Describe in detail the pathophysiological process of sickle cell anemia
Describe in detail the pathophysiological process of sickle cell anemia

SCA is characterized by abnormal hemoglobin synthesis, which results in the formation of sickle-shaped red blood cells (RBCs) (Kato, Steinberg & Gladwin, 2017). Because of their disfigured shape, sickle-shaped RBCs have a shortened life span, are unable to transport enough oxygen to the tissues in the body, and become trapped in the vasculature, resulting in vascular blockage, pain, and organ infarction (McCance, Huether, Brashers, & Rote, 2013). Sickle cells undergo hemolysis in the spleen or become blocked there, resulting in blood drawing and splenic vessel infarction (McCance, Huether, Brashers, & Rote, 2013). The resulting anemia initiates erythrocytes in the bone marrow and, to a lesser extent, in the liver. After reoxygenation and rehydration, most sickled erythrocytes return to their normal form (McCance, Huether, Brashers, & Rote, 2013).

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Nonreversible sickling is caused by irreversible plasma destruction rather than irreversible hemoglobin changes (McCance, Huether,

Describe in detail the pathophysiological process of sickle cell anemia
Describe in detail the pathophysiological process of sickle cell anemia

Brashers, & Rote, 2013). The plasma membrane loses some of its ability for active transport, allowing calcium ions to enter (McCance, Huether, Brashers, & Rote, 2013). Individuals with SCA, whose erythrocytes have an elevated proportion of hemoglobin S, may have up to 30% of their red blood cells become irreversibly sickled (McCance, Huether, Brashers, & Rote, 2013). Sickling is a rare, sporadic phenomenon that can be caused or exacerbated by one of the following stressors: low blood oxygen tension (hypoxemia), high hydrogen ion concentration in the blood (decreased PH), high plasma osmolarity, low blood volume, and low temperature (McCance, Huether, Brashers, & Rote, 2013).

The increased reduction of PO2 attributed to tenacious hypoxemia caused by stressors ultimately leads to sickling in the microcirculation of all cells that have Hb S in the site not through the body. Decline blood pH curtails hemoglobin’s affinity for oxygen (McCance, Huether, Brashers, & Rote, 2013). When decreased oxygen is picked up by hemoglobin in the lungs, the PO2 falls promoting additional sickling (McCance, Huether, Brashers, & Rote, 2013). Increased osmolarity of the plasma pulls water out of the red blood cells. This promotes sickling by increases the relative Hb S composition in the red blood cells (McCance, Huether, Brashers, & Rote, 2013).