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Kul Kel Hematologi Sem V
Kul Kel Hematologi Sem V
Kul Kel Hematologi Sem V
HEMATOLOGI
2
HEMATOPOIESIS
Blood stem cells divide into:
1.myeloid stem cells or
2.lymphoid stem cells
reticulocytes
Live 100-120 days
6
THE RED BLOOD CELL
REVIEW RED BLOOD CELL DISORDERS
MARROW PRODUCTION
ANEMIA
Concentration of Hgb
Hypochromic (Less)
Hyperchromic (More)
Normochromic (Normal)
Microcytic / Hypochromic
Chronic Blood Loss, Iron Deficiency, Thalassemia
Normocytic / Normochromic
Hemolytic, Aplastic, Myelophthisic, Acute Blood Loss, Chronic Renal Failure
ANEMIA
Aplastic Anemia
Life-threatening anemia caused by a
decrease in the bone marrow's ability to
produce all three types of blood cells — red
blood cells, white blood cells and platelets
Cause of aplastic anemia is unknown
autoimmune disease
Chemotherapy
Radiation therapy
Environmental toxins
ANEMIA
Hemolytic Anemias
Red blood cells are destroyed faster than
bone marrow can replace them.
Autoimmune disorders can produce
antibodies to red blood cells, destroying
them prematurely
Hemolytic anemias may cause yellowing of the
skin (jaundice) and an enlarged spleen.
ANEMIA
OXY-STATE DEOXY-STATE
ANEMIA
α- Thalassemia
Common in Asians
Deletion of globulin chain loci
4 possible degrees of α thalassemia:
Silent carrier, loss of a single α globulin gene
α thalassemia trait, loss of a pair of globulin gene
HbH disease, only a single gene is present
Hydrops fetalis, deletion of all α globulin
TALASSEMIA
POLYCYTHEMIA VERA
26
AKA WBCs: white blood
cells
27
WHITE BLOOD CELLS
WHITE BLOOD CELLS
Leukopenia
Decreased peripheral white cell count due to
decrease numbers of any specific types of
leukocytes
Leukocytosis
Non–neoplastic elevation of WBC count
WBC PMN Band Lymph Mono Eos Baso
J. Levine
31
WBC PMN Band Lymph Mono Eos Baso
J. Levine
32
25% 65% 8% 2%
Bone Marrow
J. Levine
33
Proliferation 25 %
34
Myeloblast
J. Levine
Promyelocyte Myelocyte
Neutrophil - Maturation Phase
65 % of myeloid cells
Neutropenia Neutrophila
Less than 1500/ml Greater than 7700/ml
Acquired
Or
Inherited
J. Levine
36
Normal ANC is 1500-7700/ml
Neutrophilia: abnormally high ANC
Shift to the left: ↑’d release of
precursors from the bone marrow
not necessarily associated with
neutrophilia
37
Chronic Stimulation
Acute shift from Excess cytokine stimulates
marginating to circulating proliferative pool
pool
↑ measured WBC, not total
WBC Causes:
Causes: Infection
Steroid treatment Down's Syndrome
Exercise Pregnancy/Eclampsia
Epinephrine Chemotherapy recovery
Hypoxia Myeloproliferative disorders
Seizures Marrow metastases
Other stress
38
WBC DISORDERS
Neutropenia
Reduction in the number of granulocytes
(<1500/µl)
Increased risk of infection
Reduced phagocytosis response
WBC DISORDERS
Neutropenia
Decreased or defective granulopoiesis
Aplastic anemia
Anti-neoplastic agents
Other drugs: chloramphenicol, sulfonamides,
chlorpromazine
Accelerated removal or destruction
Aggressive and chronic infections
Decreased Increased Shift to
Production Destruction Marginating Pool
41
WBC DISORDERS
Manifestation of Neutropenia
Infections
43
Monocyte Differentiation
into Macrophages
Differentiation
Intravascular
Maturation
Tissue:
Proliferation
Bone Marrow
Source Undetermined
44
Antigen presentation of phagocytized particles to T Cells
Cytokines/
chemokines
J. Levine
45
Follow neutrophils to sites of inflammation within 12-24h
Number 1/30th that of neutrophils
Pts w/ CGD, CHS and LAD also have defects in monocyte fxn
Chemoattractant
Phagocytosis
J. Levine
46
Low counts Elevated counts
glucocorticoids Malignancy
stress Granulomatous disease
Marrow recovery
Infections
malaria
TB
Rocky Mountain Spotted
fever
leishmaniasis
brucellosis
47
Eosinophils
Intravascular
Maturation
Tissues
Proliferation
Myelocyte Eosinophil 48
Source Undetermined (Both Slides)
Bright red granules
IgE on cell surface (not on neutrophils)
Play a key role in killing parasites
Average absolute count 200/ml
Non allergic individuals usually <400/ml
49
Conditions:
Neoplasm (Hodgkin’s disease, lymphoma other
tumors)
Allergies-drugs, environmental (grass, trees, dust)
Asthma
Collagen vascular diseases-vasculitis
Parasitic infection
Idiopathic hypereosinophilia: elevated eosinophil
count associated with organ dysfunction (GI, skin,
CNS, cardiovascular).
> 5000/µl requires treatment with
immunosuppressives and antihistamines
50
Maturation of Basophils and Mast cells
Basophil
Intravascular
Tissues
Proliferation Maturation
J. Levine
51
Basophils and mast cells
52
High count
Allergies
Low count
infection
hypersensitivity
endocrinopathies
glucocorticoids
myeloproliferative
disorders
Systemic mastocytosis
symptoms due to excess
histamine release
53
WBC DISORDERS
Reactive Leukocytosis
Increase number of WBC
Common reaction due to a variety of
inflammatory states caused by microbial or
non-microbial stimuli
Usually non-specific
NONMALIGNANT LEUKOCYTE DISORDERS
Leukemia
Malignant neoplasm of the hematopietic
stem cells
BM replaced by unregulated, proliferating,
immature neoplastic cells blood
leukemia enter spleen, lymph nodes
Most common cancer in the paediatric age
Leading cause of death in children between 3
and 14 years old
NEOPLASTIC PROLIFERATION OF WHITE CELLS
Classification of Leukemia
A. According to cell type and state of cell
maturity
Lymphocytic – immature lymphocytes and their
progenators
Myelocytic – pluripotent myeloid stem cells and
interferes with maturation of all granulocytes, RBC
and platelets
B. Acute or Chronic
Acute – immature cells (blast)
Chronic – well differentiated leukocytes
NEOPLASTIC PROLIFERATION OF WHITE CELLS
LEUCOCYTES BENIGN DISORDERS
QUALITATIVE CHANGES (MORPHOLOGY)
Congenital
Pelger-Huet anomaly
Bilobed and occasional unsegmented neutrophils
Autosomal recessive disorder
LEUCOCYTES BENIGN DISORDERS
QUALITATIVE CHANGES (MORPHOLOGY) CONTD.
Neutrophil hyper-segmentation
Rare autosomal dominant condition
Neutrophil function is essentially normal
May-Hegglin anomaly
Neutrophils contain basophilic inclusions of RNA
Occasionally there is associated leucopenia
Thrombocytopenia and giant platelet are frequent
LEUCOCYTES BENIGN DISORDERS
QUALITATIVE CHANGES (MORPHOLOGY) CONTD.
Alder’s anomaly
Granulocytes, monocytes and lymphocytes contain granules which stain
purple with Romanowsky stain
Granules contain mucopolysaccharides
LEUCOCYTES BENIGN DISORDERS
QUALITATIVE CHANGES (MORPHOLOGY) CONTD.
Chediak-Higashi syndrome
Autosomal recessive disorder
Giant granules in granulocytes, monocytes and lymphocytes
Partial occulocutaneous albinism
Depressed migration and degranulation
Recurrent pyogenic infections
Lymphoproliferative syndrome may develop
Treatment is BMT
LEUCOCYTES BENIGN DISORDERS
QUALITATIVE CHANGES (MORPHOLOGY) CONTD.
Acquired
Toxic granulation
Dohle bodies
Pelger cells
Hypersegmented neutrophils
LEUCOCYTES BENIGN DISORDERS
QUALITATIVE CHANGES (FUNCTIONAL)
Insidious onset
Incidental findings during routine exam
CHRONIC LYMPHOCYTIC LEUKEMIA
C D
Hodgkin’s Lymphoma
Disorders primarily involving the lymphoid
tissues
Anatomical spread
Morphological presence of Reed-Sternberg
cells
60-90% cure rate
ASH Teaching Slides: Blood Cells
Manifestations of Hodgkin’s
A symptoms
Painless progressive enlargement of a single or
group of nodes (neck)
May spread continuously through out the
lymphatic system
B symptoms
Fever, night sweat, weight loss
Fatigue, anemia
MALIGNANT LYMPHOMAS
Non-Hodgkin’s Lymphoma
Involves lymphoid tissue and may spread to
various tissues
Mostly B cell (80%)
Cause may be viral or genetic
EBV
Immunosuppresed patients
AIDS
After organ transplant
SCHISTOCYTES
BURR CELLS
SPUR CELLS
TARGET CELLS
HYPOCHROMIC MICROCYTIC ANEMIA
SPHEROCYTES
TEAR DROP CELLS