Erythroblastosis Fetalis (Hemolytic Disease of Newborn)

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Erythroblastosis Fetalis (Hemolytic Disease of Newborn) by Mind Map: Erythroblastosis Fetalis (Hemolytic Disease of Newborn)

1. Mother's anti Rh agglutinins remain in baby's circulation for another 1-2 days after birth.

2. Effect of anti D antibody

2.1. Inhibits the production of antigen-induced B lymphocyte antibodies in expectant mother

2.2. These antibodies also attach to D antigen receptor sites on Rh+ve fetal Rbcs

2.2.1. That may cross the placenta

2.2.2. enter into circulation of expectant mother

2.2.3. interfere with mother's immune response to D antigen

3. Mother Rh -ve Father Rh+ve Baby Rh+ve(inherited Rh+ve antigen from father)

4. Disease of fetus and newborn child, Agglutination and phagocytosis of fetus's Rbcs

5. Incidence of disease

5.1. Ist Rh+ve baby =No harm 3% of 2nd Rh+ve baby= some signs of EF 10% of 3rd Rh+ve baby= exhibit disease Incidence rises with subsequent pregnancies

6. Effect of mother's antibodies on fetus

6.1. Mother's anti-Rh antibodies diffuse slowly thorugh placental memb. into fetus's blood.

6.2. Cause agglutination of 's Rbcs

6.3. Agglutinated rbc hemolyze

6.4. Hb released into blood

6.5. Fetus's macrophages convert Hb into Bilirubin

6.6. Baby's skin turned yellow.

6.7. Jaundiced Baby

6.8. New Topic

6.8.1. Mother's antibodies may also attack other cells of body as well

7. Clinical picture of EF

7.1. Destruction of more n more Rbcs

7.2. Baby becomes anemic

7.3. Hepatospleenomegaly occurs

7.3.1. Liver and spleen enlarged

7.3.2. produce rbcs in the same manner as they produced in the middle(2nd) trimester of gestation

7.4. Hematopoeitic tissues of fetus attempt to replace hemolyzed rbcs

8. Why called so?

8.1. Attempt of rapid production of rbcs

8.2. Early forms of rbcs(mainly nucleated blast forms) pass from baby's bone marrow into its ciculatory system

8.3. Presence of these nucleated blast forms in blood is the reason of the name of this disease.

9. Cause of baby's death in EF

9.1. Main cause=Severe Anemia

9.2. Secondary cause= Kernictrus(In case if that baby survived anemia which is a very rare case)

9.2.1. Precipitation of bilirubin in neuronal cells of brain

9.2.2. destruction of many neuronal cells

9.2.3. Baby gets permanent mental impairment/damage

9.2.4. This is kernictrus

10. Treatment

10.1. Replacement of neonate's Rh+ve blood with Rh-ve blood

10.2. About 400mL of Rh-ve blood infused(1.5 or more hours required to do so) while neonate's own Rh+ve blood is being removed

10.3. That process repeated several times during first few weeks of neonate's life

10.3.1. To keep bilirubin level low

10.3.2. To prevent kernictrus

10.4. by that time, Transfused Rh-ve cells are replaced by infant's own Rh+ve cells

10.4.1. 6 or more weeks required to do so

10.4.2. Cuz by that time, mother's agglutinins had been destroyed

11. Prevention of EF

11.1. Development of Rh immunoglobulin globin/anti D antibody

11.2. in 1970s

11.2.1. Anti D antibody administered to expectant mother at 28-30 weeks of gestation

11.2.2. reduction in incidence of EF occured

11.2.3. It is also administered to Rh-ve mother delivering Rh+ve babies

11.2.3.1. New Topic

11.2.3.1.1. Prevent sensitization of mothers to D antigens

11.2.4. This step reduces the risk of development of large amounts of D antibodies during 2nd pregnancy

12. Primary culprit of EF

12.1. D antigen

12.2. D antigen causes sensitization/immunization of Rh-ve mother to Rh+ve fetus

13. Baby's main diseases in EF

13.1. Anemia

13.2. Jaundice

13.3. Kernictrus

13.4. Hepatospleenomegaly