How to instantly remember causes of normocytic anaemia

Etiologies of Normocytic Anemia Even though most cases of anemia start out in the normocytic category, there are several etiologies in which the MCV remains in the normocytic range of 80-100 fL. Increased red blood cell loss or destruction acute blood loss hypersplenism hemolytic disorders Decreased red blood cell production Marrow hypoplasia or aplasia Myelopathies Myeloproliferative diseases Pure red blood cell aplasia Chronic renal failure Liver disease Endocrine deficiency states Anemia of chronic disease Sideroblastic anemias Overexpansion of plasma volume Pregnancy Overhydration There are several etiologies of normocytic anemia, but these first few are related to diseases that lead to a decrease in the production of red blood cells. Anemia of chronic disease (AOCD) is the most common underlying etiology of chronic normocytic anemia and is the second most common type of anemia worldwide. The majority of cases of AOCD will be normocytic, but as we discussed in the last article, some will be microcytic. The pathophysiology behind anemia of chronic disease is multifaceted and is correlated with the decreased activity of the bone marrow, decreased production of erythropoietin or the body having a reduced response to a normal amount of produced erythropoietin, and shortened lifespan of red blood cells (RBCs).1 Many chronic medical conditions can be the underlying cause of AOCD. These include inflammatory diseases, cancers, infections, and systemic conditions. Several endocrine conditions such as hypothyroidism, pituitary or adrenal insufficiency, and hypogonadism all can lead to reduced bone marrow function, leading to normocytic anemia. Acute or chronic renal failure can precipitate normocytic anemia due to an excess of uremic metabolites causing the lifespan of RBCs to be decreased as well as reduced erythropoietin production. Another group of etiologies of normocytic anemia are those that cause an increase in the destruction of red blood cells or increase in the loss of red blood cells. Hemolytic anemias are often categorized as congenital or acquired. Congenital hemolytic anemias include sickle cell disease, hemoglobin C disease, RBC enzyme deficiencies, and RBC membrane disorders. The most common cause of hemolytic anemia in children is sickle cell disease, and due to the advancing treatments, this disease is becoming a common etiology of hemolytic anemia in adults. Hereditary spherocytosis is the most common RBC membrane disorder.It will often present in childhood with anemia, splenomegaly, and jaundice. Other signs and symptoms include gallstones, delayed growth, and dysmorphic features. The most common RBC enzyme deficiencies include glucose-6-phosphate dehydrogenase and pyruvate kinase deficiencies. The most common type of G6PD deficiency in the United States is the southern Mediterranean variety known as “favism,” and is less severe, but affects around ten percent of African American males. Those with G6PD may experience an acute hemolytic experience after exposure to causes of oxidative stress including sulfa medications, phenazopyridine (Pyridium), nitrofurantoin (Macrobid), or antimalarial medications. Acquired hemolytic anemias include mechanical hemolysis, autoimmune hemolytic anemia, and paroxysmal nocturnal hemoglobinuria. Medications that can cause autoimmune hemolytic anemia in predisposed individuals include methyldopa, penicillins, cephalosporins, erythromycin, acetaminophen, and procainamide. Acute normocytic anemia can occur after considerable blood loss, such as after a severe bout of gastrointestinal bleeding, bleeding from a wound, bleeding into a hip fracture, or retroperitoneal bleeding. Hypersplenism can lead to normocytic anemia after the spleen increases its size by three to four times. This can occur due to cirrhosis, myeloproliferative diseases, or chronic infection. The anemia associated with hypersplenism is often caused by the removal of red blood cells from circulation, but also by an increase in the destruction of red blood cells.