2. Hematology
• Branch of medicine that studies blood cells and blood-forming
tissue
• Includes hemostasis (the process of stopping bleeding)
• Tests can detect diseases such as
• Anemia
• Leukemia
• Hemophilia
3. Anatomy and physiology
• Hematologic system consists of the blood and the sites
where the blood is produced.
• Blood consists of plasma and blood cells.
• Because blood cells have a short lifespan, hematopoiesis
(production od blood cells in the bone marrow) is
needed.
3
4. Function of Blood
• Transporting fluids such as:
• Nutrients from digestive tract
• O2 from lungs
• Waste from cells
• Hormones
• Aids in heat distribution
• Regulates acid-base balance
5. Composition of Blood
• Plasma: liquid portion of blood w/out cells
• Contains all of the following
• Water Nutrients
• Electrolytes Metabolic waste product
• Hormones Vitamins and enzymes
• Plasma proteins such as fibrinogen, albumin and
globulin
6. Composition of Blood:
Erythrocytes
• Red blood cells are responsible for:
• Transport of oxygen and nutrients
• Removal of waste and CO2 from the cells
• Distribution of heat
• Hemoglobin:
• The O2 carrying potential.
• Has 4 subunits, each contains a hem attached to a
globin chain.
• Iron is present in the hem, hem is bind to the
oxygen
•
7. Composition of Blood: Leukocytes
• WBC are responsible for:
• Phagocytosis – to engulf and absorb waste material and
harmful microorganisms in the blood stream and tissues
• Synthesis of antibody molecules
• Inflammation process
• Production of heparin – component found in lung and liver
tissue which have the ability to prevent clotting of blood.
9. Composition of Blood: Thrombocytes
• Platelets – the smallest of the solid components of the blood
• Responsible for the clotting process
• Coagulation: term for clotting
• Embolism: a blood clot which is moving through the body
10. INTEPRETATION OF A HEMOGRAM
• The 8 parameter cell counter will give the following:
1. WBC count: white blood cell count
2. RBC count: red blood cell count
3. Hb: Hemoglobin
4. Hct: Hematocrit / Packed cell volume (PCV)
5. MCV: Mean cell volume
6. MCH: Mean cell hemoglobin
7. MCHC: Mean cell hemoglobin concentration
8. RDWt: red blood cell distribution width
• In addition to these above parameters the 18 parameter cell counter
also has White blood cell Differentials:
Neutrophils count and percentage, Lymphocyte count and percentage,
Monocytes count and percentage, Eosinophil count and percentage,
Basophils count and percentage and Pct: Plateletcrit
11. WHITE BLOOD CELL COUNT
• This is the number of white blood cells in 1 cubic mm of whole blood.
• The normal value is 4.0-11.0 million cells per microliter.
• On its own is not a useful parameter
RED BLOOD CELL COUNT
• This is the number of erythrocytes in 1 cubic mm of whole blood.
• The normal values include: Men= 4.5-6.0 million cells per microliter and
Women= 3.9-5.0 million cells per microliter
HEMOGLOBIN
• Normal hemoglobin values: Men= 13.5-17.5 g/dl and Women= 11.5- 16.0
g/dl
HEMATOCRIT/ PACKED CELL VOLUME (PCV)
• Normal PCV is Men= 0.4-0.54 L/L and Women= 0.36-0.47 L/L
MEAN CELL VOLUME (MCV)
• Indicates the average volume of a single RBC.
• It is expressed in cubic microns.
• The normal value is 80-96 fL
12. MEAN CELL HEMOGLOBIN (MCH)
• This gives an idea about the average hemoglobin content in a single red
cell.
• Normal range varies between 27 and 32 pico grams.
RED BLOOD CELL DISTRIBUTION WIDTH (RDW)
• This shows the variation in red cell size
• The normal value is 11-15%
• In iron deficiency there is increased RDW.
• In beta-Thalassaemia trait,the RDW is usually normal.
PLATELETS
• The normal platelet count is 150-400 (109/L)
DIFFERENTIAL COUNT
• Neutrophils= 3-6 (109/L),Lymphocytes= 1.5- 4 (109/L), Monocytes= 0.3-
0.6 (109/L), Eosinophils= 0.15-0.30 (109/L) and Basophils= 0-0.1 (109/L)
•
13. Definitions
• Anticoagulant: an agent that prevents the clotting of
blood.
• Examples are EDTA, Citrate and Heparin
• Capillary: small blood vessel that connects arterioles
and venules
• Hematoma: a subcutaneous mass of blood at a
venipuncture site
• Hemoglobin: the oxygen carrying molecule of red
blood cells
• Hemolysis: the breakdown of red blood cells, with the
release of hemoglobin into the plasma or serum.
Cannot use hemolyzed samples in lab tests
14. • THROMBOCYTOPENIA - Decrease in platelet count below 150 000/cu
mm of blood
• Thrombocytosis - Increase in platelet count over 450 000/cu mm of
blood
• Leukocytopenia – wbc less than the normal range in the blood
• Leukocytosis - wbc above the normal range in the blood
• PANCYTOPENIA – it is combination of anemia, thrombocytopenia and
leukocytopenia
16. Blood Types
• Four Major Groups
• A B AB O
• Blood types are inherited from your parents
• Antigen is present on the red blood cell; typing is done
w/rbc
• Antibody is present in the plasma; antibody screening
done on plasma
17. Blood Types
• O negative
• Universal donor
• It carries no antigen
• AB positive
• Universal recipient
• It carries no antibodies in the plasma
• 43% of population are O, 42% A, 12% B and 3%
AB
18. ABO & Rh compatibility
• Blood is classified according to the presence of these
antigens:
• Group A contains antigen A
• Group AB contains both antigens
• Group O contains neither antigen
• Blood plasma contains antibodies against the opposite
antigen:
• A person with Type A blood has antibodies against the B
antigen
• A person with Type AB blood has no antibodies (Universal
Recipient)
• A person with Type O blood has antibodies against the A, B
& AB antigens (Universal Donor)
19. ABO & Rh compatibility
• People with Rhesus factors in their blood are classified as "Rh
positive"
• People without the factors are classified as "Rh negative"
• Rh negative persons form antibodies against the Rh factor if they
are exposed to Rh positive blood
• Conclusion:
• Blood transfusion between incompatible groups causes an
immune response against the cells carrying the antigen, resulting
in transfusion reaction
21. Anemia
• Is a condition in which the hemoglobin concentration is lower than
normal (low RBCs).
• As a result, the amount of oxygen delivered to the tissue is lower
than normal.
• It is not a disease but a sign of underlying disorders.
22. Causes of Anemia
• Iron deficiency
• Vitamin B12 deficiency
• Infections*: HIV, tuberculosis, malaria, schistosomiasis, hookworm,
hepatitis
• Drugs: isoniazid, chloramphenicol, alcohol, zidovudine, hydroxyurea
• Chronic disease*: renal and liver disease, rheumatologic diseases,
hypothyroidism
These are common causes of anemia in adults in Africa.
23. Common signs and symptoms of anemia
• Easy fatigue and loss of energy
• Unusually rapid heart beat, particularly with exercise
• Shortness of breath and headache, particularly with exercise
• Difficulty concentrating
• Dizziness
• pale skin
• Leg cramps
• Insomnia
30. 1. IRON DEFICIENCY ANEMIA
• This is the most common type of anemia worldwide.
• Iron deficiency anemia occurs when the body iron stores become inadequate
for the need of normal RBC production.
• It is due to decreased levels of iron.
• Decreased iron leads to decreased heme and hemoglobin thus resulting in a
microcytic anemia.
• Iron deficiency anemia is a manifestation of disease, not by itself a complete
diagnosis
Anemia People with an iron deficiency may experience these symptoms:
• A hunger for strange substances such as paper, ice, or dirt (a condition called
pica)
• Upward curvature of the nails, referred to as koilonychias
• Soreness of the mouth with cracks at the corners
31. IRON METABOLISM
Irons is consumed in heme (meatderived) and non-heme (vegetablederived)
forms.
• Absorption of heme occurs in the duodenum while that of non-heme occurs
in the proximal jejunum
• Enterocytes have heme and non-heme (DMT1) transports. The heme form is
more readily absorbed.
• Absorption is facilitated by: stomach acidity (keeps iron in reduced ferrous
state Fe2+ and not ferric state Fe3+), Vitamin C (Ascorbic acid), Citrates.
• Absorption is limited by: phosphates, oxalates, tannates (tea) and pyrates
(plant food)
• Enterocytes transport iron across the cell membrane into blood via
ferroportin.
• Transferrin transports iron in the blood and delivers it to liver and bone
marrow macrophages for storage.
32. 2. ANEMIA OF CHRONIC DISEASE
• This is associated with chronic inflammation (e.g. endocarditis or
autoimmune conditions) or malignant disease.
• It is the most common type of anemia in hospitalized patients.
• Etiologies:
Infectious: TB, lung abscess, osteomyelitis, pneumonia, bacterial
endocarditis.
Non-infectious: rheumatoid arthritis, lupus, connective tissue
disease, sarcoidosis, Crohn’s disease, malignancy (carcinoma,
lymphoma, sarcoma).
33. PATHOGENESIS
• Chronic disease results in production of acute phase reactants from
the liver, including hepcidin
• Hepcidin sequesters iron in storage sites by
(1) limiting iron transfer from macrophages to erythroid precursors
(2) suppressing erythropoietin (EPO) production.
• The aim is to prevent bacteria from accessing iron, which is necessary
for their survival.
• Decreased availability of iron results in microcytic anemia.
• Other cytokines produced during inflammation reduce life span of
RBC (80 days) rendering erythropoietin inadequate.
34. • The term AA is first used by Ehrlich in 1888
• Describes a disorder of unknown etiology characterized by
• pancytopenia with
• hypo or acellular bone marrow.
• It is one of the stem cell disorders.
3. Aplastic Anemia (AA)
37. Clinical Features of AA
• History:
• Bleeding
• Symptoms of anemia
• Infections
• Drugs, chemicals or other etiologically important exposures have to be
questioned.
• Physical exam:
• Petechiae, ecchymosis
• Retinal bleeding
• Pallor
• Fever and other signs of infection
• Presence of lymphadenomegaly and /or splenomegaly are unusual (indicate
other diagnoses).
38. • LAB:
• Pancytopenia
• Reticulocytes: Low or absent
• RBC: normochrome-normocytic,or slight macrocytosis
• Neutropenia and relative lymphocytosis
• Red and white cell precursors are almost neverseen in
the peripheral smear
• Serum iron is increased
• Bone marrow :
• Aspiration; Dry tap
• Biopsy; all three cell lines are reduced or absent,
raplaced by fatty tissue, residual lymphocytes,
increased iron stores,rarely hot spots of hematopoesis
39. 4. HEMOLYTIC ANEMIA
• Due to red cell destruction and increased red cell turnover. Bone
marrow is able to compensate 5 times the normal rate.
• Clinical features: jaundice, hepatosplenomegaly, dark urine.
• Etiology can be classified as:
1. Congenital
Hemoglobinopathies: sickle cell disease*, thalassemia
Enzymopathies: G6PD deficiency*, Pyruvate kinase deficiency
Membranopathies: hereditary spherocytosis, eliptocytosis
In born errors of metabolism
2. Acquired
Microangiopathic hemolytic anemia: TTP, HUS, DIC, eclampsia, HELLP
syndrome
Autoimmune hemolytic anemia
Infections: Malaria
40. SICKLE CELL DISEASE
• A severe hemolytic anemia caused by a point mutation resulting in
the substitution of glutamate for valine on the 6th position of the
beta globin chain forming HbS.
• When deoxygenated, HbS molecules polymerize into long fibers and
cause the red blood cells to sickle
42. SICKLE CELL DISEASE
Symptoms may not appear until 6 months of age
Mortality rate children < 3 Years old is 15-35%
Early Diagnosis:
Amniocentesis,
Newborn Screen
45. 1. VASO-OCCLUSIVE CRISES
• An early presentation may be acute pain in the hands and feet:
dactylitis due to vaso-occlusion of the small vessels.
• (hand-foot syndrome)
• Severe pain in other bones e.g. femur, humerus, vertebrae, ribs,
pelvis occurs in older children/adults.
• Attacks vary from person to person.
Fever often accompanies the pain.
• Triggers of vaso-occlusive crisis include: Hypoxemia: may be due to
acute chest syndrome or respiratory complications, Dehydration:
acidosis results in a shift of the oxygen dissociation curve and
Changes in body temperature
47. Priapism
• Prolonged erection of the penis, usually without sexual arousal
• Commonly occurs in children and adolescents with SS or SC (
• Treatment is difficult
1. Opioid pain medication
2. Intravenous fluids
3. Aspiration and irrigation of the corpus cavernosum
4. Surgery
5. Blood Transfusions
6. Impotence with severe disease or recurrent episodes
48. 2. BONE MARROW APLASIA (APLASTIC CRISIS)
• This most commonly occurs following infection with erythrovirus B19
(previously called Parvovirus B19) which invades proliferating
erythroid progenitors.
• There is a rapid fall in hemoglobin with no reticulocytes in the
peripheral blood, because of the failure of erythropoiesis in the
marrow
49. 3. SPLENIC SEQUESTRATION
• Vaso-occlusion produces an acute painful enlargement of the spleen.
• There is a splenic pooling of red cells and hypovolemia, leading in
some to circulatory collapse and death.
• There will be severe hemolysis, rapid splenomegaly and a high
reticulocyte count.
• The condition occurs in childhood before multiple infarctions have
occurred.
• Multiple infarctions lead to a fibrotic non-functioning spleen
50. SPLENIC SEQUESTRATION
Sudden trapping of blood within the spleen
Usually occurs in infants under 2 years of age with SS
Spleen enlarged on physical exam, may not be
associated with fever, pain, respiratory, or other
symptoms
Circulatory collapse and death can occur in less than
thirty minutes
51. Treatments For Splenic Sequestration
• Intravenous fluids
• Maintain vascular volume
• Cautious blood transfusion
• Treat anemia, sequestered blood can be released from spleen
• Spleen removal or splenectomy
• If indicated
52. 4. HEMOLYTIC CRISIS
• Red cell half life is reduced to 10 – 20
• This results into rapid destruction rbc leading anemia
CLINICAL FEATURES
• Anaemia
• Jaundice
• Gallstones
• Cardiomegaly:CHF
• Leg ulcers
• Marrow hyperplasia
• Poor physical development
• Delayed maturation
• Subjective symptoms
54. Thalassemia
• Heterogenous group of genetic disorders which results from a
reduced rate of synthesis of alpha (coded for by 4 genes) or beta
chains (coded for by 2 genes) of hemoglobin.
• Changes in normal ratio results in each of the disorders.
• Due to inherited mutations carriers are protected against
Plasmodium falciparum malaria.
• Thalassemia are divided into alpha and beta thalassemia.
• Normally there are 3 types of hem
HbA (2 alpha, 2 beta)
HbA2 (2 alpha and 2 delta).
HbF (2alpha, 2 gamma)
55. ALPHA THALASSEMIA
• Alpha thalassemia is usually due to gene deletion, normally 4 alpha
genes are present on chromosome 16.
• One gene deleted- asymptomatic
• Two gen deleted- mild anemia with slightly increased RBC count
BETA THALASEMMIA
• Usually due to gene mutations (point mutations in promoter or splicing
sites) seen in individuals of African and Mediterranean descent.
• Two beta genes are present on chromosome 11, mutations result in
absent or diminished production of the beta-globin chain.
• Beta thalassemia minor is the mildest form of the disease and is usually
asymptomatic with an increased RBC count
56. Leukemia
Definition
It is a group of malignant disorder, affecting the blood and blood
–forming tissue of the bone marrow lymph system and spleen.
A etiology
Combination of predisposing factors including genetic and
environmental influences.
Chronic exposure to chemical such as benzene
Radiation exposure.
Cytotoxic therapy of breast, lung and testicular cancer.
57. Classification of leukaemia
1. 1. Acute lymphatic leukaemia (ALL)
Usually occurs before 14 years of age peak incidence is between
2-9 years of age, older adult
Pathophysiology
It arising from a single lymphoid stem cell, with impaired maturation
and accumulation of the malignant cells in the bone marrow.
58. Acute lymphatic leukaemia Cont.
Signs and symptoms
Anaemia, bleeding, lymphadenopathy, infection
Clinical manifestation Clinical manifestation
Fever
Pallor
Bleeding
Anorexia
Fatigue
Weakness
Bone, joint and abdominal
pain
Increase intracranial
press.
Generalized
lymphadenopathy
Infection of respiratory
tract
Anaemia and bleeding of
mucus membrane
Ecchymoses
Weight loss
Hepatomegaly
Mouth sore
59. Acute lymphatic leukaemia Cont.
Management
Diagnosis
Low RBCs count, Hb, Hct, low platelet count , low
normal or high WBC count.
Blood smear show immature lymph blasts.
Treatment
Chemotherapeutic agent, it involve three phases
1. Induction: Using vincristine and prednisone.
2. Consolidation: Using modified course of intensive
therapy to eradicate any remaining.
3. Maintenance
60. Acute lymphatic leukaemia Cont.
Treatment Cont.
Prophylactic treatment of the CNS ,
intrathecal administration and /or
craniospinal radiation with eradicate
leukemic cells.
Eat diet that contains high in protein, fibres
and fluids.
61. Acute lymphatic leukaemia Cont.
Treatment Cont.
Avoid infection (hand washing, avoid
crowds),injury
Take measure to decrease nausea and to
promote appetite, smoking and spicy and
hot foods.
Maintain oral hygiene.
62. Acute Myelogenous Leukaemia (AML)
It occurs at any age but occurs most often at adolescence and after
age of 55
Pathophysiology
Characterized by the development of immature myeloblasts in the
bone marrow.
Clinical manifestation
Similar to ALL plus sternal tenderness.
Management
Diagnosis
Low RBC, Hb, Hct, low platelet count, low to high WBC count
with myeloblasts.
63. Acute Myelogenous Leukaemia (AML) Cont.
Treatment
Use of cytarabine, 6-thioquanine, and doxorubic
The same care of client as All, plus give adequate amounts of
fluids(2000 to 3000 ml per day.)
Instruct client about medication, effects, side effects and
nursing measures
64. Chronic lymphocytic Leukaemia (CLL)
The incidence of CLincreases with age and is rare under the age
of 35.It is common in men.
Pathophysiology
It is characterized by proliferation of small, abnormal , mature
B lymphocytes, often leading to decreased synthesis of
immunoglobulin and depressed antibody response.
The number of mature lymphocytes in peripheral blood smear
and bone marrow are greatly increased
65. Chronic lymphocytic Leukaemia (CLL) Cont
Clinical Manifestation
Usually there is no symptoms.
Chronic fatigue , weakness , anorexia, splenomegaly , lymphadenopathy,
hepatomegaly.
Signs and Symptoms
Pruritic vesicular skin lesions .
Anaemia
Thrombocytopenia.
The WBC count is elevated to a level between 20,000 to 100,000.
Increase blood viscosity and clotting episode.
66. Chronic lymphocytic Leukaemia (CLL) Cont
Management
I. Persons are treated only when symptoms, particular
anaemia , thrombocytopenia , enlarged lymph nodes and
spleen appear.
I. Chemotherapy agents such as chlorambucil , and the
glucocorticoids.
I. Client and family education is that describe for AML.
67. Chronic Myelogenous Leukaemia(CML)
Occurs between 25-60 years of age. Peak 45 year
It is caused by benzene exposure and high doses of radiation.
Clinical Manifestation
There is no symptoms in disease. The classic symptoms of
chronic types of leukaemia, include:
Fatigue, weakness, fever, sternal tenderness.
Weight loss, joint & bone pain.
68. Chronic Myelogenous Leukaemia(CML) Cont.
Clinical Manifestation Cont.
Massive splenomegaly and increase in
sweating.
The accelerated phase of disease(blostic
phase) is characterized by increasing number
of granulocytes in the peripheral blood.
There is a corresponding anaemia and
thrombocytopenia.
