09 Extrinsic Hemolysis
AIHA
antibodies coat RBC. RBC removed in spleen
RBC protect themselves from complement activation: no intravascular hemolysis
Warm
Pathogenesis and Symptoms
classic symptoms of anemia
splenomegaly: macrophages hypertrophy to consume RBCs
Diagnosis
smaller, spherical, lack central pallor
macrophage can't engulf whole RBC, just takes a bite off of it: shrink in size, more dense
also inherited disease
first see if normocytic anemia, then if RC is increased (increased production), then DAT
anti IgG antibodies bind to IgG on RBC and cause them to agglutinate
not used for AIHA
take patient serum and add sample RBC. Positive if antibodies in patient serum to RBC
used for new born hemolytic disease with mother serum against D+ RBC
Causes
all these diseases involve immune system
RBC bind antibody in absence of drug: surface of RBC altered
also cephalosporin
Treatment
severe: splenectomy
Cold
symptoms of anemia plus symptoms in extremities
large antibodies, cause RBC to agglutinate, especially in extremities
IgM fix complement, leaves bound C3 on RBC
DAT positive not for IgG but only for C3
C3 doesn't get in the way of macrophages like IgG: engulf whole
intravascular hemolysis result of complement activation
instead of add IgG, add anti-C3
IgG cold association with syphilis
MAHA
intravascular hemolysis
schistocytes: arrow, look like fragments
Mechanical
very high BP causes endothelial damage
thrombus shear RBC
narrow openings, stiff tissues
Infections
either intravascular RBC rupture or removal by spleen
sickle: Higher risk of severe disease in sickle cell disease
hole in robin's shirt: Higher risk of severe disease in asplenia
cracked blood stained windows: Hemolytic anemia
yellow babe: Jaundice
Sweating robin: fever
torn robin shirt: Irregularly cycling fevers
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