Hemeonc - Acquired Anemia

Front 1

T/F Absence of anemia rules out hemolytic disorder

Back 1

F - BM can compensate

Front 2

Dx Sx and Haptoglobin levels of intravasc hemolysis

Back 2

o Dx – verified by hemoglobinemia, hemoglobinuria, hemosiderinuria
o Sx – include constitutional symptoms, tachycardia, back ache, Sx related to renal failure
o Haptoglobin – decreased

Front 3

Dx Sx and Haptoglobin levels of extravasc hemolysis

Back 3

RBCs lysed outside of vessels (often spleen):
o Sx – jaundice, splenomegaly (RBCs lysed in spleen)
o Haptoglobin – typically normal, or slightly decreased

Front 4

role of Plasma haptoglobin

Back 4

binds hemoglobin if it is free in plasma, decreased haptoglobin when bound

Front 5

• Direct Antiglobulin Test (DAT)/Coomb’s Test

Back 5

detects presence of IgG or C3 bound to RBC
o Autoimmune hemolytic anemia – hallmark is the positive Coomb’s test
o Process – wash patient’s RBCs free of plasma, add antiglobulin reagent, centrifuge, look for agglutination

Front 6

• Indirect Antiglobulin Test/Indirect Coomb’s

Back 6

detects autoimmune hemolytic anemia as well…
o Process – incubate patient’s serum with normal blood, look for reaction (x-fusion compatibility)

Front 7

• Autoimmune hemolytic anemia (AIHA) definition?

Back 7

antibody/complement binds to RBC membrane antigens => shortened RBC lifespan

Front 8

Why do you get spherocytes in warm-Ab AIHA?

Back 8

when IgG binds RBC membrane à thru spleen & engulfed by macrophages
o Spherocyte – results when part of cell membrane removed by macrophage in spleen
o Result – spherocytes eventually cleared by extravascular mechs in spleen

Front 9

etiology of warm-ab AIHA

Back 9

can be 1o idiopathic, or 2o to lymphoproliferative dz, CT dz (SLE), immune deficiency, Rx
o Immune deficiencies – including AIDS, and common variable immunodeficiency
o Drugs – classically alpha-methyldopa

Front 10

Tx of warmAb AIHA

Back 10

No therapy for well-compensated hemolytic process.

Corticosteroids – mainstay of Tx!!! Interferes w/ the synth/fxn of Fc-receptor on macros that bind/destroy Ab-coated RBCs

o RBC transfusion – only for severe refractory life-threatening cases, risk of hemolytic reaction
o Splenectomy – also for refractory, when corticosteroids fail
o IVIg – may increase RBC survival by saturating Fc receptors on macrophages, can’t deal w/ RBC
o Immunosuppressive therapy – including danazol, vinca alkaloids, rituximab (against CD20 – kill B lymphocytes)

o Folic Acid – give for all patients, to ensure RBC production