Disorders of Red and White Blood Cells

Sickle cell anemia, an inherited hemoglobin disorder, is characterized by the replacement of hemoglobin A (HbA) with hemoglobin S (HbS sickle hemoglobin). Homozygotes have all HbA replaced with HbS (HbSS) and carry the disease, whereas heterozygotes have less than 40% HbS (HbSA) and carry the sickle cell trait. HbSA occurs in about 8% to 10% of African


Siderocalcinosis of blood vessels in globus pallidus. Basophilic mineral deposits A. in the intima and media (HE), B. in full thickness of the wall, partially obliterating the lumen (Gomori iron stain) and, C. destroying the vessel's wall (Von Kossa calcium stain). D. CT scan showing mineralization in globus pallidus.

Americans. A number of situations associated with low arterial oxygen tension (chronic anemia, infection, heat stroke, physical overexertion) are apt to precipitate sick-ling of the erythrocytes.

Stroke, more often ischemic than hemorrhagic, occurs at any age from childhood to old age, and frequently is recurrent. The incidence is particularly high in children, and small infarctions may develop in the absence of clinical evidence of a stroke. The ischemic events result from occlusion of arterioles and capillaries by sludging of sickled erythrocytes, or from thrombotic occlusions of larger arteries. The cerebral pathology is characterized by small and large infarctions, often situated in the watershed region between arterial territories. Ischemic events may occur even in individuals with sickle cell trait (Fig. 4.37).

In polycythemia vera, hyperviscosity from an increased concentration of erythrocytes reduces the cerebral blood flow, leading to TIAs and eventually infarction (Fig. 4.38).

The hyperleukocytosis of leukemias is a serious risk for cerebral hemorrhage (see Fig. 4.38).

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