The goal of this program is to improve the diagnosis and management of anemia. After hearing and assimilating this program, the clinician will be better able to:
1. Determine the cause of, and provide optimal treatment for, anemia.
Diagnosis: anemia symptom (not diagnosis); mean corpuscular volume diagnostic of some types of anemia; reticulocyte count reflects response of bone marrow (BM)
Normocytic Anemia
Cause: in majority of cases, abnormality in BM
Aplastic anemia (AA): majority of cases idiopathic; drug-induced AA — causative agents include nonsteroidal anti-inflammatory drugs; management includes transfusion of red blood cells and platelets, culturing, antibiotics, and discontinuation of offending agent; some drugs and toxins cause AA based on dose; others idiosyncratic (eg, chloramphenicol); other causes — viral infection; underlying disease (eg, paroxysmal nocturnal hemoglobinuria); management — discontinue offending agent; if AA persists in patients aged >40 yr, administer antithymocyte globulin with cyclosporine and steroids; if patient aged <20 yr, BM transplantation recommended
Anemia due to myelophthisic disorders: causes include leukemia, lymphoma, myeloma, metastatic cancer, infections, and lysosomal storage diseases (eg, Gaucher disease)
Pure red cell aplasia: associated with thymoma, lymphoproliferative disorders, collagen vascular disorders, systemic lupus erythematosus, and parvovirus B19 infection
Anemia of renal failure: managed with erythropoietin; elevated hemoglobin levels due to excess administration can result in stroke, heart attack, and venous thromboembolic disease
Anemia of endocrine disorders: hypotestosteronism, hypothyroidism, and hypopituitarism
Anemia of chronic disease: associated with low iron level, total iron-binding capacity, and percent saturation and normal or high ferritin level; occurs in inflammatory and neoplastic conditions and infections; manage underlying disease
Macrocytic Anemia
Vitamin B12 deficiency: low levels of intrinsic factor (IF) can result in poor absorption of vitamin B12; administration of folic acid initially to vitamin B12-deficient individual can worsen neurologic state; deficiency occurs in absence of intact terminal ileum and stomach, strict ovo-lacto vegetarians, and individuals with pernicious anemia, gastrectomy or gastric bypass surgery, terminal ileal disease (eg, Crohn disease, carcinoid tumors, radiation enteritis, resection), and fish tapeworm infection; patient may develop immune reaction against parietal cells (antibodies against IF, antiparietal cell antibodies, and cell-mediated immunity); any disease or substance that reduces amount of stomach acid or production of IF can cause pernicious anemia; neurologic syndrome develops; dropout in dorsolateral column of spinal cord leads to ataxic gait, poor proprioception, and dementia; vitamin B12 stores thousand times daily requirement (deficiency develops over years)
Folic acid deficiency: causes include malabsorption (eg, celiac disease) and alcoholism; decreased intake causes deficiency state in weeks; folic acid absorbed in jejunum
Myelodysplasia: previous term preleukemia; often macrocytic; refractory anemia; refractory anemia with ringed sideroblasts; chronic myelomonocytic leukemia; refractory anemia poor bad (depends on chromosomal variant); incidence in older individuals increased
Other causes of macrocytosis: alcohol and drug use (eg, methotrexate, azathioprine)
Microcytic Anemia
Causes: iron deficiency; thalassemia; sideroblastic anemia
Iron deficiency: causes include blood loss in gastrointestinal tract, menstrual blood loss, pregnancy and lactation, and malabsorption
Thalassemia: chromosome 16 has 2 α-globin chains and chromosome 11, one β-globin chain; patients with β-globin chain abnormalities usually present early or have more symptoms; individuals who lose one α-globin chain can live normal lives (may be microcytic or anemic); sickle cell disease managed by increasing production of fetal hemoglobin; may cause life-long hypochromic microcytic anemia; major, intermediate, and minor categories based on disease severity; sickle cell anemia hemoglobinopathy (β-globin locus; substitution at 6-position)
Hemolytic Anemia
Causes: defects intrinsic to red blood cells (eg, enzymopathies, hemoglobinopathies) or membranes (eg, hereditary spherocytosis or elliptocytosis); cold agglutinin disease often precursor to lymphoproliferative disorders; living in warm climate helpful; warm autoimmune hemolytic anemias may be associated with drugs or underlying lymphoproliferative disorders or be idiopathic
Bayat M et al: Evaluation of clinical and laboratory data for early diagnosis of heparin-induced thrombocytopenia. Am J Health Syst Pharm, 2015 Oct 1;72(19):1649-55; Killick SB et al: British Society for Standards in Haematology. Guidelines for the diagnosis and management of adult aplastic anaemia. Br J Haematol, 2016 Jan;172(2):187-207; Koike H et al: The significance of folate deficiency in alcoholic and nutritional neuropathies: analysis of a case. Nutrition, 2012 Jul;28(7-8):821-4; Martinsson A et al: Anemia in the general population: prevalence, clinical correlates and prognostic impact. Eur J Epidemiol, 2014 Jul;29(7):489-98; Remacha AF et al: Vitamin B12 and folate levels increase during treatment of iron deficiency anaemia in young adult woman. Int J Lab Hematol, 2015 Oct;37(5):641-8; Rojas Hernandez CM, Oo TH: Advances in mechanisms, diagnosis, and treatment of pernicious anemia. Discov Med, 2015 Mar;19(104):159-68.
For this program, members of the faculty and planning committee reported nothing relevant to disclose.
Dr. Lichtin was recorded at the 28th Annual Intensive Review of Internal Medicine, held June 5-10, 2016, in Cleveland, OH, and presented by the Cleveland Clinic Foundation Center for Continuing Education. For information about upcoming activities from the Cleveland Clinic Foundation Center for Continuing Education, please visit www.clevelandclinicmeded.com. The Audio Digest Foundation thanks the speakers and the Cleveland Clinic Foundation Center for Continuing Education for their cooperation in the production of this program.
The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.
IM640902
This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.
To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.
Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.
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