Common blood disorders include anemia, bleeding disorders such as hemophilia, blood clots, and blood cancers such as leukemia, lymphoma, and myeloma.

1. PRESENTATION
ON
BLOOD DISORDERS
SUBMITTED TO: DR. PALLAVI PATHANIA
(ASSOCIATE PROFESSOR)
SUBMITTED BY: MS.REENA SHARMA(M.SC 1ST YR.)
SUBMITTED ON: 24/04/2020

2. INDEX
SR.NO CONTENT
1) Introduction
2) Anatomy and physiology of blood
3) RBC Disorders
4) WBC Disorders
5) Platelets Disorders
6) Summarization
7) Conclusion
8) Assignment
9) Bibliography

3. INTRODUCTION
Hematology is the study of blood in health
and disease. It includes problems with the red
blood cells, white blood cells, platelets, blood
vessels, bone marrow, lymph nodes, spleen,
and the proteins involved in bleeding and
clotting (hemostasis and thrombosis).

4. 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.

5. 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 liter
In females it is slightly less
and it is about 4.5 liter

6. Cont…
Reaction and pH: Blood is slightly alkaline
its pH in normal conditions is 7.4
Specific gravity:
Total blood: 1.052 to 1.06
Blood cells: 1.092 to 1.101
Plasma: 1.022 to 1.026
Viscosity: blood is five times more viscous than
water.

7. Composition of Blood

8. 1. PLASMA
It is 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+

9. 2. Protein
Normal value: 6.4 -8.3 gm%
Albumin: 55% (3-5gm% )
it 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.

10. 3.Nutrients:
These include glucose, amino acids, fats,
cholesterol, phospholipids, vitamins and minerals.
Gases: O2 & Co2
Electrolytes: Most abundant Sodium.
Amino Acids
Nitrogenous Waste
Urea
Uric Acid
Creatinine

11. 4.Blood cells:
1) Red blood cell
2) White blood cell
3) Platelet

12. 1) Red blood cell
The most abundant blood cells are the red
blood cells (RBCs), which account for
99.9 percent of the formed elements
In adult males ,4.5–6.3 million per 1
cubic ml
females, 4.2–5.5 million per 1 cubic ml

13. Cont..
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

14. RED BLOOD CELL DISODERS
1. Erythrocytosis
2. Polycythaemia vera
3. Anaemia
I. Iron deficiency anaemia
II. Anaemia owing to heamolysis
III. Sickle cell anaemia
IV. Thalassemia
V. Pernicious anaemia
VI. Aplastic anaemia

15. 1.Erythrocytosis:
A conditions with an increase in
circulating red blood cells (RBCs),
characterized by a increased
hemoglobin level.
It is of two type:
Relative
erythrocytosis
Absolute
erythrocytosis

16. Relative Erythrocytosis:
• It is apparent rise of erythrocytes
level in the blood the underlying
cause is:
• with hemoconcentration of cells.
• as a result of loss of fluid
• vomiting,
• diarrhea
• lossof electrolytes with
accompanying loss of water.

17. Absolute erythrocytosis:
This is due to increased erythropoiesis and
can be primary or secondary.
Primary erythrocytosis :
It can be a familial disorders or neoplastic.
• True idiopathic increase in the number
of circulating RBC and of the
hemoglobin level.

18. Cont..
Secondary erythrocytosis :
• The exact cause is not known.
• Absolute increased in RBC mass resultant to
enhanced production of RBC .
• Bone marrow anoxia– pulmonary dysfunction, high
altitude, CO poisoning.

19. Causes:
Smoking
A lack of oxygen, such as from
lung diseases or being in high
altitudes.
Tumors
Medications such as steroids and
diuretics

20. Pathophysiology :

21. Symptoms:
Symptoms of erythrocytosis include:
Headaches
Dizziness
Shortness of breath
Nosebleeds
Increased blood pressure
Blurred vision
Itching

22. Diagnostic evaluation:
Health history
Physical examination
RBC Count
Pulse oximetry

23. Treatment:
Treatments for erythrocytosis
include:
Phlebotomy (also called
venesection). This procedure
removes a small amount of blood
from your body to lower the
number of RBCs.

24. Cont…
Aspirin. Taking low doses of
this everyday pain reliever may
help prevent blood clots.
Medications that lower RBC
production.
These include:
Hydroxyurea (hydrea),
Busulfan (myleran)
Interferon.

25. 2.Polycythemia vera
• Chronic stem cell disorder with an insidious
onset characterized as a pan hyperplastic,
malignant and neoplastic marrow disorder.
• Absolute increase in the number of
circulating RBC and in the total blood
volume because of uncontrolled RBC
production.

26. Causes:
Causes of polycythaemia are primary or
secondary.
1. Primary polycythemia : Abnormalities in
red blood cell production cause an increase
in red cell count.
2. Secondary polycythemia : Factors
external to red blood cell production (for
example, hypoxia, sleep apnea, certain
tumors) result in polycythemia

27. Pathophysiology:

28. Clinical Manifestations:
• Asymptomatic
• Pruritis
• Vertigo
• Gastrointestinal pain
• Headache
• Paraesthesia, fatigue, weakness,
• visual disturbances, tinnitus

29. Laboratory findings
• RBC- normochromic normocytic-
>10,000.000/cubic mm
• HEMOGLOBIN: >20gm/dl
• PLATELETS- 400,000-800,000/dl
• BONE MARROW- hypercellular,
megakaryocytes are increased

30. Treatment:
• Phlebotomy
• Chemotherapy
• Radioactive phosphorus

31. 3.ANEMIA
• It can also be defined as a
lowered ability of the blood
to carry oxygen.

32. Etiology: Classification of anemia
Blood loss:
1.Acute Post haemorrhagic
2.Chronic blood loss
Deficiency of Hemopoietic factors:-
1.Iron deficiency
2.Folate and vitamin b12deficiency
3.Protein deficiency.
Bone marrow aplasia:-
1.Aplastic anaemia
2.Pure red cell aplasia

33. Cont…
Anemia due to systemic infections:
1.Due to chronic infection
2.Due to chronic renal disease
3.Due to chronic liver disease
4.Endocrinal diseases
Anemia due to bone marrow infiltration
1.Leukemia’s
2.Lymphomas
3.Myelofibrosis
4.Multiple myeloma
5.Congenital sideroblastic anemia
Anemia due to increased red cell destruction:
1.Intra-corpuscular defect
2. Extra-corpuscular defect

34. TYPES
OF
ANEMIA

35. 1.Iron deficiency anemia
• Iron deficiency is defined as a
reduction in total body iron to an
extent that iron stores are fully
exhausted and some degree of tissue
iron deficiency is present.
• Females are mostly affected.

36. Etiology:
• Chronic blood loss
• Inadequate dietary intake
• Faulty iron absorption for iron- infancy, childhood,
• Increased requirements pregnancy.

38. Clinical manifestations:
• Chronic fatigue
• Pallor of the conjunctiva, lips, and oral mucosa
• Brittle nails with spooning, cracking,
• Splitting of nail beds, koilonychia
• Palmar creases

39. Oral manifestation
• Angular cheilitis,
• Pale oral mucosa
• Oral candidiasis
• Recurrent aphthous stomatitis
• Erythematous mucositis
• Burning mouth

40. Symptoms:

41. Laboratory findings:
• Health history
• Physical examination
• RBC- 3,000,000-4,000,000/cubic
mm
• Low hemoglobin
• Low serum iron and ferritin with
an elevated total iron binding
capacity (TIBC)

42. Treatment:
• Oral iron supplementation -
Ferrous sulfate.
• High protein diet.

43. Oral Health Considerations
• Low hemoglobin levels - physician
consultation prior to surgical treatment.
• If Hemoglobin is less than 8 gm/dL,
general anesthesia should be avoided.
• Narcotic use should be limited.
• Increased risk for ischemic heart disease

44. II. Anemia Owing to Hemolysis:
• Normal RBC life span - 90 to 120 days.
• Hemolytic diseases result in anemia if the
bone marrow is not able to replenish
adequately the prematurely destroyed RBCs.
• Either inherited or acquired.

45. Cont…
3 mechanism for accelerated
destruction of RBCs:
1. Molecular defect inside the red
cell
2. Abnormality in membrane
structure and function
3. Environmental factor- mechanical
trauma

46. Clinical Manifestations:
1. Acute back pain
2. Breathlessness
3. Renal failure.
4. . Loss of stamina
5. Tachycardia
6. Haemoglobinuria

47. Physical findings:
1. jaundice of skin and
mucosae,
2. splenomegaly

48. Treatment:
Blood transfusion
Steroid therapy
Splenectomy

49. III. SICKLE CELL DISEASES
Sickle cell disease is a disorders that
affects the red blood cells, which use a
protein called hemoglobin to transport
oxygen from the lungs to the rest of the
body.
These rigid, sticky cells can get stuck in
small blood vessels, which can slow or
block blood flow and oxygen to parts of
the body.

50. Causes:
It is caused by a mutation in the gene
In sickle cell anemia, the abnormal
hemoglobin causes red blood cells to
become rigid, sticky and misshapen.

51. Pathophysiology:

52. Symptoms:
• Anemia
• Episodes of pain
• Swelling of hand and feet
• Frequent infections
• Delayed growth or puberty
• Vision problems
• infection
• Dizziness
• Fatigue

53. Laboratory finding:
• Health history
• RBC- may reach a level of 1,000,000 cells per
cubic mm.
• Decreased hemoglobin level.
• High reticulocyte count-Anemia
• Increased marrow response.
• Elevated lactic dehydrogenase and decreased
levels of hepatoglobin- confirms hemolysis

54. Radiographic features:
• HAIR – ON – END: in iron deficiency anaemia and
cyanotic congenital heart disease. Hair‐on‐end
appearance of the skull is a characteristic feature of
chronic haemolysis usually seen in patients with
thalassaemia and sickle cell anaemia.

55. Blood smear
• Typical sickle- shaped RBCs
seen

56. MANAGEMENT OF SICKLE CELL ANEMIA
ANTIBIOTIC e.g.
PENICILLIN
BLOOD
TRANSFUSION
NITRIC OXIDE
(Keep blood vessels open)
BONE MARROW
TRANSPLANT
GENE THERAPY

57. V.Thalassemia:
It is an inherited blood
disorder in which the body
makes an abnormal form of
hemoglobin. Hemoglobin is
the protein molecule in red
blood cells that carries
oxygen.

58. Types of thalassemia:
There are three main types of thalassemia
(and four subtypes):
Beta thalassemia, it occur when a gene
defect affect production of beta globin
protein.
Alpha thalassemia: it occur when a gene
defect affect production of alpha globin
protein.

59. Cont..
Thalassemia minor: in this the
defective gene received from one
parents
Thalassemia major: in this the
defective gene received from both
parents

60. Causes of thalassemia:
Mutations in the DNA
Family history of thalassemia.
Certain ancestry. Thalassemia occurs most
often in African Americans and in people of
Mediterranean and southeast Asian descent.

61. Pathophysiology:

62. Symptoms of thalassemia:

63. DIAGNOSTIC EVALUATION:
History taking
Physical examination
Heamoglobulin estimation
Periperal blood smare
Bone marrow aspiration
Serum bilirubin

64. MANAGEMENT:
Blood transfusions
Bone marrow transplant
Medications and supplements
Possible surgery to remove
the spleen or gallbladder

65. COMPLICATIONS:
IRON OVERLOAD.
INFECTION

66. VI. Anemia owing to decreased production of
RBCs
Megaloblastic (Pernicious) anemia and
vitamin B12 (Cobalamin deficiency:It
is adult form of anemia that is
associated with gastric atrophy and a
loss of intrinsic factor production in
gastric secretions.

67. Cont…
• Autoimmune disease resulting from
autoantibodies directed against intrinsic
factor (a substance needed to absorb
vitamin B12 from the gastrointestinal
tract) and gastric parietal cells.
• Vitamin B12 → erythrocyte – maturing
factor.

68. Causes:
Deficiencies of vitamin B-12:it is a
nutrient found in some foods like:
◦ Meat
◦ Fish
◦ Eggs
◦ milk.
Megaloblastic anemia caused by vitamin
B-12 deficiency is referred to
as pernicious anemia.
.

69. Cont…
Folate Deficiency: Folate is
found in foods like:
◦ Beef liver
◦ Spinach
◦ Brussels sprouts.

70. Pathophysiology:

71. Sign and symptoms :
• Shortness of breath
• Muscle weakness
• Abnormal paleness of the skin
• Glossitis (swollen tongue)
• Loss of appetite/weight loss

72. Cont…
• Diarrhea
• Nausea
• Fast heartbeat
• Smooth or tender tongue
• Tingling in hands and feet
• Numbness in extremities

73. Oral manifestation:
 Burning sensation in the tongue, lips,
buccal mucosa, and other mucosal sites.
 ‘beefy red’
 Hunter’s glossitis or Moeller’s glossitis.
 Dysphagia and taste alterations have been
reported.

74. Laboratory findings:
• SERUM: Indirect bilirubin may be elevated.
serum lactic dehydrogenase is
markedly increased.
↓- serum potassium,
cholesterol and alkaline phosphatase
• BONE MARROW-hypercellular and show
trilineage differentiation.

75. Treatment:
Weekly intramuscular injections of 1,000
μg of vitamin B12 for the initial 4 to 6
weeks, followed by 1,000 μg per week
indefinitely.
• Delayed treatment permits progression
of the anemia and neurological
complication

76. VII. APLASTIC ANEMIA:
• Aplastic anemia (AA) is a rare blood
dyscrasia in which peripheral blood
pancytopenia results from reduced or
absent blood cell production in the bone
marrow and normal hematopoietic tissue
in the bone marrow has been replaced by
fatty marrow.

77. CAUSES:
Radiation and chemotherapy treatments.
Exposure to toxic chemicals
Use of certain drugs
Autoimmune disorders
A viral infection
Pregnancy

78. Pathophysiology:

79. SYMPTOMS:
Fatigue
Shortness of breath
Rapid or irregular heart rate
Pale skin
Frequent or prolonged infections
Unexplained or easy bruising
Nosebleeds and bleeding gums

80. PREVENTION
There's no prevention for most cases of
aplastic anemia. Avoiding exposure to
insecticides, herbicides, organic solvents,
paint removers and other toxic chemicals
might lower your risk of the disease.

81. WBC
Disorder

82. 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

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

84. Cont..
Leucocytosis : increases above 11,000/ cumm
Causes:
New born
 Evening
Exercise
Stress
Pregnancy
Menstruation
 Any pyogenic infections

85. NEUTROPHILS
Size: 10-12 diameter
Nucleus: Multilobed (2-6)-PMNL
Functions:
Phagocytosis : whenever the body gets
invaded by bacteria, neutrophils are the
first to seek out to ingest and kill bacteria.
(First line defense)

86. EOSINOPHIL
Size: 10-12 diameter
Nucleus : Bilobed spectacle appearance
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)

87. BASOPHIL
Size: 10-12 m Nucleus : Bilobed
Functions:
 Liberates Histamine and ECF-A: which
leads to allergic manifestations
 Liberates Heparin : which acts as
Anticoagulant and keeps the blood in fluid
state

88. MONOCYTE
It is a Largest WBC
Size :12-18 diameter
Functions :
Active Phagocytosis and also a second line
defence
Enter the tissues to become tissue
macrophage .

89. LYMPHOCYTES
It is of 2 types:
Large Lymphocyte : 10-14 diam,
Small Lymphocyte : 7-10 diameter
Functions –
1. Produce antibodies and hence responsible for
Immunity
2. Humoral Immunity: Antibodies which are -
globulins produced by B-Lymphocytes
3. Cell-mediated Immunity: Due to T-Lymphocytes

90. Life span 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

91. White blood cell disorders:
1. Lymphoma
2. Leukaemia
3. Myelodysplastic syndrome (MDS)

92. 1.Lymphoma:
DEFINITION:
Lymphoma is cancer that begins in infection-fighting cells of
the immune system, called lymphocytes. These cells are in the
lymph nodes, spleen, thymus, bone marrow, and other parts of
the body.

93. Types :
There are two main types of lymphoma:
Most people with lymphoma have this type.
Non-
Hodgkin
Hodgkin

94. Hodgkin lymphoma :
Hodgkin’s disease: Hodgkin lymphoma,
also known as Hodgkin's disease, is a type
of lymphoma, a cancer of the lymphatic
system.
Hodgkin lymphoma is marked by the
presence of Reed-Sternberg cells, which a
physician can identify using a microscope.

95. Causes:
The exact cause is not known, but the following have been implicated:
Hodgkin lymphoma: 15 and 40 or older than 55
Gender: male, may be more common in females
weak immune system : -HIV/AIDS, Organ transplant,
Epstein-Barr,
Hepatitis C, or (HTLV-1)

96. Pathophysiology:

97. Stages of lymphoma :

98. Sign and symptoms:
Hodgkin's lymphoma may include:
Painless swelling of lymph nodes in your
neck, armpits or groin
Persistent fatigue
Fever
Night sweats
Pain following alcohol consumption

99. Diagnostic evaluation:
A physical exam
Blood tests
Imaging tests
X ray
PET scan
Removing a lymph node for testing
Removing a sample of bone marrow for
testing

100. TREATMENTS FOR HODGKIN LYMPHOMA:
Radiation therapy
Immunotherapy
Chemotherapy

101. Cont…
The most effective combination
chemotherapeutic regimen for Hodgkin
lymphoma is ABVD:
A adriamycin,
B bleomycin,
V vinblastin
D dacarbazine).

102. Cont….
MOPP regimen of
M (Mustargen) nitrogen mustard
O (Oncovin), vincristine
P procarbazine (Matulane),
P prednisone.

103. 2.Non-Hodgkin lymphoma:
Non-Hodgkin lymphoma is also a
malignancy of lymphocytes and can be
derived from B cells or T cells.
In non-Hodgkin lymphoma of Reed-
Sternberg cells are not present.
Non-Hodgkin lymphoma is more
common than Hodgkin lymphoma.
Non-Hodgkin lymphoma may arise in
lymph nodes anywhere in the body

104. Risk factors:
Non-Hodgkin lymphoma :more than 60s or
older
Some factors that may increase the risk of
non-Hodgkin's lymphoma include:
Medications that suppress your immune
system.
Infection with certain viruses and bacteria
Chemicals
Older age

105. Pathophysiology:

106. Symptoms:
• Swollen glands (lymph nodes),
often in the neck, armpit, or groin
or throughout the body that are
painless
• Cough
• Shortness of breath
• Fever
• Night sweats
• Fatigue
• Weight loss
• Itching

107. Diagnostic Evaluation:
 Additional blood tests
X-rays of the chest, bones,
liver, and spleen
 Biopsy of the lymph node

108. Treatment:
The main treatments for NON-HODGKIN LYMPHOMA are:
1. Chemotherapy
2. Radiation therapy:
3. Immunotherapy
4. Targeted therapy

109. 2.Leukemia:
Cancer of the blood cells,
usually the white blood cells.
Leukemic cells look different
than normal cells and do not
function properly.

110. Risk factors:
1. exact causes is unknown
2. Previous cancer treatment
3. Genetic disorders
4. Exposure to certain
chemical
5. Smoking
6. Family history of leukemia

111. Types of 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.

112. CONT..
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.

113. LEUKEMIA IS CLASSIFIED INTO ONE
OF THE FOUR MAIN TYPES OF
LEUKEMIA
1. Acute myelogenous leukemia (AML)
2. Chronic myelogenous leukemia (CML)
3. Acute lymphocytic leukemia (ALL)
4. Chronic lymphocytic leukemia (CL

114. 1.Acute myelogenous leukaemia (AML)
AML is a common type of leukemia. It occurs in
children and adults. AML is the most common
type of acute leukemia in adults.
The word "acute" in acute myelogenous
leukemia denotes the disease's rapid progression.
It's called myelogenous leukemia because it
affects a group of white blood cells called the
myeloid cells,

115. Cont..
2.Chronic myelogenous leukemia
(CML). This type of leukemia mainly affects
adults. A person with CML may have few or
no symptoms for months or years before
entering a phase in which the leukemia cells
grow more quickly.

116. Cont..
3.Acute lymphocytic leukemia
(ALL): This is the most common
type of leukemia in young children.
ALL can also occur in adults.

117. Cont..
4.Chronic lymphocytic leukemia
(CLL): With CLL, the most common
chronic adult leukemia, you may feel
well for years without needing
treatment.

119. Sign and symptoms:

120. Diagnosis:
 Physician examination
Blood tests and laboratory tests
Bone marrow aspiration and biopsy
 Lymph node biopsy
 Spinal tap
 Imaging procedures, such as x-ray,
ultrasound, and computed tomography (CT)

121. 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

122. 3.Myelodysplastic syndrome:
Myelodysplastic syndromes (MDS)
are a group of cancers in which
immature blood cells in the bone
marrow do not mature and therefore
do not become healthy blood cells.

123. CAUSES:
exposure to cancer treatments, such as
chemotherapy and radiation.
exposure to toxic chemicals, such as
tobacco, benzene and pesticides.
exposure to heavy metals, such as
lead.

124. Pathophysiology:

125. SYMPTOMS:
Fatigue
Shortness of breath
Unusual paleness (pallor) which occurs
due to a low red blood cell count (anemia)
Thrombocytopenia
Petechiae

126. Diagnostic Evaluation:
Full blood count
Bone marrow examination
Interphase fluorescence in situ
hybridization testing
Virtual karyotyping

127. Treatment:
The goals of therapy are to control symptoms,
improve quality of life, improve overall
survival, and decrease progression to AML.
Chemotherapy with the hypomethylating
agents to retard the progression of MDS to
AML

128. Cont…
Stimulate blood cells to mature :
Azacitidine (vidaza)
Decitabine (Dacogen)
Treat infections:
Blood transfusions

129. Platelet disorders
1. Thrombocythemia
2. Idiopathic Thrombocytopenic Purpura (ITP)
3. Haemophilia
4. Von Willebrand disease
5. Disseminated intravascular coagulation (DIC)

130. PLATELETS
(THROMBOCYTES)
Structure : It is smallest blood cells,
colorless & disc shaped (in activated from) to
sphere shaped (activated) granulated bodies.
Size : 2-5 m in diameter
Normal count: 1.5 to 4 lacs /cumm (average
2.59 lac/cumm)
Life span : 8-12 days
Destruction : Mainly in spleen

131. 1.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

132. Etiology:
Etiology is idiopathic
 The bone marrow makes too many cells
that create platelets. It's not clear what
causes this to happen.
About 90 percent of people with the
disorder have an acquired gene mutation
contributing to the disease.

134. Diagnosis
 Complete medical history
 Physical examination
 Blood counts and elevated platelet levels
Bone-marrow biopsy

136. Treatment:
Chemotherapy
 Plateletpheresis - a procedure to
remove extra platelets from the
blood

137. Bone marrow transplantation :
 BMT is a special therapy for
patients with cancer.
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.

138. 2. Idiopathic Thrombocytopenic Purpura
(ITP)
Idiopathic thrombocytopenic purpura is an immune disorder in
which the blood doesn’t clot normally. This condition is now
more commonly referred to as immune thrombocytopenia (ITP).

139. Types of thrombocytopenic purpura
1)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.

140. Cont..
2)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.

141. Cause:
The exact cause is unknown
Infection
Immune disorders
Medications - including over-the-
counter

142. Pathophysiology:

143. Symptoms:
Bruising easily
pinpoint-sized petechiae, often on the
lower legs
spontaneous nosebleeds
bleeding from the gums (for example,
during dental work)

144. Cont…
Blood in the urine
Blood in the stool
Abnormally heavy menstruation
Prolonged bleeding from cuts
Profuse bleeding during surgery
Some people with ITP have no symptoms.

145. Diagnosis
Complete medical history
 Physical examination
 Additional blood and urine tests
Bone marrow examination

146. Treatment:
Corticosteroids
Intravenous immunoglobulin (IVIg)
Rituximab (Rituxan)
Thrombopoietin receptor agonists

147. Surgery:
Splenectomy:
Lifestyle changes:
Use of protective wear
Avoidance of certain activity causing
injuries.

148. 3.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.


149. Types of Hemophilia:
Hemophilia A Or classic hemophilia : it is occur due to
deficiency of factor VIII deficiency
Hemophilia B or Christmas disease: : it is occur due to
deficiency of factor IX deficiency
Hemophilia C : : it is occur due to deficiency of factor XI
deficiency
Hegeman’s disease:: it is occur due to deficiency of factor XII
deficiency.

150. Clotting factors :

151. Causes:
Hemophilia types A
and B are inherited
diseases passed on
from a gene located on
the X chromosome.

152. Symptoms:
Excessive, uncontrollable bleeding
Bleeding may occur even if there is no
injury.
Often occurs in the joints and in the
head.
 Bruising
Bleeds easily - Tendency to bleed.
Bleeding into a joint
Heavy menstrual bleeding

154. Diagnosis test:
Complete medical history
Physical examination
Clotting factor levels
 Complete blood count (CBC)
Assessment of bleeding times
DNA testing.

155. Treatment:
Blood transfusion:
 Prophylactic (preventive)
treatment with infused clotting
factors

156. Cont…
Cryoprecipitate
Amicar (Epsilon Amino Caproic Acid)
DDAVP or Stimate (Desmopressin Acetate)

157. 4.Von Willebrand disease:
Von Willebrand disease (VWD) is a
genetic disorder caused by missing or
defective von Willebrand factor (VWF),
a clotting protein. VWF binds factor
VIII, a key clotting protein, and platelets
in blood vessel walls, which help form a
platelet plug during the clotting process.

158. Causes:
Family history
 If you have the gene for von Willebrand
disease, you have a 50% chance of transmitting
this gene to your children.

159. Symptoms :
If you have von Willebrand disease, you might have:
Excessive bleeding from an injury or after surgery
or dental work
Nosebleeds that don't stop within 10 minutes
Heavy or long menstrual bleeding
Blood in your urine or stool
Easy bruising or lumpy bruises

160. Diagnostic Evaluation
Medical history
Physical examination
Von Willebrand factor antigen
Von Willebrand factor activity
Factor VIII clotting activity

161. Treatment:
Even though von Willebrand disease has no cure, treatment
can help prevent or stop bleeding episodes.

162. Cont..
Desmopressin:
Replacement therapies: These include infusions of concentrated
blood-clotting factors containing von Willebrand factor and factor
VIII.

163. Cont..
Oral contraceptives: For women, these
can be useful for controlling heavy bleeding
during menstrual periods. The estrogen
hormones in birth control pills can boost von
Willebrand factor and factor VIII activity.

164. Cont..
Clot- stabilizing medication:
These anti-fibrinolytic medications :
Aminocaproic acid (amicar)
Tranexamic acid (Cyklokapron, Lysteda)
These can help stop bleeding by slowing the
breakdown of blood clots

165. 4.Disseminated intravascular coagulation (DIC)
DEFINITION:
Disseminated intravascular
coagulation (DIC) is a
serious disorder in which the
proteins that control blood
clotting become overactive.

166. Risk factors :
Blood transfusion reaction
Cancer, especially certain types of
leukemia
Pancreatitis
Infection in the blood
Liver disease
Pregnancy complications (such as placenta
that is left behind after delivery)

167. Pathophysiology:

168. Acute DIC
Multiple bleeding sites
 Ecchymoses of skin,
 mucous membranes Visceral
hemorrhage Ischemic tissue
Clinical findings

169. Chronic DIC
Signs of deep venous or arterial
thrombosis or embolism
Superficial venous thrombosis,
especially without varicose veins
Multiple thrombotic sites at the same
time
Serial thrombotic episodes
Cont…

170. DIAGNOSTIC EVALUATION:
LABORATORY TEST FINDINGS
Platelet count Markedly decreased
Prothrombin time Increased
Activated partial
thromboplastine time
Increased
Fibrin degradation products Markedly Increased
Fibrinogen Normal or decreased
Protein C Markedly decreased

171. TREATMENT:
Replacement
therapy
Other Treatment
Heparin therapy
Treatment of the
underlying disorder

172. COMPLICATION OF DIC:
Severe bleeding
Stroke
Ischemia of extremities or
organs

173. Summarization:
Introduction
Anatomy and physiology of blood
RBC disorders
WBC disorders
Platelets disorders
Conclusion
Summarization
Bibliography

174. Conclusion:
I conclude that the blood is a important
component in our body . Blood is a body
fluid in humans and other animals that
delivers necessary substances such as
nutrients and oxygen to the cells and
transports metabolic waste products away
from those same cells . Blood deficiency
cause many problem

176. BIBLIOGRAPHY:
Suddharth’s & brunner Textbook of medical
surgical nursing published by Wolters Kluwer
edition south Asian page no.-1170-1194
Net reference visited on 20/02/2020
www.webmd.com › ... › Reference
Net reference visited on 25/02/2020
www.slideshare.net › DRKALPAJYOTI › blood-
disord...
Net reference visited on 21/04/2020
www.slideshare.net › drvinesha › blood-and-
blood-diso...

178. Assignment
1. Write the nursing management of thalassemia.
2. Write the nursing management of leukemia.