BLOOD

PREPARED BY: GUIDED BY:

Dr. Priya Sakaria Dr. Kamal Bagda
(postgraduate 1 conservative dentistry & endodontics) Dr. Kiran Vachhani
Roll no 9 Dr. Kailash Attur
Dr. Manjusha Rawtiya 1
CONTENT
1. Introduction
2. Blood & Plasma proteins
3. Red Blood Cells
4. Erythropoiesis
5. Hemoglobin
6. ESR & PCV
7. Anemia
8. White blood cells
9. Immunity
10. Platelets
11. Hemostasis & coagulation of blood
12. Blood groups & Blood transfusion
13. Reticuloendothelial system & Tissue macrophage
14. Lymphatic system & lymph
15. Tissue fluid & edema
2
1) INTRODUCTION

3
 Plasma

Interstitial
ECF
fluid

TBW Other fluids

ICF

4
Pathological variation in TBW

Dehydration Overhydration

Heart failure, renal

Severe diarrhea disorders ,
excess sweating hypersecretion of
insufficient water intake antidiuretic
hormone

Moderate
Mild dehydration Severe dehydration
dehydration

5
2) BLOOD &
PLASMA PROTEINS

6
COMPOSITION OF BLOOD

 Blood cells which are called formed elements and the

liquid portion is known as plasma

Blood cells:
1. Red blood cells / erythrocyte
2. White blood cells/ leucocyte
3. Platelet/ thrombocyte

7
PROPERTIES OF BLOOD
Color • Red

• 450 ml in newborn
Volume • 5 L in male & 4.5 L in female

• Slightly alkaline
pH • In normal condition 7.4

Specific • Total blood- 1.052 to 1.061

gravity

Viscosity • Five times more viscous than water

8
Plasma:
Straw colored clear liquid part of blood.

Serum:
•When the blood is shed, it clots because of conversion of
fibrinogen into fibrin.
•After about 45 minutes, serum oozes out from the clot

9
PLASMA
Plasma

Solids :7 Water :
Gases
-8% 92-93%

Inorgani O2
Organic
c
substan- CO2
substan-
ces N
ces

Non- Sodium
Internal protein
Plasma Carbo- Amino Calcium
fats enzymes secretio nitrogen
proteins hydrate acid Potassi-
-n substan-
ce um etc.

10
FUNCTIONS OF BLOOD
1. Nutrient function
2. Excretory Function
3. Respiratory Function
4. Transport of Hormones and enzymes
5. Regulation of Water balance
6. Regulation of Body Temperature
7. Storage Function
8. Defensive Function

11
PLASMA PROTEINS
Types & It’s Normal Values
 Serum Albumin: 4.7 g/dL

 Serum Globulin: 2.3 g/dL

 Fibrinogen: 0.3 g/dL

 Normal A/G ratio is 2:1

Variation in protein level:

 Hyperproteinemia : Dehydration
Hemolysis
Acute infections
Leukemia
alchoholism
12
 Hypoproteinemia: Diarrhea
Haemorhhage
Burns
Malnutrition
Pregnancy
Prolonged starvation

Origin:
 Mainly from reticuloendothelial cells of liver /spleen,
bone marrow, disintegrating blood cells and general
tissue cells.

13
Functions of Plasma Proteins:
1. Role in coagulation of blood
2. Role in defence mechanism of body
3. Role in transport mechanism
4. Role in maintenance of osmotic pressure in blood
5. Role in regulation of acid-base balance
6. Role in viscosity of blood
7. Role in ESR
8. Role in suspension stability of red blood cells
9. Role in production of trephone substance
10. Role as Reserve proteins
14
3) RED BLOOD CELLS

15
Morphology:
 SHAPE : Disk-shaped & biconcave which provide some
advantages
 SIZE : 7.2 µ diameter
2.2 µ peripheral and 1µ central thickness
120 sq µ surface area
85-90 cu µ volume
 NORMAL STRUCTURE: non nucleated, thus explains the
absence of DNA

16
Properties of RBCs:

1. Rouleaux Formation

2. Specific Gravity: 1.092 – 1.101

3. Packed cell volume(Hematocrit value): is volume of

RBCs expressed in percentage.

4. Suspension Stability

17
Lifespan of RBCs:
o 120 days
o Senile RBCs are destroyed in the reticuloendothelial
system.

Fate of RBCs:

 Old RBCs becomes very fragile & are destroyed while

trying to squeeze through the smaller capillaries.

 The destruction occurs mainly in spleen .

18
 Destruction of RBC
(in spleen)

Release of Hemoglobin

Iron Globin Porphyrin

+
Apoferritin

Ferritin Protein pool Bilirubin

Stored & Reused Stored & Reused Excreted

19
Functions of RBCs:

1. Transport of O2 from lungs to tissues.

2. Transport CO2 from tissues to lungs.

3. Buffering action in blood.

4. In Blood group determination

20
Variation In Shape Of RBCs:

 The shape is altered in many conditions:

1. Crenation: shrinkage

2. Spherocytosis: Globular form

3. Elliptocytosis:

4. Sickle cell: crescentic shape

5. Poikilocytosis: flask, hammer or any other unusual

21
VARIATIONS IN NUMBER OF RBC :
Physiological Variation:

Increase in RBC count –Polycythemia:

 Age(at birth 8 to 10 millions/cu mm)

 Sex

 High altitude (7 millions/cu mm)

 Muscular Exercise (hypoxia)

 Emotional conditions (sympathetic activity)

 Increased environmental temperature

 After Meals

22
Decrease in RBC count:
1. High Barometric pressures

2. During sleep

3. Pregnancy

Pathological Variations:
Pathological Polycythemia: ↑ 7 millions/cu mm

23
Primary Polycythemia/Polycythemia Vera:
o Persistent increase in the RBC count above 14 million
/cu mm of blood.
o Associated with WBC count above 24,000/cu mm of
blood.
o Etiology: Red bone marrow malignancy.

24
Secondary Polycythemia:
o Etiology :
1. Respiratory disorders
2. Congenital heart disease
3. Chronic CO poisoning
4. Chemical poisoning like phosphorus
5. Repeated mild hemorrhages

Anemia: abnormal decrease in RBC count

25
POLYCYTHEMIA VERA

Oral menifestations:

 Erythema of oral mucosa

 Glossitis

 Erythematous and edematous gingiva.

 Spontaneous gingival bleeding can occur because the

principal sites for hemorrhage, although rare, are
reported to be the skin, mucous membrane, &
gastrointestinal tract.
26
Oral health considerations:

 Nerve block can be given.

 Gelfoam, surgicel and others can be used for clot

formation in cases of surgery.

27
Variation in size of RBCs:

 Physiologically: venous blood have slightly larger RBCs.

 Pathologically:

1. Microcytes – smaller cells

1. Iron deficiency anemia
2. Increased osmotic pressure in blood
2. Macrocytes –larger cells
1. Megaloblastic anemia
2. Decreased osmotic pressure in blood
3. Anisocytes –cells of different sizes

28
4) ERYTHROPOIESIS

29
SITE OF ERYTHROPIESIS

 In Fetal life:

1. Mesoblastic stage: from mesenchymal cells of yolk sac

( 1st trimester)

2. Hepatic stage: from liver (2nd trimester)

3. Myeloid stage: From red bone marrow & liver (3rd

trimester)

30
 In newborn babies, children & adults:

1. Upto age 20: from red bone marrow

2. After age 20: from membranous bones like vertebrae,

sternum, ribs etc & from the end of long bones.

31
 PROCESS OF ERYTHROPOIESIS/ LEUCOPOIESIS
Uncommitted pluripotent hemopoietic stem cell (UPHC)

Committed pluripotent hemopoietic stem cell(CPHC)

Lymphoid stem cell Colony forming Blastocyte

Colony forming unit -E Colony forming unit -GM Colony forming unit -M

Promyelocyte Monoblast
Megacaryocyte

Granulocyte

L R N B E M P
Neutrophil Basophil Eosinophil Monocyte Platelet
32
Lymphocyte RBCs
STAGES OF ERYTHROPOIESIS →

Changes during erythropoiesis:

1. Reduction in cell size

2. Disappearance of nucleoli and nucleus

3. Appearance of hemoglobin

4. Change in staining properties of cytoplasm

33
5) HEMOGLOBIN

34
  At birth : 25 g/dL

 After 1 year : 17 g/dL

 Puberty onwards : In Male > 15 g/dL

In Female> 14.5 g/dL

FUNCTIONS OF HEMOGLOBIN
 Transport of Respiratory gases

 Buffer action

35
STRUCTURE OF HEMOGLOBIN
 It is a conjugated protein

Heme part Protein : Globin

Four pyrole rings:tetrapyrole Four Polypeptide chains:2 and 2β

TYPES OF NORMAL HEMOGLOBIN

 Adult hemoglobin(Hb A)
 Fetal hemoglobin(Hb F)

36
ABNORMAL HEMOGLOBIN

 Hemoglobinopathies: genetic disorders > Hb S, C,E & M

 Hb in Thalassemia & related disorder: polypeptide chains

are decreased, absent or abnormal

37
ABNORMAL HEMOGLOBIN DERIVATIVES

 Abnormal Hb formed by combination of Hb with some

substances other than O2 and CO2 is called abnormal Hb
derivative.

1. Carboxyhemoglobin

2. Methamoglobin

3. Sulfhemoglobin

38
SYNTHESIS OF HEMOGLOBIN

 Synthesis of Heme: occurs from succinyl coA &

Glycine in Mitochondria

 Formation of Globin: Polypeptide chains are

produced in Ribosome.

 1 Polypeptide chains combines with 1 Heme molecule

39
DESTRUCTION OF HEMOGLOBIN

 Destroyed in reticuloendothelial system

 Globin is reused.

 Iron is stored in body

 Porphyrin is converted into Biliverdin , further Bilirubin

& excreted.

40
6) ESR & PCV
ESR : is the rate at which the erythrocytes settle
down.

PCV : is the volume of the RBCs in the blood that

is expressed in percentage .

41
ESR

allowed to
If the blood is stand the RBCs Supernatant
mixed with an undisturbed settle down layer of clear
anticoagulant on vertical due to gravity plasma
tube

42
Determination of ESR: 2 methods

1. Westergren’s method

2. Wintrobe’s method

43
Significance of determining ESR:

 Helpful in diagnosis & prognosis

44
Variation of ESR:

PHYSIOLOGICAL variation:

1. Age ↑

2. Menstruation ↑

3. Pregnancy ↑

PATHOLOGICAL variation:

1. ↑ in : TB

2. ↓ in : sickle cell anemia

45
PCV

Method of determination:

 Wintrobe’s tube is used & centrifugation is done

Normal values of PCV:

 In male: 40 to 45%

 In female: 38 to 42%

47
Significance of determining PCV:

 Diagnosis & treatment of anemia, polycythemia

 Decision of blood transfusion

 Determination of severity of dehydration & recovery

from it after treatment

Variation in PCV:

 ↑ in : Polycythemia , Dehydration

 ↓ in : Anemia

48
7) ANEMIA

49
CLASSIFICATION
1. Morphological
2. Etiological

Morphological classification:
 MCV : Mean Corpuscular Volume

 MCHC : Mean Corpuscular Hemoglobin Concentration

50
 Type of Anemia Size of RBC Color of RBC
(MCV) (MCHC)

Normocytic normochromic Normal Normal

Normocytic hypochromatic Normal Less

Macrocytic hypochromatic Large Less

Microcytic hypochromatic Small Less

51
 ETIOLOGICAL CLASSIFICATION
Type of Anemia Causes Morphology of RBC

Hemorrhagic Anemia 1. Acute hemorrhage Normocytic,normochromic

2. Chronic hemorrhage Microcytic, hypochromic
Hemolytic Anemia 1. Liver failure
2. Renal disorder
3. Hypersplenism
4. Burns
5. Infections – Malaria &
septicemia Normocytic normochromic
6. Drugs like penicillin,
antimalarial & sulfa drugs
7. Poisoning by lead, coal & tar
8. Isoagglutinins – anti-Rh
9. Hereditary disorders Sickle cell anemia: sickle shaped
& hypochromic
Thalasssemia : Small, irregular &
hypochromic
Nutrition deficiency Anemia 1. Iron deficiency Microcytic, hypochromic
2. Protein deficiency Macrocytic, hypochromic
3. Vitamin B12 deficiency Macrocytic, normochronic/
hypochromic
4. Folic acid deficiency Megaloblastic, normochromic
Aplastic Anemia Bone marrow disorder Normocytic, normochromic

Anemia of chronic disease 1. Rheumatic arthritis

2. Tuberculosis Normocytic, normochromic
3. Chronic renl failure 52
 SIGNS & SYMPTOMS OF ANEMIA

Skin & mucous membrane:

 Pale color,

 loss of elasticity ,

 thin & dry

Hair & nails :

 loss of hair with thinning & greying,

 brittle & easily breakable nails

53
Respiration:

 rate & force of respiration ↑ ,

 breathlessness & dyspnoea

Digestion :

 anorexia,

 nausea,

 vomiting,

 abdominal discomfort, constipation,

 tongue atrophy>pernicious anemia,

 necrotic lesion in mouth & pharynx> aplastic anemia

54
Metabolism :

 BMR increase in severe anemia

Kidney :

 Albuminuria is common

Reproductive system:

 menorrhagia,

 oligomenorrhea,

 amenorrhea

55
Neuromuscular system:

 headache,

 lack of concentration,

 irritability, restlessness,

 drowsiness, dizziness, fatigue

Cardiovascular system :

 ↑ in cardiac output & heart rate,

 increased velocity of blood flow

56
IRON DEFICIENCY ANEMIA

 Glossitis & stomatitis, glossodynia, angular cheilitis, erythematous

mucositis , oral candidiasis, recurrent oral ulcers & burning
mouth

 When Hb is less than 8 g/dL, general anesthesia should be

avoided.

57
HEMOLYTIC ANEMIA

 Pallor of oral mucosa, jaundice

 Paresthesia of oral mucosa

 Chronic condition : hyperplastic marrow spaces in the

mandible, maxilla & facial bones.

 Aspirin or other drugs must be avoided which triggers

hemolysis.

58
SICKLE CELL ANEMIA

 Oral menifestations

 R/E : “stepladder “ trabecular pattern

59
 Enamel hypomineralization

 Calcified canals

 Increased overbite

 Increased overjet

 Pallor of oral mucosa

 83% cases of orofacial and dental pain with no obvious

cause was detected.

60
 Delayed eruption

 Smooth tongue

61
Oral health considerations:

 The need of antibiotic prophylxis is controversial.

 Maintainence of good oral hygeine

 Aggressive treatment of oral infection

 Avoidance of use of aspirin

 Caution with respiratory-depressing conscious sedation

 Avoidance of long , stressful dental visits(nitrogen oxide-

oxygen)

62
THALASSEMIAS

Oral menifestations:
 R/E :
 Spikey shaped & short roots
 Taurodontism
 Attenuated lamina dura
 Enlarged bone marrow spaces
 Small maxillary sinuses
 Absence of inferior alveolar canal
 Thin cortex of mandible 63
 Universal class II skeletal base
relationship with a short
mandible

 Reduced posterior facial height

 Severe facial disfigurements (

chipmunk faces )

64
 Narrower maxilla

 Smaller incisor widths

 General growth retardation

 High dental caries experience

Oral health considerations

 Preanesthetic hemostatic assessment is rarely of any

clinical significant value.

65
MEGALOBLASTIC ANEMIA

Oral manifestations:

 Small & shallow ulcers

 Pt with this disease become intolerant to dentures.

 Glossitis , Glossodynia, Glossopyrosis

66
 ‘beefy red color’ either entirely or in patches scattered
all over tongue.

 Bald tongue referred as Hunter’s glossitis/ Moeller’s

Glossitis

67
PERNICIOUS ANEMIA

Oral menifestations:

 Dysphagia & taste alterations

 Complain of a burning sensation in the tongue, lips,

buccal mucosa, & other mucosal sites.

68
APLASTIC ANEMIA
Oral manifestations:

 Hemorrhage in pts with less platelet counts

 Candidiasis

 Viral infection

69
Oral health considerations:

 Neutropenia : leading to increased susceptibility to

infection

 Antifungal therapy added

 Thrombocytopenia: leads to bruising & mucosal bleeding

 Attention to details of oral hygeine

 Avoidance of minor injuries

70
8) WBC

71
 Classification

Granulocytes Agranulocytes

Neutrophils Eosinophils Basophils Monocytes Lymphocytes

72
MORPHOLOGY Bilobed
nucleus

Multilobed Nucleus
nucleus occupying
whole
cytoplasm

Bilobed
Nucleus pushed to nucleus
one side

73
NORMAL COUNT
 Total WBC count: 4000 to 11000/ cu mm of blood

VARIATIONS IN COUNT
Pathological variation:

1. Leucocytosis : infection ,allergy , common cold

2. Leucopenia : anaphylactic shock, cirrhosis of liver

3. Leukemia : characterized by abnormal & uncontrolled

↑ in WBC count more than 1,00,000 / cu mm

74
 Physiological variation:

1. Age: infant> 20,000 /cu mm

2. Sex : male> female

3. Diurnal variation : ↓ in early morning ,↑ in afternoon

4. Exercise : ↑ slightly

5. Sleep : ↓ slightly

6. Emotional conditions like anxiety: ↑ slightly

7. Pregnancy : ↑

8. Menstruation : ↑

9. Parturition: ↑
75
NEUTROPENIA

Oral health considerations:

 Prophylactic antibiotics prior to dental extractions.

 Prophylaxis with ciprofloxacin / levofloxacin is now being

recommended as a routine practice.

76
CYCLIC NEUTROPENIA
 Severe gingivitis

 Stomatitits with ulceration

 Isolated painful ulcers- lasts from 10-14 days, heals with

scarring

 With neutrophil count to normal , gingiva appears

normal.

77
 R/E : mild to severe bone loss of superficial alveolar
bone

 Pre-pubertal periodontitis – in children loss of bone

around multiple teeth.

78
CHRONIC NEUTROPENIA

Oral menifestations:

 Recurrent gingivitis

 Severe periodontitis

 Alveolar bone loss & ulceration

 Resolution of ulcer and periodontal breakdown within 2

weeks after the initiation for treatment

79
ACUTE LEUKEMIA

 Gingival hyperplasia

 Increased keratinization

 Hemorrhage

 Petechie

80
 Rapid loosening of teeth due to necrosis of PDL

 Oral mucositis, beginning with erythema & progressing

to ulceration, begins within 7 to 10 days of onset of
chemotherapy.

81
Oral health considerations:
 Prechemotherapy dental assessment
Daily preventive protocol:
 Elimination of bacterial plaque
 Application of mouthwash with nonalchoholic solution
of chlorhexidine 0.12%
 Topical application of iodopovidine followed by “swish &
swallow” with nystatin 5,00,000 units
 May require platelet transfusion prior to dental surgery
in cases of chronic leukemia
82
 FUNCTIONS OF WBC:

 Neutrophils : along with monocytes, the neutrophils

provide the first line of defense against the invading
microorganisms.

 Eosinophils : provide defense to the body by acting against

parasitic infections & allergic conditions like asthma. It is
responsible for detoxification, disintegration & removal of
foreign proteins.

83
 Basophils : plays role in healing processes & acute
hypersensitivity reactions.

 Monocytes : provide first line defense along neutrophil.

They are precursors of tissue macrophages.

 Lymphocytes: T lymphocytes & B lymphocytes plays

role in immunity

84
9) IMMUNITY

85
83
 IMMUNITY

Innate immunity Acquired immunity

Naturally present in body by birth Develops against invading microorganism

Destruction of invading microorganism by antigen presenting cells

Release of antigen
Presentation of antigen

To T Lymphocyte To B Lymphocyte

Development of cell mediated immunity Development of humoral immunity

Activation of helper T cells Activation of B cells

Activation of cytotoxic T cells Formation of plasma cells

Production of antibodies
Destruction of invading Destruction of invading
organism by direct attack organism by antibodies 86
IMMUNE DEFICIENCY DISEASES

Congenital immune deficiency diseases:

 inherited and occurs due to defects in B cell, T cell or both.

 E.g. DiGeorge’s disease (absence of thymus)

Acquired immune deficiency :

 occurs due to infection by some organisms.

 E.g. AIDS
87
AUTOIMMUNE DISEASES
 A condition in which the immune system mistakenly attacks
body’s own cells & tissues

 Normally body has tolerance against self antigen. However, in

some occasions, the tolerance fails / becomes incomplete
against self antigen. This state is called autoimmunity which
leads to activation of T lymphocytes /production of
autoantibodies from B lymphocytes.

88
Common autoimmune diseases:

 Diabetes mellitus

 Myesthenia gravis

 Grave’s disease

 Rheumatoid arthritis

89
10) PLATELETS

90
90
STRUCTURE & COMPOSITION

 Cell membrane

 Microtubules

 Cytoplasm : proteins, enzymes, hormonal substances,

platelet granules

91
NORMAL COUNT & VARIATION

Normal count : 2,00,000 - 4,00,000 /cu mm of blood

Physiological variation:

 Age :less in infant & reaches normal level at 3rd month after
birth

 Sex : reduced in female during menstruation

 High altitude: increases

 After meals : increases

90
PROPERTIES OF PLATELETS

 Adhesiveness

 Aggregation (grouping of platelets)

 Agglutination

93
FUNCTIONS OF PLATELETS

 Role in blood clotting

 Role in clot retraction

 Role in prevention of blood loss

 Role in repair of ruptured blood vessel

 Role in defense mechanism

94
LIFESPAN & FATE OF PLATELETS

Average lifespan :

 about 10 days

Fate :

 older platelets are destroyed by tissue macrophage

system in spleen.

95
PLATELET DISORDER

 Thrombocytopenia

 Thrombocytosis

 Thrombocythemia

 Glanzmann thrombasthenia

96
PRIMARY THROMBOCYTOPENIA

 Severe & profuse gingival hemorrhage

 Petechie on oral mucosa

 *tendency for excessive bleeding contraindicates any

surgical procedures, until the deficiency is compensated.

97
THROMBOCYTOSIS

 Increase in circulating platelets

 Spontaneous gingival bleeding

 Excessive and prolonged bleeding after dental surgery.

98
GLANZMANN THROMBASTHENIA
 Spontaneous bleeding from oral cavity, particularly
gingival bleeding, oftenly palatal petechie
 *use of fibrinolytic inhibitor, c-aminocaproic acid to
control postoperative bleeding.

Gingival bleeding Epistaxis menorrhagia

99
11) HEMOSTASIS &
COAGULATION OF BLOOD
Stages :

a.Vasoconstriction

b. Platelet plug formation

c. Coagulation of blood : “process in which blood

looses its fluidity & becomes a jelly like mass few
minutes after it is shed out or collected in a
container” .

100
 Injury to blood vessel & damage of endothelium

Exposure of collagen
Von willebrand factor
Adherence of platelets to collagen

Activation of platelets

Secretion of serotonin Secretion of ADP & Formation of

Thromboxane A2 prothrombin activator

Aggregation of platelets

vasoconstriction Formation of platelet plug Blood clotting

Stage 1 Stage 2 Stage 3

101
 CLOTTING FACTORS
 Factor I Fibrinogen
 Factor II Prothrombin
 Factor III Thromboplastin (tissue factor)
 Factor IV Calcium
 Factor V Labile factor(proaccelerin /accelerator globulin)
 Factor VI Presence has not been proved
 Factor VII Stable factor
 Factor VIII Antihemophilic factor(antihemophilic globulin)
 Factor IX Christmas factor
 Factor X Stuart-Prower factor
 Factor XI Plasma Thromboplastin Antecedent
 Factor XII Hegman factor (contact factor)
 Factor XIII Fibrin Stabilizing factor (Fibrinase)
102
Stage 1 Intrinsic pathway Extrinsic pathway
Endothelial damage + collagen exposure Tissue trauma + Tissue thromboplastin
Kallikrein
HMW Kinogen Glycoprotein
Phospholipid
Platelets
XII XII a
HMW Kinogen VII

XI XI a Phospholipid Xa X
Calcium

IX IX a Calcium
V
VIII
Calcium

Xa V +
+
X Thrombin Thrombin

Positive Prothrombin activator Positive

Stage 2 Feedback Feedback
Prothrombin

Thrombin

Stage 3
Fibrinogen a Fibrinogen
Polymerization

Loose strands of fibrin

Fibrin
XIII
Tight blood clot 103
Calcium
BLOOD CLOT

 Defined as the mesh of firbrin entangling RBCs,WBCs

& platelets.

 Clot retraction: The process of contraction of blood

clot & oozing of serum is called clot retraction.
 Fibrinolysis : the lysis of blood clot inside the blood
vessel is called fibrinolysis. This process requires a
substance called plasmin/plasminolysin.
ANTICLOTTING MECHANISM IN BODY

 Under physiological conditions, intravascular clotting

does not occur. It is because of presence of some
physicochemical factors in body.
 Physical factors: continuous circulation of blood.
Smooth endothelial lining of blood vessels.

 Chemical factors: heparin, thrombomodulin, inactive

clotting factor
 ANTICOAGULANTS
 The substances, which prevent or postpone coagulation of
blood, are called anticoagulants

1. Heparin

2. Coumarin derivatives

3. EDTA

4. Oxalate Compounds

5. Citrates

6. Other substances which prevent blood clotting

 Physical methods:

1. Cold

2. Collecting blood in a container with smooth surface

PROCOAGULANTS

 Thrombin

 Snake venom

 Sodium or calcium alginate

 Oxidized cellulose
TESTS FOR CLOTTING
 Bleeding time

 Clotting time

 Prothrombin time

APPLIED PHYSIOLOGY

 Bleeding diorders: Hemophilia, von Willebrand disease

HEMOPHILIA

Type Clotting factors deficiency

Hemophilia A Factor VIII

HemophiliaB Factor IX

HemophiliaC Factor XI

 Hemorrhage from many sites in oral cavity.

 Massive & prolonged gingival bleeding

MANAGEMENT
 Factor replacement
 Tranexemic acid - antifibrinolytic
 Surgifoam
 Microfibrillar collagen
 Surgical acrylic stent
 Diet restriction
 Pain control – hypnosis, intrapulpal anesthesia, diazepam
 Avoid Aspirin
 Use rubberdam
 Coumarin withdrawl
VON WILLEBRAND’S DISEASE

 Occurs due to abnormality in quality/ quantity of the

vWF.

 vWF is carrier protein for factor VIII and it is required

for normal platelet adhesion.
Oral manifestations :

 Gingival bleeding after brushing of teeth

 Profuse bleeding after any dental surgery

 *transfusions of plasma/ antihemophilic factor

12) BLOOD GROUPS &
BLOOD TRANSFUSION
ABO BLOOD GROUPS
Landsteiner’s Law: states that

1. If a particular antigen (agglutinogen) is present in the

RBCs, corresponding antibody (agglutinin) must be absent
in the serum.

2. If a particular antigen is absent in the RBCs, the

corresponding antibody must be present in the serum.
 Blood group systems: more than 20 genetically
determined blood group systems are known today. ABO
system & Rh system are most important ones.
 ABO system
Group Antigen in RBC Antibody in serum

A A Anti B (β)

B B Anti A ( )

AB A and B No antibody

O No antigen Anti A and Anti B

Determination of the ABO group:
 Also called blood grouping, blood typing or blood
matching.
 Principle of Blood Typing –Agglutination
 Requisites –suspension of a person’s RBC & testing
antisera
 Procedure –one drop of antiserum A and B are placed on a
glass slide at each end and 1 drop of RBC suspension is
mixed, slide slightly rocked for 2 minutes, observation for
clumps
 Results
Importance in blood transfusion:

 While transfusing the blood, antigen of the donor & the

antibody of the recipient are considered.

Matching & cross matching :

 Blood matching is a laboratory test done to determine the

blood group of a person.(RBCs of recipient + test sera)

 Cross matching is done when the person needs blood

transfusion.(serum of recipient & RBCs of donor)
 Transfusion reactions:

Agglutination

Hemolysis

Jaundice

Cardiac
A β B shock
Donor Recipient
Renal
shutdown
 Rh factor:

No complications
But Rh antibody is produced

First transfusion

Rh positive Rh negative

Second transfusion

Rh antigen reacts with Rh antibody

Agglutination
 Hemolytic disease of fetus & newborn –Erythroblastosis
Fetalis.

Rh –ve Mother Rh +ve fetus

First child escapes the Rh Second child if Rh +ve,

incompatibility complications. Rh antibody from mother’s
Within a month after delivery blood enters fetal blood
mother develops Rh antibody in resulting in hemolysis
her blood

1. Severe anemia &

Jaundice
2. Hydrops fetalis
3. kernicterus
 Hydrops fetalis

Kernicterus & Jaundice

Oral findings:

 Deposition of blood pigment in enamel & dentin

 Intrinsic stains

 Enamel hypoplasia

 Rh hump
 Prevention or Treatment :

i. If Rh –ve mother & Rh +ve fetus : administration of Anti

D at 28th & 34th week of gestation to mother.
Administration of anti D within 48 hours of delivery to
prevent hemolytic disease in subsequent delivery.

ii. If the baby is born with disease : exchange transfusion

of Rh negative blood into infant to replace its own
blood.
OTHER BLOOD GROUPS:

1. Lewis blood group

2. MNS blood group

3. Diego group

4. Bombay group

5. P group

6. I group etc.
BLOOD TRANSFUSION:
 It is the process of transferring blood or blood
components from one person (donor) into the
bloodstream of another person(recipient).

 Substances infused in the body instead of whole blood are

known as blood substitutes. E.g., human plasma, 5 % glucose,
0.9 % NaCl solution
 Exchange transfusion(Replacement transfusion) is the
procedure in which involves removal of patient’s blood
& replacement with fresh donor blood or plasma.
>severe jaundice, sickle cell anemia etc

 Autologous blood transfusion is the collection and

reinfusion of patient’s own blood. Also called as self
blood donation.