Anemia PDF

Anemia reduction in the HB concentration below normal range(12 to 15 g/dl-females , 13 to 17g/dl –males).may or may not be accompanied by decrease in the red cell mass. ANEMIA OF BLOOD LOSS: acute blood loss > 20% of blood volume: hypovolemic shock rather than anemia. The anemia is normocytic normoc...

Anemia reduction in the HB concentration below normal range(12 to 15 g/dl-females , 13 to 17g/dl –males).may or may not be accompanied by decrease in the red cell mass. ANEMIA OF BLOOD LOSS: acute blood loss > 20% of blood volume: hypovolemic shock rather than anemia. The anemia is normocytic normochromic plasma is restored within 2 to 3 days; reticulocytosis : 5 to 7 days. chronic blood loss iron stores are gradually depleted. Iron deficiency anemia The anemia is microcytic hypochromic Iron Deficiency Anemia Very common 25% to 50% of people in developing countries. Causes: 1. Chronic blood loss is the most important cause :peptic ulcers, colonic cancer, hemorrhoids,menorrhagia, metrorrhagia, cancers). 2. low intake 3. Increased demands (pregnancy and infancy.) 4. Malabsorption (celiac disease or after gastrectomy) iron deficiency develops insidiously. Iron stores are depleted fist, marked by : 1. a decline in serum ferritin 2. and the absence of stainable iron in the bone marrow. 3. decrease in serum iron and 4. a rise in the serum transferrin. 5. Microcytic hypochromic anemia, 6. impaired work and cognitive performance, 7. reduced immunocompetence. Clinical Features weakness, and pallor, figernails, thinning, flttening, and “spooning,” pica, the compunction to consume non food stuffs such as ice or clay. In peripheral smears red cells are microcytic and hypochromic 1. 2. 3. 4. 5. 6. Diagnostic criteria anemia, hypochromic and microcytic low serum ferritin and iron levels, low transferrin saturation, increased total iron-binding capacity, For unclear reasons, the platelet count often is elevated. Erythropoietin levels are increased, but marrow cellularity usually is only slightly increased. Normal peripheral blood film Microcytosis hypochromia There is also increased anisocytosis (variation in size) and poikilocytosis (variation in shape). Anemia of Chronic Disease Most common form of anemia in hospitalized patients. Arises from the suppression of erythropoiesis by systemic inflammation. 1. Chronic microbial infections: osteomyelitis, bacterial endocarditis&lung abscess 2. Chronic immune disorders, such as rheumatoid arthritis and regional enteritis 3. Neoplasms, such as Hodgkin lymphoma and carcinomas of the lung and breast PATHOGENESIS: high levels of plasma hepcidin, which blocks the transfer of iron to erythroid precursors by downregulating ferroportin in macrophages. The elevated hepcidin levels are caused by proinflmmatory cytokines such as IL-6, which increase hepatic hepcidin synthesis. chronic inflammation blunts erythropoietin synthesis by the kidney, the serum iron levels usually are low red cells may even be slightly hypochromic and microcytic. storage iron in the bone marrow is increased, the serum ferritin concentration is elevated, and the total iron-binding capacity is reduced. Megaloblastic Anemias Folate deficiency and vitamin B12 deficiency. Both vitamins are required for DNA synthesis. The morphologic hallmark of is the presence of megaloblasts, enlarged erythroid precursors that give rise to abnormally large red cells (macrocytes). Granulocyte precursors are also increased in size Underlying this cellular gigantism is a defect in DNA synthesis that impairs nuclear maturation and cell division the hematopoietic precursors show nuclear-cytoplasmic asynchrony ineffective hematopoiesis pancytopenia (anemia, thrombocytopenia, and granulocytopenia The bone marrow is markedly hypercellular and contains numerous megaloblastic erythroid progenitors. Megaloblasts are larger than normal erythroid progenitors (normoblasts) giant metamyelocytes. Megakaryocytes may also be abnormally large and have bizarre multilobed nuclei. Folate (Folic Acid) Deficiency Anemia Not common, 1. poor diet (vegetables and fruits) 2. increased metabolic needs (pregnant women and ,chronic hemolytic anemias). 3. Phenytoin and a few other drugs also inhibit folate absorption, while others, such as methotrexate, inhibit folate metabolism. 4. site of absorption:upper third of the small intestine;, malabsorptive disorders that affect this level of the gut, such as celiac disease and tropical sprue, PATHOGENESIS: after absorption folate is transported in the blood mainly as a monoglutamate. Within cells it is converted from dihydrofolate to tetrahydrofolate by dihydrofolate reductase Tetrahydrofolate acts as an acceptor and donor of one-carbon units in several reactions that are required for the synthesis of purines and thymidylate, the building blocks of DNA, its deficiency accounts for the defect in DNA replication that underlies megaloblastic anemia. Clinical Features: The onset is insidious, weakness and easy fatigability. sore tongue The diagnosis is by measuring serum and red cell folate and vitamin B12 levels Vitamin B12 (Cobalamin) Deficiency Anemia (Pernicious Anemia) result in a megaloblastic anemia identical to folate deficiency. However, vitamin B12 deficiency can also cause a demyelinating disorder of the peripheral nerves and the spinal cord. PATHOGENESIS: Long-standing malabsorption underlies the vast majority of cases of vitamin B12 deficiency. Pernicious anemia is the most frequent cause of vitamin B12 deficiency. autoimmune reaction against parietal cells and intrinsic factor itself, which produces gastric mucosal atrophy Autoantibodies are present in the serum and gastric juice of most patients. blocking antibodies, which disrupt the binding of vitamin B12 to intrinsic factor; intrinsic factor–B12 complex antibodies, Chronic vitamin B12 malabsorption is also seen: 1. after gastrectomy (owing to loss of intrinsic factor–producing cells) 2. ileal resection (owing to loss of intrinsic factor– B12 complex–absorbing cells), 3. and in disorders that disrupt the function of the distal ileum (such as Crohn disease, tropical sprue, and Whipple disease). 4. Particularly in older persons, gastric atrophy and achlorhydria may interfere with the production of acid and pepsin, which are needed to release the vitamin B12 from its bound form in food. The main neurologic lesions associated with vitamin B12 deficiency are: demyelination of the posterior and lateral columns of the spinal cord, sometimes beginning in the peripheral nerves. In time, axonal degeneration may supervene. The severity of the neurologic manifestations is not related to the degree of anemia. the neurologic disease may occur in the absence of overt megaloblastic anemia. Clinical Features: pallor, easy fatigability, and, in severe cases, dyspnea and even congestive heart failure. The increased destruction of erythroid progenitors may give rise to mild jaundice. symmetric numbness, tingling, and burning in feet or hands, followed by unsteadiness of gait and loss of position sense, particularly in the toes. Patients with pernicious anemia have an increased risk for the development of gastric carcinoma. The diagnostic features of pernicious anemia include : (1)low serum vitamin B12 levels, (2) normal or elevated serum folate levels, (3) serum antibodies to intrinsic factor, (4) moderate to severe megaloblastic anemia, (5) leukopenia with hypersegmented granulocytes, and (6) a dramatic reticulocytic response (within 2 to 3 days) to parenteral administration of vitamin B12