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Predisposing Age; Gender; Family history; Genetic Idiopathic autoimmune Precipitating Medication; Medical

Immune incompatibility between the mother and the fetus or blood transfusion Induced immune destruction of RBC by therapeutic drugs

Loss recognition if RBC antigen

Molecular mimicry

Polyclonal Tand B-cell activation

Binding of antibodies to RBC surface antigen

Warm antibody immunohemolytic anemia

Cold agglutinin immunohemolytic anemia

Cold hemolysin haemolytic anemia

IgG bind to erythrocyte at 37C

IgM binds to erythrocyte at 31C

IgM antibodies activate compliment

Phagucytosis of IgG coated cells

IgM binding agglutinate RBCs and rapidly attaches compliment under surface
Immune Complex B

Binds to RBC surface

Hapten Model

Autoantibody Model

Binding to cell surface

Binding to cell surface


Binding to cell surface

Drug combines with RBC membrane Induced antibody formation of IgG against the cell bounddrug

Induced IgM production Activation of RBC

Induce production of antibodies of antibodies Antibodies are directed to the RBC antigens

A, B

Rapid clearance / lysis of RBC s/sx: fever, chills, dyspnea, hypotension.

Phagocytosis for compliment and a portion of 40 antibody

Spherocyte formation in the spleen RBC sequestration in the spleen, removing them from the circulation Decreased hemoglobin levels Descreased oxygen carrying capacity of the blood If treated

s/sx: hypoxia, decreased tissue perfusion, increased RR, rapid heartbeat

If not treated Prednisone, dexamethasone, azathioprine, cyclophosphamide, danazol,cyclosporine,intravenous gamma globulin, leflunomide (primarily goal is to prevent formation of RBC antibodies.), O2 therapy, BT. Good prognosis

Rapid destruction of RBC

Release of erythropoietin

Increased bilirubin formation exceeding the rate of hepatic clearance Build up of bilirubin in the blood.

Production of RBC in the bone marrow


Defective uptake by the liver cells.



Defective conjugation

Biliary stricture Hypoxia



s/sx: RR, cold clammy skin, cyanosis, hypotension.

Icterus Hemolytic jaundice


NARRATIVE Autoimmune haemolytic anemia is an acquired disorder caused by extravascular hemolysis and is most often associated with autoimmune mechanisms, although in some instances they are mediated by drugs. There are three mechanisms of this

anemia including loss of recognition of RBC antigens, molecular mimicry, and polyclonical T- and B-cell activation causing binding of antibodies to RBC surface antigen. There are three ways of antibody response. First is the warm antibody immunohemolytic anemia in which the immunoglobulin G (IgG); the mediating antibody specific for erythrocyte antigens and has a maximum binding capacity to the surface of erythrocyte at body temperature (37C). IgG-coated RBCs bind to Fc receptors on monocytes and splenic macrophages. Attempted phagocytosis of the IgG-coated cells results in partial loss of the cell membrane causing erythrocytes to undergo spheroidal transformation. The second response is the cold agglutinin immunohemolytic anemia which is mediated by the IgM and occurs less often than warm antibody hemolysis. Cold antibodies have a RBC binding capacity that occurs at colder temperatures (lower than 31C). Autoantibody appears acutely during recovery of certain infectious disorders, including infectious monocleosis and mycoplasma pneumonia. With this condition, the anemia is self limiting and rarely produces hemolysis. IgM binding agglutinates RBCs and rapidly attaches complement on their surface. IgM is rapidly released when the blood recirculates and warms, usually before complement-mediated hemolysis can occur. However, the temporary interaction with IgM allows the deposition of C3b on the RBC surface which results in rapid phagocytosis by mononuclear phagocytes in the liver and spleen. Drug also causes induced haemolytic anemia and is classified as warm antibody type according to three mechanism: the hapten model, immune complex, and autoantibody model. The hapten model proposes that drugs combine with zrbc membrane to induce antibody formation (IgG) that is directed against the cell-bound drug. RBC destruction mostly extravascular as noted in warm antibody formation immunohemolytic anemia. The immune complex induces IgM antibody production which binds to the RBC membrane and activates complement causing hemolysis. The autoantibody model initiates production of antibodiesthat become directed against intrinsic RBC antigens particularly Rh blood groupantigens.

The third response is the cold hemolysin hemolytic anemia which involves the IgG autoantibodies and is associated with paroxysmal cold hemoglobinuria. This anemia involves acute, intermittent hemolysis and often hemoglobinuria after exposure to cold temperatures. The compliment intravascular lysis occurs when the cells begins to warm because the enzymes are more efficient at warmer temperatures. The IgM antibodies activate complement resulting in a rapid intravascular hemolsyis. Extravascular hemolysis occurs when the antibody/ complement phagocytes the RBC membrane induces damage, but not destruction, of the RBC. This damaged RBC (spherocyte) is highly susceptible to further interactions with the reticuloendothelial systems phagocytic cell in spleen, liver, or bone marrow. The spleens unique filtering system allows for prolonged contact between synthesized RBCs and complement, which efficiently removes the damaged RBC from circulation. Hemolysis leads to a decrease oxygen capacity carrying of the blood resulting to a deficiency in the amount of oxygen reaching body tissues primarily the liver. If the rate of RBC destruction is rapid, the rate of bilirubin formation may exceed the rate of hepatic clearance: the liver becomes overwhelmed which leads to a build up of bilirubin in the blood resulting in visible icterus or hemolytic anemia. Decreased oxygen levels also signals the kidneys to produce erythropoietin, an enzyme responsible for activating bone marrow to produce more RBC as a compensate. However, phagocytic mechanism again will bind to RBC surface causing destruction. Further decreased in oxygenation leads to hypoxemia and progresses to shock then death.