Term
Iron-deficiency anemia
Etiology: inadequate iron due to deficient dietary intake; decreased absorption; increased blood loss
CBC: Microcytic, hypochromic, anisocytosis, poikilocytosis
Fe studies: Decreased serum iron, serum ferritin, and percent saturation of transferrin; increased TIBC and sTfR.
Other: increased ZPP (don't use if possible lead poisoning); decreased retic hemoglobin (CHr, MCHr, RET-He); increased sTfR-F index
Classification- low expected MCV (microcytic), increased expected RDW (anisocytosis)-- maturation problem
Rx: give iron |
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Definition
Pathophysiology: less hgb produced in cell,3 stages:
-stage 1: Fe stores being depleted-serum ferritin is decreased, TfR-F index increased
-Stage 2: Fe deficient erythropoeisis; stores have been depleted, insufficient Fe for protoporphyrin IX, since protoporphyrin increased, serum iron down, TIBC increased, % sat. decreased
Stage 3: Fe deficiency anemia: hypochromic, microcytic cells, functional Fe decreases, hgb decreases.
Clinical features: from hypoxia: weakness, lethargy, headaches; from lack of Fe in tissue enzymes: koilonchia, glossitis, muscle dysfunction, gastritis, pale faced |
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Term
Sideroblastic Anemia
Etiology: Defect in enzymes needed for heme synthesis; can be hereditary or acquired (secondary to drugs/toxins, B6 deficiency or malignancy
CBC: MCV/MCHC- Dual population of normochromic and hypochromic erythrocyes
Iron: Increased serum iron and transferrin saturation; normal or decreased TIBC; increased serum ferritin; greater than/equal to 15% ringed sideroblasts
Other tests: Bone marrow shows ring sideroblasts; peripheral blood erythrocytes can contain pappenheimer bodies. |
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Definition
Pathophysiology: ineffective erythropoeisis, ringed sideroblasts, erythroid hyperplasia- RPI <2, cytoplasmic maturation problem
Clinical features: hepatosplenomegaly, usual anemic symptoms
Treatment: Hereditary treated with pyridoxine
Classification:RDW increased, MCV varies, hypochromic/normochromic, RBC inclusions help- pappenheimer bodies and coard basophillic stipling |
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Term
Anemia of chronic disease
Etiology: Impaired release of iron from mac's due to increased hepcidin induced by cytokines; inhibition of EPO production and impaired erythropoiesis; shortened erythrocyte survival
Pathophysiology: abnormal heme synthesis
CBC: Normocytic, normochromic; in long-standing cases can be microcytic, hypochromic |
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Definition
Clinical: anemia roughly correlates with the underlying disease (chronic infections, chronic inflammatory disorders, trauma, organ failure, neoplastic disorders)
Classification: Cytoplasmic maturation defect, RDW usually normal, MCV slightly low to normal
Iron: Decreased serum iron and low to normal TIBC; low/normal transferrin saturation; increased or normal serum ferritin; sTfR normal; Iron stain- decreased sideroblasts, normal to increased mac iron stores
Other tests: Increased ZPP, decreased sTfR-F index |
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Term
Anemia
Definition: Decrease in oxygen carrying and delivering capacity of the blood to the tissue because of a decrease in hemaglobin or RBC numbers; hypoxia
-Not a disease but a sign/symptom of an underlying disease or problem
-cells indicating anemia include: Hypochromic/microcytic, Macrocytic/normochromic, and normocytic/normochromic |
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Definition
Lab tests for anemia:
-CBC: includes WBC/RBC counts, hgb, hct, platelet counts, and manual differential if needed.
-Quality control: the indices E.g. Mean Cell/Corpuscular Volume ( MCV)<80fL, Mean Cell Hemoglobin Concentration (MCHC)<32 g/dL; Mean Cell Hemoglobin (MCH)<27pg; Red Cell Distribution Width (RDW)<36.4fL in females, <35.1fL in males; mean platelet volume (MPV) |
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Term
Megaloblastic macrocytic anemia- folate deficiency
Etiology: inadequate diet, increased need, malabsorption, drug inhibition, biologic competition
CBC/morphology: MCV may be increased but may not see macrocytes on blood smear
pathophysiology: decreased methylene THF, so slower DNA synthesis like in blood cells; nuclear maturation defect
clinical features: serum folate levels decrease first, 1-2 weeks, hypersegmented neuts can show before macrocytosis, alcoholism can be cause |
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Definition
megaloblastic anemia- cobalamin deficiency
etiology: malabsorption (PA), biologic competition, nutritional deficiency, impaired utilization
pathophysiology: folate trapped in methyl THF form (abnormal DNA synthesis), SAM deficiency, nerve fiber demyelination, increased homocysteine; nuclear maturation defect
clinical features: abdominal pain, neurologic symptoms
CBC: extreme anisocytosis, avg. MCV is large, RDW increased, pancytopenia: decreased RBC, WBC, platelet numbers, microbiologic or immunoassays used, Schilling test; increased MMA may be an early detector of B12 deficiency
-nuclear cytoplasmic asynchrony: nuclear maturation lags behind cytoplasmic maturity |
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Term
macrocytic megaloblastic anemias lab values
WBC count, platelet count, RBC count, hgb, hct decreased
retic. count: normal to decreased
serum cobalamin: decreased in cobalamin deficiency
serum folate: decreased in folate deficiency
FIGLU: increased in folate deficiency
MMA: increased in B12 deficiency
homocystein, serum biliruben, and LD increased
MCV: usually >110fL
RBC morphology: ovalocytes, Howell-Jolly bodies, polychromasia
Hypersegmentation of neuts present |
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Definition
Macrocytic non-megaloblastic anemias lab values
WBC and platelet count normal, RBC count, hgb and hct decreased
retic count: normal, decreased, or increased
serum cobalamin: usually normal
serum folate: normal except for alcoholism (decreased)
FIGLU, MMA, homocysteine normal
serum biliruben and LD normal to increased
MCV: >100fL
RBC morphology: polychromasia, target cells, stomatocytes (liver disease), schistocytes (hemolytic anemias)
hypersegmentation of neuts absent |
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Term
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Definition
cobalamin deficiency
Classification: ineffective erythropoiesis
Therapy: trial of intramuscular B12, retic count for following progress
Folate deficiency
anemia appears 19-20 wks after; red cell folate gives picture of 3-4 mo. folate levels
-red cell folate levels <160ng/mL reflects available folate when being made in BM, microbiologic or immunoassays used for testing
Therapy: trial with folic acid monitored by retic. response. |
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Term
Hemolytic anemia:
Etiology: destruction of RBCs exceeds production and hemolysis is the primary cause of anemia
classification: normochromic/normochromic, RPI increased, MCV- normocytic unless lots of retics, RDW increased
pathophysiology: survival defect
CBC/morphology: plasma unconjugated biliruben increased but negative biliruben in urine, poikilocytes, absent haptoglobin, hgb, hct, RBC decreased, free hgb increased, hemopexin decreased, hemosiderin in urine |
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Definition
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