Scanning electron micrograph showing a mixture of red blood<unk> s, some with round normal morphology, some with mild<unk> ng showing elongation and bending The loss of red blood<unk>  elasticity is central to the pathophysiology of<unk> . Normal red blood<unk> s are quite elastic and have a biconcave disc shape, which allows the<unk> s to deform to pass through capillaries. In<unk> , low oxygen tension promotes red blood<unk> <unk> ng and repeated episodes of<unk> ng damage the<unk>  membrane and decrease the<unk> 's elasticity. These<unk> s fail to return to normal shape when normal oxygen tension is restored. As a consequence, these rigid blood<unk> s are unable to deform as they pass through narrow capillaries, leading to vessel occlusion and ischaemia. The actual anaemia of the illness is caused by haemolysis, the destruction of the red<unk> s, because of their shape. Although the bone marrow attempts to compensate by creating new red<unk> s, it does not match the rate of destruction. Healthy red blood<unk> s typically function for 90–120 days, but<unk> d<unk> s only last 10–20 days.
Sickle cell disease
Glucose-6-phosphate dehydrogenase deficiency
Sickle cell trait
Avascular necrosis
Primary hyperoxaluria
Sick cell syndrome
Thalassemia
Hawkinsinuria