Describe in detail the pathophysiological process of sickle cell anemia
NR 507 Week 3: Discussion Part One
2. Describe in detail the pathophysiological process of sickle cell anemia
Describe in detail the pathophysiological process of sickle cell anemia
SCA is represented by abnormal hemoglobin synthesis, which leads to the production of disfigured sickle-cell shaped red blood cells (RBCs) (Kato, Steinberg & Gladwin, 2017). The sickle-shaped RBCs have a shortened life spam, and are not able to transport sufficient oxygen to the tissues in the body, and become trapped in the vasculature because of their disfigured form, resulting in vascular blockage, pain, and organ infarct (McCance, Huether, Brashers, & Rote, 2013). Sickle cells go through hemolysis in the spleen or become blockaded there, leading to blood drawing and infarct of splenic vessels (McCance, Huether, Brashers, & Rote, 2013). The anemia that follows initiates erythrocytes in the bone marrow and in utmost extent, in the liver. Most sickled erythrocytes get back their normal form after reoxygenation and rehydration (McCance, Huether, Brashers, & Rote, 2013). Nonreversible sickling is not due to nonreversible hemoglobin changes instead by irreversible plasma destruction as a result of sickling (McCance, Huether, Brashers, & Rote, 2013). The plasma membrane loses some of its capability for active transport, allowing an inflow of calcium ions (McCance, Huether, Brashers, & Rote, 2013). In individuals with SCA, in which the erythrocytes have elevated proportion of hemoglobin S up to 30 percent of the red blood cells may become irreversibly sickled (McCance, Huether, Brashers, & Rote, 2013). Sickling is infrequently, occasional phenomenon that may be initiated or supported by one of the following stressors, lowered oxygen tension PO2 of the blood (hypoxemia), elevated hydrogen ions consolidation in the blood (Decreased PH), elevated plasma osmolarity, reduced 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).
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