blood and its disorders

2. DJ COLLEGE OF DENTAL SCIENCES
AND RESEARCH
SEMINAR TOPIC – BLOOD AND
BLOOD DISORDERS
PRESENTED BY:Dr Venisha Pandita
1st Year Post Graduate
Department of Public Health
Dentistry

3. CONTENTS:













Introduction
Characteristics
Composition
Plasma proteins
Blood cells :
RBC
WBC
Platelets
Haemoglobin
Haemopoiesis
Haemostasis
Functions of blood
Blood groups

4. Disorders :
Diseases of red blood cells
 Anemia
 Polycythemia
Hemostasis and its disorders
 Thrombocytopenia
 Haemophilia
 Disseminated intravascular coagulation
Disorders of White Blood Cells
 Agranulocytosis
 Leukaemia
 Conclusion
 References


5. BLOOD:
William Harvey- father of physiology
discovered blood circulated through the body in 1628.
 It is a fluid connective tissue which transports substance from
one part of the body to another.
 It provides nutrients and hormones to the tissues and removes
their waste products.


6. CHARACTERISTICS OF BLOOD








Color:
blood is red in color.
Arterial blood is scarlet red and venous blood is purple
Volume:
Average volume of blood in a normal adult is 5 l
In females it is slightly less and it is about 4.5 l
Reaction and pH:
Blood is slightly alkaline and its pH in normal conditions is
7.4

7. 





Specific gravity:
total blood: 1.052 to 1.061
blood cells: 1.092 to 1.101
plasma:
1.022 to 1.026
Viscosity:
blood is five times more viscous than water.

8. COMPOSITION

9. 1.PLASMA:


Straw colored, nonliving part of blood.
Blood plasma is a mixture of proteins, enzymes,
nutrients, wastes, hormones and gases.

It contains :

91% Water

9% Solids : that comprises :

1% inorganic molecules: Na+,Ca2+,Cl-,
HCO3-,K+,Mg2+

10. o
8% organic molecules :7% plasma proteins
1% NPN (non –protein nitrogenous) ,
Substances,sugar,fats,enzymes and hormones

The specific composition and function of its
components are as follows:

11. 1. PROTEIN :





Normal value: 6.4 -8.3 gm%
There are three major categories of plasma
proteins, and each individual type of proteins has its
own specific properties and functions:
Albumin: 55%
3-5gm%
helps substances dissolve in the plasma by
binding to them, hence playing an important role
in plasma transport of substances such as drugs,
hormones and fatty acids.

12. Globulin : 38 %
 2-3 gm %
 alpha, beta and gamma globulins.
 eg: immunoglobulins, transport globulins
 immunoglobulins: antibiotics, attack foreign proteins &
pathogens
 transport globulins: bind small ions, hormones

Fibrinogen : functions in blood clotting
 accounts for roughly 7% of plasma proteins


13. OTHER FORMS
GLYCOPROTEIN
 LIPOPROTEIN : HDL, LDL, VLDL, Chylomicrons
 TRANSFERRIN : (mainly -globulin)-Iron binding
property
 HAPTOGLOBIN : 2 globulin - Regulates renal
threshold for hemoglobin


14. CERULOPLASMIN -(mainly 2 globulin) – binds
with copper and helps in its storage and transport .
 FETUIN –present in FOETUS, growth promoting
protein
 COAGULATION FACTORS - , -globulin
 ANGIOTENSIGEN - 2 globulin
 HAEMAGGLUTININS -antibodies against red cells
Ag
 IMMUNOGLOBULIN (Ig) - globulin


15. 2. Nutrients:

These include glucose, amino acids, fats, cholesterol,
phospholipids, vitamins and minerals.
3. Gases:

Some oxygen and carbon dioxide are transported by plasma.
4. Electrolytes:

The most abundant of these are sodium ions
5. Amino acids
6. Nitrogenous waste:
o
urea ,uric acid, creatine, creatnine

16. FUNCTIONS OF PLASMA PROTEINS:
1.
2.
3.
4.
5.
6.
7.
Helps in coagulation of blood
Helps to maintain colloidal osmotic pressure.
Helps in maintaining viscosity of blood
Provides stability to blood
Helps in maintaining the acid-base balance in the body
Immune function
Transport and reservoir function

17. BLOOD CELLS:
 Red
blood cell
 White blood cell
 Platelet

18. RED BLOOD CELLS
The most abundant blood cells are the red blood cells
(RBCs), which account for 99.9 percent of the formed
elements.
 These cells give whole blood its deep red color.
 Red blood cells contain the red pigment hemoglobin .
 No nucleus


Cell membrane : Lipids, Proteins, Spectrin, Glycophorin

No Mitochondria

No Ribosome

No Centriole
In adult males,4.5–6.3 million per 1 cubic ml
females,4.2–5.5 million per 1 cubic ml


19. HAEMOGLOBIN:
Normal values:
At birth: 23gm/dl
At the end of 3 months: 10.5gm/dl
At the end of 1 year 12.5gm/dl
Adults- males: 14-18gm/dl
females: 12-15 gm/dl

20. STRUCTURE OF HAEMOGLOBIN :
Red oxygen carrying pigment in the RBCs, there
are two parts.
 Globin (96%) and Heme (4%).
 Each heme unit holds an iron ion in such a way
that the iron can interact with an oxygen
molecule, forming oxyhemoglobin .


21. VARIETIES OF HEMOGLOBIN:
A
haemoglobin molecule in which the iron
has separated from the oxygen molecule is
called deoxyhemoglobin .
 The RBCs of an embryo or a foetus contain
a different form of hemoglobin, known
as fetal hemoglobin , which binds oxygen
more readily than does the haemoglobin
of adults.

22. Methaemoglobin - Hb with ferrous to form ferric
 Carboxyhaemoglobin -CO bound at O2 binding site
 Sulphaemoglobin n- Sulphur containing Hb usually
-Resulting from drug ingestion


23. FUNCTIONS OF HAEMOGLOBIN:
1.
2.
3.
Facilitate transport of oxygen from lungs
to tissues
Facilitate transport of CO2 from the
tissues to the lungs
It acts as an excellent acid- base buffer,
being a protein.

24. VARIATIONS
Sex :males > females
 Diurnal variation: Lowest in morning; highest in
evening
 Altitude : Increased at higher altitude
 Exercise : Increased
 Excitement :Increased


25. VARIATIONS:












Poikilocytosis :variation in shape of RBC
Anisocytosis:variation in size of RBC
Phsiological:
Diurnal variation – lowest during sleep maximum in
evening
Muscular exercise: increases
Altitude: increases
Pathological: increases
Hypoxia
Shock
dehydration
Life span : 120 days
Destruction: Mainly in spleen; liver; bone marrow

26. HAEMOPOEISIS
In order to maintain the constant blood count it is
necessary that new cells should be formed to
replace these that are destroyed. This
phenomenon of cell production is called
hemopoeisis.
 Erythropoeisis -dev of RBCs
 Leucopoeisis -dev of WBCs
 Megakaryocytopoeisis -dev of platelets

27. HAEMOPOEISIS:

28. RBC LIFE SPAN & CIRCULATION
Erythropoiesis : development of RBCs
During intrauterine life1. Mesoblastic stage:

Intravascular erythropoeisis: Upto 3 months
RBC are formed from mesoderm of yolk sac,
hence erythropoeisis occurs within the vessel.
2. Hepatic stage:

After 3 months, liver and spleen are the site of
blood formation.
3. Myeloid stage : from middle of foetal life ,occur in
bone marrow


29. 









In Children, erythropoiesis occurs in :
all bones with red marrow mainly
liver
spleen.
In adults : after 18-20 yrs
end of long bones like humerus and femur,
because shaft is converted to yellow marrow
Skull
Vertebrae
Ribs
Sternum and pelvis.

30. STAGES OF ERYTHROPOIESIS
Stem cell
Committed
cell
Haemocytoblast Proerythroblast
Developmental pathway
Early
intermediate
Late
Reticulocyte Erythrocyte
normoblast normoblast Normoblast

31. REGULATION OF ERYTHROPOIESIS
 for
erythropoiesis to proceed normally
myeloid tissues must receive adequate
supplies of amino acids, Fe, & vitamins
required for protein synthesis
 essential coenzymes: B6, B12, folic acid –
necessary for DNA replication (mitosis)
 vitamin B12: obtained from dairy products &
meat; its absorption requires presence of
intrinsic factor produced in stomach

32. LEUKOCYTES (WBCS)
Leukocytes found in blood in the following
proportions:
 Granulocytes–WBC with granules in their
cytoplasm
 60% Neutrophils
 1-4% Eosinophils
 <1% Basophils
 Agranulocytes–lack visible cytoplasmic
granules
 20 - 40% Lymphocytes
 2 - 8% Monocytes

33. 
TLC:
At birth is 20000/ ul
In adults is 4000-11000/ ul
 Leucopenia : decreases less than 4000/ cumm
Causes:
 starvation
 Typhoid fever
 Viral/ protozoal infection

34. Leucocytosis : increases above 11,000/ cumm
Causes:
 newborn
 Evening
 Exercise
 Stress
 Pregnancy
 Menstruation
 Any pyogenic / pyrogenic infections


35. 1. NEUTROPHILS
Size: 10-12 diam
 Nucleus: Multilobed (2-6)-PMNL
 Cytoplasm: Granular, Neutrophilic
 Granules: pin point granules
 neutrophilic in nature
 Contains proteins and lipids
 These granules are regarded as lysosomes as they
can lyse any type of substances using varieties of
enzymes like nucleases,glycosidases


36. Functions:
 Phagocytosis : whenever the body gets invaded by
bacteria, neutrophils are the first to seek out to
ingest and kill bacteria. (First line defense)

37. 2. EOSINOPHIL
Size: 10-12 diam
 Nucleus : Bilobed spectacle appearance
 Cytoplasm : Acidophilic, granular
 Granules: coarse, acidic
 High peroxidase content
 Lysosomal enzymes


38. Functions
Mild
phagocytic
Anti-allergic
effect: collect at the site of the tissues
where allergic reactions occur by degrading the
effects of mediators (histamine,bradykinin)
Inhibits
Kills
Mast cells degranulation
parasites

39. Eosinophilia: increase in eosinophils
Causes:
 Allergic reactions ( bronchial asthma)
 Skin diseases
 Eosinopenia: decrease
 After injection of corticosteroids


40. 3. BASOPHIL
Size: 10-12 m
 Nucleus
: Bilobed
 Cytoplasm : Basophilic
 Granules: Coarse,basic
 Plenty in no., overcrowd the nucleus
 Contain- Histamine, Heparin
Eosinophil chemotactic factor (ECF-A): chemical
mediator of immediate hypersensitivity reactions.


41. Functions:

Liberates Histamine and ECF-A: which leads to allergic
manifestations

Liberates Heparin : which acts as Anticoagulant and
keeps the blood in fluid state
Mild phagocytosis
Basophilia: increase
Chickenpox
Tuberculosis
Influenza
Basopenia : decrease
After administration of gluco-corticoids


42. 4. MONOCYTE
Largest WBC
 Size :12-18
diam
 Nucleus : Kidney shaped eccentric in position
 Cytoplasm : Clear Enzymes- proteolytic,
hydrolytic


43. Functions
 Active Phagocytosis : second line defence
 Enter the tissues to become tissue macrophage
 Kill tumor cells after sensitization by Lymphocytes.
Monocytosis:
Tuberculosis
Some leukaemia
Monocytopenia:
Hypoplastic bone marrow

44. 5. LYMPHOCYTES
2 types:
 Large Lymphocyte : 10-14
diam, precursor of
small lymphocyte
 Small Lymphocyte : 7-10 diam

45. Nucleus : Single, round, oral or indented central,
occupies whole of the cell
Nuclear chromatin is coarse and lumpy
 Cytoplasm: Only narrow ring around nucleus


46. Functions
 produce antibodies and hence responsible for Immunity
 Immunity: Resistance exhibited by the host towards the
injury caused by bacteria or foreign proteins.
 Humoral Immunity: Antibodies which are -globulins
produced by B-Lymphocytes
 Cell-mediated Immunity: Due to T-Lymphocytes
Lymphocytosis:
In children : 60 % more than neutrophils (relative
Lymphocytosis)
Lymphopenia:
AIDS
Hypoplastic bone marrow

47. LIFE SPAN AND FATE OF WBC

Neutrophils

: 2-4 days
Eosinophils
: 8-12 days (Last through
GIC or Resp. tract)

Monocyte
:
1 day in circulation

B-Lymphocytes
:
Few days or weeks

T-Lymphocytes
:
2-4 years

48. PLATELETS (THROMBOCYTES)
Structure :
General
 smallest blood cells, colorless
 disc shaped (in activated from) to sphere shaped
(activated) granulated bodies.
 Size : 2-5 m in diameter, average volume 5.8 m3
 Leishman staining : faint blue cytoplasm with
distinct reddish purple granules.
 Nucleus is not present.

49. Under Electron Microscope:
Platelet membrane: Features

Identical structure with cells membranes thickness:
60 nm

Main lipids in lipo-protein layer of cell membrane:
Phospholipids. Cholesterol, and glycolipids

Contains various receptors meant for combining with
specific substances like:

Collagen

Fibrinogen

Von-Willebrand’s factor: important role in platelet
adhesion

50. Cytoplasm : contains

Golgi apparatus

Endoplasmic reticulum

Few mitochondria

Microvesicles and microtubules:

Contractile protein –actin and myocin : helps in
clot retraction.

Glycogen

Lysosomes

51. Granules - 2 types.

Dense granules- contains

Non-proteins substances like phospholipid,
triglycerides. Cholesterol etc.

Serotonin - Vasoconstrictor agent

ADP- helps platelet aggregation

ATP- stores energy

Other adenine nucleotides

-Granules- contains secreted proteins including

Clotting factors

Platelet derived growth factor (PDGF)- stimulates
wound healing, helps in repair of damaged vessel wall

52. 
Count
Normal count: 1.5 to 4 lacs /cumm
(average 2.59 lac/cumm)

Life span : 8-12 days

Destruction : Mainly in spleen

53. VARIATIONS:
Thrombocytosis :increase in platelet count
 after administration of epinephrine
 After trauma
 Splenectomy
 Stress
 Thrombocytopenia :decrease in platelet count
 Bone marrow depression
 Hypersplenism

54. FUNCTIONS OF PLATELET
1. Hemostasis:
Spontaneous arrest of bleeding by physiological
process.



Platelet adhesion
Platelet activation
Platelet aggregation : Hemostatic plug that
prevents blood loss
2 . Blood coagulation- release of clotting factors,
Prostaglandins, Phospholipids

55. 3. Clot Retraction- 40% of original volume and
release of Thrombosthetin
4. Phagocytic functions – helps in phagocytosis
of carbon particles,viruses.

56. MECHANISM OF HAEMOSTASIS





Injury to vessel wall
initiates series of events
A. Constriction of injured blood vessel.
B. Formation of a 'temporary haemostatic plug' of
platelets.
C. Conversion of temporary haemostatic plug into
the 'definitive haemostatic clot'.
Formation of clot
Seals off the damaged blood vessel
prevents further loss of blood

57. PHYSIOLOGY OF CLOTTING MECHANISM

The clotting mechanism responsible for the
formation of fibrin involves a 'complex series' or
'cascade' of reactions. Here 'inactive' enzymes are
activated, and the activated enzymes in turn
activate other inactive enzymes.

62. ANTICOAGULANTS
Types
 Natural Anticoagulants
 Synthetic Anticoagulants
1. Heparin
 A powerful anticoagulant first isolated from liver
(hence its name)
 present in many other organs e.g. lungs.
 It facilitates the action of antithrombin III, thereby
inhibiting the active forms of clotting factors IX, X,
XI and XII.

63. Origin: Heparin is secreted by (i) granules of circulating basophils
(ii) granules of "mast cells". These cells are found in
large numbers in tissues that are rich in connective
tissue;
 Destruction: by an enzyme "Heparinase" in the
liver.
2. Anti-Thrombin or Heparin co-factor II: It inhibits
thrombin.
3. Protein C: It inactivates factors V and VIII.


64. Synthetic Anticoagulants
1. Vitamin K Antagonists: effective orally
 These
include
coumarin
derivatives
dicoumarol. and warfarin.
2. Malayan (Malaysian) Pit Viper
3. Arvin (Ancord)
e.g.

65. FUNCTIONS OF BLOOD
Transport of Respiratory gases:  Blood and particularly red cells are responsible for
transport of O2 from lungs to the tissues.
 This is done due to the presence of hemoglobin,
which combines with O2 to form oxy-Hb; Co2 from
tissue is taken up by the blood and released in the
lungs.
 Transport of Nutrition:  The substances such as glucose, fatty acids, amino
acids, vitamins, electrolytes and trace metals are
absorbed from the intensive transported to all parts
of the body for utilization and storage via blood.


66. Excretory: Blood transports urea, uric acid,
creatinine to kidney, lungs, skin, and gastrointestinal tract for excretion.
 Regulation of Body Temperature:
 Blood forms internal environment of the cell i.e.
MILLIEU INTERIUER in terms of volume,
composition, concentration, pH and temperature
which is regulated to normal physiological limits
with respect to miner changes in the body.
 This mechanism is called Homeostasis. (W. E.
Cannen).


67. Defensive Action: Blood acts as a great defensive
mechanisms through WBC s , lymphocytes
 Transport of Other Substances: Blood acts as a
vehicle through hormones, vitamins, and other
essential chemicals are transported to the various
tissues.
 Coagulation Property: It is a mechanism by which
various factors present in the blood form a cell and
thus prevent blood less
 Plasma Proteins: The plasma proteins of blood
have various functions which will be discussed
subsequently


68. BLOOD GROUPS




The chief blood groups are :
Classical ‘ABO’ blood group
Rhesus (Rh) blood group
M and N blood group

69. 1.CLASSICAL ‘ABO’ BLOOD GROUP
RELATIONSHIPS BETWEEN BLOOD TYPES AND
ANTIBODIES
Blood Type Antigens
on Red
Blood Cell
Can
Donate
Blood To
Antibodies
in Serum
Can
Receive
Blood
From
A
A
A,AB
Anti-A
A,O
B
B
B.AB
Anti-B
B,O
AB
A and B
AB
None
AB,O
O
None
A,B,AB
and O
Anti-A and
Anti-B
O

70. Blood typing is a laboratory test done to discover a person's blood
type. If the person needs a blood transfusion, cross-matching is
done following blood typing to locate donor blood that the person's
body will accept. (Illustration by Electronic Illustrators Group.)

72. 2.RHESUS (RH) BLOOD GROUP
Landsteiner and Weiner (1940)
 Present in > 85% of individuals Rh + Ve
 No corresponding Agglutinin in plasma
 Rh antigen is called D and its antibody is called
Anti-D also known as warm antibodies.


73. Rh incompatibility

74. 3. M N SYSTEM
Significance in the determination of paternity in
medico legal cases.
 M and N factors depend on two minor genes.
 Each person carries of the two of the genes of the
M and N group.
 i.e. M + M = M
N +N = N
M+ N =MN
o These are antigenic to rabbits


75. USES OF BLOOD GROUPING TESTS
Blood transfusion
 In pregnancy (Rh Incompatibility)
 Investigating cases of paternity dispute
 In forensic medicine
 Medico legal value


76. BLOOD DISORDERS
DISEASES OF RED BLOOD CELLS
(ERYTHROCYTES): Anaemia
 Iron Deficiency Anaemia
 Anaemia Of Chronic Disease
 Sideroblastic Anaemia

77. megaloblastic anaemia
 haemolytic anaemia
 sickle cell anaemia
 thalassemia
 aplastic anaemia
 Polycythemia


78. ANAEMIA

At birth, haemoglobin is 20g/dl and at 3 months
lower limit of normal is taken as 9.5g/dl. A
haemoglobin level of 12g/dl or less is usually
regarded as anaemia in adult males and less than
11g/dl is taken as anaemia in females.

79. SYMPTOMS
Pallor or lack of color
 fatigue, dizziness, headaches
 decreased exercise tolerance
 rapid heartbeat, and shortness of breath
 haemic murmurs
 Untreated anemia may progress to death from
heart failure


81. ETIOLOGICAL CLASSIFICATION OF ANEMIA

Blood loss:
Acute Post hemorrhagic
 Chronic blood loss


Deficiency of Hemopoetic factors:Iron deficiency
 Folate and vitamin b12deficiency
 Protein deficiency.


Bone marrow aplasia:Aplastic anemia
 Pure red cell aplasia


82. 
Anemia due to systemic infections:




Anemia due to bone marrow infiltration:





Due to chronic infection
Due to chronic renal disease
Due to chronic liver disease
Endocrinal diseases
Leukemia’s
Lymphomas
Myelofibrosis
Multiple myeloma
Congenital sideroblastic anemia
Anemia due to increased red cell destruction:Intra-corpuscular defect
 Extra-corpuscular defect


83. Morphological classification of anemia:-
Microcytic hypochromic
 Normocytic normochromic


Macrocytic normochromic

84. TYPES OF ANAEMIA




Macrocytic anemia: Megaloblastic anemia and nonmegaloblastic macrocyctic anemia. Primary cause of
this sort of anemia is collapse of DNA synthesis with
kept RNA synthesis that occurs due to the division of
the divisional cells.
Microcytic anemia: Sort of anemia occurs due to
hemoglobin synthesis shortage or collapse.
Normcytic anemia: Occurs when Hb levels
decreases overall. Size of RBC is often normal.
Heinz Body anemia: Considered a cell abnormality
that usually occurs in cells under anemia.

85. 


Iron-deficiency anaemia – hypochromic microcytic
anemia characterized by low serum iron, increased
serum iron-binding capacity, decreased serum
ferritin, and decreased marrow iron stores.
Megaloblastic (pernicious) anaemia –
predominant number of megaloblastic
erythroblasts, and relatively few normoblasts,
among the hyperplastic erythroid cells in the bone
marrow
Hemolytic anaemia – increased rate of erythrocyte
destruction.

86. 



Sickle cell anemia – autosomal recessive anemia
characterized by crescent- or sickle-shaped
erythrocytes and accelerated hemolysis, due to
substitution of a single amino acid - chromosome
11
Aplastic anemia – greatly decreased formation of
erythrocytes and hemoglobin, usually associated
with
pronounced
granulocytopenia
and
thrombocytopenia
Chronic anemia
Anemia of folate deficiency

87. 
Cooley's anemia (beta thalassemia) – syndrome
of severe anemia resulting from the homozygous
state of one of the thalassemia genes or one of the
hemoglobin Lepore genes with onset, in infancy or
childhood, of pallor, icterus, weakness,
splenomegaly, cardiac enlargement, thinning of
inner and outer tables of skull, microcytic
hypochromic anemia with poikilocytosis,
anisocytosis, stippled cells, target cells, and
nucleated erythrocytes

88. CAUSES




Accurate blood loss
Anemia of chronic disease
Bone marrow failure and
Plastic anemia.

89. TREATMENT



A successful treatment of anemia depends on
successful diagnosis of the cause that brings about
the disease.
There are several causes of anemia including blood
loss, cancer, a nutritional deficiency, chronic illness,
bone marrow infiltration, lower response to
erythropoietin and inflammation.
These causes can be determined with laboratory
test results and physical examination.

90. Specific treatment for anemia will be determined by
the physician based on:
 Age, overall health, and medical history
 Extent of the disease
 Tolerance for specific medications, procedures, or
therapies
 Expectations for the course of the disease
 Opinion or preference of the patient

91. 







Treatment of the causative disease
Vitamin and mineral supplements
Change in diet
Medication
Blood transfusion
Bone marrow transplant
Surgery (to remove the spleen, if related to
hemolytic anemia)
Antibiotics (if an infection is the causative agent)

92. HEMOPHILIA




Persons with hemophilia lack the ability to stop
bleeding because of the low levels, or complete
absence, of specific proteins, called "factors," in their
blood that are necessary for clotting.
Inherited bleeding or coagulation, disorder.
Proper clotting of blood helps prevent excessive
bleeding.
Types of hemophilias –
 hemophilia A - lack of factor VIII
 hemophilia B - lack of factor IX

93. CAUSES




Hemophilia types A and B are inherited diseases
passed on from a gene located on the X
chromosome.
Females carrier of hemophilia has the hemophilia
gene on one of her X chromosomes, and there is a 50
percent chance that she may pass the defective gene
to her male offspring.
Males who inherit the defective gene will develop
hemophilia.
Males with hemophilia do not pass the gene to their
sons; however, they do pass the gene to their
daughters.

94. 

Females who inherit the defective gene will become
carriers who may, in turn, have a 50 percent
chance of passing it on to their children. Although
females who inherit the gene generally have no
active problems related to hemophilia, some may
have other problems associated with bleeding,
such as excessive menstrual bleeding, frequent or
severe nosebleeds, or bleeding after dental
procedures or surgery.
In about 1/3rd of hemophilia cases, there is no
family history of the disease. These cases are due
to a new or spontaneous development of the
defective gene in the female

96. SYMPTOMS:






Excessive, uncontrollable bleeding
Bleeding may occur even if there is no injury.
Often occurs in the joints and in the head.
Bruising - Occur from small accidents, which can
result in a large hematoma.
Bleeds easily - Tendency to bleed.
Bleeding into a joint - Hemarthrosis can cause
pain, immobility, and eventually deformity if not
medically managed properly

97. 



Bleeding into the muscles - Bleeding
into the muscles can cause swelling,
pain, and redness.
Bleeding from injury or bleeding in
the brain - Bleeding from injury or
spontaneously in the brain, is the most
common cause of death in children
with hemophilia and the most serious
bleeding complication.
Other sources of bleeding - Blood
found in the urine or stool may also be
a symptom of hemophilia.
The symptoms of hemophilia may
resemble other blood disorders or
medical problems.

99. DIAGNOSIS & EFFECTS







Complete medical history and physical examination
Clotting factor levels
Complete blood count (CBC)
Assessment of bleeding times
DNA testing.
Most common cause of disability from hemophilia is
chronic joint disease or arthropathy, which is
caused by uncontrolled bleeding into the joints.
Hemorrhage – severe internal or external discharge
of blood, is a continuing problem.

100. TREATMENT

Blood transfusions

Prophylactic (preventive) treatment with infused
clotting factors

101. IMMUNE THROMBOCYTOPENIC PURPURA
(THROMBOCYTOPENIA)



Blood disorder characterized by an abnormal
decrease in the number of blood platelets, which
results in internal bleeding.
Acute thrombocytopenic purpura – Most
common in young children, the symptoms may
follow a virus infection and disappears within a year
- usually disorder does not recur.
Chronic thrombocytopenic purpura – Onset of
the disorder can happen at any age, and symptoms
can last six months or longer. Adults have this form
more often than children, and females have it 3
times more often than males.

103. CAUSES





Medications - including over-the-counter
Infection
Pregnancy
Immune disorders
However, about half of all cases are classified as
idiopathic.

104. SYMPTOMS




Internal bleeding, which may cause:
ecchymosis - bruising ,
petechiae - tiny red dots on skin or mucous
membranes
Occasionally, bleeding from the nose, gums,
digestive tract, urinary tract
Rarely, bleeding within the brain
Symptoms may resemble other blood disorders or
medical problems.

105. DIAGNOSIS





Complete medical history and physical examination
Additional blood and urine tests
Other evaluation procedures
Careful review of patient's medications
Bone marrow examination

106. TREATMENT





Treatment of the causative disease
Discontinuation of causative drugs
Treatment with corticosteroids
Treatment with medications
Lifestyle changes, such as: use of protective gear ,
avoidance of certain activity causing injuries.

107. HODGKIN'S DISEASE




Type of lymphoma, a cancer in the lymphatic
system.
Rare disease usually occurs most often in people
between the ages of 15 and 34, and in people over
age 55.
Hodgkin's disease causes the cells in the lymphatic
system to abnormally reproduce, eventually making
the body less able to fight infection.
Hodgkin's disease cells can also spread to other
organs.

109. LYMPHADENOMA – HODGKIN'S DISEASE (PSEUDOLEUKEMIA OF GERMAN AUTHORS)

110. SIGNS AND SYMPTOMS







Painless swelling of lymph nodes in neck,
underarm, and groin
Fever
Night sweats
Fatigue
Weight loss
Itching of the skin
It may resemble other blood disorders or medical
problems, such as influenza or other infections.

111. DIAGNOSIS



Additional blood tests
X-rays of the chest, bones, liver, and spleen
Biopsy of the lymph node
TREATMENT
 Radiation therapy
 Chemotherapy

112. LEUKAEMIA


Cancer of the blood cells, usually the white blood cells.
Leukemic cells look different than normal cells and do
not function properly.

113. LYMPHOCYTIC OR MYELOGENOUS LEUKEMIA



Cancer can occur in either the lymphoid or myeloid
white blood cells.
When the cancer develops in the lymphocytes
(lymphoid cells), it is called lymphocytic leukemia.
Cancer develops in the granulocytes or monocytes
(myeloid cells) – myelogenous leukemia.

114. ACUTE OR CHRONIC LEUKEMIA


Acute leukemia - The new or immature cells,
called blasts, remain very immature and cannot
perform their functions. The blasts increase in
number rapidly, and the disease progresses quickly.
Chronic leukemia - There are some blast cells
present, but they are more mature and are able to
perform some of their functions. The cells grow
more slowly, and the number increases less quickly,
so the disease progresses gradually.

115. LEUKEMIA IS CLASSIFIED INTO ONE OF THE
FOUR MAIN TYPES OF LEUKEMIAS




Acute myelogenous leukemia (AML)
Chronic myelogenous leukemia (CML)
Acute lymphocytic leukemia (ALL)
Chronic lymphocytic leukemia (CL

116. SIGNS AND SYMPTOMS




More frequent infections and fevers
Anaemia and its symptoms: pale skin, fatigue,
weakness, bleeding, bruising, fever, chills, loss of
appetite, loss of weight, swollen or tender lymph
nodes, liver, or spleen, petechiae (tiny red spots
under the skin), swollen or bleeding gums,
sweating, bone or joint pain.
Acute leukaemia: headaches, vomiting, confusion,
loss of muscle control, seizures, swollen testicles,
sores in the eyes or on the skin.
Chronic leukemia may affect the skin, central
nervous system, digestive tract, kidneys, and
testicles.

118. DIAGNOSIS







Physician examination for swelling in the: liver,
spleen, lymph nodes under the arms, in the groin,
and in the neck
Blood tests and laboratory tests
Blood tests to examine the blast (immature) blood
cells
Bone marrow aspiration and biopsy
Lymph node biopsy
Spinal tap
Imaging procedures, such as x-ray, ultrasound, and
computed tomography (CT)

119. TREATMENT







Chemotherapy
Radiation therapy
Bone marrow stem cell transplantation
Biological therapy
Platelet transfusion
Red blood cell transfusion
Medications to prevent or treat damage to other
systems of the body caused by leukemia treatment

120. NON-HODGKIN'S LYMPHOMA



Type of lymphoma, which is a cancer in the
lymphatic system.
Non-Hodgkin's disease causes the cells in the
lymphatic system to abnormally reproduce
eventually causing tumors to grow and can also
spread to other organs.
Etiology is idiopathic

121. SYMPTOMS







Painless swelling of
underarm, and groin
Fever
Night sweats
Fatigue
Weight loss
Itching of the skin
Recurring infections
lymph
nodes
in
neck,

122. DIAGNOSIS






Blood tests
X-rays of the chest, bones, liver, and spleen
Biopsy of the lymph nodes, bone marrow, and other
sites
Lymphangiograms - lymphatic system x-rays
CT scan
Ultrasonography scan
TREATMENT
 Radiation therapy
 Chemotherapy

123. THROMBOCYTHEMIA




It is a myeloproliferative blood disorder.
It is characterized by the production of too many
platelets in the bone marrow.
Too many platelets make normal clotting of blood
difficult
Etiology is idiopathic

124. SYMPTOMS








Increased blood clots in arteries and veins
Bleeding
Bruising easily
Bleeding from the nose, gums, gastrointestinal tract
Bloody stools
Hemorrhaging after injury or surgery
Weakness
Enlarged lymph nodes

125. DIAGNOSIS



Complete medical history and physical examination
Blood counts and elevated platelet levels
Bone-marrow biopsy
TREATMENT


Chemotherapy
Plateletpheresis - a procedure to remove extra
platelets from the blood

126. BONE MARROW TRANSPLANTATION
[BMT]



BMT is a special therapy for patients with cancer or
other diseases which affect the bone marrow.
A bone marrow transplant involves taking cells that
are normally found in the bone marrow (stem cells),
filtering those cells, and giving them back either to
the patient or to another person.
The goal of BMT is to transfuse healthy bone
marrow cells into a person after their own unhealthy
bone marrow has been eliminated

127. NORMAL ANATOMY

128. INDICATION

129. PROCEDURE

131. A BONE MARROW TRANSPLANT CAN BE USED
TO



Replace diseased, non-functioning bone marrow
with healthy functioning bone marrow
Replace the bone marrow and restore its normal
function after high doses of chemotherapy or
radiation are given to treat a malignancy – process
called "rescue".
Replace bone marrow with genetically healthy
functioning bone marrow to prevent further damage
from a genetic disease process

132. CONCLUSION :
Human body is an intricate system of various
tissues and organs
 Blood and lymphatic system forms an integral part
of life’s sustainance.
 As a public health dentist ,it is essential to have a
proper understanding of blood and its components
and blood related diseases so as to be well
prepared for their diagnosis and appropriate
treatment


133. REFERENCES:
Guyton C Arthur , Hall E John .Textbook of medical
physiology. 9th ed . Singapore : W B Saunders;
2000.
 Textbook of Physiology: A. K. Jain , 3rd edition
page no. 45 -110
 Essentials of Medicine: Davidson
 Essentials of Medicine :K. Sembulingam, Prema
Sembulingam , 4th edition, page no. 53-87
 Textbook of Pathology: Harsh Mohan
Malik A Neelima. Textbook of oral and maxillofacial
surgery.2nd ed:jaypee;new delhi:2010;p.205-225
