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    • #1032
      D_Juggz
      Participant

      i’ll prolly muddle this question up, but its something that i’ve come across tonight with no specific answer.

      If a pregnant woman is Rh-negative and she gets exposed to her baby’s Rh-positive blood – she develops antibodies against it, with the next child if the same thing happens her body will attack her child’s right?

      My question is will the same thing happen if the mother is Rh-positive and the baby is Rh-negative?

      (a friend told me no, because only an Rh negative person can develop antibodies, becoming sensitised to Rh-positive, while Rh-positive people can’t produce antibodies against Rh-Neg,because there are no receptors for it)

      is this right, or is it possible that the fetus’s blood attacks the mother’s causing inflammation of the placenta or something?

      thanks
      D_J πŸ˜•

    • #23366
      MrMistery
      Participant

      You need to understand that by “contact” we only mean a small amount of blood, not 2 liters πŸ˜€ πŸ˜€ If the mother is negative and the baby is positive, than all that is needed is one viable red blood cell to produce the specific response. If the situation is reversed, in the case of a contact it may kill a few red blood cells, but nothing alarming will happen

    • #23383
      D_Juggz
      Participant

      yeah i figure that, but i was just wondering if the reaction is able to occur the other way around aswell…
      i was just thinking even if there was a small rupture in the placenta, causing the baby’s blood to attack the mother’s that would stimulate an immune response from the mother would it not?

    • #23415
      Poison
      Participant
      quote :

      was just thinking even if there was a small rupture in the placenta, causing the baby’s blood to attack the mother’s that would stimulate an immune response from the mother would it not?

      The blood of the baby and the blood of the mother NEVER mixes. What do you mean by saying a small rupture?

    • #23436
      MrMistery
      Participant

      Ok, so what you need to understand is that the blood of the baby and that of the mothernever mix. It happens(though rarely) that they mix at childbirth. If what you are saying were to happen(but it doesn’t) the result would be death of the baby, the mother would be fine

    • #23441
      Poison
      Participant

      If the blood mixes, the mother’s body threats the baby like its a foreign organ.

    • #23659
      victor
      Participant

      What I think is the matter of how many blood inside the baby. The diferences between mother’s and the baby’s blood in quantity maybe one of the factor that nothing happened when Rh+ mother have an Rh- baby

    • #23669
      Poison
      Participant

      Maybe. But also think that, as I said before, the baby is like an organ of the mother. So the body prefers to kill the organ rather than killing the organism.

    • #23816
      victor
      Participant

      But, now I get a little doubt bout my statement above..I started to think that cells can reproduce in fast time…so soon or later they will be many also (not as man as mothers but I think it’s enough to create problems inside the mother’s womb)

    • #23836
      Poison
      Participant

      It causes problems. If the baby dies inside the mother, she can even die.

    • #23840
      MrMistery
      Participant

      Yes but not necessarily. Many babies are born dead

    • #23842
      Poison
      Participant

      It is necessary. I’m not talking about dead born babies. Those babies die inside the mother, couldn’t be recognized and poison the mother’s blood.

    • #23964
      victor
      Participant

      So, the conclusion is the same then…if the mother and the baby have different Rh (whoever has Rh+ or Rh-) will cause death..is it like that?

    • #23989
      Poison
      Participant

      No, Erytroblastosis fetalis only occurs if the mother is Rh- and the child id Rh+. We were talking about another situation there.

    • #24178
      victor
      Participant

      Oh, maybe it will happen in some occasion.. πŸ˜‰ wow, if like that, this is serious problem…I should not marry western girl then, because it’s said that 85% of women in western area (america) are Rh- and I have Rh+ πŸ˜†

    • #24207
      Poison
      Participant

      Preventing it is easy. A vaccine is used after the birth of the first baby. Don’t worry. Feel free to marry. πŸ˜‰

    • #24267
      b_d_41501
      Participant

      Doesn’t the mother treat the child as a foreign object and send antibodies against it?

    • #24358
      Poison
      Participant

      It is the situation for the second baby if the vaccine (as much as I know it is something that prevents antibody production.) is not used after the birth of the first baby. The first child is not under danger.

    • #24369
      b_d_41501
      Participant

      Ok, cool

    • #24458
      2810712
      Participant

      Probably as IgMs are produced first , which cannot cross human placent [ i don’t know what happens about the other animals and how the babies are saved , does anybody know ???] So, even if the mothers body treates the baby as forign , it cannot make it die…
      But please clear this one- why does ababy die when mother is Rh-ve and baby +ve???
      Does the aglgutination formed in/near placenta / umbilical cord block nutient supply???
      Please help… πŸ˜₯

      What is the effect of this phenomenon on natural selection [ today natural selection would not occur,as there are medicine to help, but if it were to happen then…] ???

      hruusheekeish

    • #24491
      Poison
      Participant
      quote :

      i don’t know what happens about the other animals and how the babies are saved , does anybody know

      Note that all the animal’s blood systems are not the same.

      quote :

      So, even if the mothers body treates the baby as forign , it cannot make it die…

      If it is the second baby, the mother can make the baby die. This is a the common result. But sometimes babies can born but there are some diseases at those babies.

      At the first baby, there are no antibodies against Rh+, while birth, blood of the baby and the mother mixes and there are some antibodies produced, And those antibodies make the second baby die or born with some abnormalities. IgG can pass through placenta. Actually erythroblastosis fetalis can also be defined as the lysis of fetal RBCs by maternal IgGs .

    • #25973
      2810712
      Participant

      [ I THINK ].But the mixing ammounts of maternal and baby’s blood are not enogh to make baby die even if all the fetal RBCs in that mixed blood blast . So, are you shure that these ammounts are large enough to make baby die…
      Please help…

      😳

      hruusheekeish

    • #25977
      MrMistery
      Participant

      Ok, here is exactly what happens if the mother is Rh- and the baby Rh+:
      1st baby: No problem, the baby is healthy. But at birth the blood of the mother is mixed with that of the baby. It really does not matter how much blood is mixed, ONE red blood cell is enough to enter the mother’s circulatory sistem for her body to produce anti-Rh anitbodies.
      2nd baby: If it is Rh+, than the antibodies created by the mother after she gave birth to the first baby will pass through the placenta and cause lysis…
      Hope it is clear

    • #26007
      victor
      Participant

      It sure is… πŸ˜‰ um, how about the 3rd? 4th? 5th?…….. πŸ˜† πŸ˜†

    • #26052
      MrMistery
      Participant

      Same as the second

    • #26069
      2810712
      Participant

      Please, try to understand my q.
      πŸ™„ See, the antibodies are present in the maternal blood and very less maternal blood mixes with the fetal blood . So, less feto- RBCs would be killed due to direct mixing of blood.
      But i wonder if the antibodies may get flushed into the fetal blood-vessels near placenta due to pressure. If the pressure and offcourse the concentration of these Abs in maternal blood is large enough to have enough Abs flushed into fetal blood then fetus may die due to erythroblastosis. But all this is my hypothesis, is it correct??? πŸ˜•
      Have u got my pt…
      πŸ˜₯

      Please help…

      hruusheekeish

    • #26128
      MrMistery
      Participant

      Man, blood does not mix, but some things, like nutrients and antibodies do cross the placenta

    • #26216
      victor
      Participant

      And the bold one mentioned above is the main problem whicg cause ErythroFeta.

    • #26233
      2810712
      Participant

      So, enough no. of Abs get flushed into fetal blood due to pressure through the placental blood vessels and they lead to the erythroblastosis. But , one pt. is that the fetus must not be in a developemental stage to raise immunoresponse agaist the maternal Abs … otherwise less erythroblastosis will occur . Right???

      hrushikesh

    • #26236
      MrMistery
      Participant

      If you remember your anatomy 101, the immune sistem of the baby is not developed even at birth. The baby takes antibodies from the mother’s milk via pinocytosis vesicles

    • #26255
      Poison
      Participant
      quote victor:

      And the bold one mentioned above is the main problem whicg cause ErythroFeta.

      Some antibodies can pass. Not all.

    • #26286
      victor
      Participant

      What do you mean ‘some’? what kind of anti that can’t pass? the one that has huge molecule structure?

    • #26325
      Poison
      Participant

      Huge molecule structures cannot pass. IMMSMR, IgG is the only one that can pass form mother to fetus by placenta.

    • #26359
      victor
      Participant

      Ow….placenta also have its limitation.. πŸ˜† hey, you try to use ‘IMMSMR’ also…that’s good… πŸ˜†

    • #26391
      Poison
      Participant

      I liked IMMSMR. πŸ˜‰

    • #26411
      victor
      Participant

      Hey how about this..huge molecules can transport through endocytosis can’t they??do placenta do endocytosis?..anyway..next time if anyone doubt, just IMMSMR… πŸ˜†

    • #26450
      Poison
      Participant

      I don’t think it can.

    • #26547
      victor
      Participant

      Hey Ozge, I’ve checked my book and I found it…yes, it’s true that only IgG can pass through placenta. The others (IgA, IgM, IgD, IgE) can’t pass. But IgM can be formed as the primary immune response.
      IgA is the main immunoglobulin from secrets such as saliva, milk, etc…it protects the mukosa from bacterias and viruses.
      IgE act as the fast response allergic because it’s contained in basophyll
      IgD act as the certain antigen response…majority contained in B limphocyte.

    • #26579
      chemistry_freako
      Participant

      hmms…why is it that only IgG can pass through?

    • #26589
      Poison
      Participant

      small molecular weight.

    • #26673
      victor
      Participant

      I think its MW (molecular weight) is 400.000 AMQ (atom mass quantity)

    • #26697
      Poison
      Participant

      It says that:
      IgA :160,000* (Looks small too but it aggregates with higher molecular weights)
      IgM: 900,000*
      IgG: 150,000*
      IgE: 200,000*
      IgD: 185,000*

      *: Daltons approximately

    • #26786
      victor
      Participant

      IgA gets in together with milk from their mom..so, no need placenta then.. πŸ˜†

    • #26795
      Poison
      Participant

      Yeah. But I haven’t seen a mother suckling a fetus. πŸ˜†

    • #26797
      victor
      Participant

      Maybe after this diagram:
      Embryo – fetus – [born] – baby

      That’s when they get the IgA.. πŸ˜†

    • #26802
      Poison
      Participant

      Good diagram. πŸ˜‰

    • #26994
      2810712
      Participant

      What is the mechanism for IgG to get into the fetus?
      Probably it is forced into the blood of fetus though the fenistrations in the maternal capillaries , so the size , shape and molecular wt. all matter.

      M I RIGHT???

      hrushikesh

    • #26997
      victor
      Participant

      Or maybe they can be carried out through endocytocys and exocytocys….

    • #27017
      Dr.Stein
      Participant
      quote 2810712:

      What is the mechanism for IgG to get into the fetus?
      Probably it is forced into the blood of fetus though the fenistrations in the maternal capillaries , so the size , shape and molecular wt. all matter.

      M I RIGHT???

      hrushikesh

      From a bleeding during the delivery. So far it was stated that IgG come into fetus via maternal-fetal circulatory system and it was not true.

    • #27050
      MrMistery
      Participant

      From what i know IgG do come into the fetus via the circulatory sistem… That is the reason why the child dies in the first part of pregnancy. If what you say were true, the child would live.
      It is true that blood cells do get inside the body of the mother at the first baby via bleeding during delivery

    • #27104
      victor
      Participant

      Hey, I’ve read that beside IgG that comes to the fetus, There’s also IgM which can be activated if there’s any antigen infection.

    • #27129
      Dr.Stein
      Participant
      quote MrMistery:

      From what i know IgG do come into the fetus via the circulatory sistem… That is the reason why the child dies in the first part of pregnancy. If what you say were true, the child would live.
      It is true that blood cells do get inside the body of the mother at the first baby via bleeding during delivery

      In erythroblastosis foetalis, the first baby is usually safe and live, because first, the contact with IgG will be happened just right when it has just been delivered. Second, the level of that IgG is just in a little number. In the second and subsequent pregnancy the level will increase and yes it will pass through placenta.

      victor: IgM is the ‘ancient’ immunoglubulin family. All that fetus has is IgM. In the development, further exposure to antigens, it will switch into IgG, IgE, or IgA depends on the purpose. IgM also appears in acute disease, after few hours or days it will switch into, mostly IgG. The clinical examination of IgM and IgG can be used to determine whether the patient is still in acute phase or chronic phase of her/his disease, respectively.

    • #27195
      victor
      Participant

      Hmm…it’s just like IgM is the master of all Igs…(maybe because of it’s pentamer valency 10 structure)

    • #27223
      Dr.Stein
      Participant

      It is NOT a master, it is just an initial, an ancient type. IgM cannot do anything if it doesn’t switched into proper IgG, IgE, or IgA. Those three types are more professional on their own purpose.

    • #27224
      iri_black
      Participant
      quote victor:

      IgE act as the fast response allergic because it’s contained in basophyll
      .

      Related to the IgE activity, why some people are more sensitive to alergens than other? Does this have to do whith the quantity or the activity of basophylls.
      Some allergies can be kept under control with certain vaccins. Does anyone know if theis vaccins contain IgE?

    • #27232
      Dr.Stein
      Participant

      I am not sure IgE is contained in basophil. Immunoglobulins are produced by B cells… πŸ˜‰

    • #27273
      iri_black
      Participant

      Ok, sorry about that πŸ™ .
      But can you answer my question? Why some people are more sensitive to allergens?

    • #27293
      victor
      Participant
      quote Dr.Stein:

      I am not sure IgE is contained in basophil. Immunoglobulins are produced by B cells… πŸ˜‰

      Maybe produced by B-cells but complexed with basophils membrane.
      Oh, yes, IgM also can be switched into IgD….so, that’s why immature B-cells contain many IgM….because they’re still not a professionals yet.. πŸ˜†

    • #27366
      Dr.Stein
      Participant

      Naah, IgD never exists alone, and it’s not a switched version from IgM, IgD always present with IgM, because there is no switching point from IgM to IgD.

      This is a simple schematic of the switching points:

      —IgM—IgD—*—IgG—*—IgA—*—IgE—

      * = switching point

      IgM/D -/-> IgD
      IgM/D —> IgG
      IgM/D —> IgA
      IgM/D —> IgE

    • #27367
      Dr.Stein
      Participant

      victor: IgE is produced by plasma cell and being attached to cells which have a receptor for it, called FCεRI, such as mast cells, basophils, eosinophils πŸ˜‰

      quote iri_black:

      Ok, sorry about that πŸ™ .
      But can you answer my question? Why some people are more sensitive to allergens?

      Allergens actually are harmless antigens (innocuous), e.g. pollens, clothes, chitin, etc, but to certain people, they become harmful and even deadly things. Allergic reactions occur when an individual produces IgE in response to such innocuous antigen(s), and subsequently encounters the same allergen(s). Their ‘sensitive’ IgE, which mainly attach on mast cells membrane surfaces, recognize those antigens and then stimulate mast cells activation and degranulation.

    • #27405
      iri_black
      Participant

      And thus the release of some mediators of inflammation, including histamine.
      And anti-histaminic drogs are the only drugs that can help….in a way πŸ™

    • #27417
      Dr.Stein
      Participant

      Do you realize that the topic of this thread is changed now? πŸ˜†

    • #27418
      iri_black
      Participant

      Yes, I do. I just got caried away I guess…. 😳 πŸ™‚

    • #27420
      Dr.Stein
      Participant

      I think I contribute on this changing too πŸ˜†

    • #27448
      b_d_41501
      Participant

      I’ll change it back then. lol. Who coined the term “Erythroblastosis Fetalis”?

    • #27485
      chemistry_freako
      Participant

      lol – sudden change back to the right track again lol

    • #27508
      Dr.Stein
      Participant
      quote b_d_41501:

      I’ll change it back then. lol. Who coined the term “Erythroblastosis Fetalis”?

      …As recently as 1946, erythroblastosis fetalis, or hemolytic disease of the newborn, affected between 0.5% and 1.0% of fetuses and newborns in the USA. It had a 50% mortality as well as significant neurologic morbidity in many survivors. Prior to 1936, four seemingly distinct neonatal syndromes had been identified: fetal hydrops; fetal erythroblastosis with massive red-cell proliferation in fetal organs; icterus gravis familiaris, a severe neonatal jaundice that often affected subsequent infants; and severe anemia in surviving infants who had not had edema or striking jaundice, which was simply called anemia of the newborn. Based on histological and hematological similarities and the familial occurrence, Diamond, Blackfan, and Baty put forth their unifying hypothesis that these four syndromes were all manifestations of an unknown single underlying disease process. They designated all of these neonatal syndromes β€œerythroblastosis fetalis”

      For complete article, click HERE πŸ˜‰

    • #27518
      b_d_41501
      Participant

      Good job, Who was the first person to be diagnosed with it?

    • #27554
      Dr.Stein
      Participant

      Is it a homework? πŸ™„ πŸ˜†

    • #27571
      victor
      Participant

      Don’t say homework b_d_ or it will become a business part??? πŸ˜†

    • #27608
      MrMistery
      Participant

      I don’t think you can be diagnosed with rytroblastosic foetails, because that means you died at birth πŸ˜†

    • #27617
      b_d_41501
      Participant

      lol. just made something up.

    • #82512
      ainda
      Participant

      The mother CAN NOT be Rh + and the baby Rh -, simply because the Rh neg allel is recessive! πŸ˜›

    • #82516
      MrMistery
      Participant

      is the mother is Dd(Rh+) and the father is both Dd(Rh+) then 1/4 of children will be dd(Rh-). Do a punner square πŸ˜‰

    • #82529
      genovese
      Participant

      Even if an RhΒ° baby developed antibodies to his Rh+ mother at the time of birth there would not be enough time to produce a clinical effect in the mother. This would be the same with subsequent pregnancies, so the Rh+ mother would never develop an Rh incompatibility problem.

      The RhΒ° babies will have been sensitized to Rh+ blood and might have a stronger reaction to it if transfused with it.

    • #82595
      Darby
      Participant

      The antibody response is to the rh markers. If you are rh-negative, those markers are "foreign," so once exposed you produce antibodies to them. If you are rh-positive, exposure to rh-negative blood doesn’t give you something to make antibodies to.

      I have to disagree about blood mixing, though. The tearing free of the placenta mixes exposes the mother to the fetus’ blood pretty reliably. There are also many instances of what would otherwise be minor exposures during pregnancy, as well as cases of maternal rejection of rh-positive fetuses in a first pregnancy.

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