tonystep1's version from 2017-08-02 00:06


Question Answer
Iron Deficiency AnemiaChronic blood loss (Menstrual blood loss is the most common source. In the absence of menstrual bleeding, GI blood loss is most likely.)/// Dietary deficiency/increased iron requirements (Infants and toddlers-Occurs especially if the diet is predominantly human milk (low in iron).) Adolescents-Rapid growth increases iron requirements Pregnant women-Pregnancy increases iron requirements
Sideroblastic AnemiaHereditary or acquired-Acquired causes include drugs (chloramphenicol, INH, alcohol), exposure to lead, collagen vascular disease, and neoplastic disease (myelodysplastic syndromes).
Anemia of Chronic DiseaseOccurs in the setting of chronic infection (e.g., tuberculosis, lung abscess), cancer (e.g ., lung, breast, Hodgkin's disease) , inflammation (rheumatoid arthritis, systemic lupus erythematosus [SLE ] ) , or trauma. The release of inflammatory cytokines has a suppressive effect on erythropoiesis.
Aplastic Anemiaa. Idiopathic-maj ority of cases b. Radiation exposure c. Medications-e .g. , chloramphenicol, sulfonamides, gold, carbamazepine d. Viral infection-e.g. , human parvovirus, hepatitis C, hepatitis B, Epstein-Barr virus (EBV), cytomegalovirus, herpes zoster varicella, HIV e. Chemicals-e.g., benzene, insecticides
Vitamin 812 Deficiencyl. Pernicious anemia (lack of intrinsic factor)-most common cause in the Western hemisphere 2. Gastrectomy 3. Poor diet (e.g. , strict vegetarianism) ; alcoholism 4. Crohn's disease, ileal resection (terminal ileum) 5. Other organisms competing for vitamin B12 a. Diphy llobothrium latum infestation (fish tapeworm) b. Blind-loop syndrome (bacterial overgrowth)
Folate Deficiencyl. Inadequate dietary intake such as "tea and toast" (most common cause) 2. Alcoholism 3. Long-term use of oral antibiotics 4. Increased demand 5. Pregnancy 6. Hemolysis 7. Use of folate antagonists such as methotrexate 8. Anticonvulsant medications (phenytoin) 9. Hemodialysis
Hemolysis due to factors external to RBC defects• Immune hemolysis • Mechanical hemolysis (e.g., prosthetic heart valves, microangiopathic hemolytic anemia) • Medications, burns, toxins (e.g. , from a snake bite or brown recluse spider) ; infection (malaria, clostridium), and so on
Hemolysis due to intrinsic RBC defects• Hemoglobin abnormality: sickle cell anemia, hemoglobin C disease, thalassemias • Membrane defects: hereditary spherocytosis, paroxysmal nocturnal hemoglobinuria • Enzyme defects: glucose-6-phosphate dehydrogenase (G6PD) deficiency, pyruvate kinase deficiency


Question Answer
reticulocyte index <2 // microcytic anemia (MCV < 80) // Low Fe// High TIBCIron deficiency anemia
reticulocyte index <2 // microcytic anemia (MCV < 80) // Normal Fe // Normal TIBCThalassemia or Ring sideroblastic anemias
reticulocyte index <2 // microcytic anemia (MCV < 80) // Low Fe // Low TIBCAnemia of Chronic Disease
reticulocyte index <2 // macrocytic anemia (MCV > 100) // Hi or nl Fe // Low or nl TIBC vitamin B12 deficiency or folate deficiency
reticulocyte index <2 // macrocytic anemia (MCV > 100) // normal folate & B12 levelsLiver disease
reticulocyte index <2 // normocytic anemia (MCV 80-99)Aplastic anemia • BM fibrosis • Tumor • Anemia of chronic disease • Renal failure
reticulocyte index > 2 // normocytic anemia (MCV 80-99)suspect Hemolytic anemia or acute blood loss


Question Answer
a. Decreased serum ferritin b. Increased TIBC c. Elevated transferrin levels d. Decreased serum iron e. Microcytic, hypochromic RBCs on peripheral smearIron Deficiency Anemia
a. Hemoglobin electrophoresis-Hb F is elevated.b. Peripheral blood smear-microcytic hypochromic anemiabeta Thalassemia
a. Hemolytic anemia, splenomegaly b. Significant microcytic, hypochromic anemia c. Hemoglobin electrophoresis shows Hb Halpha Thalassemia Hb H disease-mutation/deletion of three a loci
a. Characterized by mild microcytic hypochromic anemia b. Common in African-American patientsa-thalassemia trait (or minor)-mutation/deletion of two a loci
a. increased serum iron and ferritin, normal TIBC b. ringed sideroblasts in bone marrowSideroblastic Anemia
a. Low serum iron, low TIBC, and low serum transferrin levels occur. b. Serum ferritin levels are increased.Anemia of Chronic Disease
a. Normocytic, normochromic anemia b. bone marrow biopsy for definitive diagnosis-this reveals hypocellular marrow and the absence of progenitors of all three hematopoietic cell lines.Aplastic Anemia
l. Peripheral blood smear a. Megaloblastic anemia-macrocytic RBCs (MCV > 1 00) b. Hypersegmented neutrophils c. Serum vitamin B12 level i s low ( < 1 00 pg/mL)Vitamin B12 Deficiency
l. hemolysis and reticulocytosis 2. Elevated reticulocyte count 3. Peripheral smear Schistocytes("trauma" or mechanical hemolysis)
l. hemolysis and reticulocytosis 2. Elevated reticulocyte count 3. Peripheral smear Spherocytes or helmet cells suggestextravascular hemolysis (depending on the cause)
l. hemolysis and reticulocytosis 2. Elevated reticulocyte count 3. Peripheral smear Sickled RBCssickle cell anemia
l. hemolysis and reticulocytosis 2. Elevated reticulocyte count 3. Peripheral smear Heinz bodies & "bite cells"G6PD deficiency
RBC osmotic fragility to hypotonic saline//Elevated reticulocyte count, elevated MCHC//Peripheral blood smear would reveal spherocytes (sphere-shaped RBCs).//Direct Coombs test result is negativeHereditary Spherocytosis
Direct Coombs test RBCs are coated with IgG (positive direct Coombs test)Warm Autoimmune Hemolytic Anemia (AIHA)
Direct Coombs test RBCs are coated with complement aloneCold Autoimmune Hemolytic Anemia (AIHA)
Ham's test: The patient's cells are incubated in acidified serum, triggering the alternative complement pathway, resulting in lysis of abnormal cells but not normal cells.Paroxysmal Nocturnal Hemoglobinuria (PNH)
Sugar water test: The patient's serum is mixed in sucrose...hemolysis ensuesParoxysmal Nocturnal Hemoglobinuria (PNH)
Serum vitamin B12 level is low ( < 1 00 pg/mL)//Schilling test adding intrinsic factor improves serum vitamin B12 levels.pernicious anemia is present
Serum vitamin B12 level is low ( < 1 00 pg/mL)//Schilling test adding intrinsic factor does not improve serum vitamin B12 levelsmalabsorption is the problem


Question Answer
Iron Deficiency AnemiaOral iron replacement (ferrous sulfate)
Thalassemia major (Cooley's anemia; homozygous ,beta-chain thalassemia)Frequent PRBC transfusions are required to sustain life.
Thalassemia minor (heterozygous ,beta-chain thalassemia)usually not necessary (Patients are not transfusion-dependent.)
Thalassemia intermediaPatients usually are not transfusion-dependent
Alpha Thalassemia Silent carriers-mutation/deletion of only one a locusNo treatment necessary
a-thalassemia trait (or minor)-mutation/deletion of two a lociNo treatment necessary
Hb H disease-mutation/deletion of three a lociFrequent PRBC transfusions are required to sustain life. Splenectomy is sometimes helpful.
Sideroblastic AnemiaRemove offending agents. Consider pyridoxine
Anemia of Chronic DiseaseNo specific treatment is necessary other than treatment of the underlying process. Do not give iron. The anemia is usually mild and well-tolerated
Aplastic Anemial. Bone marrow transplantation 2. Transfusion of PRBCs and platelets, if necessary (use judiciously) 3. Immunosuppression
Vitamin 812 DeficiencyParenteral therapy is preferred-cyanocobalamin (vitamin B 12) I M once per month
Folate Deficiencyoral folic acid replacement
Hemolytic Anemiasl. Treat underlying cause. 2. Transfusion of PRBCs if severe anemia is present or patient is hemodynamically compromised. 3. Folate supplements (folate is depleted in hemolysis
Sickle Cell Anemia Patient Advisea. Avoid high altitudes (low oxygen tension can precipitate crisis) . b. Maintain fluid intake (dehydration can precipitate crisis) . c. Treat infections promptly (infection/fever can precipitate crisis). d. Early vaccination for S. pneumoniae, H. influenzae, and Neisseria meningitidis
Sickle Cell Anemia Management of painful crisesa. Hydration-oral hydration if mild episode, otherwise give IV fluids (normal saline) b. Morphine for pain control-do not underestimate patient's pain. c. Keep the patient warm. d. Supplemental oxygen if hypoxia is present
Sickle Cell Anemia Preventive MedicationsProphylactic penicillin for children until 6 years of age-start at 4 months//Hydroxyurea
Hereditary SpherocytosisSplenectomy is the treatment of choice
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency l. Avoid drugs that precipitate hemolysis. 2. Maintain hydration. 3. Perform RBC transfusion when necessary
Warm AIHAa. Glucocorticoids are the mainstay of therapy. b. Splenectomy-Use for patients whose condition does not respond to glucocorticoids c. Immunosuppression (azathioprine or cyclophosphamide) may be beneficial. d. RBC transfusions-if absolutely necessary e. Folic acid supplements
Cold AIHAa. Avoiding exposure to cold-prevents bouts of hemolysis and anemia b. RBC transfusions-if absolutely necessary c. Various chemotherapeutic agents d. Steroids are not beneficial
Paroxysmal Nocturnal Hemoglobinuria (PNH)l. Glucocorticoids (prednisone) are the usual initial therapy, but many patients do not respond. 2. Bone marrow transplantation