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Autoimmune Hemolytic Anemia (AIHA) MNEMONICS

AIHA

Caused by autoantibodies that react with RBCs at temperatures ≥ 37° C (warm agglutinin disease) or < 37° C  (cold agglutinin disease)

Extravascular hemolysis: occurs in the spleen (this is why you don’t see fragmented RBC in the smear)

Coombs (+)

Warm Agglutinin Disease:

Causes Mnemonic

L ymphoma

S ystemic Lupus erythematosus (SLE)

C LL

D rugs: penicillin, phenytoin, rifampin, alpha-methyldopa.

Tx

Best initial tx: Prednisone

Severe, Acute hemolysis & no response to Prednisone: IVIG

Recurrent episodes: splenectomy

No control of hemolysis after splenectomy: Rituximab, Azathioprine, Cyclophosphamide or Cyclosporine.

Cold Agglutinin Disease:

Causes Mnemonic: MEW

Numbness or mottling of colder parts of the body: nose, ears, toes, fingers

Tx

Warm up

Rituximab

Sometimes plasmapheresis

Stop Ab production: Cyclophosphamide, Cyclosporine

Steroids, splenectomy DO NOT WORK here

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Anti-Platelet Drugs

ASA / Aspirin : inhibits the synthesis of thromboxane A2 ( thromboxane A2 is an arachidonate product that causes platelets to change shape, release their granules, and aggregate) by irreversible acetylation of the enzyme cyclooxygenase

Clopidogrel & Ticlopidine : reduce platelet aggregation by inhibiting the ADP pathway of platelets. These drugs are thienopyridine derivatives that achieve their antiplatelet effects by irreversibly blocking the ADP receptor on platelets.

Abciximab, Eptifibatide & Tirofiban : target the platelet IIb/IIIa receptor complex. The IIb/IIIa complex functions as a receptor mainly for fibrinogen and vitronectin but also for fibronectin and von Willebrand factor. Activation of this receptor complex is the “final common pathway” for platelet aggregation.

Dipyridamole : vasodilator that inhibits platelet function by inhibiting adenosine uptake and cyclic GMP phosphodiesterase activity.

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