys
for elimination
o
Hormones from endocrine glands to target organs
10

11. Cont’d….
2.Regulations
o
Appropriate body temperature by absorbing and distributing
heat to other parts of the body
o
Maintaining body PH in the body tissues using buffer
system.
o
Maintaing adequate fluid volume in the circulatory volume.
11

12. 3. protection
o
Hemostasis


o
Activating plasma proteins and platelets.
Initiating clot formation when a vessel is broken.
infection : Synthesizing and utilizing antibodies.

Activating complement proteins. Activating WBCs to
defend the body against foreign invaders.

13. Composition of Blood

2 major components

Liquid = plasma (55%)

Formed elements (45%)

Erythrocytes / red blood cells (RBCs)

Leukocytes / white blood cells (WBCs)

Platelets, fragments of megakaryocytes in marrow (
thrombocytes ).

14. Components of Whole Blood
Plasma (55% of
whole blood)
Buffy coat:
leukocyctes and platelets Formed
(<1% of whole blood)
element
s
1 Withdraw blood
and place in tube
2 Centrifuge
Erythrocytes
(45% of whole
blood)
14

15. Cont’d……
Capillary
tube
Plasma 55%
Buffy coat
RBCs =45%
Plug
15

16. 4. Plasma constituents

Blood plasma : straw colored sticky fluid, includes:


Water = 90-92%.
Proteins = 6-8%. Albumin,globilin and clotting
proteins

Organic nutrients – glucose, carbohydrates, amino acids

Electrolytes – sodium, potassium, calcium, chloride,
bicarbonate.
16

17. 
Non protein nitrogenous substances – lactic acid, urea,
creatinine.

Respiratory gases – oxygen and carbon dioxide.

Plasma proteins

Albumins:

accounts 60% of Wt,Most abundant plasma protein.

Carrier to shuttle molecules through the circulation
17

18. 


Important blood buffer.
maintain osmotic pressure of the blood.
Globulins : Accounts 36% of the plasma protein.



α and β globulins have role in transport.
γ globulins are in immuno globulins( IgG, IgA).
Clotting proteins : account for 4%
‾
Fibrinogen and Prothrombin.
18

19. 
Serum: Plasma with clotting
factors removed, yellowish color.

Determined by means of
electrophoresis
19

20. Cont’d……..

Formed elements

Comprise 45% of blood

Erythrocytes, leukocytes, and platelets make up the formed
elements

Only WBCs are complete cells

RBCs have no nuclei or organelles, and platelets are just
cell fragments.
20

21. Cont’d…….

Most formed elements survive in the bloodstream
for only a few days.

Most blood cells do not divide but are renewed by
cells in bone marrow.
21

23. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Blood
45%
55%
Plasma
Formed elements
Platelets
Red blood cells
(4.8%)
(95.1%)
White blood cells
Electrolytes
(0.1%)
Water
(92%)
Proteins
Wastes
(7%)
Nutrients
Gases
Vitamins
Hormones
Neutrophils
Eosinophils
Basophils
Monocytes
Lymphocytes
(54–62%)
(1–3%)
(<1%)
(3–9%)
(25–33%)
Albumins
Globulins
Fibrinogen
N2
O2
CO2

24. 5. Red Blood Cells ( RBCs)

Shape: flexible biconcave cell that is thinner at the center
and thicker at the edges

Diameter: ~ 7.5 um
- Mature, No nucleus and organelles.

Has greater surface area/volume ratio, Therefore, can
bend and twist to pass through the narrow capillaries very
easily.
24

25. 25

26. 
The major forms of cell in the blood.

The average number of RBCs are 5 million/ mm3
blood or 5 x106 / μl of blood.

Lack of mitochondria.

Each RBC contains 280 million haemoglobin.

Half-life app.120 days.
26

27. Hematocrit (Hct) / Packed cell volume
(PCV)


1.
Hematocrit (Ht): is the percentage by volume of packed RBC.
Procedure :
Centrifuge of un –coagulated blood at a high speed (10-15 min).
2.
RBC precipitate down to the bottom.
3.
The plasma portion remains floating.

The cells that settle down to the bottom (mainly RBCs) form the
hematocrit or packed cell volume (PCV).
27

28. 
Normal value:



Males: 47%
5%
Females: 42%
5%
HCT increase in
polycythemia and
dehydration states.

Decrease in anemia
28

29. Function of RBCs :
1.
Carries hemoglobin that in turn transports respiratory
gases (O2 and CO2).
2.
Carbonic anhydrase (CA): An enzyme located in RBC
membrane.

CO2 + H2O
CA
H2CO3 = HCO-3 + H+

CA increases the rate of this reaction 5000 fold.

Good to transport CO2 from the tissues to the lung very fast.

30. 
Haemoglobin : Consists of globulin and heme.

Globulin

Two alpha(α) chain polypeptide

Two beta(β) chain polypeptides

Heme: Each heme is present in one peptide chain and
contains an iron {Fe++} that combines reversibly with one
molecule of O2.
30

31. 
Each polypeptide has one heme group, each heme with
Fe2+ carries one O2 molecule, total = 4- O2 molecules
Are carried with in Hb molecule.

1g Hb binds with 1.34 ml O2

15g Hb/dl x 1.34 ml O2 = 20.1 ml O2/100 ml blood.
31

32. 32

33. 33

34. 
The polypeptide chain (the Globin unit) determines the
physical characteristics of the Hb-molecule. Thus, there
exists:
a. Adult Hb (Hb A): 2α + 2β
b. Fetal Hb (Hb-F): 2α + 2γ
c. Sickle cell (Hb-S): glutamic acid is replaced by
valine at Beta- chain so on.
34

35. 
Saturation of Hb: refers to the number of O2 molecules
combined with Hb.

The Hb molecule combine maximally with 4 molecules of
O2 in a cascade manner(100%saturated),by Oxygenation
reaction, each binding facilitates further binding of O2.

50 % saturation: means that Hb binds with 2 molecules of
O2.
35

36. Hematopoiesis/ hemopoieisis

RBC and other blood cells
are produced in the Bone
marrow.

All cells emerge from undifferentiated (uncommitted ) stem
cells in the Bone marrow.

Stem cells: All formed elements derived from single
population
36

37. 
Stem cells: All formed elements derived from single population

Proerythroblasts : Develop into red blood cells

Myeloblasts: Develop into basophils, neutrophils,
eosinophils

Lymphoblasts: Develop into lymphocytes

Monoblasts: Develop into monocytes

Megakaryoblasts: Develop into platelets
37

38. Hematopoiesis

39. Erythropoiesis.
A. Embryonic life: RBC are produced in the liver,
spleen and lymph nodes.
B. Infants (5 years old): Red bone marrow of all cells.
C. Adults (after age 20): Membranous bones like
ribs, sternum, vertebrae and pelvic bones.
- But not in long bones like femur or tibia (fat).
39

40. 
Stem cells differentiate to produce committed stem cells called
hematocytoblasts that in turn produce :
1. Proerythroblast: where Hb synthesis begins, big nucleus.
2. Basophile erythroblast: cell divide, continues
3. Polychromatophil erythroblast: Hb synthesis increases and
fills the cytoplasm, nucleus size decreases.
40

41. 4. Ortochromatic erythroblast: Nucleus decreases.
5. Reticulocytes: Contains Hb, no nucleus and the cell is
expelled from the bone to circulation.
6. Erythrocytes: Mature form of RBC without nucleus,
filled with Hb.
41

42. 42

43. 
Physiological Mechanism
1.
Low oxygen(Hypoxia ) that occurs in the kidney cells.
2.
Kidney then produce a hormone called erythropoietin.
3.
Erythropoietin is transported by the blood to bone
marrow.
4.

Bone marrow produces and releases a increased RBC .
Increased or adequate O2 then blocks the formation of more RBC.

44. 44

45. 45

46. Organs involved in erythropoiesis

Kidney : Erythropiotein

Liver : Store protein, vit.B12& folic acid ,Synthesize globin
, Produce Erythropiotein 10%.

Bone Marrow: Site of RBCs formation

Stomach: intrinsic factor.

Small Intestine: absorption of Iron, vitamins, and amino
acids.
46

47. Substances necessary for RBC maturation
A. Vitamin B12: requires intrinsic factor for absorption
-
Important for DNA synthesis and thus for cell division.

Deficiency of Vit B12 : Megaloblastic anemia.

Characterized : macrocytic cells (big Hb in
cytoplasm) Because of their big size, the cells rupture
when passing through the capillary wall.
47

48. 
Insufficient of intrinsic factor causes , Maturation failure
for Vit. B12 is call pernicious anemia.
B. Folic acid: important in DNA synthesis.
c. Iron: Necessary for RBC formation.
D.Trace elements : (Co, Vit. Copper etc).
48

49. Destruction of RBCs

The absence of nucleus in erythrocytes prevents them
from synthesizing proteins and other important
substances necessary for survival.

The cells become weak and fragile and die after about
120 days.
49

50. 
The older red cells are phagotizised by macrophage cells of the
reticuloendothelial system that are located in the liver, spleen,
and bone marrow cells.

The macrophages release the Hb-molecule that is broken down
into:
a. its protein part (Globin) and
b. Heme part
50

51. 
Steps in the destruction of RBC:
1. RBC = Globin + Heme
2. Globin = Broken to AA‟s > used for protein synthesis
3. Heme = Fe2+ + poryphrine rings.
4. Fe 2+ = stored in the liver > used for new Hb synthesis.
5. Pyrol rings > oxidation to green pigment called
Biliverdin and later reduced to bilirubin.
51

52. a.
Bilirubin + serum albumin > reach liver.
b.
Bilirubin conjugates with glucuronic acid in liver.
C.
Liver releases bilirubin as bile to Small intestine.
Bacteria's change bilirubin into:
D.


Strrcobilinogen > stercobilin , feces (brown color).
Uribilinogen > Urobilin > Urine (yellow).
52

53. Life Cycle of a Red Blood Cell

54. 54

55. Clinical correlations:
Anemia
A decrease in;
1- RBC number or/and
2- Hb content Below the normal for that sex and age.
1.Decreased RBC Number.
- Blood loss : e.g, hemorrhage
- A plastic anemia: bone marrow destruction (X-ray)
- Maturation failure anemia: pernicious anemia.
55

56. 
Microcytic Hypochromic Anemia: Low levels of
hemoglobin in RBCs due to chronic blood loss
resulting in low Fe2+ levels in newly produced
RBCs.
2. Hemolytic Anemia: Different abnormalities of
RBCs that make RBCs fragile and rupture easily.
56

57. 
Hereditary Spherocytosis: RBC develop as small
spherical cells . These spherical cells easily rupture by
slight compression.



Sickle-cell Anemia:
Genetic mutation causing abnormal beta chains.
HgS exposed to low O2 concentrations, it precipitates into
long crystals that cause the cells to become sickle-shaped.
57

58. Effects of Anemia
•
Due to decrease O2 supply to tissues.
1- Fatigue, muscle weakness
2- Mental effects: lack of concentration and dizziness , even Faintining
3- CVS effects: tachycardia, palpitation, heart failure if not treated
4- nausea & anorexia
5- Retarded growth in children
58

59. Polycethemia

is abnormal increase of RBC in the circulation.

Two types
1.
Polycethemia Vera (8-9 million)

Tumerous or cancerous production causes highly engorged blood.

genetic mutation in the hemocytoblastic cell line that
increases RBC production. Hematocrit values can reach
70%
59

60. 2. Secondary Polycethemia;


Mostly Physiologic
Increase in RBC production due to hypoxic tissues.
e.g. high altitudes.
60

61. Effect of polycethemia on the circulatory
system
1. Increased viscosity causes sluggish blood movement.
2.thrombosis and obstruction of different blood vessels.
3.decreased blood flow to tissues and Decreased delivery of
O2 to tissues.
4.Hct increases and so blood volume, blood pressure and work
of the heart increases.

RX: aim to remove RBC by; phlebotomy, blood donation
61

62. 6.Blood Groups

Erythrocytes contain genetically determined surface
antigens( agglutinogens).

Blood plasma contains antibodies(agglutinins )that react
with specific antigens.

Blood is named according to surface antigens that are
present.
62

63. Types of blood group

In humans, there are two known blood groups that
are clinically important:
a. The ABO-Blood groups
b. The Rh- Blood group factors
63

64. ABO Blood Group

In the ABO system, blood is classified primarily on the
Basis of the A and B antigens present on the surface of
red blood cell membranes (erythrocytes).

Secondly, blood is classified on the basis of the naturally
occurring antibodies (agglutinins) in the serum .

A person whose red cells possess the A -antigen has antiB antibody in his serum and is classified as Blood group A.
64

65. 
If B antigen is present in the Red cell membranes, Anti-A
antibody is present in his serum and the person is designated
as Blood group B.

If Both AB antigens are present on Red cells, then he has
no antibody, so is AB blood group.

If No antigens are present on red cells, he is O Type and
has both anti A and B antibody in his serum.
65

66. 
ABO Blood Group

4 blood types – A, B, AB, O

Types are identified by antigens located on the RBC surface.
66

67. 67

68. ABO-blood group
68

69. 
Typing and cross-matching – process by which blood
type is identified and donor blood is tested for possible
transfusion.

Transfusion:

Type O is a Universal Donor.

Type AB is the Universal Recipient.
69

70. 
Blood group O

Universal Donor.

No antigens on their cell-membrane surfaces and therefore
can not agglutinate if transfused to any blood types.

Receive only from persons with blood group “O” only
because , they have anti- A & anti-B antibodies in the
plasma.
70

71. 
Blood group AB

Universal recipient

they have no antibodies in their blood to cause
agglutination reactions.

Have antigen A and B, AB can donate blood only to a
person with blood AB, not to other.
71

72. 

Method of blood typing
Procedures:
1. On a slide at opposite ends , drops of anti- A antibody and
Anti-B antibody are added at opposite sides.
2. 2-3 drops of Blood (RBC‟s) are added on the prepared
antibodies and changes for agglutination are observed after
a few minutes.
72

73. A.
If agglutination occurs on anti-A antibody (sera), then
the blood is Blood Group A.
B.
If agglutination occurs on anti-B antibody , the blood is
Blood Group B.
C.
If there is agglutination in both A and B-antibodies, then
it is Blood Group AB.
D.
If no agglutination occurs, then it is Blood Group O.
73

74. 74

75. Agglutination Reaction
75

76. Donators and Recipients

Donators
1.
2.
3.
4.

O can donate blood to group A, B, AB, and O
A
“
A & AB only
B
“
B & AB only
AB
“
AB only
Recipients
1.
2.
3.
4.
O can receive blood from group
A
“
B
“
AB
“
O only
A & O only
B & O only
A, B, O, & AB
76

77. RH Blood Group

Named after Rhesus monkey.

Consists of over 50 related antigens, the most clinically
significant is D,C,E,c ,d and e.

The type D antigen is more antigenic and widely prevalent
in the population.

Rh+, having type D antigen, 85% of the population

Rh-,lack of type D antigen , 15% of the population
77

78. •
A person with Rh negative(-)blood does not have Rh
antibodies naturally in the blood plasma.
•
If they receive blood that is Rh positive (+) , antibodies
form but not a problem.
•
The second exposure can produce a transfusion reaction
(Hemolysis and possible kidney damage).
78

79. Rh incompatibility

Father Rh + = Rh + means he has D antigen on his RBC
membrane.

Mother Rh- = No Rh factor(no D antigen).
Marriage:
1.
Rh+ father X Rh- mother = Rh + fetus.
2.
During birth through placenta , Rh+ blood (antigens) of
the fetus leak (enter) to mothers blood and sensitizes her.
79

80. 3. Mother „s blood produces anti-Rh antibodies (anti-D
antibodies ) against the Rh+ blood.
4.
During the 2nd pregnancy and there after, the Anti-Rh+
antibodies (agglutinins) enter into the fetus and
agglutinate or hemolyze the RBC’s the fetus.
80

81. 
This type of hemolytic disease is called Erythroblastosis
fetalis.

If the baby is born alive from the incidence, then there is a
higher risk of being Anemic and jaundiced.
81

82. 
Prevention
•
Shortly after each birth of an Rh+ baby, the mother is given
an injection of anti-Rh antibodies (or Rhogam).

These passively acquired antibodies destroy any foetal
cells that got into her circulation before they can elicit an
active immune response in her.
82

83. Bio 130 Human Biology

84. Erythroblastosis Fetalis
19-84

85. 7. White Blood Cells( Leukocytes ) and
immune response
85

86. Properties

The only formed element that are complete cells.

Normal number: 4000-10,000 / mm3 of blood

Mobility: Are highly mobile and reach tissue fluids.

When infection occurs, WBC increase in number e.g.,
Neutrophils.

Life span : Many (not all) live only a few days, may be
b/s of their engagement with pathogens.

Grouped into two main categories.
86

87. 
Granulocytes : contain specialized membrane-bound
cytoplasmic granules.

Contain cytoplasmic granules that stain specifically
(acidic, basic, or both) with Wright‟s stain

Are larger and usually shorter-lived than RBCs.

Have lobed nuclei, Are all phagocytic cells.

include neutrophils, eosinophils and basophiles.
87

88. 
Agranulocyte : Lack obvious granules; Lymphocytes
and Monocytes.
88

89. Granulocytes
1.Neutrophils: Make up 60 to 70% of WBC‟s.

Diameter of 10-15 μm, Phagocytic

First to arrive at infections.

Nucleus 2-5 lobes (increase with cell age)

Increase: stress, burns and bacterial infections.

Decrease: Radiation exposure, B12 deficiency.
89

90. 2.Eosinophils : Account for 1-4% of WBCs

10 –12 um in diameter, Nucleus 2–3 lobed

Increase: allergic reactions, parasitic infections and
autoimmune disease.
1. Kill parasitic worms
2. Destroy antigen-antibody complexes.
3. Inactivate some inflammatory chemical of allergy (histamine).
90

91. 3. Basophils: Account for 0.5% -1% of WBCs.

Liberate heparin and histamines during allergic reactions.

Intensify inflammatory response

Increase: Allergic reactions, leukemia, cancers,
hypothyroidism.

Decrease: Pregnancy, ovulation, stress, hyperthyroidism
91

92. Agranulocyte
1.

Lymphocytes: Make up 20 to 25% WBC‟s
Small: 6-9 um in diameter, Large: 10-14 um, Nucleus is
round or slightly indented.

B cells produce antibodies.

T cells attack viruses, cancer cells, and transplanted tissues

Natural killer cells attack infectious microbes and tumor
cells.
92

93. 
2. Monocytes

Account for 4-8% of WBCs and the largest WBCs.

They leave the circulation enter tissue and differentiate
into macrophages.

Activate lymphocytes to mount an immune response.

Phagocytize bacteria, dead cells, and other debris.
93

94. 94

95. mobility through the tissues
1. Diapedesis: WBC Squeeze out through the capillary pore (e.g.
Neutrophils, Monocytes ).
2. Amoeboid motion: Produce pseudopodia and reach the microbes
in the tissues
3. Chemotaxis: WBC are attracted by chemicals or toxins produced
by the microbe or inflamed tissues
4.Phagocytosis: engulfing and destroying e.g., Neutrophils,
macrophages .
95

96. 96

97. Clinical correlation

Leukemia (increased WBC No):

cancerous production of WBC.

These occurs:
a. in the bone marrow
b. in the lymph.

Their increased production takes the space of platelets &
RBC causing anemia + impaired blood clotting
97

98. 
Leucopenia: Decreased production of WBC
- Bone marrow stops producing them
- Drug poison, X-rays
98

99. Practical hematology/leukocyte differential

Lists the different percentages of leukocytes

↑Neutrophils : Bacterial Infection

↑ Lymphocytes: Viral Infection

↑ Monocytes: Chronic Infection

↑ Basophils: Allergic Rxns

↑Eosinophils: parasitic infections
99

100. 8. Platelets and Hemostasis
100

101. Platelets/Thrombocytes

Small, non nucleated (anucleated), round/oval cells/cell
fragments.

Their size ranges 1-4 m in diameter.

The cytoplasm stain pale blue and contain many pink
granules.

They are produced in the bone marrow by fragmentation of
megakaryocytes, which are large and multinucleated cells.
101

102. •
Their primary function is preventing blood loss from
hemorrhage by forming a platelet plug
•
Normal value – 150,000 to 300,000/mm3.

Platelets have a life span of approximately 10 days.

Senescent platelets are removed by the spleen.
102

103. 
Attracted to hemorrhage.

Plugs leaks.

Promotes constriction of blood vessel.

Triggers inflammation.

Initiates clotting.
103

104. Hemostasis
•
•
Hemostasis refers to the stoppage/arresting of bleeding.
Actions that limit or prevent blood loss include:
•
Blood vessel spasm
•
Platelet plug formation
•
Blood coagulation
104

105. 105

107. 

Blood coagulation
Triggered by cellular damage and blood contact with
foreign surfaces.
•
•
A blood clot forms
Causes the formation of clot via a series of reactions
which activates the next in a cascade
•
Occurs extrinsically or intrinsically.
107

108. 
Extrinsic clotting mechanism
•
Triggered when blood contacts damaged blood vessel
walls or tissues.
•
Chemical outside of blood vessel triggers blood
coagulation.
•
Triggered by tissue thromboplastin (factor III) (not
found in blood).

109. •
A number of events occur that includes factor VII, factor X, factor V,
factor IV, and factor II (prothrombin).

Intrinsic clotting mechanism

Triggered when blood contacts a foreign surface
•
Chemical inside blood triggers blood coagulation
•
Triggered by Hageman factor XII (found inside blood)
•
Factor XII activates factor XI which activates IX which joins with
factor VIII to activate factor X.

110. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Extrinsic Clotting
Mechanism
Intrinsic Clotting
Mechanism
Blood contacts
foreign surface
Tissue damage
Releases
Activates
Tissue thromboplastin
(Factor lll)
Activates (Ca+2)
Hageman Factor Xll
Activates
Factor Vll
Factor Xl
Activates (Ca+2)
Activates
Factor X
Factor lX
Activates
Factor V
(Ca+2)
Factor Vlll
platelet phospholipids
Factor X
Activates (Ca+2)
Activates
Factor V
(Ca+2)
Prothrombin
activator
Converts
Thrombin
(Factor lla)
Prothrombin
(Factor ll)
Converts
Fibrinogen
(Factor l)
Fibrin
Factor Xlll
Stabilizes
Fibrin
clot
110

111. 111

112. Fate of Blood Clots
•
After a blood clot forms it retracts and pulls the edges of a
broken blood vessel together while squeezing the fluid
serum from the clot.

Platelet-derived growth factor stimulates smooth muscle
cells and fibroblasts to repair damaged blood vessel walls.

Plasmin digests the blood clots.
112

113. Clinical correlations
1. Hemophilia A: Deficiency of Factor VIII accounts for
85% cases. Almost exclusively in males.

Females are usually carriers, caused by a gene mutation
on the “X” chromosome. Occurs in about 1/10,000 male
births

Other Hemophilias account for another 15% ,Hemophilia B (Factor
IX),Hemophilia C (Factor XI) and Hemophilia D (Factor XII)
113

114. 2.Thrombocytopenia: Abnormally low levels of platelets.
Usually below 50,000/ μl of blood.
3.Thrombus: Abnormal clot that develops in a blood vessel.
4.Embolus: Free thrombic clots carried in the blood that
usually get caught in arterioles in the brain, kidney, and
lungs.
114

115. Practical hematology/Tests for
Bleeding
1. Bleeding time : The time interval that takes between start of
bleeding (oozing) until arrest of blood. Normal duration : 36 min
2. Clotting time: The duration of time it takes for the blood to
clot (normal duration is 3-8 min).
3.Prothrombin time: Deals with the duration of formation of
Prothrombin after addition of oxalate and Ca2+ ions to the
blood.

116. 
Reading assignment on immunity
116