hypoproliferative anemias Flashcards
hypoproliferative anemia
ineffective erythropoiesis +/- hematopoiesis
Nutritional anemia, marrow failure, anemia of chronic disease and renal failure
Iron deficiency anemia vs anemias of chrinic disease
Iron deficiency:
no bone marrow iron stores, serum ferritin low, serum iron low, TIBC high, transferrin saturation low
Anemia of chronic disease: increased storage iron, decreased sideroblastic iron, increased serum ferritin, decreased serum iron, dec/normal TIBC and trasnferrin saturation
ferritin is iron stores, transferritin is the binding molecule for iron
iron is consumed in heme (meat), and non-heme (veg). Absorption occurs in the duodenum, enterocytes have heme/non heme iron DMT1 transporters. Enterrocytes transfer iron to blood via ferroportin. transferrin transports iron in the blood and delivers it to liver and bone marrow macrophage for storage
stored iron is bound to ferritin, preventing free radical formation
Iron deficincy anemia
decreased levels of iron –> decreased heme–> decreased hemoglobin –> microcytic anemia
iron is depleted in the diet, lost in chronic blood loss or by malabsorption leading to decreased iron stores and incorporated into hemoglobin. common nutriotional disorder, GI blood los and and lowered GI cells to uptake iron
storage iron is gone–> low ferritin and low serum iron’
compensatory increase in trasferritin to catch any iron out there
decreased saturation of trasferritin (T saturation)
Anemia of chronic disease
chronic inflammation (common in hospitalized patients) lead to release of hepcidin. Hepcidin sequesters iron by limiting iron transfer from macrophages to erythroid precursors (sideroblasts) AND suppressing EPO. Trying to prevent bacteria from gaining access to iron.
decreased iron –> decreased heme–> decreased Hgb–> microcytic anemia
increased ferritin, decreased TIBC, decreased serum iron and decreased saturation, increased marrow iron stores, decrecrased sideroblastic iron
seen in inflammatory, infectious, and neoplastic conditions
anemia of renal failure
decreased EPO production secondary to kidney disease leads to decreased EPO
Normocytic, normochromic with echinocytes (burr cells)
Seen in chronic renal disease
megaloblastic anemia
Folate or vitamin B12 deficiency leading to impaired DNA synthesis (specifically thymidine) which produces nuclear to cytoplasmic asynchronia in erythroid and granulocytic maturation
Macrocytic anemia, macroovalocytes, hyper segmented neutrophils, NC asynchrony in marrow
Seen in pernicious anemia (atrophic gastritis leading to vitamin B 12 deficiency neuro deficits in B 12 deficiency
macrocytic/megaloblastic anemia
Anemia with high MCV, most commonly due to folate or vitamin B12 deficiency (megaloblastic anemia)
Folate and B12 are necessary for synthesis of DNA precursors
Folate comes into the body via THF, then methylated as M-THF, then demethylated by vitamin B12 and transfers vmethyl group to homocysteine producing methionine
lack of folate or vitamin b12 impairs synthesis of DNA precursors, impared division and enlargement of RBC precursors–> megaloblastic anemia
impaired division of granulocytic precursors leads to hyper segmented neutrophils
Megaloblastic change in rapid dividing cells (alcoholic liver disease and drugs cause Macrocytic anemia)
Folate deficiency
folate deficiency is from fresh foods, absorbed in the jejunum, folate deficiency develops within months as body stores are minimal poor diet (alcoholics and old people) increased demand (pregnancy, cancer, hemolytic anemia) folate antagonists (methotrexate)
Macrocytic RBCs, hypersegmented PMNs, glossitis, decreased serum folate, increased serum homocysteine, normal methylmalonic acid)
Vitamin B12 deficiency
Dietary vit B12 is complexed to animal derived proteins
Salivary gland enzymes (amylase liberate B12) then B12 immediately bind R binder and carried to stomach
Pancreatic proteases in the duodenum detach vit B12 from R binder
Vit B12 binds intrinsic factor in parietal cells in the small bowel. B12/intrinsic factor can be absorbed in the illeum
LARGE stores of vit B12, takes years to develop, pernicious anemia (loss of parietal cells). pancreatic insufficiency and damage to terminal illeum,
Macrocytic RBCs with hypersegmented neeutrophils, glossitis, subacute combine degeneration of the spinal cord
increased methylmalonic acid–> spinal cord involvement
increased homocysteine (thrombosis)
Aplastic anemia
Suppression of bone marrow pluripotent stem cells likely by autoreactive T cells
Normocytic normochromic
exposure to toxins, drugs, infectious agents, pancytopenia
myelophthisic anemia
cytopenia related to marrow infiltration by a carcinoma or storage disorder
Tear drop cells, leukoerythroblastic reaction
Associated with metastatic carcinoma
Pure red cell aplasia
Autoimmune destruction of erythroid precursors in the marrow
Thymic hyperplasia or thymoma, large granular lymphocytic leukemia or autoimmune disease
