Blood

BLOOD
PRESENTED BY-
DR. MEENAL ATHARKAR
MDS
DEPT OF CONSERVATIVE
DENTISTRY AND
ENDODONTICS

CONTENTS
1. Introduction
2. Properties of blood
3. Composition of blood
 Blood cells
 Plasma
 Serum
4. Functions of blood

CONTENTS
5. Genesis of blood cells
6. Erythropoiesis
7. Red blood cells
8. Hemolysis and fragility of red blood cells
9. Hemoglobin and iron metabolism
10.Erythrocyte sedimentation rate
11. Packed cell volume
12. Blood indices

CONTENTS
13. White blood cells
▫ Neutrophils
▫ Eosinophil
▫ Basophil
▫ Monocytes
▫ Lymphocytes
14. Platelets

CONTENTS
15. Leukemia
16. Anemia
17. Blood groups
18. Blood transfusion
19. Blood volume
20.Clinical relevances
21. References

Introduction
• BLOOD is a connective tissue in fluid form.
• It is known as
▫ Fluid of life because it carries oxygen from lungs to other parts
of body and carbon dioxide from all parts of body to lungs.
▫ Fluid of growth because it carries nutritive substances from the
digestive system and hormones from endocrine glands to all the
tissues.
▫ Fluid of health because it protects the body against the diseases
and gets rid of the waste products and unwanted substances by
transporting them to excretory organs.

1. Colour - Red , Arterial blood- scarlet red because it contains more
oxygen, venous blood- purple red because it contains more carbon
dioxide.
2. Volume – In adults, average blood volume is 5 L.
In new born it is 450 mL, which increases during
growth and reaches 5L in puberty.
In females-4.5 L.
It is 8% of body weight of normal healthy young adult
weighing,70 kg .
3. Reaction & pH- slightly alkaline in nature, pH- 7.4.
Properties of blood

Properties of blood
4. Specific gravity-
1. Of total blood: 1.052- 1.061
2. Of blood cells: 1.092- 1.101
3. Of plasma : 1.022- 1.026
5. Viscosity – 5 times more viscous than water due to presence of
blood cells and plasma proteins.

Composition of blood
A. Blood cells (formed elements)– RBC, WBC, platelets(45%)
B. Plasma (liquid protein)(55%)
C. Serum

Composition of blood
A.BLOOD CELLS: They are of three types
-Red blood cells (Erythrocytes)
-White blood cells (Leukocytes)
-Platelets (Thrombocytes)
B.PLASMA: It is a straw colored clear liquid part of the blood.
Normal plasma volume is 3 Litres.
If plasma is allowed to clot, fluid left behind after
clotting is serum

• Plasma proteins are:
1. serum albumin (4.7 g/dL)
2. serum globulin (2.3 g/dL)
3. fibrinogen (0.3 g/dL)
Total =( 6.4-8.3 g/dL)
ALBUMIN/GLOBULIN RATIO:
- It is the ratio between plasma level of albumin and globulin.
- normal A/G ratio is 2:1.
- It is an important indicator of some diseases of liver and
kidney.

Properties of plasma proteins:
1. Molecular weight: Albumin- 69000
Globulin- 156000
Fibrinogen- 400000
2. Oncotic pressure: The oncotic pressure exerted by the proteins
in the plasma is called colloidal oncotic (osmotic) pressure.
: it is 25 mm Hg.
: Albumin plays an important role in exerting
oncotic pressure.
3. Specific gravity: 1.026
4. Buffer action: The plasma proteins have 1/6 of total buffering
action of the blood.

ORIGIN OF PLASMA PROTEINS
o In Embryo
▫ mesenchyme cells ( Albumin is synthesized first)
Adults
▫ reticuloendothelial cells of liver and also from spleen, bone
marrow, disintegrating blood cells, general tissue cells.

Functions of plasma proteins
• Role in coagulation of blood- fibrinogen
• Role in defence mechanism of body- gamma globulins act as
antibodies
• Role in transport mechanism- albumin, alpha and beta globulins
transport hormones, enzymes, etc throughout the body.
• Role in maintenance of osmotic pressure in blood- the size of plasma
proteins is large so that they cannot pass through the capillary
membrane easily and remain in the blood and exert colloidal oncotic
pressure.
• Role in regulation of acid- base balance- 15% of buffering capacity of
blood

• Role in viscosity of blood- Albumin provides maximum viscosity to
the blood
• Role in erythrocyte sedimentation rate (ESR)- globulin and
fibrinogen accelerate the tendency of rouleaux formation by RBCs
which is essential for ESR.
• Role in suspension stability of RBCs- globulin and fibrinogen
• Role in production of trephone substances- trephone substances
which are essential for nourishment of tissue cells in culture are
produced by leukocytes from plasma proteins.
• Role as reserve proteins- during fasting or in adequate protein
intake

Functions of blood
• Nutritive function- glucose, aminoacids, lipids and vitamins derived from
digested food are absorbed from gastrointestinal tract and carried by blood to
different body parts for growth and production of energy.
• Defensive function- WBCs
- Neutrophils, Monocytes- engulf bacteria by phagocytosis
- Lymphocytes- development of immunity
- Eosinophils- detoxification, disintegration and removal of
foreign proteins.
• Respiratory function- transport of respiratory gases is done by blood.
• Transport of hormones and enzymes- blood transports hormones released from
ductless (endocrine) glands to their target organs.

Functions of blood
• Excretory function- waste products from tissues are removed by blood
and carried to excretory organs like kidney, skin, liver, etc for excretion.
• Regulation of water balance- water content in blood is freely
interchangable with interstitial fluid.
• Regulation of acid balance- plasma proteins and hemoglobin act as
buffers.
• Regulation of body temperature-blood has high specific heat which is
responsible for maintaining the thermoregulatory mechanism in the body
that is the balance between heat loss and gain in the body.
• Storage function- blood serves as a readymade source for subtances like
proteins, sodium, potassium which are used by the body in conditions like
starvation, fluid loss, electrolyte loss, etc.

RED BLOOD CELLS (ERYTHROCYTES)
• Non nucleated
• Red color of RBC is due to red pigment hemoglobin
• Normal range- adult males- 5 millions /cu. mm
- adult females- 4.5 millions / cu. mm
Plays a vital role in transport of gases.
Size and shape: biconcave disc
diameter- 7.8 micrometers
volume- 90-95 cu. Mm
the RBC is a bag that can be deformed into any
shape but this deformation does not occur as the cell has great
excess of cell membrane for the quantity of material inside.

• Quantity of hemoglobin in cells
- upto 34 grams in each 100 millilitres of cells.
- when hematocrit and quantity of hemoglobin in each
respective cell are normal, the whole blood contain average
- 15 grams per 100 millilitres ( men)
- 14 grams per 100 millilitres (women)

ERYTHROPOIESIS
• Definition:Erythropoiesis is the process of the origin, development
and maturation of erythrocytes
• Site of erythropoiesis:In fetal life-
1. Mesoblastic Stage- During the first two months of intrauterine
life, primitive and nucleated RBCs are produced in yolk sac.
2. Hepatic Stage- During middle trimester of gestation , liver is
the main organ that produces RBCs. Spleen and lymphoid organs
are also involved in erythropoiesis.
3. Myeloid Stage- During the last three months of intrauterine
life, the RBCs are produced from red bone marrow and liver.

ERYTHROPOIESIS
• IN NEWBORN BABIES, CHILDREN AND ADULTS- RBCs are produced
only from the red bone marrow only.
1. Up to the age of 20 years: red bone marrow of all bones (long bones
and all the flat bones).
2. After the age of 20 years: marrow of 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 looses the
erythropoietic function.
In adults, liver and spleen may produce the blood cells if the bone marrow
is destroyed or fibrosed.
Though bone marrow is the site of production of all blood cells,
comparatively 75% of the bone marrow is involved in the production of
leukocytes and only 25% is involved in the production of erythrocytes.

Process of erythropoiesis:
• The cells of CFU-E pass
through different stages and
finally become matured RBCs.

STAGES OF ERYTHROPOIESIS
1. Proerythroblast ( megaloblast)- first cell, 20 u in diameter. Its
nucleus is large and occupies the cell completely. Nucleoli are
present. It does not have hemoglobin.
2. Early normoblast (basophil erythroblast)- it is smaller than
proerythroblast , 15 u in diameter. Its cytoplasm stains with
basic dyes. In nucleus, nucleoli disappear.
3. Intermediate normoblast (polychromatic erythroblast)- it is
smaller than early normoblast , 10-12 u in diameter. Nucleus
present. Hemoglobin starts appearing. Cytoplasm stains both
acidic and basic stains.

STAGES OF ERYTHROPOIESIS
4. Late normoblast (orthochromatic erythroblast)- 8-10 u in diameter.
Nucleus becomes very small (ink spot nucleus). Quantity of hemoglobin
increases so the cytoplasm becomes acidophillic. Nucleus disappears.
5. Reticulocyte (immature RBC)- slighty larger than matured RBC.
Endoplasmic reticulum is reabsorbed. Cells pass from bone marrow
into blood by diapedesis. Cytoplasm contains reticular network or
reticulum. In new born babies, reticulocyte count is 2-6% and later falls
to 1% of RBCs.
6. Mature erythrocyte- 7.2 u in diameter. Reticular network disappears.
Biconcave shape . Hemoglobin present.
It requires seven days for the development and maturation of RBCs from
proerythroblast.

FACTORS NECESSARY FOR
ERYTHROPOIESIS
• 1. General factors
▫ i. Erythropoietin
▫ ii. Thyroxine
▫ iii. Hemopoietic growth factors- interleukin 3,6,11
▫ iv. Vitamins- B,C,D,E

.
• 2. Maturation factors
▫ Vitamin B12- Synthesis of DNA in RBCs
- deficiency leads to failure of maturation of RBCs,
intrinsic factor of castle
folic acid
• 3. Factors necessary for hemoglobin formation.
▫ 1.proteins and amino acids
▫ 2. Iron
▫ 3. Copper
▫ 4. Cobalt and nickel
▫ 5. Vitamins
FACTORS NECESSARY FOR
ERYTHROPOIESIS

Role of erythropoietin- regulation of RBC
production

PROPERTIES of RBCs
1. ROULEAUX FORMATION- when blood is
taken out of blood vessel,RBCs pile up one
above another like pile of coins

. PROPERTIES of RBCs
2. SPECIFIC GRAVITY- 1.092- 1.101
3. PCV- proportion of blood occupied by RBCs expressed in
percentage.i.e, 45%.
4. SUSPENSION STABILITY- during circulation, RBCs remain
suspended uniformly in blood.

LIFESPAN OF RBC-average- 120 days, senile RBCs
are destroyed in reticuloendothelial system
• Lifespan of RBCs is determined by radioisotope method, RBCs
are tagged with radioactive substances like radioactive iron or
radioactive chromium. The life of RBCs is determined by
studying the rate of loss of radioactive cells from circulation.

Destruction of RBCs:
- occurs in capillaries of red pulp
of spleen.
- when cells become older, cell
membrane becomes fragile so
these cells are destroyed while
trying to squeeze through
capillaries.
- spleen- graveyard of RBCs.
- daily 10% senile RBCs are
destroyed which releases 0.6 g/Dl
of hemoglobin into plasma.

FUNCTIONS OF RBCs
• 1. Transport of Oxygen from the Lungs to the Tissues (97%)
• 2. Transport of Carbon Dioxide from the Tissues to the Lungs
(30%)
• 3. Buffering Action in Blood- hemoglobin
• 4. In Blood Group Determination- RBCs carry antigen like A
antigen, B antigen, RH factor.

Variations in RBCs: 1.Number-
A. Physiological
• Increase: age Decrease: high
barometric
sex sleep
high altitude pregnancy
muscular exercise
emotional conditions
increased environmental
temperature
after meals

B. Pathological
1. Polycythemia 2. Anemia
(abnormal increase in RBC count) (abnormal decrease in
(>7 millions/ cu mm) RBC count)
Primary Secondary
>14 millions/ secondary to diseases-
cu mm emphysema,
carbon monoxide
poisoning

Variations in RBCs
2. Shape-
• Crenation- shrinkage in hypertonic
solution
• Spherocytosis- globular form in
hypotonic solution
• Elliptocytosis- elliptical shape in
anemia
• Sickle cell- crescentic shape in sickle
cell anemia
• Poikilocytosis- unusual shapes due to
deformed cell membrane

Variations in RBCs
3. Size-
• Under physiological conditions, the size of RBCs in venous blood
is slightly larger than those in arterial blood.
• Under pathological conditions,
microcytes- iron deficiency anemia
macrocytes- megaloblastic anemia
anisocytes- pernicious anemia

Variations in RBCs
4. Structure-
• Punctate basophilism-striated RBCs
in lead poisoning
• Ring in RBC- rings/ twisted strands
(goblet ring) in some anemia
• Howell- Jolly Bodies- some nuclear
fragments present in ectoplasm of
RBCs in some anemias.

Hemolysis and Fragility of RBCs:
• Hemolysis- It is the destruction of formed elements that is the
process which involves the breakdown of RBC and liberation of
hemoglobin.
• Fragility- The susceptibility of RBC to form hemoglobin or
tendency to break easily.
- two types:1. osmotic – due to exposure to hypotonic
saline
2. mechanical- due to mechanical trauma

HEMOGLOBIN & Iron metabolism
• Hemoglobin (Hb) is the iron containing colouring matter of red
blood cell (RBC).
• It is a chromo protein forming 95% of dry weight of RBC and
30% to 34% of wet weight.
• Molecular weight of hemoglobin is 68,000

HEMOGLOBIN content
• Average hemoglobin (Hb) content in blood is 14 to 16 g/dL.
:AGE:
▫ At birth : 25 g/dL
▫ After 3rd month : 20 g/dL
▫ After 1 year : 17 g/dL
 At the time of birth, hemoglobin content is very high because of
increased number of RBCs .
:SEX:
 Adult males- 15 g/ dL
 Adult females- 14.5 g/ dL

Functions of hemoglobin:
• Transport of respiratory gases
1. Transport of oxygen from lungs to tissues
2. Transport of carbon dioxide from tissues to lungs
• Buffer action

Structure of hemoglobin:
• Hemoglobin is a conjugated protein.
• It consist of protein combined with iron containing pigment.
• Globin- protein part
• Heme- iron part
• Heme forms a part of – myoglobin(oxygen binding pigment in
muscles)
-neuroglobin(oxygen binding pigment in
brain)
• Iron- present in ferrous (Fe++) form (unstable)

Structure of hemoglobin:
• Porphyrin- The pigment part of heme.
- It is formed by four pyrrole rings (tetrapyrrole)
which are attached to one another by methane (CH4) bridges.
• Globin- contains 4 polypeptide chains.
1. Two are α-chain – 141 aa
2. Two are β-chain – 146 aa

Types of normal hemoglobin:
• Adult (HbA): globin contains 2 alpha and 2 beta chains
: less affinity towards oxygen.
• Fetal (HbF): globin contains 2 alpha and 2 gamma chains
: more affinity towards oxygen.

Abnormal hemoglobin:
A} Hemoglobinopathies-( genetic diorders)
1. hemoglobin S- sickle cell anemia
- beta chains- abnormal
2. hemoglobin C- mild hemolytic anemia , spleenomegaly
3. hemoglobin E- mild hemolytic anemia , spleenomegaly
4. hemoglobin M- methemoglobin is present
- mutation in genes of alpha, beta chains
B} Hemoglobin in thalassemia and related disorders:
- alpha thalassemia- alpha chains- decreased, absent or abnormal
- beta thalassemia- beta chains- decreased, absent or abnormal

Abnormal hemoglobin derivatives:
• Carboxyhemoglobin
• Methemoglobin
• sulfhemoglobin

FORMATION OF HEMOGLOBIN:
• Synthesis of hemoglobin begins in proerythroblasts and
continues even into the reticulocyte stage of RBC.
• Therefore, when reticulocytes leave the bone marrow and pass
into blood stream, they continue to form minute quantities of
hemoglobin for another day or so untill they become mature
erythrocytes.

FORMATION OF HEMOGLOBIN:
• Basic chemical steps in formation of hemoglobin are:
(mitochondria)
1) 2 Succinyl CoA + 2 Glycine- Pyrrole Molecule
( krebs metabolic cycle)
2) 4 Pyrroles combine - Protoporphyrin IX
ferrochelatase
3) Protoporphyrin IX + Iron(Fe++)---------- Heme Molecule
4) Each heme molecule + long polypeptide chain HEMOGLOBIN
(globin) CHAIN

• There are different types of hemoglobin chains: alpha, beta,
gamma, delta chains.
• Most common in adult human beings- hemoglobin A(2 alpha, 2
beta chains)
• Each hemoglobin molecule can transport total four molecules of
oxygen (8 atoms of oxygen)
• The types of hemoglobin chains in the hemoglobin molecule
determine the binding affinity of hemoglobin for oxygen.
• The heme portion is synthesized in mitochondria and globin in
ribosomes.
• Each polypeptide chain combines with one heme molecule. Thus
after the complete configuration, each hemoglobin molecule
contains 4 polypeptide chains and 4 heme molecules.

Combination of hemoglobin with oxygen:
• Most important feature- to combine loosely and reversibly to
oxygen.
• Oxygen does not combine with two positive bonds of iron in
hemoglobin molecule.
• Instead, it binds loosely with one of the so called co-ordination
bond so that it is easily reversible.
• Furthermore, this oxygen does not become ionic oxygen and
remains as molecular oxygen and is carried to the tissues where
because of readily reversible state it is released into tissue fluids
in the form of molecular oxygen(O2) only.

Destruction of hemoglobin:
• When the RBCs are destroyed, hemoglobin is released into the
plasma.
• This hemoglobin is phagocytized almost immediately by
macrophages i.e. Kupffer cells in liver and macrophages of
spleen and bone marrow.
• During next few hours to days, hemoglobin is degraded and split
into globin, iron and porphyrin.

Destruction of hemoglobin
blood
bone marrow
new RBC

IRON metabolism
• Human body needs iron for oxygen transport.
• Total quantity of iron in body- 4-5 gm,
65%- in form of Hb,
4 %- myoglobin(muscles)
1%- intracellular oxidative Heme compounds,
0.1%- combined with protein transferrin in blood plasma,
15-30% -stored in reticuloendothelial system & liver, in form
of ferritin

Transport and storage of iron:
• When iron is absorbed from small intestine, it immediately
combines in blood plasma with beta globulin, apotransferrin to
form transferrin which is then transported into plasma.
• In the cell cytoplasm, iron combines mainly with a protein,
apoferritin to form ferritin. Varying quantities of iron can
combine in clusters of iron radicals with this large molecule. The
iron stored as ferritin is called as storage iron.
• Smaller quantities of iron in the storage pool are in an extremely
insoluble form called hemosiderin.

• When the quantity of iron in the plasma falls low, some of the
iron in the ferritin storage pool is removed easily and
transported in the form of transferrin in the plasma to the areas
of the body where it is needed.
• Iron is stored in large quantities in reticuloendothelial cells and
liver hepatocytes.
• In males, about 1 mg of iron is excreted everyday through faeces.
• In females, the amount of iron loss is very much high( almost 25
mg during menstrual cycle)

Normal values of some important
substances in blood

Erythrocyte Sedimentation Rate
• Definition: Rate at which the erythrocytes settle down.
• ESR is also called sedimentation rate, sed rate or Biernacki
reaction( first demonstrated by Edmund Biernacki in 1897)
• Normally, RBCs remain suspended uniformly in circulation-
suspension stability of RBCs.

Determination of ESR:
• 2 methods:
Westergren’s method- Westergren’s tube is used.
 Wintrobe’s method- Wintrobe’s tube is used.

Determination of ESR
westergren’s method wintrobe’s method
• 1.6 mL of blood is mixed with
0.4 mL of 3.8% sodium citrate
(anticoagulant) and loaded in
the Westergren tube.
• Blood :anticoagulant is 4:1
• Reading is taken at the end of 1
hour.
• Determines - ESR
• 1 mL of blood is mixed with
anticoagulant (EDTA) and
loaded in the Wintrobe tube.
• Reading is taken after 1
hour.
• Determines- PCV & ESR

Normal values of ESR
• By Westergren Method
1. In males : 3 to 7 mm in 1 hour
2. In females : 5 to 9 mm in 1 hour
3. Infants : 0 to 2 mm in 1 hour
• By Wintrobe Method
1. In males : 0 to 9 mm in 1 hour
2. In females : 0 to 15 mm in 1 hour
3. Infants : 0 to 5 mm in 1 hour

Variations of ESR
PHYSIOLOGICAL:
• 1. Age: ESR is less in children and infants because of more number
of RBCs.
• 2. Sex: It is more in females than in males because of less number
of RBCs.
• 3. Menstruation: The ESR increases because of loss of blood and
RBCs
• 4. Pregnancy: From 3rd month to parturition, ESR increases up to
35 mm in 1 hour because of hemodilution.

PATHOLOGICAL :
ESR increases in
1. Tuberculosis
2. All types of anemia except
sickle cell anemia
3. Malignant tumors
4. Rheumatoid arthritis
5. Rheumatic fever
6. Liver diseases.
ESR decreases in
1. Allergic conditions
2. Sickle cell anemia
3. Peptone shock
4. Polycythemia
5. Severe leukocytosis

Factors affecting ESR
• Increasing ESR
1. Specific gravity of RBC
2. Rouleaux formation
3. Increase in size of RBC
• Decreasing ESR
1. Viscosity of blood
2. RBC count

Packed cell volume (PCV)
• Definition: It is the proportion of blood occupied by RBCs,
expressed in percentage.
• It is the volume of RBCs packed at the bottom of a hematocrit
tube when the blood is centrifuged.
• also called hematocrit value or erythrocyte volume fraction
(EVF).

METHOD of determination of PCV
blood mixed with anticoagulant (EDTA/HEPARIN)
hematocrit/wintrobe’s tube
centrifuged at speed of 3000 revolutions per minute
for 30 minutes
RBCs packed at the bottom, plasma remains above
•In between RBCs and plasma, there is a white buffy coat which is
formed by WBCs and platelets.
•In laboratories with modern equipments, hematocrit is calculated
indirectly by autoanalyzer

PCV: • Normal PCV
▫ Males: 40-45%
▫ Females: 38- 42%

Significance of determining PCV
1. Diagnosis and treatment of Anemia, Polycythemia
2. Determination of extent of dehydration and recovery from
dehydration after treatment
3. Decision of blood transfusion

Variations In PCV
• Increases in
1. Polycythemia
2. Dehydration
3. Dengue shock syndrome
• Decreases in
1. Anemia
2. Cirrhosis of liver
3. Pregnancy
4. Haemorrhage due to
ectopic pregnancy

Blood indices
• Blood indices have got diagnostic value in determining types of
anemia.
• The number, shape, volume and color of RBCs indicate the
quality of blood. So these features are named as blood indices.
• These are calculations derived from RBC count, hemoglobin
content of blood & PCV.

Different blood indices:
1. Mean corpuscular volume (MCV)
2. Mean corpuscular hemoglobin (MCH)
3. Mean corpuscular hemoglobin concentration (MCHC)
4. Color index (CI)

1} Mean corpuscular volume( MCV)
• avg. volume of single RBC
• expressed in cubic microns (cu µ)
• normal-90 cu µ (78 to 90 cu µ).
• When MCV is normal, the RBC is called normocyte.
• When MCV increases, the RBC is called macrocyte
• When MCV decreases, the RBC is called microcyte
• In pernicious anemia, megaloblastic anemia, RBCs – macrocyte
• In iron deficiency anemia RBCs- microcytic

2} Mean corpuscular hemoglobin(MCH)
• MCH is the quantity or amount of hemoglobin present in one
RBC.
• It is expressed in micromicrogram or picogram (pg).
• Normal value of MCH is 30 pg (27 to 32 pg).

3} Mean corpuscular hemoglobin concentration:
• It is the concentration of hemoglobin in one RBC.
• It is the amount of hemoglobin expressed in relation to the
volume of one RBC.
• unit of expression is percentage.
• Most important absolute value in the diagnosis of anemia.
• Normal value - 30% (30% to 38%).

• MCHC normal, RBC- normochromic
• MCHC decreases, RBC- hypochromic.
▫ In pernicious anemia and megaloblastic anemia,
RBCs may be normochromic or hypochromic.
▫ In iron deficiency anemia, RBCs are hypochromic.
A single RBC cannot be hyperchromic because, the amount
of hemoglobin cannot increase beyond normal.

4} COLOR INDEX (CI)
• It is the ratio between the percentage of hemoglobin and the
percentage of RBCs in the blood.
• Normal color index is 1.0 (0.8 to 1.2).
• It is useful in determining the type of anemia.
• Increases -macrocytic (pernicious) anemia and megaloblastic
anemia.
• Decreases- iron deficiency anemia.
• Normal -normocytic normochromic anemia

Formation of the multiple different peripheral blood cells
from the original pluripotent hematopoietic stem cell
(PHSC) in bone marrow

WHITE BLOOD CELLS (WBCs)( leucocytes)
Introduction:
• mobile units of body’s protective system
• Leukocytes are transported to the areas of serious infection and
inflammation, thereby providing a rapid and potent defense
against infectious agents.
• They are colorless, nonnucleated
• (leuko = white/colorless).
• Total WBC count is 4000-11000 cu/ mm of blood

WBCs differ from RBCs in these aspects:
• Larger in size
• Irregular in shape
• Nucleated
• Many types
• Granules present in some types of WBCs
• Lifespan is shorter
• Less in number.

CLASSIFICATION
• Based on the presence or absence of granules in the cytoplasm,
the leukocytes are classified into two groups:
Granulocytes . Agranulocytes
1. Neutrophils 1. Monocytes
2. Eosinophils 2. Lymphocytes
3. Basophils

Genesis of WBCs( LEUKOPOIESIS):
• Differentiation of pluripotent hematopoietic stem cell into different types
of committed cells occurs.
• Aside from those cells committed to form RBCs, two major lineages of
WBCs are formed, the myelocytic(myeloblast) and
lymphoblastic(lymphoblast)
• Formed partially
1. In bone marrow- granulocytes ,monocytes & few lymphocytes
2. In lymph tissue- lymphocytes and plasma cells
(lymph glands,spen,thymus,tonsils and various pockets of lymphoid
tissue elsewhere in body, such as in bone marrow and peyer’s patches
underneath the epithelium in the gut wall.
WBCs are stored in bone marrow and released into circulation when needed

Types of leukocytes:
N
Neutrophils
fine granules stain with
eosin/methylene blue
stain
Violet color with
leishman stain
multilobed(increased
number of lobes
determine more age)
Young-no lobes
Old- 2-3 lobes
1
10-12 u
2-5
2-5
days
50-70%
3000-6000
Per cu mm
Eosinophils
Large granules with eosin
stain
Pink/red color
Bilobed/ spectacular 10-14 u 7-12
days
2-4%
150-450
Per cu mm
Basophils
Coarse granules with
methylene blue stain
Purple blue color
Bilobed 8-10 u 12-15
days
0-1%
0-100
Per cu mm
Monocytes
No clear granules Horseshoe/bean/oval/ro
und/ kidney shaped
14-18 u 2-5
days
2-6%
200-600
Per cu mm
Lymphocyte
s
No clear granules Oval/ bean/
Kidney shaped
2 types
Large-10-12 u
Small-7-12 u
½-1
day
20-30%
1500-2700
Per cu mm
Type Features of cytoplasm Nucleus Diameter Lifespa
n
Concentration/
absolute value

Different types of leukocytes:

Life span of WBCs
• #Granulocytes once released from bone marrow – 4-8 hrs
circulating in the blood & another 4-5 days in tissues.
 In times of serious infection- lifespan is shortened to only few hours
because they proceed rapidly to site of infection – perform their
function– & are self destroyed
#Monocytes – 10-20 hrs in blood
tissues swell to much lager sizes to become
tissue macrophages (live for months)
#Lymphocytes- weeks or months

Functions of WBCs
1} NEUTROPHILS:
• Provide 1st line defence against invading organisms.
• Free cells, they wander in the body.
• Granules contain enzymes like proteases, myeloperoxidases, elastases,
metalloproteinases which destroy micro- organisms.
• It also contain antibody- defensin which is active against bacteria and
fungi.
• Membrane contain enzyme NADPH oxidase which is responsible for
bactericidal action of neutrophils.
• They secrete platelet activating factor.
• First, neutrophils engulf bacteria and then destroy them by
phagocytosis.

2} EOSINOPHILS:
• defence against parasitic infection.
• Eosinophil count increases also during allergic diseases like asthma.
• Eosinophils are responsible for detoxification, disintegration and
removal of foreign proteins.
• Cytotoxic substances present in granules are:
• Eosinophil peroxidase- helminths, bacteria, tumor cells
• Major basic protein(MBP)- helminths( ballooning and detachment of
tegumental sheath)
• Eosinophil cationic protein(ECP)- neurotoxin, more toxic than MBP
against helminths(complete disintegration)
• Eosinophil derived neurotoxin-myelinated nerve fibres.
• Cytokines- interleukin 4, 5 accelerate inflammatory responses

3} BASOPHILS:
• Important role in healing processes.
in allergy or acute hypersensitivity reactions (allergy). This is
because of the presence of receptors for IgE in basophil membrane.
Release of some important substances from their granules such as:
1. Heparin: prevents the intravascular blood clotting.
2. Histamine( slow-reacting substances of anaphylaxis), bradykinin
and serotonin: produce the acute hypersensitivity reactions by
causing vascular and tissue responses.
3. Proteases, myeloperoxidase, cytokines: accelerates inflammatory
responses

• 4} MONOCYTES:
• Motile and phagocytic.
• Provide 1st line defense against invading organisms.
• Monocytes secrete-interleukin I, colony stimulating factor, platelet
activating factor.
• 5} LYMPHOCYTES:
• 2 types-
• T lymphocytes- responsible for cellular immunity.
• B lymphocytes- responsible for humoral immunity.

MECHANISM OF ACTION:
NEUTROPHILS:
infected area chemoattractants chemotaxsis
neutrophils move by diapedesis
towards site of infection
neutrophils surround the area and get adhered to the infected tissues
each neutrophil holds 15-20 micro organisms
engulf bacteria
phagocytosis

EOSINOPHILS:
granules
cytotoxic substances like MBP, ECP, cytokinessubstances
Released over the invading parasites
Substances become lethal and destroy parasites

BASOPHILS AND MAST CELLS:
IgE antibody binds with mast cells & basophils
specific antigen of IgE Ab reacts with the Ag
cause mast cell or basophil to rupture
release large quantities of histamine ,bradykinin ,serotonin ,heparin
,slow reacting subs of anaphylaxis & large number of lysosomal
enzymes cause local & vascular tissue reactions

Variations:
• Leukocytosis: increase in number of WBCs.
• Leukopenia: decrease in number of WBCs.
• Granulocytosis: it is the abnormal increase in number of
granulocytes.
• Granulocytopenia: it is the abnormal decrease in number of
granulocytes.
• Agranulocytosis: it is a condition in which there is absolute lack of
granulocytes.

Variations
phsiological pathological
• Age- 20000/ cu mm(infants) 1) leukocytosis: increase in total WBC count
-10000-15000/ cu mm - infections
(children) - allergy
-4000-11000/ cu mm - common cold
(adults) - tuberculosis
• Sex- more in males. - glandular fever
• Diurnal variations-afternoon 2) leukocytopenia: decrease in WBC count
(maximum) - anaphylactic shock
- early morning - cirrhosis of liver
( minimum) - disorders of spleen
• Exercise- increases - pernicious anemia
• Stress- increases -typhoid
• Pregnancy, menstruation, -paratyphoid
Parturition- increases - viral infections
• Sleep- decreases

Properties of WBCs:
• Diapedesis: neutrophils, monocytes.
• Ameboid movement: neutrophils, macrophages
• Chemotaxis: Attraction of WBCs at the site of injury by chemical
substances released at the site of injury.

PLATELETS ( Thrombocytes)
• Introduction- they are small, colorless, non nucleated and
moderately refractive bodies.
• - considered as fragments of cytoplasm.
• Size- diameter- 2.5 u (2-4 u)
• - volume- 7.5 cu u (7-8 cu u)
• Shape- spherical, rod , oval, disc shaped, dumbell, comma, cigar
shape , etc.

• Composition- cell membrane- contains phospholipids,
glycoproteins, cholesterol, proteins, etc.
• - microtubules- form a ring around cytoplasm below
cell membrane made up of tubulin.
• - cytoplasm- contain cellular organelles, golgi
apparatus, endoplasmic reticulum, mitchondria, microtubule,
microvessels, filaments, granules, proteins, enzymes, hormonal
substances.
• Normal count- 2,50,000/ cu mm (average)
• (2,00,000- 4,00,000 / cu mm)

GLYCOPROTEINS
• prevent the adherence of platelets to normal endothelium,
but accelerate the adherence of platelets to collagen and
damaged endothelium in ruptured blood vessels.
• Glycoproteins also form the receptors for adenosine
diphosphate (ADP) and thrombin.

PHOSPHOLIPIDS
• accelerate the clotting reactions. The phospholipids form the
precursors of thromboxane A2 and other prostaglandin-related
substances

CYTOPLASM
contains the cellular organelles, Golgi apparatus, endoplasmic
reticulum, mitochondria, microtubule, microvessels, filaments
and granules. Cytoplasm also contains some chemical substances
such as proteins, enzymes, hormonal substances.

PROTEINS
• 1. Contractile proteins i. Actin and myosin: which are
responsible for contraction of platelets.
ii. Thrombosthenin: Third contractile protein, which is
responsible for clot retraction.
• 2. von Willebrand factor: Responsible for adherence of
platelets and regulation of plasma level of factor VIII.

.
• 3. Fibrin-stabilizing factor: A clotting factor.
• 4. Platelet-derived growth factor (PDGF): Responsible for
repair of damaged blood vessels and wound healing. It is a
potent mitogen (chemical agent that promotes mitosis) for
smooth muscle fibers of blood vessels.

.
• 5. Platelet-activating factor (PAF): Causes aggregation of
platelets during the injury of blood vessels, resulting in
prevention of excess loss of blood.
• 6. Vitronectin (serum spreading factor): Promotes adhesion of
platelets and spreading of tissue cells in culture.
• 7. Thrombospondin: Inhibits angiogenesis (formation of new
blood vessels from pre-existing vessels).

Enzymes
1. Adensosine triphosphatase (ATPase)
2. Enzymes necessary for synthesis of prostaglandins.

Hormonal Substances
1. Adrenaline
2. 2. 5-hydroxytryptamine (5-HT; serotonin)
3. Histamine.

Other Chemical Substances
1. Glycogen
2. Substances like blood group antigens
3. Inorganic substances such as calcium, copper, magnesium and
iron.

Platelets granules
1. Alpha granules
2. Dense granules

Development of platelets:
• Platelets are formed from bone marrow.
• Pluripotent stem cell gives rise to the colony forming unit-
megakaryocyte (CFU-M).
• This develops into megakaryocyte.
• 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.

PROPERTIES of platelets
1. Adhesiveness
2. Activation
3. Aggregation
4. Agglutination

FUNCTIONS of platelets
1. Blood clotting
2. Clot retraction
3. Prevention of blood loss (Hemostasis)
4. Repair of ruptured blood vessels
5. Defence mechanism

Activators
• 1. Collagen, which is exposed during damage of blood vessels
• 2. von Willebrand factor
• 3. Thromboxane A2
• 4. Platelet-activating factor
• 5. Thrombin
• 6. ADP
• 7. Calcium ions
• 8. P-selectin: Cell adhesion molecule secreted from endothelial cells
• 9. Convulxin: Purified protein from snake venom

Inhibitors
• 1. Nitric oxide
• 2. Clotting factors: II, IX, X, XI and XII
• 3. Prostacyclin
• 4. Nucleotides which breakdown the ADP.

LIFESPAN AND FATE of platelets
• Average lifespan of platelets is 10 days. (8 and 11 days)
• Platelets are destroyed by tissue macrophage system in spleen.
• So, splenomegaly (enlargement of spleen) decreases platelet
count and splenectomy (removal of spleen) increases platelet
count.

Variations in platelets:
physiological pathological
• Age- less in infants 1) thrombocytosis:(increases)
reach normal after conditions-allergy, hemorrhage,
3rd month of birth. Bone fractures, surgical operations,
• Sex- no difference splenectomy, rheumatic fever,
( in females it is trauma.
reduced in menstruation) 2) thrombocytopenia:(decreases)
• High altitude- increases conditions-acute infections,
• After meals- increases acute leukemia, pernicious anemia,
chicken pox, small pox, typhoid,
tuberculosis, purpura.

Leukemia:
• Uncontrolled production of white blood cells can be caused by
cancerous mutation of a myelogenous or lymphogenous cell.
• This causes leukemia, which is usually characterized by greatly
increased numbers of abnormal white blood cells in the
circulating blood.
• Types of Leukemia:
• Leukemias are divided into two general types:
• lymphocytic leukemias
• myelogenous leukemias

• lymphocytic leukemias:
• caused by cancerous production of lymphoid cells, usually
beginning in a lymph node or other lymphocytic tissue and
spreading to other areas of the body.
• myelogenous leukemia:
• begins by cancerous production of young myelogenous cells in the
bone marrow and then spreads throughout the body so that white
blood cells are produced in extramedullary tissues like lymph
nodes, spleen, liver.

• In myelogenous leukemia,
• the cancerous process occasionally produces partially differentiated
cells, resulting in what might be called neutrophilic leukemia,
eosinophilic leukemia, basophilic leukemia, or monocytic leukemia.
• the leukemia cells are bizarre and undifferentiated and not identical to
any of the normal white blood cells.
• Usually, the more undifferentiated the cell, the more acute is the
leukemia, often leading to death within a few months if untreated.
• With some of the more differentiated cells, the process can be chronic,
sometimes developing slowly over 10 to 20 years.
• Leukemic cells, especially the very undifferentiated cells, are usually
nonfunctional for providing the normal protection against infection.

Oral manifestation of leukemia:
• Gingival hyperplasia
• Petechiae
• Ulceration of mucosa
• Gingiva are boggy, edematous and deep red
• In severe cases teeth may be almost hidden
• Rapid loosening of teeth

Effects on the body:
• The first effect of leukemia is metastatic growth of leukemic cells in abnormal areas of the body.
• Leukemic cells from the bone marrow may reproduce so greatly that they invade the surrounding
bone, causing pain and, eventually, a tendency for bones to fracture easily.
• Almost all leukemias eventually spread to the spleen,lymph nodes,liver,and other vascular regions,
regardless of whether the origin of the leukemia is in the bone marrow or the lymph nodes.
• Common effects in leukemia are the development of infection, severe anemia, and a bleeding tendency
caused by thrombocytopenia (lack of platelets).
• These effects result mainly from displacement of the normal bone marrow and lymphoid cells by the
nonfunctional leukemic cells.
• the most important effect of leukemia on the body is excessive use of metabolic substrates by the
growing cancerous cells.
• The leukemic tissues reproduce new cells so rapidly that tremendous demands are made on the body
reserves for foodstuffs,specific amino acids,and vitamins.
• Consequently,the energy of the patient is greatly depleted, and excessive utilization of amino acids by
the leukemic cells causes especially rapid deterioration of the normal protein tissues of the body.
• Thus,while the leukemic tissues grow, other tissues become debilitated. After metabolic starvation has
continued long enough, this alone is sufficient to cause death.

ANEMIA
Anemia is the blood disorder, characterized by the reduction in:
• 1. Red blood cell (RBC) count
• 2. Hemoglobin content
• 3. Packed cell volume (PVC).
It means deficiency of hemoglobin in the blood, which can be
caused by either too few RBCs or too little hemoglobin in the
cells.

It occurs because of:
• 1. Decreased production of RBC
• 2. Increased destruction of RBC
• 3. Excess loss of blood from the body
 caused either by inherited disorders or environmental influences
such as nutritional problem, infection and exposure to drugs or
toxins.

.CLASSIFICATION OF ANEMIA:
• „Anemia is classified by two methods:
• 1. Morphological classification
• 2. Etiological classification.
1) „MORPHOLOGICAL CLASSIFICATION:
• Morphological classification depends upon the size and color of RBC.
• Size of RBC is determined by mean corpuscular volume (MCV).
• Color is determined by mean corpuscular hemoglobin concentration (MCHC).
• By this method, the anemia is classified into four types :
• 1. Normocytic Normochromic Anemia Size (MCV) and color (MCHC) of RBCs are
normal. But the number of RBC is less.
• 2. Macrocytic Normochromic Anemia RBCs are larger in size with normal color. RBC
count is less.
• 3. Macrocytic Hypochromic Anemia RBCs are larger in size. MCHC is less, so the cells
are pale (less colored).
• 4. Microcytic Hypochromic Anemia RBCs are smaller in size with less color.

• 2) ETIOLOGICAL CLASSIFICATION:
• On the basis of etiology (study of cause or origin), anemia is
divided into five types:
• 1. Hemorrhagic anemia
• 2. Hemolytic anemia
• 3. Nutrition deficiency anemia
• 4. Aplastic anemia
• 5. Anemia of chronic diseases.

1) Hemorrhagic anemia:
• Caused due to excessive loss of blood
• It occurs both in acute and chronic hemorrhagic conditions.
• 1) Acute hemorrhage:
• Acute hemorrhage refers to sudden loss of a large quantity of
blood as in the case of accident.
• RBCs are normocytic and normochromic.
• Decreased RBC count causes hypoxia, which stimulates the bone
marrow to produce more number of RBCs. So, the condition is
corrected within 4 to 6 weeks.

• 2) Chronic hemorrhage:
• It refers to loss of blood by internal or external bleeding, over a
long period of time.
• It occurs in conditions like peptic ulcer, purpura, hemophilia and
menorrhagia.
• Due to continuous loss of blood, lot of iron is lost from the body
causing iron deficiency.
• This affects the synthesis of hemoglobin resulting in less
hemoglobin content in the cells.
• RBCs are microcytic and hypochromic

2) Aplastic anemia(bone marrow aplasia):
• due to the disorder of red bone marrow.
• Red bone marrow is reduced and replaced by fatty tissues.
• Bone marrow disorder occurs in the following conditions:
• i. Repeated exposure to Xray or gamma ray radiation.
• ii. Presence of bacterial toxins, quinine, gold salts, benzene,
radium, etc.
• iii. Tuberculosis.
• iv. Viral infections like hepatitis and HIV infections.

3) Hemolytic anemia:
• Hemolysis means destruction of RBCs.
• Anemia due to excessive hemolysis which is not compensated by
increased RBC production is called hemolytic anemia.
• It is classified into two types:
• A. Extrinsic hemolytic anemia.
• B. Intrinsic hemolytic anemia.

• A. Extrinsic hemolytic anemia:
• It is caused by destruction of RBCs by external factors.
• Healthy RBCs are hemolized by factors outside the blood cells
such as antibodies, chemicals and drugs.
• also called autoimmune hemolytic anemia.

• Causes-
• i. Liver failure
• ii. Renal disorder
• iii. Hypersplenism
• iv. Burns
• v. Infections – hepatitis, malaria and septicemia
• vi. Drugs – Penicillin, antimalarial drugs and sulfa drugs
• vii. Poisoning by lead, coal and tar
• viii. Presence of isoagglutinins like anti Rh
• xi. Autoimmune diseases – rheumatoid arthritis and ulcerative colitis

• B. Intrinsic hemolytic anemia:
• It is caused by destruction of RBCs because of the defective RBCs.
• There is production of unhealthy RBCs, which are short lived and
are destroyed soon.
• Intrinsic hemolytic anemia is often inherited
• It includes sickle cell anemia and thalassemia, heriditary
spherocytosis, erythroblastosis fetalis.
• Because of the abnormal shape in sickle cell anemia and
thalassemia, the RBCs become more fragile and susceptible for
hemolysis.

• 1] sickle cell anemia:
• Sickle cell anemia is an inherited blood disorder
• characterized by sickleshaped red blood cells.
• It is also called hemoglobin SS disease or sickle cell disease.
• It is common in people of African origin.
• Sickle cell anemia is due to the abnormal hemoglobin called
hemoglobin S (sickle cell hemoglobin). In this, αchains are normal
and βchains are abnormal.
•

• The molecules of hemoglobin S polymerize into long chains and precipitate
inside the cells.
• Because of this, the RBCs attain sickle (crescent) shape and become more
fragile leading to hemolysis.
• Sickle cell anemia occurs when a person inherits two abnormal genes (one
from each parent).
• In children, hemolyzed sickle cells aggregate and block the blood vessels,
leading to infarction (stoppage of blood supply).
• The infarction is common in small bones.
• The infarcted small bones in hand and foot results in varying length in the
digits.
• This condition is known as hand and foot syndrome.
• Jaundice also occurs in these children.

• 2] hereditary spherocytosis:
• the red cells are very small and spherical rather than being
biconcave discs.
• These cells cannot withstand compression forces because they do
not have the normal loose,baglike cell membrane structure of the
biconcave discs.
• On passing through the splenic pulp and some other tight vascular
beds, they are easily ruptured by even slight compression.

• 3] thalassemia:
• Thalassemia is an inherited disorder,
• characterized by abnormal hemoglobin.
• It is also known as Cooley’s anemia or Mediterranean anemia.
• It is more common in Thailand and to some extent in
Mediterranean countries.
• Thalassemia is of two types:
• i. αthalassemia
• ii. βthalassemia.

• The βthalassemia is very common among these two.
• In normal hemoglobin, number of α and β polypeptide chains is
equal.
• In thalassemia, the production of these chains become
imbalanced because of defective synthesis of globin genes.
• This causes the precipitation of the polypeptide chains in the
immature RBCs, leading to disturbance in erythropoiesis.
• The precipitation also occurs in mature red cells, resulting in
hemolysis

• α-Thalassemia:
• in fetal life or infancy.
• αchains are less, absent or abnormal.
• In adults, βchains are in excess and in children, γchains are in excess.
• This leads to defective erythropoiesis and hemolysis.
• The infants may be stillborn or may die immediately after birth.
• β-Thalassemia:
• βchains are less in number, absent or abnormal with an excess of α-
chains.
• The αchains precipitate causing defective erythropoiesis and hemolysis.

4) Nutrition deficiency anemia:
• Iron deficiency anemia: RBCs are microcytic,hypochromic. Features
are brittle nails,brittle hair, atrophy of papilla in tongue, dysphagia.
• Protein deficiency anemia:RBCs are macrocytic and hypochromic.
• Pernicious anemia( addison’s anemia): due to deficiency of vitamin
B12. RBCs are macrocytic, normochromic or hypochromic. It is
common in old age. It is more common in females. features are lemon
yellow colored skin, red sore tongue, parasthesia and ataxia.
• Megaloblastic anemia:due to deficiency of vitamin B9 i.e. folic acid.
RBCs are megaloblastic and hypochromic

5)Anemia caused due to chronic diseases:
• It is the second common type of anemia (next to iron deficiency anemia).
• It is characterized by short lifespan of RBCs, caused by disturbance in iron metabolism or resistance to
erythropoietin action.
• Anemia develops after few months of sustained disease.
• Common causes anemia of chronic diseases:
• i. Noninfectious inflammatory diseases such as rheumatoid arthritis (chronic inflammatory
autoimmune disorder affecting joints).
• ii. Chronic infections like tuberculosis (infection caused by Mycobacterium tuberculosis) and abscess
(collection of pus in the infected tissue) in lungs.
• iii. Chronic renal failure, in which the erythropoietin secretion decreases (since erythropoietin is
necessary for the stimulation of bone marrow to produce RBCs, its deficiency causes anemia).
• iv. Neoplastic disorders (abnormal and disorganized growth in tissue or organ) such as Hodgkin’s
disease (malignancy involving lymphocytes) and cancer of lung and breast.
• RBCs are generally normocytic and normochromic in this type of anemia. However, in progressive
disease associated with iron deficiency the cells become microcytic and hypochromic.

Effect of anemia on function of circulatory system:
• In severe anemia, the blood viscosity may fall to as low as 1.5
times that of water rather than the normal value of about 3.
• This decreases the resistance to blood ﬂow in the peripheral blood
vessels, so that far greater than normal quantities of blood ﬂow
through the tissues and return to the heart, thereby greatly
increasing cardiac output.
• increased pumping workload on the heart.

Signs
1. Pallor - mucous membranes, conjunctivae and skin.
2. cardiovascular system -tachycardia, collapsing pulse,
cardiomegaly, midsystolic flow murmur, dyspnoea on
exertion, and in the case of elderly, congestive heart failure

.
3. CNS-attacks of faintness, giddiness, headache, tinnitus,
drowsiness, numbness and tingling sensations of the hands and
feet.
4. Ocular manifestations- Retinal haemorrhages
5. Reproductive system -Menstrual disturbances such as
amenorrhoea and menorrhagia and loss of libido

.
6. Renal system- Mild proteinuria and impaired concentrating
capacity of the kidney
7. Gastrointestinal system- Anorexia, flatulence, nausea,
constipation and weight loss may occur.

Symptoms
• Tiredness, easy fatiguability, generalised muscular weakness,
lethargy and headache.
• In older patients, there may be symptoms of cardiac failure,
angina pectoris, intermittent claudication, confusion and
visual disturbances

Oral manifestations of anemias:
• Pernicious anemia:
• Glossitis
• Painful and burning lingual sensation
• Beefy red tongue
• Apthous ulcers( rare)
• Atrophy of tongue known as bald tongue
• Loss of taste
• Burning sensation of mucosa in some cases

• Aplastic anemia:
• Petechiae purpuric spots or frank hematomas of oral mucosa
• Ulcerative lesions of oral mucosa or pharynx
• Thalassemia:
• Oral mucosa may exhibit characteristic anemic pallor observed on
the skin.

• Sickle cell anemia:
• Bone changes in dental radiographs.
• Morphological alterations in the nuclei of epithelial cells in
scrapings of oral mucosa
• Erythroblastosis fetalis:
• Deposition of blood pigment in enamel, dentin of developing teeth
giving them green, brown or blue hue.
• Enamel hypoplasia

• Iron deficiency anemia:
• Cracks or fissures at corners of mouth
• Glossitis(smooth,red, painful tongue)
• Atrophy of filliform papillae and then fungiform papillae

BLOOD GROUPS
• Discovered by Austrian Scientist Karl Landsteiner, in 1901.
• He was honored with Nobel Prize in 1930 for this discovery
ABO system & Rh system.

Blood grouping
• 21 different systems. Common ones are:
 ABO System
 Rh system
 Lewis system
 MNS system
 P system
 Kell system
 Duffie system
 Lutheran system

Landsteiner’s law
• 1. If a particular agglutinogen (antigen) is present in the RBCs,
corresponding agglutinin (antibody) must be absent in the
serum.
• 2. If a particular agglutinogen (antigen)is absent in the RBCs,
the corresponding agglutinin(antibody) must be present in the
serum.

BLOOD GROUP SYSTEM:
ABO SYSTEM:
• A group
• B group
• AB group
• O group

Ag & Ab present in ABO blood group system

Compatibility between different blood groups
Donor’
s group
Recipient’s group
A
(Aβ)
B
(Bα)
AB
(AB nil)
O
(nil αβ)
O
A X X
B X X
AB X X X
158
“O”=Universal Donor “AB”= Universal Recipient

Blood typing, grouping
• Blood typing is done on the basis of agglutination.
• Agglutination means the collection of separate particles
like RBCs into clumps or masses.
• Agglutination occurs if an antigen is mixed with its
corresponding antibody which is called isoagglutinin

Complications of mismatched blood
transfusion

Rh factor
• This antigen was discovered by Landsteiner and Wiener.
• It was first discovered in Rhesus monkey and hence the name
‘Rh factor’.
• There are many Rh antigens but only the D antigen is more
antigenic in human.
 85%- Rh positive, 15%- Rh negative

Rh factor:
• It is an antigen present in RBC.
• The persons having D antigen are called Rh positive and those
without D antigen are called Rh negative.
• There is no anti D present.

Inheritance of Rh factor
• Rhesus factor is an inherited
dominant factor. It may be
homozygous Rhesus +(DD)
or heterozygous Rhesus
+(Dd). Rhesus- occurs only
with complete absence of D
(dd).

Hemolytic disease of the newborn
(ERYTHROBLASTOSIS FETALIS):
• Abnormal hemolysis of RBC.
• Due to Rh incompatibility.
• Disorder in fetus characterised by presence of erythroblasts in blood.
• When mother is Rh negative and fetus is Rh positive, usually the first
child escapes these complications as Rh antigen cannot pass from fetal
blood to mother’s blood through placental barrier.
• But at the time of parturition, Rh antigen from fetal blood leaks into
mothers blood because of severance of umbilical cord.
• Within a month of delivery, mother develops Rh antibody in her blood.
• If the conceives again and the fetus is Rh positive again then Rh
antibody from mother’s blood crosses placenta and enters fetal blood.
• This causes hemolysis and then jaundice in fetus.

Treatment of erythroblastosis fetalis:
• If mother is Rh negative and fetus is found to be Rh positive then anti
D should be administered to the mother at 28th and 34th weeks of
gestation.
• If Rh negative mother delivers Rh positive baby then anti D should be
administered to the mother within 48 hours of delivery. This develops
passive immunity.
• If the baby is born with this disease then treatment is done by exchange
transfusion method. Rh negative blood is transfused into the infant. It
will take atleast 6 months for the infant’s new Rh positive blood to
replace the transfused Rh negative blood. By this time, Rh antibody
molecules derived from mother will get destroyed.

BLOOD TRANSFUSION
• Blood transfusion is the process of transferring blood or blood
components from one person (the donor) into the bloodstream of
another person (the recipient).
• Transfusion is done as a life-saving procedure to replace blood cells
or blood products lost through bleeding.
• It is necessary in condition like-
anemia burns
hemorrhage surgery
trauma

Precautions to be taken before blood
transfusion
1. Donor must be healthy, without any diseases like:
▫ Sexually transmitted diseases such as syphilis
▫ Diseases caused by virus like hepatitis, AIDS, etc.
2. Only compatible blood must be transfused
3. Both matching and cross-matching must be done
4. Rh compatibility must be confirmed

Precautions to be taken while transfusing blood
1. Apparatus for transfusion must be sterile
2. Temperature of blood to be transfused must be same as the
body temperature
3. Transfusion of blood must be slow. The sudden rapid infusion
of blood into the body increases the load on the heart,
resulting in many complications.

Hazards of blood transfusion
1. Reactions due to mismatched (incompatible) blood
transfusion – transfusion reactions
2. Reactions due to massive blood transfusion
3. Reactions due to faulty techniques during blood transfusion
4. Transmission of infections

Exchange transfusion
• It is the procedure which involves removal of patient’s blood
completely and replacement with fresh blood or plasma of the
donor
• It is otherwise known as replacement transfusion.
• It is an important life-saving procedure carried out in
conditions such as severe jaundice, sickle cell anemia,
erythroblastosis fetalis, etc.

Autologous blood transfusion
• It is the collection and reinfusion of patient’s own blood.
• It is also called self blood donation.
• The conventional transfusion of blood that is collected from
persons other than the patient is called allogeneic or
heterologous blood transfusion.
• Used for planned surgical procedures.
• Prevents the transmission of viruses such as HIV or hepatitis
B. It also eliminates transfusion reactions

Transfusion reactions:
• ABO SYSTEM: fever, hives(skin itching), renal failure, shock,
death
• Rh SYSTEM: fever, hives(skin itching), renal failure, shock, death
: Erythroblastosis fetalis

Blood substitutes
• Fluids infused into the body instead of whole blood are known
as blood substitutes.
• Commonly used blood substitutes are:
1. Human plasma
2. 0.9% sodium chloride solution (saline) and 5% glucose
3. Colloids like gum acacia, isinglass, albumin and animal
gelatin.

BLOOD VOLUME
• Total amount of blood present in the circulatory system, blood
reservoirs, organs and tissues together constitute blood
volume.
• In a normal young healthy adult male weighing about 70 kg,
the blood volume is about 5 L.
• It is about 7% of total body weight.
• It ranges between 6% and 8% of body weight.
• In relation to body surface area, blood volume is 2.8-3.1 litres
per square metre.

Variations in blood volume:
PHYSIOLOGICAL:
1)Age – increases as age advances. 8)Posture-standing erect for long
2)Sex- more in males time reduces blood volume by 15%
3)Surface area of the body- 9)Stress- increases
directly proportional 10) High altitude- increases
4)Body weight-
directly proportional
5)Atmospheric temperature-
warm- increases
cold- decreases
6)Pregnancy-early stages-
20-30 % increase
7)Exercise- increase

Variations in blood volume:
PATHOLOGICAL:
Hypervolemia(increased)
1. Hyperthyroidism
2. Hyperaldosteronism
3. Cirrhosis of liver
4. Congestive cardiac failure
Hypovolemia(decreased)
1. Hemorrhage or blood
loss
2. Fluid loss
3. Hemolysis
4. Anemia
5. Hypothyroidism

REGULATION of blood volume
• Hypothalamus 2 mechanism renal &
hormonal
• When BV increases—loss of fluid from the body.
• When BV decreases– retention of water.
• Hypothalamus regulates the extracellular fluid (ECF) volume
and blood volume by acting mainly through kidneys and sweat
glands and by inducing thirst.

Clinical relevance-
• General restorative procedures do not pose a significant risk
of bleeding.
• Care should be taken to avoid injuring the gingiva while
placing rubber dam clamps, matrices and wedges.
• A rubber dam should be used to prevent laceration of soft
tissues by the cutting instruments.

.
• Saliva ejectors and high-speed suction can injure the mucosa in
the floor of the mouth and cause hematoma or ecchymosis;
thus, they should be used carefully.
• Endodontic therapy is preferred over extraction whenever
possible in these patients.

.
• Endodontic therapy does not usually pose any significant risk
of bleeding and can be performed routinely.
• Endodontic surgical procedures may require factor
replacement therapy.

.
• Dentists must be aware of the impact of bleeding disorders on
the management of their patients.
• Proper dental and medical evaluation of patients is therefore
necessary before treatment, especially if an invasive dental
procedure is planned.
• Regular dental visits usually every 6 months will help identify
problems early, reinforce prevention, and emphasis the
importance of reducing the intake of food and drink
containing high levels of sugar or acid.

References:
1.Guyton and Hall /textbook of medical physiology/13th edition
2. K.Sembulingam/Essentials of medical physiology/6th edition.
3. Shafer’s textbook of oral pathology/ 6th edition.

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