Hematology Picture
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HEMATOLOGY AND ONCOLOGY
CELLULAR ELEMENTS •
THE RED CELLS
Erythropoiesis •
stem cell proerthroblast
orthocromatophil ic
reticulocy te
basophilic
polychromat ophilic
Mature RBCs
Monocyte Development
stem cell
monoblast
promonocyte
Monocyte
Lymphocyte Development
Stem cell
lymphoblast
prolymphocyte Lymphocyte
The production of platelets is THROMBOPOIESIS
Plasma
Plasma
Sites of formation of hematopoietic cells
Differentiation pathway of hematopoietic cells
) HEMOGLOBIN ) Hb
Different Hemoglobin Types Hb type
% at birth
Embryonic type
Embryonic Hb may be present at birth in small percentage. Fetal type(α2γ 2) 45-90% Adult type A1 (α2β 2) A2 (α δ )
10-55% 0-1.5%
% After 2 years Major embryonic Hb are not present after 3rd month of gestation. 3% 95% 1.5-3.5%
Proportions of the various human hemoglobin polypeptide chains .through early life
valueHematocrit
IRON DEFICIENCYANEMIA
Iron Metabolism
Spooning of the nails
Atrophic glossitis
HEMOLYTIC ANEMIA
BILIRUBIN METBOLISM
HEMOGLOBIN
GLOBIN
AMINOACIDS
HEME
IRON
PROTOPORPHYRIN
HEME OXYGENASE BILIVERDIN BILIVIRDIN REDUCTASE UNCONGUGATED BILIRUBIN
UNCONGUGATED BILIRUBIN
FREE UNCONGUGATED BILIRUBIN
ALBUMIN BOUND BILIRUBIN
ALBUMIN BOUND BILIRUBIN
DETACHED FROM ALBUMIN
LIGAND Y&Z PROTEIN SMOOTH ENDOPLASMIC R
URIDINE DIPHOSPHATEGLUCORYL TRANSFERASE E CONGUGATED BILIRUBIN
INTESTINE
URINE
CONGUGATED BILIRUBIN
B-GLUCURONIDASE E UNCONGUGATED BILIRUBIN
INTESTINAL BACTERIAL FLORA E-COLI STECOBILINOGEN
OXYDIZED ENTEROHEPATIC CIRCULATION STERCOBILIN
]G6PD deficiency[
]G6PD deficiency[
fava beans
SICKLE CELL ANEMIA
INHERITANCE
PATHOPHYSIOLOGY
)Bone infarction)head necrosis
THALASSEMIA SYNDROMES
Geographical distribution
MODE OF TRANSMISSION
PATHOPHYSIOLOGY OF ΒTHALASSEMIA MAJOR
CLINICAL MANIFESTATION OF Β - THALASSEMIA MAJOR
Target cells
RADIOLOGIC INVESTIGATION Plain x ray skull • There is maxillary over growth, prominent widening of the diploic spaces, with hair standing on end appearance.
Desferal pump
HEMORRHAGIC DISEASES
Introduction
Blood within the vascular tree remains fluid throughout life
If a blood vessel is damaged a rapid localized
RESPONSE OF BLOOB CLOT FORMATION will occur.
Introduction
Failure of clotting leads to
MECHNISMIS OF HEMOSTASIS
Formation of a haemostatic plug fibrinogen
Primary homeostasis
GPIIB,IIIA Aggregation adhesion
activation
Secondary homeostasis FIBRIN CLOT FORMATION
release
Dr:Mohamed El-shanshory
Factor level activity &severity type
Activity Type of hemorrhage %
severe
<1%
Spontaneous;hemarthrosis; deep tissue hemorrhage
moderate
1 -5%
Bleeding following mild to moderate trauma
mild
5–25% Bleeding following moderate to severe trauma
High risk 30-50% carrier female
Gynacologic & obestatric hemorrhage
Gene therapy
PURPURAS
Pathogenesis • ITP is an autoimmune
Bleeding time
THROMBOCYTOPENIA
PURPURIC SPOTS
HENOCH – SCHOENLEIN PURPURA
BLOOD TRANSFUSION
GROWTH FACTORS
Apharesis •
CELLULAR ELEMENTS •
THE RED CELLS
Erythropoiesis •
stem cell proerthroblast
orthocromatophil ic
reticulocy te
basophilic
polychromat ophilic
Mature RBCs
Monocyte Development
stem cell
monoblast
promonocyte
Monocyte
Lymphocyte Development
Stem cell
lymphoblast
prolymphocyte Lymphocyte
The production of platelets is THROMBOPOIESIS
Plasma
Plasma
Sites of formation of hematopoietic cells
Differentiation pathway of hematopoietic cells
) HEMOGLOBIN ) Hb
Different Hemoglobin Types Hb type
% at birth
Embryonic type
Embryonic Hb may be present at birth in small percentage. Fetal type(α2γ 2) 45-90% Adult type A1 (α2β 2) A2 (α δ )
10-55% 0-1.5%
% After 2 years Major embryonic Hb are not present after 3rd month of gestation. 3% 95% 1.5-3.5%
Proportions of the various human hemoglobin polypeptide chains .through early life
valueHematocrit
IRON DEFICIENCYANEMIA
Iron Metabolism
Spooning of the nails
Atrophic glossitis
HEMOLYTIC ANEMIA
BILIRUBIN METBOLISM
HEMOGLOBIN
GLOBIN
AMINOACIDS
HEME
IRON
PROTOPORPHYRIN
HEME OXYGENASE BILIVERDIN BILIVIRDIN REDUCTASE UNCONGUGATED BILIRUBIN
UNCONGUGATED BILIRUBIN
FREE UNCONGUGATED BILIRUBIN
ALBUMIN BOUND BILIRUBIN
ALBUMIN BOUND BILIRUBIN
DETACHED FROM ALBUMIN
LIGAND Y&Z PROTEIN SMOOTH ENDOPLASMIC R
URIDINE DIPHOSPHATEGLUCORYL TRANSFERASE E CONGUGATED BILIRUBIN
INTESTINE
URINE
CONGUGATED BILIRUBIN
B-GLUCURONIDASE E UNCONGUGATED BILIRUBIN
INTESTINAL BACTERIAL FLORA E-COLI STECOBILINOGEN
OXYDIZED ENTEROHEPATIC CIRCULATION STERCOBILIN
]G6PD deficiency[
]G6PD deficiency[
fava beans
SICKLE CELL ANEMIA
INHERITANCE
PATHOPHYSIOLOGY
)Bone infarction)head necrosis
THALASSEMIA SYNDROMES
Geographical distribution
MODE OF TRANSMISSION
PATHOPHYSIOLOGY OF ΒTHALASSEMIA MAJOR
CLINICAL MANIFESTATION OF Β - THALASSEMIA MAJOR
Target cells
RADIOLOGIC INVESTIGATION Plain x ray skull • There is maxillary over growth, prominent widening of the diploic spaces, with hair standing on end appearance.
Desferal pump
HEMORRHAGIC DISEASES
Introduction
Blood within the vascular tree remains fluid throughout life
If a blood vessel is damaged a rapid localized
RESPONSE OF BLOOB CLOT FORMATION will occur.
Introduction
Failure of clotting leads to
MECHNISMIS OF HEMOSTASIS
Formation of a haemostatic plug fibrinogen
Primary homeostasis
GPIIB,IIIA Aggregation adhesion
activation
Secondary homeostasis FIBRIN CLOT FORMATION
release
Dr:Mohamed El-shanshory
Factor level activity &severity type
Activity Type of hemorrhage %
severe
<1%
Spontaneous;hemarthrosis; deep tissue hemorrhage
moderate
1 -5%
Bleeding following mild to moderate trauma
mild
5–25% Bleeding following moderate to severe trauma
High risk 30-50% carrier female
Gynacologic & obestatric hemorrhage
Gene therapy
PURPURAS
Pathogenesis • ITP is an autoimmune
Bleeding time
THROMBOCYTOPENIA
PURPURIC SPOTS
HENOCH – SCHOENLEIN PURPURA
BLOOD TRANSFUSION
GROWTH FACTORS
Apharesis •
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