This document provides an overview of the composition and functions of blood. It discusses the main components of blood including plasma, red blood cells, white blood cells, and platelets. It describes the properties of each component as well as their roles in nutrition, respiration, immunity, temperature regulation, and other vital functions. The document also examines the processes of erythropoiesis, coagulation, and the determination of blood groups. In summary, it serves as a comprehensive review of the makeup and workings of the circulatory fluid known as blood.

1. BLOOD
Prepared by :-
Dr.Nidhi Ruparelia
Guided by :-
Department of conservative dentistry and
endodontics

2. CONTENT
INTRODUCTION
PROPERTIES
COMPOSITION
FUNCTIONS
RBC
ERYTHROPOIESIS
WBCs
PLATELETS

3. COAGULATION OF BLOOD
BLOOD GROUPS
BLOOD DISORDERS
COMPLICATIONS

4. INTRODUCTION
Blood is a connective tissue in fluid form.
It is considered as ‘Fluid of Life’ because it
carries oxygen from lungs to all parts of the
body and carbon dioxide from all parts of
the body to the lungs.
It is called as ‘Fluid of Growth’ because it
carries nutritive substances from the
digestive system,and hormones from
endocrine glands, to all the tissues.

5. It is also called ‘Fluid of health’ because it
protects the body against the diseases and
gets rid of waste products and unwanted
substances by transporting them to
excretory organs like kidneys.
So basically, blood is a body fluid in
humans and other animals that delivers
necessary substances such as Nutrients &
Oxygen to the cells & transports Metabolic
waste products away from the cells.

6. PROPERTIES OF BLOOD
 COLOR
 VOLUME
 pH
 SPECIFIC GRAVITY
 VISCOSITY

7.  COLOR :-
Blood is red in color.
Arterial blood is scarlet red because it contains more oxygen.
Venous blood is purple red because of more carbon dioxide.
 VOLUME :-
Average volume of blood – 5 L
Femles – 4.5 L
It is 8% of body weight in young adult weighing about 70 kg
 pH and REACTION :-
Blood is slightly alkaline and is Ph is 7.4

8.  SPECIFIC GRAVITY :-
Specific gravity of total blood :- 1.052 – 1.061
Specific gravity of blood cells :- 1.092 – 1.101
Specific gravity of plasma :- 1.022 – 1.026
 VISCOSITY :-
Blood is 5 times more viscous than water.
It is mainly due to RBCs and Plasma Proteins

9. COMPOSITION OF BLOOD
Blood contains Blood cells which are formed elements and liquid
portion known as Plasma.
BLOOD CELLS
3 Types of cells are present in the blood :-
1. Red blood cells / Erythrocytes
2. White blood cells / Leukocytes
3. Platelets / Thrombocytes

10. BLOOD PLASMA

11. HEMATOCRIT VALUE
Volume of red blood cells expressed in % is called
Hematocrit value / packed cell volume.
Plasma = 55%
RBCs = 45%

12. PLASMA
 It is straw – colored clear liquid part of blood.
 It contains 91-92% water and 8-9% solids
Plasma
Solids
[7-8%]
Water
[92-93%]
Gases
[O2, CO2, N2]
INORGANIC SUBSTANCES
Sodium
Calcium
Potassium
magnesium
ORGANIC SUBSTANCES
Plasma proteins
Amino acids
Carbohydrates
Fats

13. SERUM
Serum is straw colored clear fluid that oozes from blood clot.
When blood is shed/collected in container
It clots
[because fibrinogen is converted to fibrin]
Blood cells are trapped in fibrin forming blood clot.
after 45 mins
Serum oozes out
For clinical significance,
Serum is seperated from blood cells & clotting elements by
centriguging.

14.  Volume of serum is same as plama = 55%
 Serum is same as plasma in all other constituents except
FIBRINOGEN {absent in serum bcoz it’s converted to fibrin
during clotting}
SREUM = PLASMA - FIBRINOGEN

16. FUNCTIONS OF BLOOD
1. Nutritive function
2. Respiratory function
3. Excretory function
4. Transport of hormones and enzymes
5. Regulation of water balance
6. Regulation of acid-base balance
7. Regulation of body temperature
8. Storage function
9. Defensive function

17. NUTRITIVE FUNCTION
 Nutritive substances like glucose, amino acids, lipids ,
& vitamins are derived from digested food are
absorbed from GIT & carried by blood to different parts
of body for growth and production of energy.
RESPIRATORY FUNCTION
 Transport of respiratory gases is done by the blood.
 It carries oxygen from alveoli of lungs to different
tissues & CO2 from tissues to alveoli.

18. EXCRETORY FUNCTION
 Waste products formed in the tissues during various
metabolic activities are removed by blood, & carried to
the excretory organs like kidney, skin, liver, etc. for
excretion.
TRANSPORT OF HORMONES & ENZYMES
 Hormones which are secreted by ductless glands are
released directly into the blood.
 The blood transport of these hormones to their target
organ/tissues.
 Blood also transports enzymes.

19. REGULATGION 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.
REGULATION OF ACID – BASE BALANCE
 Plasma proteins & hemoglobin act as buffers & help
in the regulation of acid – base balance.

20. REGULATION OF 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 & heat gain in the body.
STORAGE FUNCTION
 Water and some important substances like proteins,
glucose, sodium, & potassium are constantly required
by the tissues.
 Blood serves as readymade source for these
substances & are taken from blood during conditions
like starvation, fluid loss, electrolyte loss etc.

21. DEFENSIVE FUNCTION
 Blood plays an important role in the defense of the
body.
 The White blood cells are responsible for this function.
 Neutrophils & Monocytes engulf the bacteria by
phagocytosis.
 Lymphocytes are involved in development of immunity.
 Eosinophills are responsible for detoxification ,
disintegration & removal of foreign proteins.

23. RED BLOOD CELLS / ERYTHROCYTES
 RBCs are the non-nucleated formed elements in the blood.
 Red color of RBCs is due to presence of Hemoglobin.
 They play a vital role in transport of gases.
 They are in large number as compare to other two blood cells.
NORMAL VALUE :-
 4 – 5.5 Million/cumm
 Adult males = 5 Million/cumm
 Adult females = 4.5 Million/cumm

24. FUNCTIONS OF RBCS
1. Transport oxygen from lungs to the tissues
(oxyhemoglobin).
2. Transport carbon-dioxide from tissues to lungs
(carboxyhemoglobin)
3. Hemoglobin acts as a buffer and regulates the
hydrogen ion concentration (acid base balance)
4. Carry the blood group antigens and Rh factor

25. MORPHOLOGY OF RBCS
 Normally RBCs are disk shaped and biconcave
{dumbell}
 Central portion is thinner and periphery is thicker.
 Biconcave contour of RBCs has some mechanical &
functional advantages.

26. ADVANTAGES
 Biconcave shape helps in equal and rapid diffusion of
oxygen & other substances into interior of cells.
 Large surface area is provided for absorption / removal
of different substances.
 Minimal tension is offered on the membrane when the
volume of cell alters.
 Because of biconcave shape, while passing through
capillaries , RBCs squeeze through capillaries very
easily without getting damaged.

27. PROPERTIES OF RED BLOOD CELLS
 Roulexux Formation
When blood is taken out of blood vessels the RBCs pile
up one above another like pile of coins.
This property is called ROULEAUX Formation.
 Specific gravity
Specific gravity of RBCs is 1.092-1.01
 Packed cell volume
PCV is the proportion of the blood occupied by RBCs expressed
in percentage, also called hematocrit value.

28. Suspension stability
During circulation,
The RBCs remain suspended uniformly in the blood.
This property of RBCs is called suspension stability.

29. LIFESPAN OF RBCs
 Average lifespan of RBCs is about 120days.
 After the lifetime the senile RBCs are destroyed in
reticuloendothelial system.
FATE OF RED BLOOD CELLS
 When the cells become older , 120 days, the cell
membrane becomes more fragile.
 Diameter of capillaries is less or equal to that of RBCs
 Younger RBCs pass through capillaries easily &
because of fragile nature, older cells are destroyed
while trying to squeeze through capillaries.

30. HEMOGLOBIN

31. GLOBIN
 Each hemoglobin molecule is composed of two types
of globins organized into four subunits.
 Hemoglobins are classified into different types,
depending on the combination of the two sets of globin
units.
 Most of the hemoglobin present in adult humans
comprises 2 α globins and 2 β globins.

32. Heme
 The heme group bound to each globin is an organic
macromolecule with an iron at the center.
 The heme group comprises a structure called the
porphyrin ring, which is formed by the combination of
four heterocyclic rings called pyrroles.
 When the heme is bound to an oxygen molecule or
carbon dioxide molecule, it is termed oxyhemoglobin,
or carbaminohemoglobin respectively.
 When the heme groups of a hemoglobin molecule are
not bound by any molecule, it is referred to as
deoxyhemoglobin.
 It is oxyhemoglobin that imparts a bright red color to
blood.

33. ERYTHROPOIESIS
hemocytoblast
Proerythroblast
Early
erythroblast
Late
erythroblast
Normoblast
Reticulocyte
Erythrocyte

34. ERYTHROPOIESIS
 Erythropoiesis is the process of the origin,
development and maturation of the erythrocytes.
SITE OF ERYTHROPOIESIS
Upto the age of 20yrs, RBCs are produced from RED BONE
MARROW of all bones.
After 20yrs RBCs are produced from all the Membranous bones
and ends of long bones.

35. MEGALOBLAST
INK SPOT NUCLEUS
BASOPHILLIC
ERYTHROBLAST
POLYCHROMATIC ERYTHROBLAST

36. WHITE BLOOD CELLS / LEUKOCYTES
 White blood cells or leukocytes are the colorless and
nucleated formed elements of blood .
 Compared to RBCs , WBCs are large in size and
lesser in number.
Normal count
Total WBC count [TC] : 4000-11,000/cumm of blood

37. CLASSIFICATION
GRANULOCYTES
 Neutrophils - 40-70%
 Eosinophils- 1-4%
 Basophils- <1%
AGRANULOCYTES
 Monocytes - 4-8%
 Lymphocytes- 20-45%

38. NEUTROPHILLS
 Neutrophills are also known as polymorphonuclear leukocytes
because the nucleus is multilobed.
 The number of lobes vary from 1-6.
 The granules are fine or small in size.
 When stained with Leshiman’s stain
[which contains acidic eosin and basic methylene blue],the
granules take both the stains equally.
So , the granules appear Violet in color.

39. EOSINOPHILLS
 Eosinophills have coarse granules in the cytoplasm, which stain
pink or red with eosin.
 Nucleus is bilobed and spectacle shaped.
 Diameter is between 10-14 micron.

40. BASOPHILLS
 Basophills also have coarse granules in the cytoplasm and the
granules stain Purple Blue with Methylene Blue.
 Nucleus is bilobed.
 Diameter of the cell is 8-10micron.

41. MONOCYTES
 Monocytes are the largest WBCs with diameter of 14-18 micron.
 The cytoplasm is clear without granules.
 The nucleus is round, oval, horseshoe shaped, bean shaped or
kidney shaped.
 The nucleus is placed either in the centre of the cell or pushed
to the one side and large amount of cytoplasm is seen.

42. LYMPHOCYTES
 Lymphocytes also do not have granules in cytoplasm.
 The nucleus is oval, bean shaped or kidney shaped and
occupies the whole of the cytoplasm.
A rim of cytoplasm may or may not be seen.
Depending on size, lymphocytes are divided into two types:
Large
lymphocytes
(10-12micron)
Small
lymphocytes
(7-10micron)
T lymphocytes
(cellular
immunity)
B lymphocytes
(humoral
immunity)

43. lymphocyte

44. PATHOLOGICAL VARIATIONS
o LEUKOCYTOSIS
• Increase in WBCs count
• Occurs in conditions like – infections, allergy, TB.
o LEUKOPENIA
• Abnormally low WBC count.
• Occurs in conditions like –
1. Anaphylactic shock
2. Cirrhosis of liver
3. Viral infection
o LEUKEMIA
• Cancerous conditions involving abnormal and uncontrolled increase in
WBCs count.
• More than 1,000,000/cumm.

45. PLATELETS

46. PLATELETS / THROMBOCYTES
 Platelets are the formed elements of the blood.
 They are small, colorless, non nucleated and moderately
refractive bodies which are considered to be the fragments of
cytoplasm.
SHAPE OF PLATELETS
Normally, platelets are of several shapes, eg:-
Spherical, rod shaped, & become oval or disk shaped when
inactivated.
Sometimes have dumb-bell shape, comma shape, cigar shape or
any other unusual shape.

47. NORMAL COUNT
Normal count is 1,50,000 – 4,50,000/microliter of blood.
Platelets are less in infants ( 1,50,000-2,00,000/cumm)
But, reaches normal level at 3rd month after birth.

48. FUNCTIONS OF PLATELETS
 ROLE IN BLOOD CLOTTING
 ROLE IN CLOT RETRACTION
(Actin, myosin and thrombosthenin)
 ROLE IN PREVENTION OF BLOOD LOSS
 ROLE IN REPAIR OF RUPTURED BLOOD VESSELS
 ROLE IN DEFENSE MECHANISM

49. COAGULATION OF BLOOD

50. COAGULATION OF BLOOD
 Coagulation or clotting is defined as the process in which blood
looses its fluidity and becomes a jelly like mass, few minutes
after it is shed out or collected in a container.
 Coagulation of blood occurs through a series of reactions due to
the activation of group of substances. The substances
necessary for clotting are called clotting factors

51.  13 clotting factors are identified
CLOTTING FACTORS
FACTOR I – Fibrinogen
FACTOR II – Prothrombin
FACTOR III – Thromboplastin
FACTOR IV – Calcium
FACTOR V – Labile factor
FACTOR VI – presence not been proved
FACTOR VII – Stable factor
FACTOR VIII – Antihemophillic factor
FACTOR IX – Christmas factor
FACTOR X – Stuart-power factor
FACTOR XI – Plasma thromboplastin
antecedent
FACTOR XII – Hegman factor
FACTOR XIII – Fibrin stabilizing

52. STAGES OF BLOOD CLOTTING
STAGES OF
BLOOD
CLOTTING
FORMATION
OF
PROTHROMBI
N ACTIVATOR
CONVERSION OF
PROTHROMBIN
INTO THROMBIN
CONVERSION OF
FIBRINOGEN
INTO FIBRIN
INTRIN
SIC
PATH
EXTRI
NSIC
PATH

54. BLOOD GROUPS

55.  BLOOD GROUPS are determined by the Presence Of Antigen
In RBC Membrane.
ABO BLOOD GROUPS
 Blood groups depends upon the immunological reaction
between antigen and antibody.
 Landsteiner found two antigens on the surface of RBCs and
named them as A antigen and B antigen.
 These antigens are also called AGGLUTINOGENS because of
their capacity to cause agglutination of RBCs.
 He noticed the corresponding antibodies or AGGLUTININS in
the plasma and named them as Anti A and Anti B.
 A particular agglutinogen and the corresponding agglutinin
cannot be present together.
 If present, it causes Clumping Of The Blood.

56. LANDSTEINER’S LAW
 Landsteiner’s law states that:-
• If a particular antigen (agglutinogen) is present in the RBCs ,
corresponding antibody (agglutinin) must be absent in the
serum.
• If a particular antigen is absent in the RBCs, the corresponding
antibody must be present in the serum.

57. ABO SYSTEM
 Based on presence or absence of antigen A and antigen B,
Blood group is divided into 4 groups:-
1. ‘A’ GROUP
2. ‘B’ GROUP
3. ‘AB’ GROUP
4. ‘O’ GROUP
 The blood having antigen A is called A group, this group has B
antibody in the serum.
 The group with antigen B and alpha antibody is called B group.

59. RH FACTOR
 Rh factor is the Antigen Present In RBC.
 The antigen was discovered by Landsteiner and
Wiener.
 It was discovered in Rhesus monkey and hence the
name Rh factor.
 The persons having D antigen are called if Rh
positive and those without D antigens are called Rh
negative.

60. IF RH POSITIVE BLOOD IS TRANSFUSED TO RH
NEGATIVE PERSON FOR THE FIRST TIME, THEN
ANTI D IS FORMED IN THAT PERSON.
ON, THE OTHER HAND , THERE IS NO RISK OF
COMPLICATIONS , IF RH POSITIVE PERSON
RECEIVES THE NEGATIVE BLOOD.

61. ERYTHROBLASTOSIS FETALIS
 Hemolytic disease is the disease in fetus and newborn
characterized by Abnormal Hemolysis Of Rbcs.
 Hemolytic disease leads to erythroblastosis fetalis.
 Erythroblastosis fetalis is a disorder in the fetus
characterized by the Presence Of Erythroblast In The
Blood.
 It is due to Rh incompatibility i.e. the difference
between the Rh blood group of mother and baby.

62.  When a Mother Is Rh Negative and Fetus Is Rh
Positive usually the first child escapes the
complications of Rh incompatibility.
 This is because the Rh antigen cannot pass from fetal
blood into mother’s blood through the placental barrier.
 However, at the time of parturition, the Rh antigen
from fetal blood may leak into mother’s blood because
of placental detachment .
 During post partum period i.e. within a month after
delivery, the mother develops Rh antibody in her
blood.

63. RH FACTOR AND PREGNANCY

64.  When the mother concieves for the Second Time and if
the fetus happens to be Rh positive again,
the Rh antibody from mother’s blood crosses the
placental barrier ,
enters the fetal blood ,
causes Agglutination Of Fetal Rbcs,
resulting in Hemolysis.
 The severe hemolysis in the fetus causes jaundice.

65.  Rh+ Mother With Rh- Baby–
No Problem
 Rh- Mother With Rh+ Baby–
Problem
 Rh- Mother With Rh- Father–
No Problem
 Rh- Mother With Rh- Baby-- No
Problem

66. BLEEDING DISORDERS

67. BLEEDING DISORDERS
Hemophillia
Purpura
Von-Willebrand disease
Thrombosis
Thrombocytopenia
Anaemia
Leukemia

69. HEMOPHILIA
 Hemophilia is a group of sex-linked inherited blood
disorders, characterized by Prolonged Clotting Time.
 However, the Bleeding Time Is Normal.
 Usually, it affects males with Females Being The
Carrier.
Types of Hemophilia:
1. Hemophilia A / classic hemophilia : due to
deficiency of factor VIII. 85% people are affected.
2. Hemophilia B / Christmas disease: due to
deficiency of factor IX. 15% of people are affected.
3. Hemophilia C / Factor XI : due to deficiency of
factor XI it is very rare bleeding disorder.

71. SYMPTOMS OF HEMOPHILIA
 Spontaneous bleeding
 Prolonged bleeding due to cuts, extraction and surgery
 Hemorrhage in GIT and Urinary Tracts.
 Bleeding in joints followed by swelling and pain
 Appearance of blood in urine.

72. MANAGEMENT OF HAEMOPHILIC PATIENTS
 Mild haemophilics can be easily managed and can
effectively undergo even surgical endodontics without
factor replacement therapies.
 Severe hemophilia can pose significant health hazard
and needs thorough preparation to meet any
exigencies arising during the treatment.
 If suspicion of bleeding is raised, the next step is blood
investigations:
1. Complete Blood Count/ Platelet Count
2. Bleeding Time

73.  Formocresol can be used as mummifying agent to
control and eliminate bleeding from the canals.
 Local Tranexamic acid can be applied whenever there
is silght injury to gingiva.

74. MANAGEMENT OF HAEMOPHILIA- A
 Management of Haemophilia A requires:
increasing factor VIII levels,
replacing factor VIII and
inhibiting fibrinolysis.
 Desmopressin is a vasopressin agonist that raises
factor VIII levels by 3-4 folds by encouraging the body
to produce endogenous factor VIII.
 The dose given is either 0.3 ug/kg I.V. or S.C. 30-60
minutes prior to surgical procedure or 300ug
intranasally.

75.  Anti- fibrinolytic agents like Tranexamic acid and
Epsilon Aminocaprioic Acid (EACA) can be used to
protect the formed clot.
 Tranexamic Acid is given systemically in a dose of
1g(30mg/kg) orally, 4 times/day starting at least one
day preoperatively especially for surgical procedures.
 If bleeding starts or is expected to start, Factor VIII
must be replaced to a level adequate to ensure
hemostasis. One unit of Factor VIII concentrate per
kilogram of body weight elevates the Factor VIII level
by 2%.

76.  The local hemostatic measures recommended are:
 Surgicel [Absorbable Hemostat Wrap]
 Oxidized cellulose,
 Fibrin glue
 Tranexamic acid,
 Collagen,
 Cyanoacrylate,
can also be helpful.
o Local Use Of Fibrin Glue and Swish And Swallow
Rinse Of Tranexamic Acid before and after the
procedure is also suggested as a cost-effective
alternative.

77. LOCAL HEMOSTATIC MEASURES

78. ENDODONTIC CONSIDERATIONS
 Nerve blocks like inferior alveolar block, lingual infiltration are
usually contraindicated until and unless the factor levels are
raised above 30% by replacement therapy, else extravasation
of blood in oropharyngeal area or in pterygoid plexus can be
life threatening.
 Acetaminophen and Narcotics are prefebly used for
postoperative pain while Aspirin or any other Non-steroidal
anti-inflammatory drug should be avioded because of their
effect on platelet aggregation.
 Rubber dam should be used to prevent laceration of soft
tissue by rotary instruments.
 Sodium Hypochlorite should be used for irrigation in all cases
followed by use of Calcium hydroxide paste to control
bleeding.

79.  Apex locator should be used to measure working length instead
of IOPA as repeated placement of films can lead to injury and
bleeding in mucosa.
 Intracanal injection of local anaesthetic solution containing
Adrenaline or Topical application of adrenaline can be used to
minimise bleeding.

80. PURPURA

81. PURPURA
 Purpura is a disorder characterized by prolonges bleeding
time. However, clotting time is normal.
 Characteristic feature – spontaneous bleeding under the skin
from ruptured capillaries.
 Causes small tiny hemorrhagic spots in many area of the
body , called Purpuric spots(purple colored patch like
appearance).
CLASSIFICATION
THROMBO
CYTOPENIC
PURPURA
IDIOPATHIC
THROMBO
CYTOPENIC
PURPURA
THROM
BASTENIC
PURPURA

82. THROMBOCYTOPENIC PURPURA
 Due to deficiency of platelets
IDIOPATHIC THROMBOCYTOPENIC PURPURA
 Cause is unknown
 It is believed that platelet count decreases due to the
development of antibodies against platelets.
THROMBASTHENIC PURPURA
 Due to structural or functional abnormality of platelets.
 Defective clot retraction.

83. CLINICAL CONSIDERATIONS
 ITP is a common childhood disease with low morbidity
and mortality, with or without hemorrhage.
 Dental procedures can be performed in patients with
platelet counts above 50,000/mm3.
 For patient with low platelet count, blood transfusion or
previous corticosteriod treatment is necessary.
 Prescription of antiplatelet drugs, such as acetylsalicilic
acid and ibuprofen must be avoided.

85. VON - WILLEBRAND DISEASE
 Von Willebrand disease is an inherited disease marked by vWF
deficiency.
 It is considered the most common congenital bleeding disorder.
 Three types of vWD with different subtypes and different
patterns of inheritance have been recognized:
 Type 1 (mild)
 Type 2 (moderate)
 Type 3 (severe)
 Patients with vWD are diagnosed via
 Prolonged bleeding time,
 Prolonged aPTT, and
 Low levels of vWF antigen.

87. CLINICAL CONSIDERATIONS
 Desmopressin acetate is usually the treatment of
choice for patients with the mild to moderate form of
Vwd.
 Laboratory investigations are necessary prior to any
dental procedures that are likely to cause bleeding.
These tests include the aPTT, bleeding time, and
factor VIII level in the plasma.
 The severe form of vWD requires replacement therapy
with factor concentrate that is rich in vWF because
there is no recombinant therapy for vWF.

88.  Postoperatively,
it is recommended that the patient avoid any
analgesic medications that increase the possibility of
bleeding.
Such as Aspirin and other Non Steroidal Anti-
Inflammatory Drugs (eg, ibuprofen and naproxen
sodium).
 Paracetamol (acetaminophen) can be used safely.

89.  Dental care providers must attempt to minimize trauma to the
soft tissues during placement of rubber dams, clamps,
interdental wedges, and matrix bands.
 Although it is preferable to use a supragingival margin over a
subgingival one, crowns and fixed partial dentures are
associated with a low risk of bleeding.
 Dental procedures, such as Atraumatic Restorative
Treatment, Air Abrasion, And Chemomechanical Caries
Removal Agents should be considered.
 Root canal treatment is considered safe. Bleeding from the
vital pulp might prolong pain, which can be eliminated by
irrigation with 4% sodium hypochlorite and the administration
of calcium hydroxide.

90. THROMBOSIS

91. THROMBOSIS
 Thrombosis s the formation of a blood clot inside a blood
vessel, obstructing the flow of blood through the circulatory
system.
 When a blood vessel (a vein or an artery) is injured, the body
uses platelets and fibrin to form a blood clot to prevent blood
loss. A clot, or a piece of the clot, that breaks free and begins to
travel around the body is known as an Embolus.
 Thrombosis may occur in veins (Venous thrombosis) or in
arteries(Arterial Thrombosis)
 Venous thrombosis leads to congestion of the affected part of
the body, while Arterial thrombosis affects the blood supply
and leads to damage of the tissue supplied by that artery.

92. Signs And Symptoms
 Deep Vein Thrombosis
 Pain
 Swelling of the affected extremity/area with erythema and
warmth over the vicinity of the clot
 Discoloration including a bluish or suffused color

93. 0

94. THROMBOCYTOPENIA
 Thrombocytopenia is a condition in which you have a low
blood platelet count. Platelets (thrombocytes) are colorless
blood cells that help blood clot. Platelets stop bleeding by
clumping and forming plugs in blood vessel injuries.
 You can get thrombocytopenia if your body doesn't make
enough of platelets, or if they're destroyed faster than they can
be made.

97. ANEMIA
 Anemia is a blood disorder characterized by the reduction in:
1) Red blood cells
2) Hemoglobin content
3) Packed cell volume
 Decrease in the total amount of red blood cells(RBCs) less
than 4 million/uL or their content of hemoglobin in blood less
than 12 gm/dL, or a lowered ability of the blood to
carry oxygen.
GRADING
MILD
8-12 GM/DL
MODERATE
5-8 gm/dL
SEVERE
5 gm/dL
-a.k.jain

98. Etiological classification of Anemia
Hemorrhagic
Anemia
Hemolytic
Anemia
Nutritional
deficiency
Anemia
Aplastic Anemia
Anemia of
chronic
disease
-K sembulingam

99. Hemorrhagic
Anemia
• Acute
• Chronic
Hemolytic
Anemia
• Intrinsic
• Extrinsic
• Sickle cell
• Thalassemia
Nutritional
Deficiency
• Iron
Deficiency
• Protein
Deficiency
• Pernicious (Vit
B12)
• Megaloblastic
(Folic Acid)
Aplastic
Anemia
Due to disorder
of Red Bone
Marrow
Anemia of Chronic
Disease
Chron’s disease
Rheumatiod arthritis
Liver cirrhosis
-K sembulingam

100. HEMOLYTIC ANEMIA
Extrinsic Hemolytic Anemia
• Also Autoimmune hemolytic Anemia
Intrinsic Hemolytic Anemia
• Sickle Cell Anemia (a- chains are normal and B-
chains are abnormal)
• Thalessemia
• i) a- thalassemia
• ii) b- thalassemia

101. SICKLE CELL ANEMIA
 Sickle cell anemia is inherited blood disorder characterized by
sickle-shaped red blood cells.
 It is also called Hemoglobin SS disease or Sickle cell disease.
 Sickle cell anemia is due to the abnormal hemoglobin called
Hemoglobin S.
 It occurs when a person inherits two abnormal genes
(one from each parent).
 The RBCs attain sickle (crescent) shape and become more
fragile leading to hemolysis.
-K sembulingam

102.  Since patients with SCA may be considered
immunocompromised and infections can trigger a
sickle cell crisis, these patients usually require
aggressive treatment of infections, including the use of
systemic antibiotics.
 Pulpal necrosis may occur in patients with sickle cell
anemia.
 The vasoocclusive aspects of the disease can result in
tissue and bone necrosis and pulpal necrosis in an
otherwise intact and healthy tooth.

103.  Nonsurgical root canal treatment of asymptomatic
necrotic teeth prior to the development of acute
symptoms and infection is indicated.
 The use of a local anesthetic with no vasoconstrictor
(or minimal vasoconstrictor) may be advisable for
nonsurgical procedures since the microvasculature is
often already compromised by SCA.

104. THALASSEMIA
 Thalassemia is inherited disorder characterized by abnormal
hemoglobin. It is also known as Cooley’s anemia or
Mediterranean anemia.
 They are of two types:
I. α- thalassemia
II. β-thalassemia ( more commom)
 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.
 It causes precipitation of polypeptide chains in immature
RBCs, leading to disturbance in erythropoiesis.
-K sembulingam

105.  It occurs in fetal life or infancy. In this α-chains are less, absent
or abnormal.
 In Adults, B- chains are in excess.
 In Children, γ chains are in excess.
 The Presentation Of Individuals With Alpha-thalassemia
Consists Of:
 Fatigue, Weakness, Or Shortness Of Breath.
 A Pale Appearance Or A Yellow Color To The Skin (Jaundice)
 Irritability.
 Deformities Of The Facial Bones.
 Slow Growth.
 A Swollen Abdomen.
 Dark Urine.

106. DIAGNOSIS
 Diagnosis is primarily by laboratory evaluation
and molecular diagnosis.
 Alpha-thalassemia can be mistaken for iron-deficiency
anaemia on a full blood count or blood film, as both
conditions have a microcytic anaemia. Serum
iron and Serum ferritin can be used to exclude iron-
deficiency anaemia.

107. Β-THALASSEMIA
 In β – thalassemia , β – chains are less in number , absent or
abnormal with an excess of α- chains. The body's inability to
construct new beta-chains leads to the underproduction of HbA
TYPES OF THALASSEMIA
 Beta Thalassemia Minor - heterozygous disorder resulting in
mild hypochromic, microcytic hemolytic anemia.
 Beta Thalassemia Major - homozygous disorder resulting in
severe transfusion-dependent hemolytic anemia.

108. BETA THALASSEMIA MINOR
 Caused by heterogenous mutations that affects beta globin
synthesis.
 Have one normal beta gene and one mutated beta gene.
 Usually presents as Mild, Asymptomatic hemolytic anemia.
 Hemoglobin level in 10-13 g/dL range with normal or slightly
elevated RBC count.
 Normally requires no treatment.
-Textbook of medical physiology- guyton and hall

109. BETA THALASSEMIA MAJOR
 Characterized by severe Microcytic, Hypochromic
anemia.
 It is detected in early in childhood as:
 Infants fail to thrive.
 Have pallor, variable degree of jaundice, abdominal
enlargement, and hepatosplenomegaly.
 Hemoglobin level is between 4 and 8 gm/dL.
 Severe anemia causes marked bone changes due to
expansion of marrow space for increased
erythropoiesis.

110.  Characteristic changes in skull, long bones, and hand bones
are seen.
 Have protrusion of upper teeth and Mongoloid facial features.
 Regular transfusions required and usually begins around one
year of age and continues throughout the life.
 Bone marrow transplants may be future treatment.
-Textbook of oral medicine and radiology - ghom

111. LABORATORY DIAGNOSIS OF THALASSEMIA
 Need to start with patient's individual history and family
history. Ethnic background important.
 On physical examination following may be observed:
 Pallor indicating anemia.
 Jaundice indicating hemolysis.
 Splenomegaly due to pooling of abnormal cells.
 Skeletal deformity, especially in beta thalassemia major.
 There would be decrease in hemoglobin, hematocrit, MCV, and
MCH. Normal to slightly decreased MCHC.
 Will see microcytic, hypochromic pattern.

112. IRON DEFICIENCY ANEMIA
 It is the most common type of anemia.
 It developes due to inadequate availability of iron for
hemoglobin synthesis.
 RBCs are Microcytic and Hypochromic.
 CAUSES:
• Loss of blood
• Decrease intake of iron
• Poor absorbtion of iron from intestine
• Increased demand for iron in conditions like growth and
pregnancy

113. FEATURES OF IRON DEFICIENCY ANEMIA
o Brittle nails
o Spoon-shaped nails(koilonychias)
o Brittle hair
o Atrophy of papilla in tongue
o Dysphagia

114. MEGALOBLASTIC ANEMIA
 Loss of vit B12, folic acid or intrinsic factor from stomach
mucosa can lead to slow production of erythroblasts in the bone
marrow.
 As a result, the red blood cells grow too large, with odd shapes
and are called MEGALOBLASTS.
 The erythroblasts cannot proliferate rapidly enough to form
normal number of red blood cells and those red cells that are
formed are mostly oversized, have bizarre shapes, and fragile
membrane.
 These cells rupture easily, leaving the person in dire need of
adequate number of red cells.

115. LEUKEMIA

116. LEUKEMIA
 A malignant progressive disease in which the bone marrow and
other blood-forming organs produce increased numbers of
immature or abnormal leucocytes.
 These suppress the production of normal blood cells, leading to
anemia and other symptoms.
 There Are Four Main Types Of Leukemia:
 Acute myeloid leukemia (AML)
 Chronic myeloid leukemia (CML)
 Acute lymphocytic leukemia (ALL)
 Chronic lymphocytic leukemia (CLL)

118. CLINICAL CONSIDERATIONS

119. Patient During Chemotherapy
• The most appropriate time to schedule patient for treatment
is after patient’s blood count has recovered, usually prior to
next chemotherapy session.
HOW TO MANAGE BLEEDING?
• Use of haemostatic agent such as Epinephrine to reduce blood
flow.
• Platelet Transfusion may be required.

120. ANTICOAGULANT THERAPY AND BLEEDING
DISORDERS
 Management of patients on anticoagulant therapy depends on
the: type of anticoagulant, reason for anticoagulant therapy,
and type of procedure planned.
 The International normalized ratio (INR) value is the
accepted standard for measuring prothrombin time (PT).
 Nonsurgical root canal treatment does not usually require
modification of anticoagulant therapy, although it is important to
ascertain that the patient’s INR is within the therapeutic range,
especially if a nerve block injection is required.
 Periapical surgery may present a greater challenge for
hemostasis even for patients well maintained within the
therapeutic range .

121.  The clear field visibility normally required for proper
surgical management of the root end may not be
possible in patients on anticoagulant therapy.
 Consultation with the patient’s physician is required to
assist in developing an appropriate treatment plan.
 Low-dose aspirin therapy is known to increase
bleeding time by irreversibly inhibiting platelet
aggregation.
 Hence, No treatment modifications should be
necessary for nonsurgical root canal procedures.

122.  However, surgical procedures require evaluation of
the reason and the necessity of aspirin therapy.
 It has been a common practice to advise patients to
discontinue aspirin therapy for 7 to 10 days
prior to an oral surgical procedure.
 At low-dose therapeutic levels (<100 mg/day),
aspirin may increase bleeding time and potentially
complicate surgical procedures.

123. ALLERGY TO MATERIALS USED IN ENDODONTIC
THERAPY
 True allergic reactions are characterized by one or more of the
following signs and symptoms:
 skin rash,
 swelling,
 urticaria,
 chest tightness,
 shortness of breath,
 rhinorrhea, and
 conjunctivitis.
 Type I (immediate or anaphylactic, IgE-mediated) and
Type IV (delayed, cell-mediated) are the two types of allergic
reactions most likely to be encountered as a result of exposure
to a substance used in endodontic treatment.

124.  Type I hypersensitivity requires :
 previous exposure to the antigen and can occur after
a single prior exposure or multiple prior exposures to
the allergen.
 The reaction occurs shortly after exposure and can
rapidly progress to life-threatening anaphylaxis.

125.  Type IV hypersensitivity
typically appears 48 to 72 hours after exposure and is
mediated by T lymphocytes in contrast to the humoral
immune system (antibody)-mediated Type I reaction.
 Contact dermatitis is a classic Type IV reaction.
 When materials used in endodontic treatment come in
contact with the periapical tissues (either intentionally
or inadvertently), there is the potential for a delayed
Type IV hypersensitivity reaction.

126.  The primary drug treatments for acute anaphylactic
reactions are epinephrine and H1 antihistamines.
 During an anaphylactic attack, you might receive
cardiopulmonary resuscitation (CPR) if you stop
breathing or your heart stops beating. You might also
be given medications, including:
 Epinephrine (adrenaline) to reduce your body's
allergic response
 Oxygen, to help you breathe
 Intravenous (IV) antihistamines and cortisone to
reduce inflammation of your air passages and improve
breathing
 A beta-agonist (such as albuterol) to relieve
breathing symptoms

127. REFERENCES
 Essentials of Medical Physiology - by Sembulingam
 Textbook of physiology by AK Jain
 Ingle's Endodonics - by John I. Ingle
 Burket's Oral Medicine - by Michael Glick
 Textbook Of Oral Medicine With Free Book On Basic Oral
Radiology by Ghom Anil Govindrao