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10 Cards in this Set

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Presentation- Weakness, fatigue, lightheadedness, tachycardia, shortness of breath, or worsening of angina. “PICA” symptoms – unusual cravings to chew dirt, clay, or ice(most common). Since heme can not be made, cells are small from less hemoglobin per cell (low MCV). The reticulocyte count is low since erythrocytes are produced in lower numbers. Ferritin (the storage form of iron) is usually the best indicator of iron storage levels. A high total iron binding capacity and a low serum iron level also indicate iron deficiency.
Iron Deficiency
Pathology/Etiology- Loss of iron needed for heme production in erythrocytes. Women lose iron during menses, pregnancy, lactation, or occult hemorrhage. Men lose iron from occult hemorrhage, almost always from the GI tract. Iron deficiency anemia in men and post-menopausal women requires a work-up to exclude GI malignancy.

Anemia from decreased production(Low reticulocyte count)

Microcytic Anemias
Presentation- Can be mild and asymptomatic, or can be very severe.
In severe thalassemia, symptoms include weakness, fatigue, lightheadedness, tachycardia, and shortness of breath – evident after six months. In most cases, low MCV with a low reticulocyte count. I
Thalassemia
Pathology/Etiology- Mutations in either the alpha or beta globin chain resulting in decreased production of hemoglobin(Hb), and subsequently decreased erythrocyte production. Thalassemia is more common in people of Southeast Asia, African, or Mediterranean descent.

n beta thalassemia there is increased Hb A2 (α2σ2) on Hb electrophoresis. Definitive diagnosis of alpha-thalassemia requires DNA analysis.

Anemia from decreased production(Low reticulocyte count)

Microcytic Anemias
Presentation- Symptoms include weakness, fatigue, lightheadedness, tachycardia, and shortness of breath. Also, peripheral neuropathy and abnormal balance may be present in B12 deficiency (NOT folate deficiency). Since the erythrocytes are blocked from dividing, they tend to be abnormally large (high MCV). The reticulocyte count is still low since erythrocytes are released into the circulation in reduced numbers.
Folate/B12 Deficiency
Pathology- Loss of folate and/or B12 leads to decreased DNA synthesis in all hematopoietic cells. Therefore, granulocytes and platelets can also be decreased, not just erythrocytes. Neurons affected in B12 deficiency (NOT in folate deficiency). Folate deficiency most commonly results from poor diet (alcoholics, anorexia/bulemia), while B12 deficiency results from acquired poor absorption (loss of intrinsic factor in pernicious anemia, or GI damage as in sprue or Crohn’s disease). Occurs equally in men or women.

Macrocytic Anemias
Causes of Macrocytic anemias
Causes of Macrocytic anemias

1. B12 deficiency
2. Folate deficieny
3. myelodyplastic syndromes(see Myeloid lecture)
4. medications (such as chemotherapy drugs),
5. hypothyroidism,
6. liver disease.
Causes of Normocytic anemias
Causes of Normocytic anemias-

Low erythropoietin states (e.g. renal disease), aplastic anemia, bone marrow infiltration (such as multiple myeloma), infection (such as Parvovirus B19 or HIV), medications.
Presentation- Symptoms include weakness, fatigue, lightheadedness, tachycardia, and shortness of breath. Also, jaundice may occur. The reticulocyte count is high, and the MCV is also often high (due to increased number of reticulocytes). LDH and indirect bilirubin are high, and haptoglobin is low. The direct Coomb’s test is positive.
Immune Hemolytic Anemia
Pathology- Acquired hemolytic anemia is usually an auto-immune condition, where antibody deposition on the red blood cells shortens their survival.

Anemias from increased destruction - hemolysis (High reticulocyte count)
Presentation- Normocytic anemia with a high reticulocyte count. Hb S with some Hb F (higher Hb F results in less symptoms) on hemoglobin electrophoresis. Pain crises may cause abdominal pain (splenic infarction), chest pain and shortness of breath from acute chest syndrome, stroke or seizures, leg ulcers, priapism, and bone necrosis. Infections with encapsulated organisms such as pneumococcus.
Non-immune Hemolytic Anemia
Sickle Cell Anemia
Pathology- A mutation in the β globin chain results in an abnormal hemoglobin that will aggregate when the intracellular oxygen concentration is low. These aggregates cause red cells to “sickle”, which leads to intravascular occlusion from these sickled red cells, which then causes hypoxia and pain. 8% of the African-American population is heterozygous for Hb S, 0.25% is homozygous.

Sickling episodes may be precipitated by infection, trauma, stress, high altitude.

Anemias from increased destruction - hemolysis (High reticulocyte count)
Red cell enzyme abnormalities
Red cell enzyme abnormalities – Example -Glucose-6-phosphate dehydrogenase deficiency
The most common inherited hemolytic anemias are glucose-6-phosphate dehydrogenase deficiency (Asian, Mediterranean or African descent). Lack of this enzyme leads inability of red cell to eliminate free radicals, which damage the red cell membrane, and hence shortens red cell survival. Typically, induced by infections or medications, but certain subtypes can manifest after ingestion of Fava beans.
Red cell membrane abnormalities
Red cell membrane abnormalities- Example - Hereditary spherocytosis, paroxysmal nocturnal hemoglobinuria
Microangiopathic Hemolytic anemia
Microangiopathic Hemolytic anemia- caused be intravascular destruction of red cells, e.g. Thrombotic thrombocytopenia purpura, hemolytic uremic syndrome