Scenario 6
A child asks his prents why his blood type is different from his parent.Father’s and mother’s blood types are A and B respectively, while her blood type is O.
Step 1 : Clarifying unfamiliar terms
1.respectively
2.blood type
3.blood type is A
Answer :
1.Belonging to each other
2.specific characteristic of someone’s blood
3.eritrosit contain aglutinogen A and anti B in plasm
Step 2 : Pribloem definition
1.Blood type is determined by ?
2.What’s the function we must know know our blood type ?
3.Beside O, can the child get another Blood type?
4.Why the children’s blood type difference with her parents ?
5.What’s the effect if the children have difference blood type?
6.How the shape’s process of agglutinin and aglutinogen ?
7.What’s the factors that influence blood type ?
8.What’s the test can determined the blood type?
9.is it normal if the children have Blood type that’s different with the parent?
10.What’s the factors that influence the making process of agglutinin and aglutinogen ?
11.What’s the contain of agluinin and aglutinigen ?
Step 3 : Brainstorming
1.Based on agglutinin and aglutinogen
2.-preparing blood tranfussion
-prevent blood’s coagulation
-safe pregnancy
3.Yes
4.-Because the parents have different genotip
-the genotip is heterozygote
-blood junction
5.-The child will be surprised
-The child can’t take blood tranfussion from her parents
6.Aglutinogen create agglutinin
7.herediter
8.Take the selulin in our blood
9.Normal
10. Antigen can enter to our body by food, bacteria, etc.
11.Aglutinogen : contain stranger molecul and gamma globulin
Step 4 : Analyzing the problem
1.*Kaltzeiner classified blood type based on aglutiogen and agglutinin :
-A =aglutinogen A and aglutinin anti A
-B=aglutinogen B and aglutinin anti B
-O=no aglutinogen and agglutinin anti A and B
-AB=aglutinogen A and B and no agglutinin
*Aglutinin and aglutinogen is shape in 2-8 month in postnatal
*We can check the Rh type
Problem : Mom’s blood type is B, Dad’s blood type is AB, why thechild is O?
Answer: -maybe the child is not their”real child”
-the child get the aglutinogen and agglutinin from another factors like food,bacteria
-There is DNA’s obstruction (on the 9 chromosome)
2.-For the safety recipient, we don’t give the wrong blood type if we check it first
-Related to rhesus for the safety pregnancy
3.Blood junction :
Dad : IA IO
Mom : IB IO , so the result of junction is : IA IB (AB), IA IO(A),IB IO(B),IO IO(O), and the children can get O blood type.
4.(Clear)
5.(Clear)
6.It’s related to the function of aglutinogen and agglutinin, aglutinogen is for create aglutinin and both of it is for determinedthe blood type
7.(Clear)
8.-Take the blood and mix with selulin A or B
-DNA test
-Based on “D” factor
-Aglutinogen in eritrosit, ex. M,N,S
-System of protein serum
-System enzyme in eritrosit
-Antigen in leucosit
-Rhesus test, by mixig the blood with “something substance” and if there is a coagulation, so the blood type is Rh(+)
9.The parent’s have heterozygote’s genotype (Look at nmber 3 on blood junction)
10.The another factor can influence the aglutinogen
11.-Aglutinin contain protein molecul that have paretop
-Agltinogen contain stranger molecul that have the specific reaction from leucosyte
-Aglutinogen A cotain enzyme glycosiltranferase with the specific contained is glutiasetil glukosamin in glikoprotein chain
-Aglutinogen B contain enzim galaktosa and same in glikoprotein
-Gamma globulin produced by bound marrow and limp
Step 5 :Formulating Learning Issues
1.The specific making process of aglutinogen and agglutinin
2.The scheme of blood junction
3.Blood test and Rh test
4.Blood type and rhesus(ABO+MNS)
5.Factor that influence the difference of blood type
6.Disease of blood type
Step 6 :Self study
Step 7 :Reporting
Agglutination
Sometimes when the blood of two people is mixed together, it clumps or forms visible islands in the liquid plasma--the red cells become attached to one another.
When different types of blood are mixed within the body, the reaction can be a bursting of the red cells as well as agglutination. Different types of blood are recognized on the molecular level and sometimes rejected by being destroyed and ultimately filtered out by the kidneys in order to expel them from the body along with urine. In the case of a transfusion mistake, there can be so much of the wrong type of blood in the system that it can result in kidney failure and death. This is due to the fact that when the kidneys try to filter the blood, they essentially become clogged as they are overwhelmed and cease being effective filters. Additionally, there is a rapid depletion of blood clotting factors which causes bleeding from every body orifice. In the United States, about 1 in 12,000 units of whole blood transfused is given to the wrong person. Depending on the blood types of the donor and the recipient, this can result in death or no problems at all.
The compositional difference between blood types is in the specific kinds of antigens found on the surface of the red cells. Antigens are relatively large protein molecules that provide the biological signature of an individual's blood type.
Within blood, there are substances called antibodies which distinguish particular antigens from others, causing bursting or agglutination of the red cells when alien antigens are found. The antibodies bind to the antigens. In the case of agglutination, the antibodies "glue" together the antigens from different red cells thereby sticking the red cells together (as shown below on the right).
As agglutination proceeds, millions of red cells are glued together into clumps. This is not the same thing as clotting. When agglutination occurs, the blood mostly remains liquid. With clotting, however, it does not.
The specific types of antigens on our red blood cells determine our blood types. There are 29 known human blood systems, or groups, for which each of us can be typed. As a result, there is one or more antigens for each of these blood groups. Since many of these blood systems also are found in apes and monkeys, it is likely that they evolved prior to the time that we became a separate species.
Rh Blood Types
Rh blood types were discovered in 1940 by Karl Landsteiner and Alexander Wiener. This was 40 years after Landsteiner had discovered the ABO blood groups. Over the last half century, we have learned far more about the processes responsible for Rh types. This blood group may be the most complex genetically of all blood type systems since it involves 45 different antigens on the surface of red cells that are controlled by 2 closely linked genes on chromosome 1.
The Rh system was named after rhesus monkeys, since they were initially used in the research to make the antiserum for typing blood samples. If the antiserum agglutinates your red cells, you are Rh+ . If it doesn't, you are Rh- . Despite its actual genetic complexity, the inheritance of this trait usually can be predicted by a simple conceptual model in which there are two alleles, D and d. Individuals who are homozygous dominant (DD) or heterozygous (Dd) are Rh+. Those who are homozygous recessive (dd) are Rh- (i.e., they do not have the key Rh antigens).
Clinically, the Rh factor, like ABO factors, can lead to serious medical complications. The greatest problem with the Rh group is not so much incompatibilities following transfusions (though they can occur) as those between a mother and her developing fetus. Mother-fetus incompatibility occurs when the mother is Rh- (dd) and her fetus is Rh+ (DD or Dd). Maternal antibodies can cross the placenta and destroy fetal red blood cells. The risk increases with each pregnancy. Europeans are the most likely to have this problem--13% of their newborn babies are at risk. Actually only about ½ of these babies (6% of all European births) have complications. With preventive treatment, this number can be cut down even further. Less than 1% of those treated have trouble. However, Rh blood type incompatibility is still the leading cause of potentially fatal blood related problems of the newborn. In the United States, 1 out of 1000 babies are born with this condition.
Rh type mother-fetus incompatibility occurs only when an Rh+ man fathers a child with an Rh- mother. Since an Rh+ father can have either a DD or Dd genotype, there are 2 mating combinations possible with differing risks as shown below. Regardless of the father's genotype, if he is Rh+ and the mother is Rh-, doctors assume that there will be an incompatibility problem and act accordingly.
Keep in mind that only the Rh+ children (Dd) are likely to have medical complications. When both the mother and her fetus are Rh- (dd), the birth will be normal.
The first time an Rh- woman becomes pregnant, there usually are not incompatibility difficulties for her Rh+ fetus. However, the second and subsequent births are likely to have life-threatening problems for Rh+ fetuses. The risk increases with each birth. In order to understand why first born are normally safe and later children are not, it is necessary to understand some of the placenta's functions. It is an organ that connects the fetus to the wall of the uterus via an umbilical cord. Nutrients and the mother's antibodies regularly transfer across the placental boundary into the fetus, but her red blood cells usually do not (except in the case of an accidental rupture). Normally, anti-Rh+ antibodies do not exist in the first-time mother unless she has previously come in contact with Rh+ blood. Therefore, her antibodies are not likely to agglutinate the red blood cells of her Rh+ fetus. Placental ruptures do occur normally at birth so that some fetal blood gets into the mother's system, stimulating the development of antibodies to Rh+ blood antigens. As little as one drop of fetal blood stimulates the production of large amounts of antibodies. When the next pregnancy occurs, a transfer of antibodies from the mother's system once again takes place across the placental boundary into the fetus. The anti-Rh+ antibodies that she now produces react with the fetal blood, causing many of its red cells to burst or agglutinate. As a result, the newborn baby may have a life-threatening anemia because of a lack of oxygen in the blood. The baby also usually is jaundiced, fevered, quite swollen, and has an enlarged liver and spleen. This condition is called erythroblastosis fetalis . The standard treatment in severe cases is immediate massive transfusions of Rh- blood into the baby with the simultaneous draining of the existing blood to flush out Rh+ antibodies from the mother. This is usually done immediately following birth, but it can be done to a fetus prior to birth. Later, the Rh- blood will be replaced naturally as the baby gradually produces its own Rh+ blood. Any residual anti-Rh+ antibodies from the mother will leave gradually as well because the baby does not produce them.
Erythroblastosis fetalis can be prevented for women at high risk (i.e., Rh- women with Rh+ mates or mates whose blood type is unknown) by administering a serum (Rho-GAM ) containing anti-Rh+ antibodies into the mother around the 28th week of pregnancy and again within 72 hours after the delivery of an Rh+ baby. This must be done for the first and all subsequent pregnancies. The injected antibodies quickly agglutinate any fetal red cells as they enter the mother's blood, thereby preventing her from forming her own antibodies. The serum provides only a passive form of immunization and will shortly leave her blood stream. Therefore, she does not produce any long-lasting antibodies. This treatment can be 99% effective in preventing erythroblastosis fetalis. Rho-GAM is also routinely given to Rh- women after a miscarriage, an ectopic pregnancy, or an induced abortion. Without the use of Rho-GAM, an Rh- woman is likely to produce larger amounts of Rh+ antibodies every time she becomes pregnant with an Rh+ baby because she is liable to come in contact with more Rh+ blood. Therefore, the risk of life-threatening erythroblastosis fetalis increases with each subsequent pregnancy.
Anti-Rh+ antibodies may be produced in an individual with Rh- blood as a result of receiving a mismatched blood transfusion. When this occurs, there is likely to be production of the antibodies throughout life. Once again, Rho-GAM can prevent this from happening.
Mother-fetus incompatibility problems can result with the ABO system also. However, they are very rare--less than .1% of births are affected and usually the symptoms are not as severe. It most commonly occurs when the mother is type O and her fetus is A, B, or AB. The symptoms in newborn babies are usually jaundice, mild anemia, and elevated bilirubin levels. These problems in a baby are usually treated successfully without blood transfusions.
ABO system
The ABO system is the most important blood-group system in human-blood transfusion. The associated anti-A and anti-B antibodies are usually Immunoglobulin M, abbreviated IgM, antibodies. ABO IgM antibodies are produced in the first years of life by sensitization to environmental substances such as food, bacteria, and viruses. The O in ABO is often called 0 (zero, or null) in other languages.
History of Blood Transfusions
Long before the phenomenon of blood antigen-antibody interaction was discovered, surgeons experimented with human transfusions in an attempt to save the lives of patients who were dying from severe blood loss and the resulting shock. The first attempt may have been an English physician during the mid-17th century who infused a wounded soldier with sheep blood. Not surprisingly, the soldier suffered a painful death. The first successful transfusion of human blood to another human was done by a British doctor in 1818 in order to save the life of a woman who was hemorrhaging following childbirth. By the mid 19th century, European and American doctors used transfusions in a last ditch attempt to save soldiers and other patients with horrendous wounds. They usually transferred blood directly from a healthy individual to their patient via a rubber tube with hypodermic needles at each end. This occasionally resulted in success but more often than not killed the recipient. The results seemed to be random. Doctors in the 19th century also experimented with a variety of blood substitutes, including milk, water, and even oils.
It was the discovery of the ABO blood types in 1900 that finally led us to understand how to consistently use transfusions to save lives. Even with this knowledge, however, life threatening reactions still occur in about 1 out of 80,000 transfusions in developed nations. The ABO blood group and its central role in transfusion failures is described in the next section of this tutorial.
Blood Tests
Reticulocyte Count
Blood cells are formed in the bone marrow. Reticulocytes are the young RBCs that are not yet mature, but have been released by the bone marrow to enter into your bloodstream. Daniel Ryan, M.D., professor of pathology and laboratory medicine at the University of Rochester Medical Center explains in "Williams Hematology," that the reticulocyte count is used to help determine if RBCs are being destroyed and whether bone marrow is functioning properly.
PT and PTT
PT stands for prothrombin time and PTT is the partial thromboplastin time. According to Diana Nicoll, M.D., Ph.D., associate dean of the University of California, both of these blood tests evaluate whether or not you can create blood clots within the normal amount of time.
ABO Typing
Ravindra Sarode, M.D., director of transfusion medicine and hemostasis laboratory at the University of Texas Southwestern Medical Center writes in "The Merck Manual for Healthcare Professionals," that ABO typing is the blood test that determines what type of blood you have. This is crucial in the event that you need a blood transfusion. If you receive the wrong blood type, your immune system will destroy the transfused blood. This can be a life-threatening condition.
Rh Typing
Rh typing identifies whether or not you have the Rh(D) antigen on your RBCs. Sarode explains that if you do not have this antigen (substance) on your RBCs, you are called Rh negative which means that, in cases where transfusion is needed, you will always need Rh-negative blood. If you have the Rh(D) antigen, you are Rh positive and can be transfused with Rh negative or Rh positive blood. This blood test also identifies the Rh type of a fetus and mother.
REFERENCES
- E.A. Letsky; I. Leck, J.M. Bowman (2000). "Chapter 12: Rhesus and other haemolytic diseases". Antenatal & neonatal screening (Second ed.). Oxford University Press.
- Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1.
- Blood Transfusion Division, United States Army Medical Research Laboratory (1971). Selected contributions to the literature of blood groups and immunology. 1971 v. 4
- Hardison, R. (1999). "The Evolution of Hemoglobin: Studies of a very ancient protein suggest that changes in gene regulation are an important part of the evolutionary story". American Scientist 87 (2): 126.
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