NR 507 Week 2 Assignment; Hematological and Cardiovascular Disorders

Anemia Classi昀椀ca琀椀on Anemias can be classi昀椀ed into 3 categories based on the average size of the RBCs (MCV): • Microcy琀椀c anemia (MCV100 fL) describes RBCs that are large. • Normocy琀椀c anemia (MCV 80-99 fL) describes RBCs that are normal in size. Microcy琀椀c Hypochromic Microcy琀椀c Normochromic Microcy琀椀c Hyperchromic Iron de昀椀ciency Anemia of in昀氀amma琀椀on and chronic disease Hereditary spherocytosis Sideroblastic Thalassemia Anemias can also be classi昀椀ed according to the color of the RBCs: • Hypochromic anemia describes RBCs with less hemoglobin than normal. As a result, the RBCs appear pale in color (MCHC is low). • Hyperchromic anemia describes RBCs with more hemoglobin than normal. As a result, the RBCs a ppear a dark hue or red than normal cells (MCHC is high). Macrocy琀椀c Anemias As you should recall, macrocy琀椀c anemias result from condi琀椀ons whereby the RBCs are large (MCV>100 dL ). Macrocy琀椀c anemias are categorized as megaloblas琀椀c and non-megaloblas琀椀c: • Megaloblas琀椀c: Folate de昀椀ciency and vitamin B12 de昀椀ciency • Non-megaloblas琀椀c: Liver disease, myelodysplas琀椀c syndrome, increased re琀椀culocyte count (hemorrhage) In this sec琀椀on, we will explore the macrocy琀椀c, hypochromic, megaloblas琀椀c anemias which are caused from folate and vitamin B12 de昀椀ciencies. Folate and cobalamin (vitamin B12) are required for red blood cell DNA synthesis; therefore, a de昀椀ciency in either results in impaired DNA replica琀椀on of the RBC. This causes the erythroblasts to con琀椀nue to increase in size (macrocy琀椀c) instead of undergoing cell division. B12 De昀椀ciency (Pernicious Anemia) Pernicious anemia (PA) results from the autoimmune destruc琀椀on of the gastric parietal cells which decreases the secre琀椀on of intrinsic factor. Intrinsic factor, as you probably recall, binds to B12 in the stomach and travels through the small intes琀椀ne. When the complex reaches the ileum, it is broken and B12 is absorbed into the blood. Why is this important? Because B12 is needed for DNA matura琀椀on and condensa琀椀on. As a result, a de昀椀ciency leads to immature RBCs, lack of func琀椀onal hemoglobin, and decreased nerve cell myelina琀椀on. This gene琀椀cally induced autoimmune condi琀椀on is especially prevalent in individuals of English, Irish or Scandinavian ancestry. • Hemoly琀椀c disease of the newborn (Rh incompa琀椀bility issue occurring in Rh-mothers and their Rh+ fetus): This condi琀椀on also links back to our Module 1 discussion on the Type 2 Cytotoxic hypersensi琀椀vity reac琀椀on. Refer to the clinical applica琀椀on case under Module 1, Type 2 Cytotoxic reac琀椀on to review the underlying pathophysiology occurring with hemoly琀椀c anemia. Regardless of the cause of the hemolysis, the underlying pathophysiology does not change. • Autoimmune reac琀椀ons: these can be either congenital or idiopathic in nature. • Drug-induced: note that drugs are chemicals and they autoxidize (self-destruct, especially over 琀椀me and/or with exposure to heat, moisture) to form H2O2 (hydrogen peroxide, a free radical) which causes Fe +2 to oxidize to form Fe +3; and as men琀椀oned earlier, this form of iron cannot bind O2 as well. In addi琀椀on, hydrogen peroxide can also a琀琀ack and oxidize cell membranes to weaken them. In any of the above situa琀椀ons, there is a premature destruc琀椀on/lysis of RBCs due to enzymes or toxins produced by the infec琀椀ous