Question

1. Identify all anatomical structures related to and/or that are being affected based on the patient case information. (i.e. tissues, organs, vessels, brain components, membranes)
2. Explain how the anatomical structures and their physiological function/dysfunction are interrelated normally and what is going wrong with the structures in this current patient case information.
3. Identify and explain possible a diagnosis and what can be done to fix or reverse the current situation described in the patient case information. Please be specific and detailed.

Patient Case (Initial Review):

Donna is a 35 year old female who is married and has a 5 year old daughter. Donna recently found out she was pregnant, but last week at 12 weeks she started to spot and went to see the doctor. At the doctors, Donna found out she was having a miscarriage and the doctors decided to look at her blood type and seemed very alarmed and asked her who her doctor was for her first child. Her blood type was A-.

Answer 1

This this is classic case of haemolytic disease of newborn (HDN) specifically erythroblastosis Fetalis.

It is it is used to be a major cause of fetal loss and death among newborn babies.

During pregnancy e some of mother's antibodies are transported across the present and enter the fetal circulation. This is necessary because by the time of birth newborns have only primitive immune system, and the continuing presence of maternal antibodies helps ensure that they survive the immune system matures. Downside to this protection is that by targeting foetal RBC maternal antibodies can also cause HDN. Major cause of HDL and is incompatibility of the RH blood group between the mother and the foetus.

Pregnancy is at risk of SDN are those in which an RH negative mother become pregnant within rhd positive children. The Mother's immune response to the fetal D antigen is to form antibodies against it. These antibodies are usually of the of the IgG type, the type that is transported across the Placenta and hence delivered to the fetal circulation. HDN can also be caused by an incompatibility of Ab blood group. Arises when a mother with blood type O becomes pregnant with the foetus with different blood type.

But in all cases the the incompatibility is RH factor the Mother's blood group is A negative.

Sensitization occurs during the first pregnancy.

Sensitization to an antigen occurs when the immune system Encounters and antigen for the first time and Mount an immune response. In the case of HDN caused by RH incompatibility, and RH negative mother made first encounter the antigen while being pregnant with an Rh D positive child or by receiving a blood transfusion or Rh D positive blood. Once a mother has been sensitized to the D antigen, her Serum will contain anti D. The direct coombs test confirms the presence of Anti D and hence that the mother has been sensitized.

Only small fetal blood need enter the Mother's circulation for sensitisation to occur. Typically this occurs during the delivery of the first born Rh D positive children. Foetal membrane hemorrhage is commonly during labour and is increased during a prolonged for complicated labour which in turn increases the risk of sensitization. Sensitization can also occur earlier in the pregnancy, example during A prenatal forbleeding miscarriage. It may also occur during medical procedures termination of pregnancy or chronic villus sampling. The risk of sensitization to the Rh D antigen is decreased if the foetus is abo incompatible this is because any fetal cells that leak into the maternal circulation are rapidly destroyed by the court and maternal and or ndb reducing the likelihood of maternal exposure to the D antigen.

HDN occurs in subsequent pregnancies

Initially the maternal anti D that is formed at the time of sensitisation is of the IgM type, which cannot cross the placenta. In subsequent pregnancies, repeat encounter with the Rh D antigen stimulates the Rapid production of type Ig G anti D, which can be transported across the placenta and enter the fetal circulation. Once in the fetal circulation, Anti D attaches to the Rh D antigens found on the fetal RBC making them to be destroyed.

The rate of haemolysis determines whether the nature of HDN is mild, moderate,or severe. In mild cases, the small increase in the rate of haemolysis is tolerated by the foetus. At birth and during the newborn period symptoms include mild anaemia and jaundice both of which are resolved without treatment.

Cases where there is Greater increase in the rate of haemolysis, the level of bilirubin May still remain low during the pregnancy because of the ability of the plasenta to remove Billirubin from the fetal circulation. However, after birth the neonat's immature liver is unable to metabolize the increased amount of Billirubin that instead accumulates in his or her blood. Within 24 hours of birth the level of bilirubin May rise dramatically. If levels continue to rise in May and the brain to cause kernicterus a potentially fatal condition that leaves permanent neurological damage in the babies that survive.

Anyone greater Rapid and prolonged destruction of RBC Leads to severe anaemia in the foetus. The liver, spleen, and other organs increase the production of RBC is to compensate for their loss. The drive to produce RBC is causes the liver and spleen to increase in size (hepatosplenomegaly), and liver dysfunction can occur. Immature RBCs( erythroblasts) spill into circulation, giving house to the alternative name of this disease erythroblastosis Fetalis. Complication of severe HDN is hydrops Fetalis in which the fetal tissue becomes Swollen. This condition is usually fatale in utero or soon after birth.

The coombs test Rh incompatibility between mother and foetus.

Direct coombs test helps in diagnosis of HDN.

Direct coombs test Detect maternal anti D antibodies that have already band fetal RBCs.

Indirect coombs test helps in prevention of HDN.

The indirect coombs test find antibody D antibody in the Mother's serum. If these two come into contract with fetal RBCs would hemolyzed them and hence cause HDN. But finding maternal and TB before fetal RBC have been attacked, treatment can be given to prevent or limit seviarity of HDN.

Treatment treatment of HDN of the newborn.

Once HDN is diagnosed treatment may be needed.

Intrauterine blood transfusion of RBC into the baby circulation:-

This is done by placing a needle through the Mother's uterus and into the abdominal cavity of the foetus or directly into the vein in the umbilical cord. It may be necessary to give a sedative medication to keep the baby from moving. Intrauterine transfusions may need to be repeated.

Early delivery of the foetus develops complication:-

If the foetus has mature lungs, labour and delivery may be induced to prevent worsening of HDN.

Prevention of HDN

Fortunately HDN is very preventable disease. Because of the advance in prenatal care, nearly all women with RH negative blood are identified in early pregnancy by blood testing. If mother is RH negative and has not been sensitized, she is usually given ajwain called RH immunoglobulin, also known as RhoGAM. This is specifically developed blood product that can prevent and RH negative mothers antibodies from being able to react to RH positive cells. Many Womens are are given that drug around 28th week of pregnancy. After the baby is born, women should receive a second dose of the drug within 72 hours, if baby is RH positive. If your baby is RH negative she does not need another dose.

The womens antibody should be suppressed and the appropriate drug for suppression of the immune system should be given to two women while she is pregnant to prevent II pregnancy from HDN.