HEMATOLOGY

AND
ONCOLOGY
 CELLULAR ELEMENTS
•
THE RED CELLS
 Erythropoiesis
• stem cell
proerthroblast basophilic polychromat
ophilic

orthocromatophil reticulocy Mature RBCs

ic te
 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 % After 2 years
Embryonic Embryonic Hb Major embryonic
type may be present Hb are not
at birth in present after 3rd
small month of
percentage. gestation.
Fetal type(α2γ 2) 45-90% 3%
Adult type
A1 (α2β 2) 10-55% 95%
A2 (α δ ) 0-1.5% 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 HEME

AMINOACIDS PROTOPORPHYRIN
IRON

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 INTESTINAL BACTERIAL FLORA E-COLI

UNCONGUGATED BILIRUBIN 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 Β-
THALASSEMIA 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
Primary homeostasis fibrinogen
GPIIB,IIIA
Aggregation

adhesion
release
activation

Secondary homeostasis

FIBRIN CLOT
FORMATION
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% Gynacologic & obestatric
carrier female hemorrhage
Gene therapy
PURPURAS
 Pathogenesis
• ITP is an autoimmune
Bleeding time
THROMBOCYTOPENIA
PURPURIC SPOTS
HENOCH – SCHOENLEIN
PURPURA
BLOOD TRANSFUSION
GROWTH FACTORS
 Apharesis
•