2. DEPARTMENT OF PUBLIC
HEALTH DENTISTRY
SEMINAR
BLOOD
Presented By:-
Dr. Amrita Rastogi
M.D.S 1st Year

3. CONTENTS
• INTRODUCTION
• PROPERTIES OF BLOOD
• FUNCTIONS OF BLOOD
• FORMATION OF BLOOD
• COMPOSTION OF BLOOD
Plasma
Red Blood Cells
White Blood Cells
Platelets

4. • HEMOSTASIS
• BLOOD GROUPING
• BLOOD TRANSFUSION
• ROLE OF PUBLIC HEALTH DENTIST
• CONCLUSION
• REFERENCES

5. INTRODUCTION
• Blood is a complex, living tissue that contains many cell types
and proteins. A transporter, regulator, and defender, blood
courses through the body carrying out many important
functions.
• Blood, fluid pumped by the heart that circulates throughout the
body via the arteries, veins, and capillaries . An adult male of
average size normally has about 6 quarts (5.6 litres) of blood.
The blood carries oxygen and nutrients to the body tissues and
removes carbon dioxide and other wastes. The colourless fluid
of the blood, or plasma, carries the red and white blood cells,
platelets, waste products, and various other cells and
substances.

6. • Blood is the only tissue that flows throughout our body. This
red liquid carries oxygen and nutrients to all parts of the body
and waste products back to our lungs, kidneys and liver for
disposal. It is also an essential part of our immune system,
crucial to fluid and temperature balance, a hydraulic fluid for
certain functions and a highway for hormonal messages.
• Blood is a wonderful tissue may be the easiest to transplant
(transfuse).

7. PROPERTIES OF BLOOD
Color
– Oxygen-rich blood is scarlet red bright crimson.(arterial
blood)
– Oxygen-poor blood is purple red. (Venous blood)
– Red color comes from the several million red cells, present
in it.
Volume
− In a normal adult is 5 ltrs in women & 5.5 ltrs in men and
represents about 8% of total body weight.
Reaction and pH
– Blood is slightly alkaline and its pH in normal conditions is
7.4.

8. Specific gravity
– total blood :1.052 to 1.061
– blood cells : 1.092 to 1.101
– plasma : 1.022 to 1.026
Viscosity
− Blood is 5 times more viscous than water mainly due to red
blood cells and plasma proteins.
Temperature
− 38 ◦c or 100.4 F

9. FUNCTIONS OF BLOOD
•NUTRIENT FUNCTION.
•RESPIRATORY FUNCTION.
•EXCRETORY FUNCTION.
•TRANSPORT OF HORMONES AND
ENZYMES.
•REGULATION OF WATER BALANCE.
•REGULATION OF ACID BASE
BALANCE.
•REGULATIONOF BODY TEMPERATURE
STORAGE FUNCTION.
•DEFENCIVE FUNCTION.

10. 1. NUTRIENT FUNCTION
Nutritive substances like glucose, amino acids, lipids and
vitamins derived from digested food are absorbed from
gastrointestinal tract and carried by blood to different parts of
the body for growth and for production of energy.
2. RESPIRATORY FUNCTION
Transport of respiratory gases is done by the blood. It carries
oxygen from alveoli of lungs to different tissues and carbon
dioxide from tissues to alveoli.

11. 3. EXCRETORY FUNCTION
Waste products formed during various metabolic activitiesfrom
the tissues are removed by blood and carried to the excretory
organs like kidney, skin, liver, etc.
4. TRANSPORT OF HORMONES AND ENZYMES
The hormones and some of the enzymes are carried by blood
to different parts of the body from the source of secretion.

12. 5. REGULATION OF WATER BALANCE
Water content of the blood is freely interchangeable with interstitial
fluid. This helps in the regulation of water content of the body.
6. REGULATION OF ACID BASE BALANCE
The plasma proteins and hemoglobin act as buffers and help in
regulation of acid base balance.

13. 7. REGULATIONOF BODY TEMPERATURE
Because of the high specific heat of blood, it is responsible for
maintaining the thermoregulatory mechanism in the body, i.e.
the balance between heat loss and heat gain in the body.
8. STORAGE FUNCTION
Water and some important substances like proteins, glucose,
sodium and potassium are constantly required by the tissues.
Blood serves as a readymade source for these substances. And,
these substances are taken from blood during the conditions
like starvation, fluid loss, electrolyte

14. 8.DEFENCIVE FUNCTION.
Immunological functions, including circulation of white blood
cells, and detection of foreign material by antibodies.

15. FORMATION OF BLOOD
• In foetus - bone marrow,liver & spleen
• In adults- bone marrow.
• In children, blood cells are actively produced in marrow
cavities of all the bones
• 75% of the cells - white blood cell producing myeloid series &
25% are maturing red cells
• Bone marrow contains pluripotent stem cells that differentiate
into progenitor cells that in turn differentiate into various
differentiated types of blood cells.

16. BONE MARROW
• The bone marrow is present in the bone cavities.
• It can be considered as one of the largest organs in the body,
and also one of the most active.
• In children, blood cells are produced in the marrow cavities of
all the bones.
• Gradually, it gets replaced by fat (yellow marrow).
• In the adult blood cells are produced in the bone marrow of
selected bones (e.g. backbone – vertebral column, ribs, bones
of the skull, etc.)

18. HEMATOPOIESIS
Hematopoiesis is the process which includes
origin, development and maturation of all the
blood cells.
Hematopoiesis is the process which includes
origin, development and maturation of all the
blood cells.

19. • STEMCELLS
• The stem cells are the primitive cells in the bone marrow,
which give rise to the blood cells. As the stem cells can give
rise to different types of blood cells, these are called
pluripotent hemopoietic stem cells (PHSC). In the earlier
stages, the stem cells are not designed to form a particular type
of blood cell. And it is also not possible to determine the blood
cell to be developed from these stem cells.

20. So at this stage, the cells are called uncommitted pluripotent
hemopoietic stem cells (Uncommitted PHSC). When the
cells are designed to form a particular type of blood cell, the
stem cells are called committed pluripotent hemopoietic
stem cells (Committed PHSC). The committed stem cells are
of two types namely:
1. Lymphoid stem cells (LSC) which give rise to lymphocytes.
2. Colony forming blastocytes, which give rise to the blood cells
other than lymphocytes.

21. When grown in cultures, these cells form colonies hence the
name colony forming blastocytes. There are different units of
colony forming cells as follows:
a. Colony Forming Unit-Erythrocytes (CFU-E).The stem cells of
this unit develop into erythrocytes.
b. Colony Forming Unit-Granulocytes/ Monocytes (CFU-GM).
These cells give rise to granulocytes (neutrophils, basophils
and eosinophils) or Monocytes.
c. Colony Forming Unit-Megakaryocytes (CFU-M).From these,
platelets are developed.

22. BLOOD CELLS - TYPICAL COUNT
• Total Erythrocytes = 5,000,000,000 cells/ml blood
– RBC count = 5,000,000/mm3
• Total leukocytes = 7,000,000 cells/ml blood
– WBC count = 7,000/mm3
• Differential White Blood Cell Count
(% Distribution of Types of Leukocytes)
Polymorphonuclear granulocytes Mononuclear agranulocytes
Neutrophils 60-70% Lymphocytes 25-33%
Eosinophils 1-4% Monocytes 2-6%
Basophils 0.25-0.5%
• Total Platelets = 250,000,000/ml blood
– Platelet count = 250,000/mm3

24. UNCOMMITTED PLEURIPOTENT HAEMOPOIETIC STEM CELL
COMMITTED PLEURIPOTENT HAEMOPOIETIC STEM CELL
M
LYMPHOID STEM CELL
COLONY FORMING BLASTOCYTE
C F U-E CF U-GM C F U-M
GRANULOCYTES MEGAKARYOCYTE
L R N B E P

25. ERYTHROPOIESIS
Erythropoiesis is the process by which the origin,
develop-ment and maturation of erythrocytes occur.

26. Site of erythropoiesis in fetal life
During embryonic life, erythropoiesis occurs in three stages.
i) Mesoblastic stage: During the first two months of
intrauterine life, the primitive red blood cells are produced from
mesenchyme of yolk sac.
ii) Hepatic stage: From third month of intrauterine life,
liver is the main organ that produces red blood cells. Some
erythrocytes are also produced from spleen and lymphoid organs.
iii) Myeloid stage: During the last three months of intra
uterine life, the red blood cells are produced from red bone
marrow and liver.

27. In post natal life and In adults
1. Up to age of 5 to 6 years: The red blood cells are produced in
red bone marrow of all bones.
2. From 6th year up to 20th year: The red blood cells are
produced by red bone marrow of long bones and all the
membranous (flat) bones.
3. After the age of 20 years: The red blood cells are produced
from all membranous bones like vertebra, sternum, ribs, scapula,
iliac bones and skull bones and from the ends of long bones.
After 20 years of age, the shaft of the long bones becomes yellow
bone marrow because of fat deposition and lose the
erythropoietic function.
During disorders of bone, the RBC’s are produced in spleen.

28. Stages of Erythropoiesis
CELL DIAMETER NUCLEUS CYTOPLASM
CELL DIAMETER NUCLEUS CYTOPLASM
15-20 μm Big & strongly Very scanty & basophilic
15-20 μm Big & strongly Very scanty & basophilic
basophilic No Hb.
basophilic No Hb.
11-16 μm Smaller Scanty & basophilic.
11-16 μm Smaller Scanty & basophilic.
No Hb.
No Hb.
10-12 μm Smaller & Hb starts to appear,
10-12 μm Smaller & Hb starts to appear,
Denser cytoplasm polychromatic.
Denser cytoplasm polychromatic.
8-10 μm Ink spot Plentiful, eosinophilic.
8-10 μm Ink spot Plentiful, eosinophilic.
nucleus increase in Hb.
nucleus increase in Hb.
8-10 μm Absent Some RNA still present.
8-10 μm Absent Some RNA still present.
7.5 μm Absent Hb++.
7.5 μm Absent Hb++.

29. Factors Affecting Erythropoiesis
• General factors
– Erythropoietin
– Thyroxine
– Hemopoietic growth factors
– Vitamins
• Maturation factors
– Vitamin B12
– Intrinsic Factor of Castle
– Folic Acid
• Factors necessary for Hb formation
– First class proteins & amino acids
– Iron
– Copper
– Co ,Ni
– vitamins

30. LEUKOPOIESIS
Leukopoiesis is the development and maturation of leukocytes.

31. STEM CELLS
The committed pluripotent stem cell gives rise to colony forming
unit and lymphoid stem cell.
• COLONY FORMING UNIT
• Different colony forming units are:
1. Colony forming unit-Erythrocytes (CFU-E)
2. Colony forming unit-Granulocytes and Monocytes (CFU-GM)
3. Colony forming unit-Megakaryocytes (CFU-M)
• DEVELOPMENT OF GRANULOCYTES
• Granulocytes are formed in bone marrow. The colony forming
unit-granulocyte-monocyte (CFU-GM) gives origin to
myeloblast. From myeloblast, three types of cells are formed.
1. Neutrophil myelocyte
2. Eosinophil myelocyte and
3. Basophil myelocyte

32. • Neutrophil: Neutrophi myelocyte develops into neutrophils
metamyelocyte that forms neutrophil.
• Basophil: Basophil myelocyte is converted into basophil
metamyelocyte that is developed into basophil.
• Eosinophil: Eosinophil myelocyte is converted into
eosinophils myelocyte and this forms eosinophil.
DEVELOPMENT OF AGRANULOCYTES
Formation of Monocytes
Monocytes are also developed from bone marrow; stem cell is
colony forming unit-granulocyte-monocyte [CFU-GM] that
develops into myeloblast. The myeloblast is converted into
monoblast, which develops into monocyte.

33. Formation of Lymphocytes
The stem cells for lymphocytes are in the bone marrow. The
pluripotent stem cell gives origin to colony forming units
(CFU) and lymphoid stem cells (LSC). The Lymph stem cells
give origin to Lymphoblast, which develop lymphocytes.
These lymphocytes are released from bone marrow into the
circulation. Then, some of lymphocytes enter the thymus. In
thymus, these lymphocytes are processed and come out of
thymus as lymphocytes. The remaining cells enter liver and
bone marrow and are processed as B lymphocytes.

34. THROMBOPOIESIS
DEVELOPMENT OF PLATELETS
• Platelets are formed from bone marrow. The pluripotent stem
cell gives rise to the CFU-M. This develops into
megakaryocyte. The cytoplasm of megakaryocyte form
pseudopodium. A portion of pseudopodium is detached to
form platelet, which enters the circulation
• Production of platelets is influenced by colony stimulating
factors and thrombopoietin. Colony stimulating factors are
secreted by monocytes and T lymphocytes. Thrombopoietin is
a glycoprotein like erythropoietin. It is secreted by liver and
kidneys.

35. • Factors regulating Thrombopoiesis
– Interleukins --IL3, IL6, IL11
– CSF’s
– Thrombopoietin—liver & kidney
– TGFβ

36. COMPOSTION OF BLOOD

37. • Blood contains the blood cells which are called formed
elements and the liquid portion known as plasma.
• Blood is a specialized type of connective tissue in which living
blood cells, (formed elements), are suspended in a non living
fluid matrix called plasma.
– Cellular Part (Formed Elements)
– Non cellular part (Plasma)
• 55 % plasma
– Plasma is the straw-colored liquid in which the blood cells
are suspended.
• 45 % formed elements
– Red blood cells (Erythrocytes)
– White blood cells (leukocytes)
– Platelets (thrombocytes)

39. PLASMA
• Plasma is the relatively clear liquid water , sugar, fat, protein
and salt solution which carries the red cells, white cells,
platelets, and some other chemicals.
• Normally, 55% of our blood's volume is made up of plasma.
About 95% of it consists of water.
• As the heart pumps blood to cells throughout the body, plasma
brings nourishment to them and removes the waste products of
metabolism.

41. Organic Substances of Plasma
The following are the organic substances of the plasma.
1. Proteins: Proteins present in plasma, albumin, globulin &
fibrinogen are specifically known as plasma proteins.
2. Carbohydrates: The carbohydrate is present in plasma mainly
in the form of glucose.
3. Fats: The lipid substances present in plasma are the neutral
fats, phospholipids and cholesterol.
4. Amino acids: Plasma contains both essential and non essential
amino acids.
5. Non protein nitrogenous substances: The plasma also contains
some non protein nitrogenous substances like ammonia,
creatine, creatinine, xanthine, hypoxanthine, urea and uric
acid.

42. 6. Internal secretions: The plasma contains many hormones.
7. Enzymes: The enzymes like amylase, carbonic anhydrase,
alkaline phosphatase, acid phosphatase, lipase, esterase,
protease and transaminase are present in plasma.
8. Antibodies: The plasma contains many antibodies, which are
called immunoglobulins

43. Inorganic Substances of Plasma
ION SYMBOL CONC
(mmol/l)
Sodium Na+ 135-146
Potassium K+ 3.5-5.2
Calcium Ca++ 2.1-2.7
Chloride Cl- 98-108
Hydrogen
Carbonate HCO3- 23-31
Phosphate PO4-- 0.7-1.4
• GASES PRESENT IN PLASMA:
– O2 & CO2

44. Red Blood Cells
• Red cells, or erythrocytes , are relatively large
microscopic cells without nuclei.
• Red cells normally make up 40-50% of the total blood
volume.
• They transport oxygen from the lungs to all of the
living tissues of the body and carry away carbon
dioxide.
• The red cells are produced continuously in our bone
marrow from stem cells at a rate of about 2-3 million
cells per second.

45. • Hemoglobin is the gas transporting protein molecule that
makes up 95% of a red cell.
• Each red cell has about 270,000,000 iron-rich hemoglobin
molecules.
– People who are anemic generally have a deficiency in red
cells.
• The red color of blood is primarily due to oxygenated red
cells.

46. Morphology
• Shape : circular, biconcave (dumb bell shaped)
• Size : 7.2 μm
• Thickness : 2.2 μm, 1 μm
• Volume : 90-95 μm3
• Surface area : 130 μm2
• Avg. count
– Male : 5-6 million/mm3
– Female : 4.5-5.5 million/mm3
– Infant : 6-7 million/mm3

47. Structure
• Cell membrane consists of lipid and protein molecules.
• Blood group antigens are present on the surface.
• Spectrin is a contractile protein present on the cell membrane
which help to keep the biconcave shape.
• Metabolic needs are met by glucose.
• Normally, the red blood cells are disc shaped and biconcave
(dumb-bell shaped). The biconcave contour of red blood cells
has the following mechanical advantages.
1. It helps in equal and rapid diffusion of oxygen other
substances into the interior of the cell.
2. Large surface area is provided for absorption removal of
different substances.

48. 3. Minimal tension is offered on the membrane wh the volume of
cell alters.
4. While passing through minute capillaries, these cells can
squeeze through the capillaries very easily.

49. Properties Of Rbc’s
1. ROULEAUX FORMATION
When blood is taken out of the blood vessel, the red blood cells
pile up one above another like the pile of coins. This property
of the red blood cells is called rouleaux (pleural = rouleau)
formation.
2. SPECIFICGRAVITY
The specific gravity of red blood cell is 1.092 to 1.101.
ROULEAUX
FORMATION
ROULEAUX
FORMATION

50. 3. PACKED CELL VOLUME
When the blood is collected in a centrifuge tube along with
proper anticoagulant and centrifuged for a period of 30
minutes at a speed of 3000 rpm (revolutions per minute),the
red blood cells settle at the bottom of the tube leaving the clear
plasma at the top. The red blood cells form 45% of the total
blood. This is called the packed cell volume or hematocrit.
The volume of plasma is 55%.
4. SUSPENSION STABILITY
During circulation, the red blood cells remain suspended
uniformly in the blood. This property of the red blood cells is
called the suspension stability.

51. FUNCTIONS
• Transport of Hb
• Exchange of CO2 – carbonic anhydrase
• Acid base buffer – Hb
• Blood group antigens

52. Life Span and Fate of RBC’s
• Average life span of red blood cell is about 120 days. The
senile blood cells are destroyed in reticuloendothelial system.
• When the cells become older (120 days), the cell membrane
becomes more and more fragile. The diameter of the
capillaries is less or equal to that of red blood cell. The
younger red blood cells can pass through the capillaries easily.
However, because of the fragile nature, the older cells are
destroyed while trying to squeeze through the capillaries. The
destruction occurs mostly in the capillaries of spleen because;
the splenic capillaries have a thin lumen. So, the spleen is
usually called Graveyard of red blood cells.

53. • The destroyed red blood cells are fragmented. From the
fragmented parts, the hemoglobin is released. The iron and
globin parts of the hemoglobin are separated with the
production of bilirubin. Iron combines with the protein apo
ferritin to form ferritin, which is stored in body. Globin also
enters the protein depot the bilirubin is excreted by liver
through bile.
• Daily 10% red blood cells, which are senile, get destroyed in
normal young healthy adults. This causes release ofabout0.6 g
% of hemoglobin into the plasma. From this 0.9 to 1.5mg%
bilirubin is formed.

54. Variations In RBC Structure
• In Number
• In Size
• In Shape
• In Structure

55. PHYSIOLOGICAL VARIATIONS
• Increase in count--Physiological Polycythemia
– Age
– Sex
– High altitude
– Muscular exercise
– Emotional conditions
– Increased environmental temperature
– After meals
• Decrease in count
– High barometric pressure
– After sleep
– Pregnancy

56. PATHOLOGICAL VARIATIONS
• Pathological Polycythemia
– Primary Polycythemia – Polycythemia Vera
– Secondary Polycythemia
• Anemia

57. Variations In RBC Size
• Microcytes
– Iron deficiency anemia
– Prolonged forced breathing
– Increased osmotic pressure in blood
• Macrocytes
– Megaloblastic anemia
– Muscular exercise
– Decreased osmotic pressure in blood
• Anisocytes
– Pernicious anemia

58. Variations In RBC Shape
1. Crenation: Shrinkage -- hypertonic solution
2. Spherocytosis: Globular -- hypotonic solution
3. Elliptocytosis: Elliptical -- certain anemias
4. Sickle cell: Crescentic -- sickle cell anemia
5. Poikilocytosis: flask, hammer, unusual shape--deformed cell
membrane

59. Variations In RBC Structure
1.Punctate Basophilism(In this condition, dots of basophilic
materials (porphyrin) appear in the red blood cells giving a
stripped appearance. This occurs in conditions like lead
poisoning.)
2. Ring(Ring or twisted strands of basophilic material appearing
at the periphery of the red blood cells. This is also called the
Goblet ring. This appears in the red blood cells in certain types
of anemia)

60. 3. Howell-Jolly Bodies(In certain types of anemia, some nuclear
fragments are present in the ectoplasm of the red blood cells.
These nuclear fragments are called Howell-Jolly bodies.)

61. Hemoglobin
• Hemoglobin is a conjugated protein. It consists of a protein
combined with an iron containing pigment. The protein part is
globin and the iron containing pigment is heme.
IRON
• It is present in ferrous (Fe++) form. It is in unstable or loose
form. Under certain conditions, the iron may be present in
ferric (Fe+++) state, which is a stable form.
PORPHYRIN
• The pigment part is called porphyrin. This is formed by four
pyrole rings (tetrapyrole) called, I, II, III and IV. The pyrole
rings are attached to one another by methane (CH4) bridges.
The iron is attached to N-of each pyrole ring and N-of globin
molecule.

62. GLOBIN
• This contains four polypeptide chains. Among the four
polypeptide chains, two are alpha chains and two are beta
chains.
• Molecular weight of the polypeptide chains:
• Alpha chains : 15,126
• Beta chains : 15,866
• Number of amino acids in the polypeptide chains:
• Alpha chains : 141
• Beta chains : 146

64. • Structure of Haem
In a haem molecule, there are four pyrrole structures The four
pyrroles are linked up with one another by methane(= CH - )
bridges, to form, what is known as porphyrin.
There are various types of porphyrins. The particular type of
porphyrin found in hemoglobin is called protopor­phyrin
III
and as it contains an iron in the central part of the molecule, it
is called iron protoporphyrin. Haem is iron protoporphyrin.
Properties of Hb
1. Oxygen affinity
Properties of Hb
1. Oxygen affinity
2. Haem-haem interaction
2. Haem-haem interaction

65. DERIVATIVES OF HEMOGLOBIN
Hemoglobin readily combines with gas or any other substances to
form some products, which are called the derivatives of
hemoglobin. The following are the derivatives of hemoglobin.
1. OXYHEMOGLOBIN
This is formed by the combination of hemoglobin with oxygen
by the physical process of oxygenation. Oxyhemoglobin is an
unstable compound and the combination is reversible, i.e. the
oxygen can be released from this compound. The iron remains
in ferrous state in this compound.
2. REDUCED HEMOGLOBIN OR FERROHEMOGLOBIN
When O2 is released from oxyhemoglobin, it is called reduced
hemoglobin or ferrohemoglobin.

66. 3. CARBHEMOGLOBIN
It is the derivative of hemoglobin with carbon dioxide. Carbon
dioxide can be released easily from this. The affinity of
hemoglobin for carbon dioxide is 20 times more than for
oxygen.
4. CARBOXYHEMOGLOBIN
The combination of hemoglobin with carbon monoxide produces
this. The affinity of hemoglobin for carbon monoxide is 200
times more than its affinity for oxygen.
5. SULFHEMOGLOBIN
It is formed by the combination of hemoglobin with hydrogen
sulfide.

67. 6. NITROUS OXIDE HEMOGLOBIN
It is produced when hemoglobin combines with nitrous oxide.
7. METHEMOGLOBIN OR FERRIHEMOGLOBIN
It is formed when blood is treated with potassium ferricyanide. It
is a stable compound. The iron is in ferric form.

68. TYPES OF HEMOGLOBIN
1.Adult hemoglobin-HbA —globin contains 2 α
and 2 β chains
2.Fetal hemoglobin-HbF -- 2 α and 2 γ chains
instead of β chains.
Fetal Hb
Adult Hb

69. NORMAL VALUES
• Average hemoglobin (Hb) -- 14 to 16 gm%.
• At different ages:
– At birth : 25 gm%
– After 3rd month : 20 gm%
– After1 year : 17 gm%
– Sex :
– In adult males : 15 gm%
– In adult females : 14.5 gm%

70. • SYNTHESIS OF HEMOGLOBIN
– Starts in proerythroblastic stage.
– Appears only in Intermediate normoblast stage
– Heme—Acetic acid & glycine -- mitochondria
– Globin -- ribosomes
• DESTRUCTION OF HEMOGLOBIN
– IRON: Stored in body as ferritin and hemosiderin and
reutilized for synthesis of new Hb.
– GLOBIN: Utilized for resynthesis of hemoglobin.
– PORPHYRIN: Converted into a green pigment - biliverdin.

71. ABNORMAL HEMOGLOBIN
• Due to gene mutation -- structural variation in polypeptide chains.
• In hemoglobinopathy, structural abnormality in polypeptide
chains.
– Hemoglobin S --sickle cell anemia. α chains normal & β
chains abnormal.
– Hemoglobin C --hemoglobin C disease. β chains abnormal.
– Hemoglobin E --hemoglobin E disease. β chains are abnormal.
• In thalassemia, polypeptide chains are decreased, absent or
abnormal.
– In α thalassemia, α chains are decreased, absent or abnormal
and
– In β thalassemia, β chains are decreased, absent or abnormal.

72. • Abnormalities of an individuals hemoglobin value can indicate
defects in red blood cell balance.
• Both low and high values can indicate disease states

73. ERYTHROCYTE SEDIMENTATION RATE
• Also known as: Sed Rate; Sedimentation Rate;
Westergren Sedimentation Rate.
• The erythrocyte sedimentation rate (ESR or sed
rate) is a relatively simple, inexpensive, non-specific
test that has been used to
detect inflammation associated with conditions
such as infections, cancers and autoimmune
diseases.
• Determination
– Westergren’s Method
– Wintrobe’s Method

74. Variations of ESR
Physiological
• Age: Less in children & infants
• Sex: F>M
• Menstruation: Increased
• Pregnancy: Increased
Pathological
Increases- TB, Anemias, Malignant tumours, RA, RF, and
Liver diseases.
Decreases – Allergic conditions, Sickle cell An, Peptone
shock, Polycythemia and Extreme Leukocytosis

75. FACTORS AFFECTING ESR
1. Specific gravity of RBC’s :
– ESR increased
2. Rouleaux formation -- Increases ESR.
– Albumin and globulin accelerate rouleaux formation.
3. Increased size of RBC’s -- ESR increased.
4. Viscosity of blood: ESR is reduced when viscosity more.
5. Number of RBC’s :
– number more -- ESR decreased.
– RBC count less -- ESR increased.

76. PACKED CELL VOLUME
• The hematocrit (Ht or HCT, British English
spelling haematocrit), also known as packed cell
volume (PCV) or erythrocyte volume fraction (EVF), is
the volume percentage (%) of red blood cells in blood. It is
normally 45% for men and 40% for women.

77. • The packed cell volume (PCV) can be determined
by centrifuging heparinized blood in a capillary tube (also
known as a microhematocrit tube) at 10,000 RPM for five
minutes.This separates the blood into layers. The volume of
packed red blood cells divided by the total volume of the
blood sample gives the PCV. Since a tube is used, this can be
calculated by measuring the lengths of the layers.
• With modern lab equipment, the hematocrit is calculated by
an automated analyzer.

78. • SIGNIFICANCE OF DETERMINING PCV
– Determination of anemia
– Determination of polycythemia
– Extent & recovery from dehydration.
– Decision of blood transfusion
• VARIATIONS IN PCV
– PCV increases in polycythemia and dehydration.
– Decreases in anemia, pregnancy and cirrhosis of liver.

79. Blood Indices
• Different Blood Indices
– Mean Corpuscular Volume (MCV)
– Mean Corpuscular Hemoglobin (MCH)
– Mean Corpuscular Hemoglobin Concentration (MCHC)
– Color Index (CI)

80. MEAN CORPUSCULAR VOLUME (MCV)
Average volume of a single red blood cell
– Normal MCV = 90 cu μ (78to 90 cu μ).
– When increased-- macrocyte
• pernicious anemia
• megaloblastic anemia
– When decreased—microcyte
• microcytic anemia

81. MEAN CORPUSCULAR HEMOGLOBIN (MCH)
Quantity or amount of Hb present in one RBC
– Normal value of MCH is 30 pg (27 to32pg)
– Decreases or remains normal
• pernicious anemia
• megaloblastic anemia
– RBC’s are macrocytic & normochromic or hypochromic
– Decreases in hypochromic anemia.
– Normal MCH -- normochromic state.

82. MEAN CORPUSCULAR HEMOGLOBIN
CONCENTRATION (MCHC)
Conc of Hb in one RBC -- amount of Hb expressed in relation
to vol of one RBC.
– Most important absolute value in diagnosis of anemia.
– Normal value of MCHC is 30% (30 to 38%)
– Decreased in iron deficiency anemia -- RBC’s are
microcytic and hypochromic.

83. COLOUR INDEX (CI)
Ratio between % of Hb and % of RBC’s in blood.
Avg Hb content in 1 cell of a patient compared to avg Hb
content in 1 cell of a normal person.
– Normal colour index is 1.0 (0.8to 1.2).
– Useful in determining type of anemia.
– Raised in pernicious anemia and megaloblastic anemia.
– Reduced in iron deficiency anemia.
– Normal in normocytic normochromic anemia.

84. WHITE BLOOD CELLS
White Blood Cells: Battling Blood Cells

85. • Leukocyte is the colourless and nucleated formed element of
blood. Leukocytes play very important role in defense
mechanism of the body.
• Depending upon the presence or absence of granules in the
cytoplasm, the leukocytes are classified into 2 types namely-

86. White cells, or leukocytes , exist in variable numbers and types
but make up a very small part of blood's volume--normally only
about 1% in healthy people.
Leukocytes are not limited to blood.
They occur elsewhere in the body as well, most notably in the spleen, liver, and lymph
glands.

87. • NEUTROPHILS
• Size : 10- 14 μm diameter
• Nucleus : purple, multilobed
• Lobes :2,3 upto 5 or more. Young cell—less lobes. Arneth
Count
• Cytoplasm :blue , granular
• Granules : fine, amphophilic /neutrophilic, have lytic enzyme
1. Primary/azurophilic /lysosomal --phagocytosis
2. Secondary – inflammation
• Life span :2-5 days

88. • Functions : phagocytosis – 1st line of
defense
• Neutrophilia:
– Physiological cause :
• exercise
• lactation
• pregnancy
– Pathological cause :
• acute pyogenic infection
• Neutropenia:
– Causes :
• typhoid and viral fever
• bone marrow depression

89. • EOSINOPHILS
• Size : 10- 14 μm diameter
• Nucleus : purple, bilobed
• Cytoplasm : acidophilic
• Granules : coarse, bright red, have lysozymes
– Major basic proteins (MBP) - histaminase
– Eosinophil peroxidase (EPO)– histamine secretion
– Cationic proteins -neurotoxin
• Life span : 7-12 days

90. • Functions :
– limit allergic intensity
• eg Bronchial asthma, hay fever
– mild phagocytosis
• Eosinophilia :
– Causes :
• allergic conditions
• parasitic infections
• Eosinopenia :
– Causes :
• injection Of corticosteroids

91. • BASOPHILS
• Size : 10-14 μm diameter
• Nucleus : bilobed, S shaped
• Cytoplasm : basophilic, granular
• Granules : coarse, purple/ blue, plenty, contain
– Heparin
– Histamine
– Hyaluronic acid
– Proteases & myeloperoxidases
• Life span : 12-15 days

92. • Functions :
– librates histamine
– librates heparin
– mild phagocytosis
• Basophilia :
– Causes :
• chicken pox
• small pox
• tuberculosis
• influenza
• Basopenia
– Causes :
• administration of glucocorticoids

93. • LYMPHOCYTES
• Can be classified in two ways
– Based on structure :
a) large : 10-14 μm
b) small : 7-10 μm
– Based on maturation :
a) T Lymphocytes –80%
b) B Lymphocytes -15%
c) NK Cells-5%
• T cells – CD4 & CD8
• Life span : ½-1 day

94. • Function of T cells :
– secrete lymhokines
– induction of apoptosis in target cells
– create pores by perforin in target cells
• Function of B cells :
– produce plasma cells- immmunoglobins
• Nk cells/ large granular lymphocytes
– attack cancer cells and viruses
• Lymphocyte mediated immunity
• Cell mediated immunity
• Humoral immunity - Ag-Ab

95. • MONOCYTES
• Size : 10- 18 μm diameter (largest)
• Nucleus : pale , round/kidney shaped
• Cytoplasm : clear , pale blue , agranular
• Life span : 48-72 hrs in blood & 3 months in tissues.
• Reticuloendothelial system :
blood monocytes + tissue macrophages

96. • Functions :
– phagocytosis – 2nd line of defense
– secretions of chemical activators of inflammation
• IL-1,TNFβ, binding proteins like transferrin, lysozyme,
proteases, acid hydrlase
– lymphocyte mediated immunity – antigen presenting cells
– role in tissue repair

97. PROPERTIES OF WBC’s
1. Diapedesis
2. Ameboid Movement
– Neutrophils,
– Monocytes
– Lymphocytes
3. Chemo taxis
4. Phagocytosis
– Neutrophils
– Monocytes

98. VARIATIONS IN WBCs
Normal Count – 4000-11000/cmm of blood
Leucocytosis –­ in WBC count above 11000/cmm of blood
Leucopenia – ¯ in WBC count below 4000/cmm of blood
PHYSIOLOGICAL VARIATIONS :-
1)Diurnal :- WBC count > in the evening than in the morning
2)Meals , Pregnancy, Fear, pain, anxiety & Exercise ­ the count
3)Age :- Newborn :-20000/cmm of blood
Lymphocyte :- 40% to 60%

99. PATHOLOGICAL VARIATIONS :-
1)­ in Neutrophils – Acute infection , haemorrhage , operations ,
tissue damage
2) ­ in Eosinophils – Allergy,Parasitic infections
3) ­ in Monocytes – Chronic infections
)­ in lymphocyte – Whooping cough , Tuberculosis , leprosy
5) ­ in Basophils – Lead poisoning
LEUKOPENIA
1) ¯ in Neutrophils – Viral infections
2) ¯ in Eosinophils – Cortisol therapy
3) Bone marrow depression causes in ¯ neutrophil , eosinophil ,
basophil , monocyte

100. LEUKEMIA
• Group of disorders characterised by malignant
transformation of blood –forming cells
• Proliferation of leukaemic cells –Primarily in the bone
marrow
• Classification –
1)On the basis of cell types predominantly involved :-
a) Myeloid
b) Lymphoid
2) On the basis of natural history of disease :-
a)Acute
b)Chronic

101. • Account for 4% of all cancer deaths
• Incidence higher in men than in women
• Causes:-
# Genetic factors
# Environmental factors
# Infection

102. PLATELETS
Platelets: Sticky Situations
Platelets or thrombocytes are small colourless,
non nucleated and moderately refractive
bodies. These formed of blood are considered
to be the fragments of plasm. Their diameter is
2.5 microns (2 to 4) and, the lume is 7.5 cubic
microns (7 to 8 cubic microns). Normally, the
platelets are spherical or rod shaped and
become oval or disc shaped when inactivated.
Some say the platelets are of dumb bell,
comma, cigar or other unusual shape.
Platelets or thrombocytes are small colourless,
non nucleated and moderately refractive
bodies. These formed of blood are considered
to be the fragments of plasm. Their diameter is
2.5 microns (2 to 4) and, the lume is 7.5 cubic
microns (7 to 8 cubic microns). Normally, the
platelets are spherical or rod shaped and
become oval or disc shaped when inactivated.
Some say the platelets are of dumb bell,
comma, cigar or other unusual shape.
Platelets

103. • Size : 2-4 μm diameter (Smallest)
• Count : 1.5- 4 lakh/μl
• Shape : spherical, oval/ rounded granulated
• Structure : non-nucleated mass of protoplasm
disc like -- inactive
spherical--active
• Life span : 8 -12 days
• Destruction : Spleen

104. PROPERTIES OF PLATELETS
1. ADHESIVENESS
When platelets come in contact with any wet surface, rough surface, these are
activated and stick to the surface. The factors, which cause adhesiveness,
are collagen, thrombin, ADP, Thromboxane A2, calcium ions and von
Willebrand factor.
2. AGGREGATION (GROUPING OF PLATELETS)
The activated platelets group together and become sticky. The stickiness is
due to ADP and thromboxane A2.
3. AGGLUTINATION
Agglutination is the clumping together of platelets. The agglutination of
platelets occurs due to the actions of platelet agglutinins.

106. Functions
1. ROLE IN BLOOD CLOTTING
The platelets are responsible for the formation of intrinsic
prothrombin activator. This substance is responsible for the
onset of blood clotting.

107. 2. ROLE IN CLOT RETRACTION
In the blood clot, the blood cells including platelets are entrapped
in between the fibrin threads. The cytoplasm of platelets
contains the contractile proteins namely actin, myosin and
thrombosthenin. The contractile proteins are responsible for
clot retraction.
3. ROLE IN PREVENTION OF BLOOD LOSS
(HEMOSTASIS)
Platelets accelerate the processes of hemostasis by three ways:
a. Platelets secrete 5 HT, which causes the constriction of blood
vessels.
b, Due to the adhesive property, the platelets can seal the damage
in blood vessels like capillaries.
c, By formation of temporary plug also platelets seal the damage
in blood vessels.

108. 4. ROLE IN REPAIR OF RUPTURED BLOOD VESSEL
The platelet derived growth factor (PDGF) formed in cytoplasm
of platelets is useful for the repair of the endothelium and
other structures of the ruptured blood vessels.
5. ROLE IN DEFENSE MECHANISM
By the property of agglutination, platelets encircle the foreign
bodies and kill them by the process of phagocytosis.

109. VARIATIONS
PHYSIOLOGICAL
• Age: Platelets are less in infants (1,50,000 to 2,00,000/ cu
mm) and reaches normal level at 3rd month after birth.
• Sex: There is no difference in the platelet count I between
males and females. In females, it is reduced I during
menstruation.
• High altitude: Platelet count is increased in high I altitude.
• After meals: After taking food, the platelet count is increased.

110. • PATHOLOGICAL VARIATIONS
• Thrombocytosis :
– Causes :
• After trauma
• Splenectomy
• Stress
• Hemorrhage
• Bone fractures
• Rheumatic fever and
• Thrombocytopenia :
– Causes :
• Acute infections
• Acute leukemia
• Aplastic and pernicious
anemia
• Splenomegaly
• Scarlet fever
• Typhoid and
• Tuberculosis

111. • Thrombocythemia -
• Occurs in
Carcinoma
Chronic leukemia and
Hodgkin's disease.

112. HEMOSTASIS
• The term hemostasis means
prevention of blood loss. Whenever
a vessel is servered or ruptured,
hemostasis is achived by :-
Eventual growth of fibrous
tissue into blood clot

113. 1.VASOCONSTRICTION:
• Immediately after injury, there is constriction of blood vessel
and this decreases loss of blood from the damaged vessel.
Usually, arterioles and small arteries constrict. The
vasoconstriction is purely a local phenomenon. When the
blood vessels are cut, the endothelium is damaged and the
collagen is exposed. The platelets adhere to this collagen, and
get activated. The activated platelets secrete serotonin and
other vasoconstrictor substances. These substances cause
constriction of the blood vessels. The adherence of platelets to
the collagen is accelerated by von Willebrand factor.

114. • This factor acts as a bridge between a specific glycoprotein
present on the surface of platelet and collagen fibrils. The
platelet aggregation is also accelerated by another factor called
platelet activating factor (PAF) secreted by neutrophils,
monocytes and platelets.

115. 2. FORMATION OF PLATELET PLUG
• When platelets adhere to the collagens of ruptured blood
vessel, these platelets secrete ADP and thromboxane A2.
These two substances attract more and more platelets and
activate them. So, more platelets aggregate and form a
temporary loose plug, which closes the vessel am prevents the
blood loss.

116. 3. COAGULATION OF BLOOD
• During this process, the fibrinogen is converted into fibrin.
The fibrin threads get attached to the loose platelet plug,
which blocks the ruptured part of blood vessels and prevents
blood loss completely.
• When blood is shed out or collected in a container, it looses its
fluidity and becomes a jelly like mass after few minutes. This
process is called coagulation or clotting of blood. The clot is a
mesh of thin fibrils entangling the blood cells. These fibrils
consist of fibrin which is formed from fibrinogen.

117. CLOTTING FACTORS
FACTORS NAME
I Fibrinogen
II Prothrombin
III Thromboplastin
IV Calcium
V Proaccelerin, labile factor
VII Stable factor, proconvertin
VIII Antihaemophilic factor (AHF),
IX Christmas factor
X Stuart – Power factor
XI antihaemophilic factor C
XII Hageman factor
XIII Fibrin stabilizing factor

118. OTHER FACTORS
HMN-K Pre kallikrein,
Pre-K feltcher factor
Ka Kallikrein
PL Platelet phospholipids

119. STAGES OF CLOTTING
• Formation of prothrombin activator
– Extrinsic pathway-- initiated by tissue thromboplastin.
– Intrinsic pathway-- initiated by factor XII
• Conversion of prothrombin into thrombin
• Conversion of fibrinogen into fibrin
• During the process of blood clotting, the clotting factors,
which are in inactive forms, are converted into active forms.
And their enzymatic actions produce the successive reactions
one after another in a cascading manner.
Thus, the various reactions involved in blood clotting are
explained by enzyme cascade theory

120. Coagulation Cascade

121. CLOT FORMATION

122. Role of Thrombin

123. BLOOD CLOT
• The fibrin threads run in all directions. The red blood cells,
white blood cells and the platelets get entrapped within the
meshwork of fibrin. The entire mass of fibrin meshwork and
the blood cells entrapped within this is called blood clot. The
external blood clot is also called scab.
• This blood clot adheres to the opening of damaged blood
vessel and prevents blood loss.
• Red blood cell and white blood cells are not necessary for
clotting process. However, when clot is formed, these cells are
trapped in it. The trapped red blood cells are responsible for
the red color of the clot.

124. CLOT RETRACTION
• After the formation, the blood clot starts contracting. After
about 30 to 45 minutes, a straw coloured fluid called serum
oozes out of the clot. The process involving contraction of
blood clot and oozing of serum is called clot retraction. The
contractile proteins namely, actin, myosin and thrombosthenin
present in cytoplasm of platelets are responsible for clot
retraction.
Lysis Of Blood Clot
• The lysis of blood clot inside the blood vessel is called
fibrinolysis. This occurs by a substance known as plasmin or
fibrinolysin.

125. Significance of Lysis of Clot
• In certain organs, particularly the heart, the blood may
obstruct the minute blood vessel leading to cardial infarction.
The lysis of blood clot allows reopening of affected blood
vessels and prevents the development of infarction. The
fibrinolytic enzymes like streptokinase used for the lysis of
blood clot during the treated early stages of myocardial
infarction.

126. Why circulating blood does not clot?
1. Continuous movement of blood
2. Smooth endothelium lining
3. Circulatory anticoagulants
4. Fibrinolytic mechanism
5. All the clotting factors are in inactive form

127. • Role of Ca-
First two steps in the intrinsic pathway, calcium ions are required for the
promotion of all reactions in blood coagulation.
Therefore in the absence of calcium ions, clotting will not occur.
Thus, coagulation in vitro can be prevented in vitro (eg. for storage in
the blood bank) by removal of the calcium ions.
The use of oxalates and citrates as in vitro anticoagulants is based on this
principle.

128. • Role of vit K-
• Vitamin K is a complex naphthoquinone derivative.
• It is obtained from food as well as synthesized by bacterial
flora in the gut.
• In the liver, synthesis of the following factors is dependent
upon vitamin K:
– Coagulant like prothrombin
– Factor VII, IX, X, and
– Circulatory anticoagulant protein.
• Deficiency of vitamin K causes prolonged prothrombin time
and blood clotting time

129. • Role of liver-
Liver plays following significant role in the coagulation
mechanism:
• Synthesis of procoagulants – factor V, VII, IX, X, prothrombin
and fibrinogen.
• Removal of activated procoagulants from the blood
• Synthesis of anticoagulants like heparin, antithrombin C and
protein C.
Liver failure can cause:
• Bleeding disorders due to hypercoagulability of the blood
• Uncontrolled excessive clotting inside blood vessels where
clotting is not only unwanted but also dangerous.

130. ANTI-COAGULANTS
• Invivo:
– Heparin-
– Coumarin derivatives- Dicoumoral and Warfarin inhibit action of vit k
– Genetically engineered steptokinase for treating intravascular clots
• Invitro:
– Heparin-
– EDTA – remove calcium from blood .
– Oxalate compounds- calcium oxalate
– Citrates – Na, NH3,K citrate
– ACD, CPD

131. TESTS FOR CLOTTING
Three tests are available to test the process of coagulation of
blood.
• BLEEDING TIME
This is the time interval from oozing of blood after a cut or injury
till arrest of bleeding. The normal duration of bleeding time is
3 to 6 minutes. It is prolonged in purpura.
• Screening for – platelet disorders and Willebrand’ s disease
• DUKES method
• Ivy method

132. • CLOTTING TIME
The time interval from oozing of blood after a cut or injury till
the formation of clot is called clotting time. The normal
duration of the clotting time is 3 to 8 minutes. And it is
prolonged in hemophilia.
• Wright s capillary tube method: 1-3 min
• Lee & White method: 5-11 min

133. • PROTHROMBIN TIME
Blood is collected and oxalated so that, the calcium is
precipitated and prothrombin is not converted into thrombin.
Thus, the blood clotting is prevented. Then a large quantity of
tissue thromboplastin with calcium is added to this blood.
Calcium nullifies the effect of oxalate.
And, the tissue thromboplastin activates prothrombin and blood
clotting occurs. During this procedure, the time taken by blood
to clot after adding tissue thromboplastin is called prothrombin
time. Prothrombin time indicates the total quantity of
prothrombin present in the blood.
The normal duration of prothrombin time is about 12 seconds.
The prothrombin time is prolonged in deficiency of
prothrombin and other factors like factors I, V, VII and X.
However, it is normal in hemophilia.

134. BLEEDING DISORDERS
• Hemophilia
– Def of factor VIII
– Secondary hemostatic mechanism faulty
– CT increased but BT, PT normal, Platelet aggregatation normal
• Purpura
– Primary hemostatic mechanism faulty
– Prolonged BT but normal CT, PT, APTT
– Spontaneous bleeding from capillaries-- small tiny hemorrhagic spots
in body -- purpuric spots – PURPURA
• von Willebrand disease
– excessive bleeding even with a mild injury.
– reduction in platelet adhesion and 2O deficiency of factor VIII --
excessive bleeding

135. THROMBOSIS
Coagulation of blood inside the blood vessels is called
thrombosis or intravascular blood clotting. Normally, blood
does not clot in the blood vessel because of the following
reasons.
1. All the clotting factors are in inactive form.
2. Smooth endothelial lining of the blood vessels does not allow
the formation of clot.
3. Continuous movement of blood does not allow clot formation.
4. The natural anticoagulants like heparin present in the blood
prevent blood clotting.

136. CAUSES OF THROMBOSIS
1. Injury to Blood Vessels: During infection or mechanical
obstruction, the endothelial lining of the blood vessel is
damaged and this initiates the thrombosis.
2. Roughened Endothelial Lining: In infection, damage or
arteriosclerosis, the endothelium becomes rough and this
initiates clotting.
3. Sluggishness of Blood Flow: Decreased rate of blood flow
causes aggregation of platelets and formation of thrombus.
Slowness of blood flow occurs in reduced cardiac action,
hypotension, low metabolic rate, prolonged confinement to
bed and immobility of limbs.

137. 4. Agglutination of Red Blood Cells: Agglutination of red blood
cells can occur by the foreign antigens or toxic substances.
The blood clotting occurs inside the blood vessel during the
agglutination of the red blood cells.
5. Toxic Thrombosis: Thrombosis is common due to action of
chemical poisons like arsenic compounds, mercury, poisonous
mushrooms and snake venom.
6. Congenital Absence of Protein C: Protein C is a circulating
anticoagulant, which inactivates factors V and VIII. The
thrombosis occurs in the absence of this protein. Congenital
absence of protein C can cause thrombosis and death in
infancy.

138. COMPLICATIONS OF THROMBOSIS
• Thrombus
• Embolism and Embolus
– lungs (pulmonary embolism)
– brain (cerebral embolism) or
– heart (coronary embolism).
• Infarction and Infarct

139. BLOOD GROUPING

140. • Around 30 different common antigens and hundreds of rare ones
• 21 different systems. Common ones are:
• ABO System
• Rh system
• Lewis system
• MNS system
• P system
• Kell system
• Duffie system
• Lutheran system
• ABO system & Rh system
– Karl Landsteiner – 1900 & 1940

141. Landsteiner -1901
• Landsteiner laws:
– If a particular antigen is present in the RBC , corresponding
antibody must be absent in the plasma
– If the particular antigen is absent in the RBC, the
corresponding antibody must be present in the plasma.
GGeenneetticicss o off B Blolooodd T Tyyppeess
Our blood type is established before we are BORN, by specific
GENES inherited from our parents.
We inherit one gene from our MOTHER and one from our
FATHER.
These genes determine our blood type by causing proteins called
AGGLUTINOGENS to exist on the surface of all of our red
blood cells.
Our blood type is established before we are BORN, by specific
GENES inherited from our parents.
We inherit one gene from our MOTHER and one from our
FATHER.
These genes determine our blood type by causing proteins called
AGGLUTINOGENS to exist on the surface of all of our red
blood cells.

142. ABO blood grouping system

143. • Blood group A If you belong to
the blood group A, you have A
antigens on the surface of your
RBCs and B antibodies in your
blood plasma.
• Blood group B If you belong to
the blood group B, you have B
antigens on the surface of your
RBCs and A antibodies in your
blood plasma.

144. Blood group O
If you belong to the blood group
O (null), you have neither A or B
antigens on the surface of your
RBCs but you have both A and B
antibodies in your blood plasma.

146. Rh Blood Group
Rh FACTOR
• Rh factor is an antigen present in red blood cell. The antigen
was discovered by Landsteiner and Wiener. Since it was first
discovered in rhesus monkey, it was named as Rh factor.
There are many Rh antigens but only the D is more antigenic.
• The persons having D antigen are called Rh positive and those
without D antigen are called Rh negative. Among Asian
population, 85% of people are Rh positive and 15% are Rh
negative.

147. Percentage of People Belonging
to Different Blood Groups
Population A B AB O
Europeans 42 9 3 46
Asians 25 25 5 45
Asians
25%
5% 25%
45%
A
B
AB
O
Europeans
42%
3% 9%
46%
A
B
AB
O
AAssiiaann ppooppuullaattiioonn –– 8855%% RRhh ++vvee aanndd 1155%% RRhh --vvee

148. • According to above blood grouping
systems, you can belong to either of
following 8 blood groups:

150. Erythroblastosis Fetalis

151. • Importance of blood grouping
– For blood transfusion
– In criminal practice or in forensic medicine
– In study of anthrophology
– Predominance of certain diseases
– In the study of disputed paternity.

152. BLOOD TRANSFUSION
Blood transfusion is defined as the process of
receiving blood products into one’s circulation
intravenously. this is usually done as a life saving
maneuver to replace blood cells or blood products
lost through severe bleeding, during surgery when
severe blood loss occurs or to increase the blood
count in an anaemic patient.
Transfusions usually involve the use of two sources of
Blood – one’s own (autologous transfusion) or
Someone else’s (allogenic transfusion).
Blood transfusions involves the use of whole blood ,
Red blood cells, white blood cells, plasma, clotting
Factors and platelets.

153. Who can give you blood?
People with TYPE O blood are called
Universal Donors, because they
can give blood to any blood type.
People with TYPE AB blood are
called Universal Recipients,
because they can receive any blood
type.
Rh +  Can receive + or -
Rh -  Can only receive -
Universal Donor
Universal Recipient

154. • When conducting a blood transfusion, it
is important to carefully match the donor
and recipient blood types. If the donor
blood cells have surface molecules that
are different from those of the recipient,
antibodies in the recipient's blood
recognize the donor blood as foreign.
This triggers an immune response
resulting in blood clotting.
• If the donor blood cells have surface
molecules that are the same as those of
the recipient, the recipient's body will not
see them as foreign and will not mount
an immune response.

155. Indications for transfusion of whole blood or its derivatives
• WHOLE BLOOD TRANSFUSION
Loss of whole blood due to--
– Accidental injuries
– During and after major surgery
PACKED CELL TRANSFUSION :
Patients with severe anaemia - Hb conc < 4 gms%
Patients suffering from agranulocytosis.

156. • LEUKOCYTE TRANSFUSION :
• Patients with decreased immunity (increased susceptibility for
infections) or
• Patients suffering from agranulocytosis.
• PLATELET TRANSFUSION
– Disorders due to Thrombocytopenia.

157. • TRANSFUSION OF COAGULATION FACTORS
– Factors VIII or AHG -- hemophilic patient
– Factor IX -- patient suffering from Christmas disease.
– Factors obtained in concentrated form from fresh plasma
(human) by way of cryoprecipitation.

158. Precautions while
Blood transfusion
Precautions while
Blood transfusion
BBEEFFOORREE DDUURRIINNGG AAFFTTEERR
No
No
communicable
diseases
communicable
diseases
Matching ABO &
Rh compatibility
Matching ABO &
Rh compatibility
VVoolluummee o ovveerrllooaadd Observation for
Observation for
delayed effects
delayed effects
Metabolic
side effects
Metabolic
side effects

159. Complications of Blood Transfusion
• Can be of different types:
– Transfusion reactions
– Transmission of diseases
– Reaction caused by massive transfusion
– Complication of IV fluid administration

160. • Transfusion reactions:
– Incompatibility
– Allergic reactions
– Sensitization to leukocytes & platelets
• Transmission of diseases:
– Serum hepatitis
– AIDS
– Bacterial infections

161. • Reaction due to massive transfusion :
– Acid-base imbalance
– Hyperkalemia
– Hypothermia
• Complication of general IV fluid
administration:
– Thrombo embolism
– Air embolism

162. ROLE OF PUBLIC HEALTH DENTIST
Dental professionals can play an important role in early
detection and referral of patients with hypertension and
prehypertensives. During their practice, dentists come across
significant number of patients with undetected high BP or
uncontrolled hypertension and also known hypertensives.
These patients are at high risk for various complications as
well as for acute medical problems when receiving dental
treatment.
Dental practitioners as other healthcare workers confront a
identified risk of occupational exposure to blood-borne
pathogens like the Human Immunodeficiency Virus (HIV), the
hepatitis B virus (HBV), and the hepatitis C virus (HCV).

163. LIST OF BLOOD DONATION AGENCIES IN INDIA
• Blood Cross Society
• Indian Red Cross Society
• friends2support
• ISBTI- Indian Society of Blood Transfusion &
Immunohaematology
• Sankalap Indian Foundation
• Sujla Blood doner

164. CONCLUSION
• The function of the circulation is to service the needs of the
tissues to transport nutrients to the tissues, to transport waste
products away, to conduct harmones from one part of the body
to another and the ability to provide immunity to the body.
• In general to maintain an appropriate environment in all the
tissue fluids for optimal survival and function of the cells.
• Disorders of the blood can influence dental treatment . The
dentist should be able to detect abnormalities by history,
clinical examination, and screening laboratory tests .
• Patients with disorders of the blood may be susceptible to
abnormal bleeding, delayed wound healing, infection, or
mucosal ulceration.

165. • Only those who have had bloodborne pathogen training should
clean up a blood spill, because they understand the hazards
and how to keep them selves safe while properly handling the
clean-up process.
• Wear appropriate protective equipment. At a minimum you
must wear gloves and eye protection during spill clean-up to
protect yourself from exposure.
• Use disposable towels to soak up most of the blood and
properly dispose of immediately after use.

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