Blood ppt

1. PRESENTER :
S LIPI PRAKASH

2. CONTENTS
1. INTRODUCTION
2. PLASMA
3. ERYTHOCYTES
4. WHITE BLOOD CELLS
5. PLATELETS
6. HEMOSTASIS AND BLOOD COAGULATION
7. CLINICAL CONSIDERATION OF BLOOD IN
CONSERVATIVE DENTISTRY AND ENDODONTICS

3. INTRODUCTION
Blood is a fluid connective tissue present in the circulatory system .
It is red in color due to the presence of hemoglobin
The normal blood volume in adults is around 5L
Blood is made up of –
 FLUID COMPONENT – Plasma (constitutes 55% of blood)
FORMED ELEMENTS- ( constitutes 45% of blood)
-Erythrocytes [RBCs]
-Leukocytes [ WBCs]
-Thrombocytes [ Platelets]
Dr. A K Jain Human physiology for BDS fifth edition

4. PLASMA
It’s a fluid portion of blood
Normal volume is 3500mL
Mainly composed of - water (91%)
- other substances are : Inorganic substances
like Na+ ,K+, Ca++ ions , iron , copper
Organic substances like proteins , lipids ,
glucose, urea , creatinine
Serum is plasma without clotting factors
Plasma proteins :are the proteins present in plasma
Important plasma proteins are – Albumin , Globulin , Fibrinogen
and Prothrombin

5. FUNCTIONS OF PLASMA PROTEINS-
1. Maintenance of colloidal osmotic pressure
2. Maintenance of viscosity of blood
3. Buffering action
4. Protein reserve
5. Immunity
6. Blood clotting
7. Transport
Dr. A K Jain Human physiology for BDS fifth edition

6. ERYTHROCYTES
They are the most abundant cells present in
blood.
Normal life span of an RBC is 120 days. They
lack nucleus , mitochondria or ribosomes and
hence mature RBCs cannot divide .
They contain hemoglobin
Normal erythrocyte count –
Males- 5- 5.5 million cells/mm cube
Females- 4.5 – 5 million cells/mm cube
Infants – 6- 7 million cells /mm cube
BICONCAVE SHAPE

7. Functions: The functions of RBCs are mainly due to the presence of
hemoglobin.
They include:
Transport of oxygen from lungs to tissues
Transport of carbon dioxide from tissues to lungs, and
Regulation of acid-base balance
ERYTHROPOIESIS :
It is the process of formation of RBCs
It starts in the 3rd week of IUL in the mesoderm of the yolk sac
From the 3rd month of IUL, erythropoiesis takes place in the liver and spleen
After 5th month of IUL the fetal bone marrow starts producing RBCs
By birth, the bone marrow becomes the only place of erythrocytes production
Dr. A K Jain Human physiology for BDS fifth edition

8. STAGES OF ERYTHROPOIESIS:
The various stages between stem cell and matured red blood cell are as
follows:
1.Proerythroblast
2.Early normoblast
3.Intermediate normoblast
4. Late normoblast
5. Reticulocyte and
6.Matured erythrocyte.
Dr. A K Jain Human physiology for BDS fifth edition

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

10. CHANGES DURING ERYTHROPOIESIS:
During this process four important changes are noticed.
1. Reduction in size of the cell (from the diameter of 25 m to 7.2 m)
2. Disappearance of nucleoli and nucleus
3. Appearance of hemoglobin and
4. Change in the staining properties of the cytoplasm
Dr. A K Jain Human physiology for BDS fifth edition

11. FACTORS INFLUENCING ERYTHROPOIESIS:
1.ERYTHROPOIETIN :
 Glycoprotein hormone that stimulates Erythropoiesis.
 It increases RBC production , enhances synthesis of Hb, hastens maturation of
RBC
 It is mainly formed in kidney and partly by liver
2. ANDROGENS:
 They stimulate erythropoiesis. Therefore men have higher RBC count compared to
women
3. ESTROGENS:
 They have inhibitory effect on erythropoiesis by suppression of erythropoietin
production
Dr. A K Jain Human physiology for BDS fifth edition

12. 4. HORMONES:
Throxine , Cortisol and growth hormone are necessary for RBC production .
Interleukin 1, 5 and 3 , granulocyte-macrophage colony stimulating factor (GM-CSF)
and BPA all act as local hormones and helps in conversion of stem cells to progenitor
cells.
5. DIETARY FACTORS:
Iron is necessary for Hb synthesis
VitB12 and Folic acid necessary for maturation of RBC
Vit B6 , Vit C , Copper, and Cobalt act as cofactors
6. INTRINSIC FACTORS
 Helps in the absorption of Vitamin B12
Dr. A K Jain Human physiology for BDS fifth edition

13. FATE OF RBC:
Lifespan of RBC is 120 days
The destruction occurs mostly in the capillaries of spleen - graveyard of red blood
cells
The old and fragile RBC is phagocytosed by reticuloendothelial system
In the reticuloendothelial cells , they are broken down and Hb is
released
Subsequently, Hb is broken down into heme and globin
Globin is added to the amino acid pool
Iron liberated from heme is used again for the synthesis of new Hb
The remaining portion of heme is called biliverdin.
It is reduced to bilirubin in the liver and secreted through bile

14. HEMOGLOBIN:
Hemoglobin is a conjugate protein present in the RBC
It is a globular molecule made up of 4 subunits. Each subunit contains a heme
moiety conjugated to a polypeptide
4 polypeptides form the globin portion of Hb molecule
There are 2 pairs of polypeptides in each Hb molecule . In a normal adult Hb (HbA),
two types of polypeptide chains are alpha chains and beta chains. Therefore HbA is
alpha2 beta2
Human fetus has HbF. It has alpha2 and gamma 2 polypeptide chains
Fetal hemoglobin is replaced by adult Hb soon after birth.
 Oxygen binding capacity of fetal Hb is greater than adult Hb. This helps in the
movement of maternal to fetal circulation

15. NORMAL VALUE:
MALES= 14-18g/ dL
FEMALES= 12-16g/ dL
INFANTS= UPTO 20g/Dl
It is required for
(i) transport of oxygen
(ii) transport of carbon dioxide and
(iii)it also behaves as a blood buffer.
Derivatives of haemoglobin-
Oxyhaemoglobin, Carboxyhaemoglobin, Carbaminohaemoglobin
Methaemoglobin or ferrihaemoglobin, Deoxyhemoglobin, glycohemoglobin
D. Venkatesh Basics of medical physiology third edition

16. BLOOD GROUP
Based on the presence or absence of A and B antigens on the red cell membrane
individually or in group,There are four blood groups.

17. APPLIED PHYSIOLOGY:
ANEMIA:
Decrease in RBC count, hemoglobin and/or haematocrit values resulting in lower
ability for the blood to carry oxygen to body tissues.
If Hb values- in men- <13.5gm/dL and in women-<12gm/dL, then they are anemic
Depending on the cause of anemia, they are classified
1. Anemia due to decreased RBC formation
2. Anemia due to increased RBC destruction
3. Anemia due to blood loss
 ANEMIA DUE TO DECREASED RBC FORMATION
a) Iron deficiency anemia:
b) Vitamin B12 and folic acid deficiency
c) Pernicious anemia
d) Aplastic anemia

18. ANEMIA DUE TO INCREASED RBC DESTRUCTION :
a) Thalassemia
b) Sickle cell anemia
c) Hereditary spherocytosis
d) Glucose-6-phosphate dehydrogenase deficiency
 ANEMIA DUE TO BLOOD LOSS
a) Acute blood loss
b) Chronic blood loss
 MORPHOLOGICAL CLASSIFICATION
a) Microcytic hypochromic anemia
b) Normocytic normochromic anemia
c) Macrocytic anemia

19. PATHOPHYSIOLOGY-
Decrease in RBCs, Hb levels
Diminished oxygen carrying capacity
Hypoxia and hypoxia induced effects on organ function
Signs and symptoms of anemia
CLINICAL MANIFESTATION :
Seen only in moderate and severe anemia
Patients have :
Pallor, Dyspnea, Palpitations, and heart murmurs
Headache, vertigo , restlessness and muscle weakness

20. ORAL MANIFESTATIONS:
In Iron deficiency anemia – the mucous membrane of oral cavity and
esophagus are atrophic and show loss of keratinization.
A smooth red painful tongue with atrophy of filiform and fungiform papillae is seen
In Pernicious anemia – There is gradual atrophy of tongue resulting in a bald
tongue which is often referred to as Hunter’s glossitis or Moeller’s glossitis
In sickle cell anemia – includes osteoporosis and loss of trabeculation of the
jawbones with the appearance of large irregular spaces and morphological alterations in
nuclei of oral epithelial cells
In aplastic anemia – Spontaneous gingival hemorrhages, lack of resistance to
infection , ulcerative lesions of oral mucosa and pharynx.

21. POLYCYTHEMIA
A condition where RBC count is increased above 8 million cells/ mm3
There are two types of polycythemia :
1. Polycythemia Vera
 It is produced due to genetic abnormality. The blast cells start producing too many
cells.
 This increases the hematocrit value , total blood volume and viscosity of blood .
2. Secondary polycythemia
 Physiological polycythemia occurs at high altitude due to hypoxia
 Pathological polycythemia occurs in pulmonary disease, hydronephrosis of kidney
and tumors of the liver and kidneys
Dr. A K Jain Human physiology for BDS fifth edition

22. HEMOGLOBINOPATHIES:
The defects are due to the abnormalities in the polypeptide chain.
The abnormal hemoglobins produced are HbS, HbC, and HbE
HbS – In this type of hemoglobin , valine replaces glutamic acid at the sixth position
in the beta chain .
When HbS is exposed to hypoxia , it becomes insoluble leading to a change in the
shape of RBC
The homozygous individuals suffer from this condition leading to sickle cell anemia.
They are less flexible than normal RBCs. This leads to blocking of capillaries
The heterozygous individuals have sickle cell trait

23. THALASSEMIA
In this condition, alpha and beta chains of globin are normal, but they are produced in
less number or absent.
The decrease in alpha chain synthesis is called alpha thalassemia
Alpha thalassemia is of two types- 1. alpha thalassemia major 2. alpha thalassemia
minor
Beta thalassemia is caused due to reduced synthesis of beta chains
It is of two types 1. Beta thalassemia major 2. Beta thalassemia minor
In beta thalassemia major , the patients suffer from anemia due to rapid destruction of
RBC’s
They need frequent blood transfusion
There is increased bone marrow activity , leading to frontal bossing , splenomegaly ,
repeated fever , prominent cheekbones, depression of the bridge of the nose, unusual
prominence of maxillary anterior teeth
Dr. A K Jain Human physiology for BDS fifth edition

24. WHITE BLOOD CELLS
Leukocytes are also called white blood corpuscles. The fundamental
job of the WBCs is to provide defense against Bacteria, Fungus,
parasite and Virus
1.Total WBC count (TC): 4,000 to 11,000 cells/cu. mm of blood
2. Differential WBC count (DC):
Polymorphonuclear granulocytes Mononuclear agranulocytes
Neutrophils 60-70% Lymphocytes 25-33%
Eosinophils 1-4% Monocytes 2-6%
Basophils 0.25-0.5%
D. Venkatesh Basics of medical physiology third edition

25. VARIATIONS IN THE COUNT OF WBC’s
Leukocytosis is a condition where total count (TC) of WBC is > 11,OOO/μl.
In leukopenia, TC of WBC is <4000/μl.
FACTORS HELPING THE PROLIFERATION OF LEUKOCYTES
For WBC proliferation, growth factors are required. These growth factors are:
(i) Interleukins : Interleukin-1,-3,-6 convert pleuripotent uncommitted stem cells to
committed stem cells
(ii) CSF-GM :Stimulates the production of neutrophils, monocytes, eosinophils,
erythrocytes and megakaryocytes
(iii) CSF-G : Stimulates the production of neutrophil
(iv) CSF-M : Stimulates the production of monocytes
(v) Prostaglandins, cortisol , adrenocorticotropic hormone play an important role in
control of leukopoiesis.
D. Venkatesh Basics of medical physiology third edition

26. LEUKOPOIESIS : Leukopoiesis is the development of leucocytes.

27. NEUTROPHILS
Size : 10- 14 µm diameter
Nucleus : purple, multilobed
Lobes : 2,3 up to 5 or more. Young cell—less lobes.
Granules : fine, amphophilic /neutrophilic, have lytic enzyme
1. Primary/azurophilic /lysosomal –bacterial destruction.
2. Secondary – lactoferrin – inhibits growth
Functions - Most important function of the neutrophil is to attack and destroy the
invading bacteria.

28. • Neutrophilia: Neutrophilic leukocytosis is a condition where the differential count
(DC) of neutrophil is> normal plus the TC is > normal.
– Physiological cause :
• exercise
• lactation
• pregnancy
– Pathological cause :
• acute pyogenic infection
• Neutropenia: In neutropenia, neutrophil count is < normal.
– Causes :
• typhoid and viral fever
• bone marrow depression
D. Venkatesh Basics of medical physiology third edition

29. EOSINOPHILS.
• Size : 10- 14 µm diameter
• Nucleus : purple, bilobed
• Cytoplasm : acidophilic
• Granules : coarse, bright red
• contains- major basic proteins (MBP) - histaminase
– Eosinophil peroxidase enzyme (EPO) – antibacterial

30. Functions :
– limit allergic intensity ,eg Bronchial asthma, hay fever
– mild phagocytosis
• Eosinophilia : Eosinophilia is a condition where DC of eosinophil is
greater than normal or absolute count of eosinophils is more than
500/μl.
• allergic conditions
• parasitic infections
• Eosinopenia :
• injection Of corticosteroids
D. Venkatesh Basics of medical physiology third edition

31. BASOPHILS
• Size : 10-14 µm diameter
• Nucleus : bilobed, S shaped
• Cytoplasm : basophilic, granular
• Granules : coarse, purple/ blue, plenty, contain Heparin, Histamine, Hyaluronic
acid, protease
Functions :liberate heparin which is anticoagulant, histamin produces allergic reaction
• Basophilia :
• chicken pox
• small pox
• tuberculosis
• influenza
• Basopenia
• administration of glucocorticoids

32. MONOCYTES
Size : 10- 18 µm diameter (largest)
• Nucleus : pale , round/kidney shaped
• Cytoplasm : clear , pale blue , agranular
• Life span : 48-72 hrs in blood & 3 months in tissues.
• Functions :
– phagocytosis – 2nd line of defense
– antigen presenting cells (APC).
– role in tissue repair
D. Venkatesh Basics of medical physiology third
edition

33. LYMPHOCYTES
 Size : 9-18 µm diameter
 Nucleus : heterochromatic nuclei
 Life span : 12-24 hours
Small Lymphocytes;The cells are 6–9 μm in diameter.They have ovoid
or kidney shaped nucleus Nucleus is usually eccentrically placed and
occupies about 90% of the cell area
Large Lymphocytes;The cells are 10–15 μm in diameter The nucleus is
homogenous.Nucleus is usually oval or kidney shaped and eccentrically
placed

34. • PHYSIOLOGICAL VARIATIONS
1.Age : In infants -- 20,000 per mm3
In children-- 10,000 to 15,000 per mm3
2. Sex: slightly more in males. In females, increases during
menstruation, pregnancy and parturition.
3. Diurnal variation: Min in early morning & max in afternoon.
4. Exercise: Increased
5. Sleep: Minimum.
6. Emotional conditions: like anxiety - count increased.
7. Pregnancy: Increased

35. Leukemias
Leukemia is a malignancy (cancer) of the hematopoietic tissue, characterized by
uncontrolled proliferation of abnormal white blood cells in the bone marrow and
peripheral blood
Leukemia can be (1) acute or (2) chronic.
Acute myeloblastic (AML), Acute lymphoblastic (ALL), Chronic myeloid (CML),
Chronic lymphocytic leukemias(CLL)
ACUTE MYELOID LEUKEMIA – Malignant transformation of undifferentiated
precursors of myeloid series
-WBC count upto 1 lakh
-Gingival hyperplasia is most common
-More than 30 % myeloblasts are present in blood and bone marrow

36. ACUTE LYMPHOBLASTIC LEUKEMIA – Malignant transformation of
undifferentiated precursors of lymphoid series
-Common in young adults and children
CHRONIC LYMPHOBLASTIC LEUKEMIA – Malignant transformation of well
differentiated cells of lymphoid series
-Common in elder age group
-WBC counts upto 5 lakhs/mm cube
CHRONIC MYELOD LEUKEMIA – Malignant transformation of well
differentiated cells of the myeloid series
-Common in middle age
-Gingival hyperplasia is common

37. PLATELETS
 Small colorless, nonnucleated and moderately refractive bodies.
Diameter is 2.5 microns (2 to 4microns)
Volume is 7.5 cubic microns (7 to 8 cubic microns).
Spherical or rod shaped and become oval or disc shaped when inactivated. Sometimes,
the platelets are of dumb bell, comma, cigar or any other unusual shape.
Normal platelet count is 2,50,000 (2,00,000 to 4,00,000)/ cubic mm of blood.
 Lifespan of platelets is 10 days. Platelets are destroyed by tissue macrophage system
in spleen.
Dr. A K Jain Human physiology for BDS fifth edition

38. PROPERTIES OF PLATELETS
1. ADHESIVENESS
When platelets come in contact with any wet and rough surface, these are activated and
stick to the surface. The factors, which cause adhesiveness are thrombin, ADP,
Thromboxane A2, calcium ions and Von Willebrand factor.
2. AGGREGATION (GROUPING OF PLATELETS)
The activated platelets group together and the stickiness is due to ADP and
thromboxane A2.

39. PHYSIOLOGICAL VARIATIONS
1. Age: Platelets are less in infants (1,50,000 to 2,00,000/ cu mm) and reaches normal
level at 3rd month after birth.
2. Sex: In females, it is reduced during menstruation.
3. High altitude: Platelet count is increased in high altitude.
4. After meals: After taking food, the platelet count is increased
DEVELOPMENT OF PLATELETS
Platelets are formed from bone marrow. The pluripotent stem cell gives rise to the CFU-
M. This develops into megakaryocyte. The cytoplasm of megakaryocyte form
pseudopodium. A portion of pseudopodium is detached to form platelet, which enters
the circulation .
Dr. A K Jain Human physiology for BDS fifth edition

40. FUNCTIONS OF PLATELETS
1. ROLE IN BLOOD CLOTTING- responsible for the formation of intrinsic prothrombin
activator.
2. ROLE IN CLOT RETRACTION- The cytoplasm of platelets contains the contractile proteins
namely actin, myosin and thrombosthenin and are responsible for clot retraction.
3. ROLE IN PREVENTION OF BLOOD LOSS (HEMOSTASIS)
a. Platelets secrete 5 HT, which causes the constriction of blood vessels.
b. Due to the adhesive property, the platelets can seal the damage in blood vessels like
capillaries.
c. By formation of temporary plug also platelets seal the damage in blood vessels.

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

42. PATHOLOGICAL VARIATIONS
Decrease in platelet count is called thrombocytopenia and it occurs in the following
conditions:
1. Immune thrombocytopenic purpura
2. Infections- measles, HIV
3. Bone marrow infiltration
4. Disseminated intravascular coagulopathy(DIC)
5. Pregnancy
6. Aplastic anaemia
Dr. A K Jain Human physiology for BDS fifth edition

43. The increase in platelet count is called thrombocytosis, occurs in the following
conditions:
1. Allergic conditions
2. Asphyxia
3. Hemorrhage
4. Bone fractures
5. Surgical operations
6. Splenectomy
7. Rheumatic fever and
8. Trauma (wound or injury or damage produced by external force).
Dr. A K Jain Human physiology for BDS fifth edition

44. Idiopathic Thrombocytopenic Purpura;
PALATAL PETECHIAE
PETECHIAL RASH AND
ECCHYMOSIS
BLEEDING GUMS

45. HEMOSTASIS AND BLOOD
COAGULATION:
 The variety of body mechanism which try
to arrest bleeding is called hemostasis.
Hemostasis is achieved by several
mechanism :
Vascular spasm or vasoconstriction
Formation of platelet plug
Formation of a blood clot as a result of
blood coagulation
Deposition of fibrous tissue in the clot and
permanent closure of defect in blood vessel
D. Venkatesh Basics of medical physiology third edition

46. • Coagulation of blood is a vital physiological process.
• Immediately following vascular damage, platelet plug (temporary hemostatic
plug) formation occurs at the site of injury that immediately stops bleeding.
• The definitive hemostasis is the coagulation of blood,
• Coagulation of blood occurs due to activation of clotting factors (coagulation
proteins) that are normally present in their inactive form in plasma.
Blood Coagulation

47. CLOTTING FACTORS-
• Coagulation of blood depends
on a series of chemical
reactions involving clotting
factors.
• There are known 12 clotting
factors that were depicted
earlier as factors I to XIII
(factor VI absent)

48. The formation of prothrombin activator requires 12 different coagulation factors. They
are as under:
Factor 1- fibrinogen: It’s a plasma protein and it is acted upon by thrombin to form
insoluble fibrin clot. Absence of factor 1 is termed as afibrinogenmia
Factor 2- prothrombin: its an inactive precursor of thrombin .It is formed in the liver
with the help of vitamin K
Factor 3- Thromboplastin:This converts prothrombin to thrombin in the presence of
factors 5, 7 , 10 and calcium and phospholipids
Factor 4 – Calcium: Ionic calcium is required for clotting.This is required for the
formation of prothrombin activator, for the conversion of prothrombin to thrombin and
formation of insoluble fibrin clot
Factor 5- labile factor: This is required for the conversion of prothrombin to thrombin
by tissue extract and plasma factors
Factor 6- Absent

49. Factor 7 – stable factor (proconvertin): This is required for the formation of
prothrombin activator from tissue extracts
Factor 8- Antihemophilic factor A: This is required for the formation of prothrombin
activator by tissue extract
Factor 9- Christmas factor (antihemophilic factor B): This is needed for the
formation of prothrombin activator from blood constituents.
Factor 10- Stuart-power factor- This is also required for the formation of prothrombin
activator
Factor 11-Plasma thromboplastin antecedent
Factor 12 –Hageman factor
Factor 13- Fibrin stabilizing factor : This is a plasma protein which causes
polymerization of soluble fibrin to produce insoluble fibrin

50. MECHANISM OF BLOOD COAGULATION
Blood coagulation occurs in three major stages:
Stage 1: Activation of Stuart-Prower factor
(formation of prothrombin activator)
Stage 2: Formation of thrombin from
prothrombin
Stage 3: Formation of fibrin from fibrinogen

51. Activation of Stuart-Prower Factor
(Factor X)
• Activation of Stuart-
Prower factor or factor
X is the key to blood
coagulation.
• Factor Xa activates
prothrombin to form
thrombin. Therefore,
this process is also
called prothrombin
activation.
• This is achieved by
two pathways: the
intrinsic pathway and
the extrinsic pathway

52. ABNORMALITIES OF COAGULATION
Hemorrhagic disorders are broadly classified into inherited and acquired defects.
1. Acquired defects are more common than inherited defects and platelet defects are
more common than the coagulation defects.
2. Deficiencies of factor VIII (hemophilia) and factor IX (Christmas disease) are
more common inherited coagulation defects.
3. The common acquired defects are thrombocytopenia,vitamin K deficiency,
disseminated intravascular coagulation and liver failure resulting in clotting defects.

53. CHEMICAL AGENTS TO PREVENT BLOOD CLOTTING—ANTICOAGULANTS
1. HEPARIN
2. COUMARIN DERIVATIVES
3 EDTA
4. OXALATE COMPOUNDS
5. CITRATES
Some snake venom, peptone and hirudin (from leach) are also the known anticoagulants
SUBSTANCES WHICH HASTEN BLOOD CLOTTING—PROCOAGULANTS
1. THROMBIN
2. SNAKE VENOM
3. EXTRACTS OF LUNGS AND THYMUS
4. SODIUM OR CALCIUM ALGINATE
5. OXIDIZED CELLULOSE

54. TESTS FOR CLOTTING
■ BLEEDING TIME-This is the time interval from oozing of blood after a cut or
injury till arrest of bleeding. The normal duration of bleeding time is 3 to 6 minutes. It
is prolonged in purpura.
CLOTTING TIME-The time interval from oozing of blood after a cut or injury till the
formation of clot is called clotting time. The normal duration of the clotting time is 3 to
8 minutes. And it is prolonged in hemophilia
PROTHROMBIN TIME -The normal duration of prothrombin time is about 12
seconds. The prothrombin time is prolonged in deficiency of prothrombin and other
factors like factors I, V, VII and X

55. APPLIED PHYSIOLOGY-
BLEEDING DISORDERS:
1. HEMOPHILIA-
 Hemophilia major is due to deficiency of factor 8
 It is a sex- linked hereditary disease which occurs exclusively in males
 Females are carriers
 Clotting time is prolonged and bleeding time is normal in hemophilia
 Hemophilia A
• It is due to deficiency of factor VIII.
• It is an X-linked recessive hereditary disease
 Soft tissue hematomas and hemarthroses
 In mild to moderate cases, continuation of hemorrhage secondary to trauma
or surgery is the feature.

56. Diagnosis
• Patients have prolonged Activated
partial thromboplastin time
(APTT).
• Prothrombin time and bleading
time are normal.
• Assay of factor VIII in plasma is
diagnostic
Treatment
• The treatment consists of transfusion of
fresh blood (as on storage factor VIII is
rapidly lost), or transfusion of
factorVIII-concentrate.
• Fresh-frozen plasma and
cryoprecipitate both contain factor
VIII.

57. Christmas Disease (Hemophilia B)
Christmas disease or hemophilia-B occurs due to deficiency of factor-IX
(antihemophilic factor-B or Christmas factor). This is a sex-linked recessive
hemorrhagic disease.
Treatment
The specific treatment of hemophilia B is the replacement of factor IX.
VITAMIN K DEFICIENCY –
 It is necessary for the formation of five clotting factors – prothrombin, factor 7,
factor 9, factor 10 and protein C in the liver .
 Absence of vitamin K leads to deficiency of these factors and defective clotting.

58. von Willebrand Disease
von Willebrand disease (vWD) is the most common inherited bleeding disorder that
occurs due to deficiency of von Willebrand factor (vWF)
Clinical Features
• Mucocutaneous bleeding , Epistaxis, easy bruising, hematoma, menorrhagia and GI
bleeding are common.
• In severe cases patient suffer from hemarthroses and muscle hematomas.
Diagnosis
• Increase in bleeding time which is a standard screening test for vWD.

59. CLINICAL CONSIDERATIONS OF BLOOD IN CONSERVATIVE
DENTISTRY AND ENDODONTICS
1.SICKLE CELL ANAEMIA:
• Sickle Cell Anaeima is a potential risk factor for pulpal necrosis in clinically intact
permanent tooth.
• Asymptomatic pulpal necrosis resulting from infarction involve periapical and
appear as radiolucent areas
Suggested steps to be followed for the dental treatment of sickle cell anemia patients
• Consulting the physician before performing dental procedures
• Avoding salicylates in pain management
• Avoiding elective dental surgical procedures
Pulpal necrosis with sickle cell anaemia Shafers Textbook of oral pathology

60. THALASSAEMIA
• The bone marrow expansion affecting the maxilla
leads to varying degrees of protrusion,spacing,rotation
of anterior teeth and malocclusion.
• Teeth may be discoloured and have short roots( To be
considered during root canal treatment)
• There is increased risk of caries,which might be due to
reduced salivation due to deposition of iron in the
salivary glands because of secondary
haemochromatosis,which can additionally cause pain
in glands
Shafers Textbook of oral pathology
Superior Repositioning of the Maxilla in Thalassemia-Induced Facial Deformity: Report of 3 Cases and a

61. Erythroblastosis fetalis
 Teeth will have green, brown or blue
hue by deposition of blood pigment in
the enamel and dentin of the
developing teeth.
 But here stain does not involve teeth or
portions of teeth developing after
cessation of hemolysis shortly after
birth.
 Also ground sections of these teeth
will be positive for bilirubin

62. HEMOLYTIC JAUNDICE
• Hemolytic jaundice is common in
newborn
• One of the manifestations of these
disorders is the elevated serum levels of
bilirubin (hyperbiliru-binemia)
• When hyperbilirubinemia occurs during
the period of dental development, these
teeth can develop a green coloration.
Shafers Textbook of oral pathology
Superior Repositioning of the Maxilla in Thalassemia-Induced Facial Deformity: Report of 3 Cases and a
Review of the Literature

63. Thrombocytopenia
• Non-steroidal anti-inflammatory drug are contraindicated and the patient may be
given acetaminophen for pain management. Post-operative antibiotics are advised as
this will reduce the late bleeding due to the infection
• Nerve-block anesthetic injections are contraindicated unless there is no better
alternative
.
• The finish line for crown preparations for these patients should be preferably
supragingival, so as to reduce the chances of gingival bleeding
• In case of surgical procedures the patients require infusion of 1 bottle platelet rich
plasma prior to procedure and tranexamic acid post-operatively.

64. Endodontic Treatment in the Patients with Bleeding Disorders
• Non-surgical endodontic treatment is generally low risk for patients with bleeding
disorders’
• Electronic apex locator is preferred over radiographic technique as it reduces the
need of IOPA x-ray, which can traumatize the soft tissue during placement and lead
to prolonged bleeding.
• The use of rubber dam is almost mandatory to prevent laceration of soft tissues. But
care to be taken to minimize trauma to the soft tissues during placement of rubber
dams clamps.
• High-speed vacuum evacuators and saliva ejectors can cause trauma to the floor of
mouth thereby leading to haematoma formation. So they should be used very
carefully in those patients. with a gauze swab in the floor of the mouth
• In surgical endodontic treatment the consultation of the patient’s hematologist
should be considered

65. PAIN MANAGEMENT;
• Dental pain can usually be controlled with a minor analgesic such as
paracetamol (acetaminophen) in the patients with bleeding disorders
• NSAIDs produce a systemic bleeding tendency by reversibly inhibiting
platelet cyclooxygenase
• The risk of systemic bleeding with NSAIDs is enhanced by concomitant use
of alcohol or anticoagulants, and associated by conditions such as,liver
disease, and other hemorrhagic diatheses (e.g., hemophilia, von
Willebrand's disease)

66. ENDODONTIC TREATMENT CONSIDERATIONS LOCAL
ANESTHESIA;
• In the patients with bleeding disorders, the inferior alveolar nerve- block are
contraindicated because of the risk of hematoma formation
• There is an 80% chance that a patient with hemophilia will develop a hematoma
following the administration of an inferior alveolar nerve block injection without
prior factor VIII infusion.
• The Preoperative prophylactic coverage should be discussed with the patient’s
hematologist prior to any local anesthesia in the floor of the mouth or lingual
infiltration for the same reason
• Mental nerve block injection in the mandibular arch is considered safe
• Other local anesthetic techniques, such as intra-pulpal, intra-ligamentary, and buccal
infiltration, are safer, The alternative techniques, including sedation with diazepam
or nitrous oxide oxygen analgesia can be employed to reduce need of anesthesia.
A Review on Endodontic Treatment in the Patients with Bleeding Disorders

67. HEMOPHILIA
• There is generally no contraindication for performing endodontic treatment in
hemophiliac patients. but instrumentation and filling should never be done beyond
the apical region of a vital tooth.
• Non-vital teeth should be treated at least 2 to 3 mm short of the radiographic apex.
• Severe haemophiliac patients endodontic treatment can be usually carried out under
antifibrinolytic cover (usually tranexamic acid).
• Endodontic surgeries must be carefully planned ;Desmopressin and tranexamic acid
are primary alternatives. Desmopressin can be given as a slow intravenous infusion
over 20 min of 0.3-0.5µg/kg, 30 to 60 minutes prior to the surgical procedure.
• Intranasal administration as a spray of 1.5mg per ml is an alternative,
• Mild haemophiliacs can effectively undergo surgical endodontics without the need
for factor replacements
Endodontics for the haemophiliac, a multidisciplinary perspective

68. • Systemically Tranexamic acid, is given in dose of 1 g , 4 times a day starting at least
1 day preoperatively for surgical procedures.
• Local use of fibrin glue and/or swish and swallow rinses of tranexamic acid before
and after the procedure is a cost-effective solution.
• Infection induces fibrinolysis and so antimicrobials such as amoxicillin 500 mg
three times daily should be given postoperatively for a full course of 7 days to
reduce risk of secondary haemorrhage.
Endodontics for the haemophiliac, a multidisciplinary perspective

69. HEMOSTATIC AGENTS IN ENDODONTIC SURGERY
 Adequate hemostasis is a critical step in endodontic surgery.
 It facilitates the procedure and affects the success and prognosis of the operation.
HEMOSTATIC AGENTS USED IN ENDODONTICs;
1. Aluminum chloride
2. Ferric Sulphate
3. BotroClot
4. Epinephrine Impregnated Gauze
5. Electrocauterization
Aluminum Chloride versus Electrocauterization in Periapical Surgery: A Randomized Controlled
Trial

70. Aluminum chloride placed into the bone defect for 2 minutes and removed with
the help of a dental curette and sterile saline
Hemostatic Agents in Periapical Surgery: A Randomized Study of Gauze Impregnated in
Epinephrine versus AluminumChloride
Aluminum Chloride versus Electrocauterization in Periapical Surgery: A Randomized Controlled
Trial
Application of the aluminum chloride

71. Frozen paper point
The paper point,is sprayed with endo frost spray and placed inside the root canal
system beyond physiological terminus for about 20-30 seconds.
The frozen paper point will constrict the blood vessels, allowing a clot to form more
quickly and stop the bleeding. After removal of paper point the bleeding has stopped.
Endo frost spray
A simple technique for management of
apical bleeding

72. PLATELET RICH FIBRIN
PRF is a biomaterial derived from the patients own blood , containing a high
concentration of platelets , leukocytes, and growth factors
The applications of platelet-rich fibrin (PRF) in regenerative endodontics are
numerous.
Bains et al. employed it as the agent for repairing iatrogenic perforation of the
pulpal floor of the mandibular first molar when used in combination with MTA
 PRF is ideal for the revascularization of immature permanent teeth with necrotic
pulps by providing a scaffold rich in growth factors, enhancing cellular
proliferation and differentiation
Evidence of progressive thickening of dentinal walls, root lengthening, regression
in the periapical lesion, and apical closure was reported by Shivashankar et al.,
following the use of PRF on a tooth with pulpal necrosis and open apex
Platelet rich fibrin used in regenrative endodontics and current uses , limitations

73. PLATELET RICH PLASMA
PRP (Platelet-Rich Plasma):PRP is also derived from the patient's blood and contains a
high concentration of platelets and growth factors.
In conservative dentistry and endodontics, PRP can be used similarly to PRF for tissue
regeneration and wound healing.However,
 PRP is typically more liquid in consistency compared to PRF and may require
activation with thrombin or calcium chloride before use.
PRP is used in procedures such as bone grafting, sinus augmentation, and periodontal
surgery to promote tissue regeneration and enhance wound healing.
Platelet rich plasma and regenrative dentistry

74. CONCLUSION
In conclusion, a comprehensive understanding of
blood-related considerations in dentistry is essential
for providing high-quality, safe, and patient-centered
dental care. By incorporating appropriate
techniques and precautions, dental professionals
can ensure positive treatment experiences and
contribute to overall patient health and well-being.

75. 1.Hemostatic Agents in Periapical Surgery: A Randomized Study of Gauze Impregnated
in Epinephrine versus AluminumChloride
Aluminum Chloride versus Electrocauterization in Periapical Surgery: A Randomized
Controlled Trial
2.Endodontics for the haemophiliac, a multidisciplinary perspective
3.A Review on Endodontic Treatment in the Patients with Bleeding Disorders
4.Shafers Textbook of oral pathology
5.Superior Repositioning of the Maxilla in Thalassemia-Induced Facial Deformity:
Report of 3 Cases and a Review of the Literature
6.D. Venkatesh Basics of medical physiology third edition
7.Dr. A K Jain Human physiology for BDS fifth edition
8.A simple technique for management of apical bleeding
9. Platelet rich fibrin used in regenrative endodontics and current uses , limitations