PATHOPHYSIOLOGY OF ERYTHROBLASTOSIS FETALIS AS A RESULT OF Rhesus Factor (Rh)-ISOIMMUNIZATION MADE RIDICULOUSLY RIDICULOUS (with bits of explanations)

by Ralph R. delos Santos Bachelor of Science in Nursing Pamantasan ng Lungsod ng Maynila

Gravida 1 (First Pregnancy)

Rh(+) Fetus Rh(-) Pregnant Mother forms antiRh antibody as a result of exposure to Rh(+) Fetal Blood (may be due to Fetal-Maternal Transfusion) Rh(-) Pregnant Mother Tissue Hypoxia Hypoxemia Decreased Oxygenation

Motor Dysfunction Shift to Anaerobic Metabolism Deposition of Heme in the Basal Ganglia Lactic Acidosis

ERYTHROBLASTOSIS FETALIS a.k.a Hemolytic Anemia of the Newborn

KERNICTERUS Formation of antiRh antibody in the mothers serum Anti-Rh antibody may be IgG (the smallest antibody) THIS CAN CROSS THE PLACENTA AND MAY ENTER THE FETAL CIRCULATION! Anti-Rh antibody may be IgM (the largest antibody) and this cant cross the placenta (will not be transferred from mother to fetus) unless there is fetal-maternal transfusion

FOR THE NEXT PREGNANCY, AGAIN WITH Rh(+) FETUS Anti-Rh antibody, formed by the mother, enters the fetal circulation and binds with Rh antigens on the surface of fetal erythrocytes Jaundice

Antigen-Antibody reaction causes erythrocyte destruction a.k.a Hemolysis

Hemolysis causes the release of Hemoglobin metabolite such as Heme

Hyperbilirubinemia or too much bilirubin in the blood

Excess Heme will be metabolized further into Bilirubin