Professional Documents
Culture Documents
ANEMIA
lungs
Hb + O2 HbO2
tissues
HEMOGLOBIN
↓ proliferation
By external agents, physical
or chemical (e.g. ionizing
radiation, marrow toxins
Marrow
damage Hereditary or acquired
or defect aplastic anemia
Maturation
defect
Iron deficiency and the
anemia of chronic disease
Microcytic
Impaired globin chain
(hypochromic synthesis
(thalassemias)
Impaired porphyrin
synthesis
ANEMIA Membrane defects (e.g.
hereditary
Phagocytosis by spherocytosis)
reticuloendothelial
cells Heinz body associate
(e.g. G6PD deficiency)
Hemoglobin discorders
(e.g. sickle cell)
Accelerated Red cell
fragmentation DIC
Hemolysis
syndromes Vasculitis
syndromes
Sickle cell
An autosomal
recessive inherited
defect
The disease is
chronic and lifelong.
Lifespan is often
shortened with
sufferers living to an
average of 40 years.
OVERVIEW
The polymerization of deoxygenated HbS is the
primary indispensable event in the molecular
pathogenesis of sickle cell disease
HbS polymerization is associated with increased
red cell density (dense erythrocytes) as well as
red cell membrane damage favoring the
generation of distorted rigid sickle cells and
contributing to vaso-occlusion and premature
red cell destruction (hemolytic anemia).
OVERVIEW
NORMAL SC TRAIT
A S A A A S A A
A S A A S S S A
• Ulcers on the Legs. Sickle cell ulcers (sores) usually begin as small,
raised, crusted sores on the lower third of the leg. Leg sores occur more
often in males than in females and usually appear between the ages of
10 and 50. The cause of leg ulcers is not clear. The number of ulcers can
vary from one to many. Some heal rapidly, but others persist for years or
come back after healing.
Weakness Slowed
and physical Damage Damge Damage Brain Damage
lassitude development to heart to lungs to damage to abd Kidney
muscle muscles organs damage
Impaired and
mental joints
function
Heart pneumonia paralysis Kidney
Abd
Failure Rheumatism pain failure
DEATH
Who Is At Risk for Sickle Cell Anemia?