Rh-positive Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Rh-positive and links to relevant pages within the course.
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|Treatment for ITP|
Treatment guidelines recommend that patients receive treatment if they have any of the following: Significant bleeding risk <20 x 109/L platelets and moderate bleeding <10 x 10 9/L platelets with no bleeding symptomsCorticosteroids are effective treatments for 50 - 80% of individuals with either acute or chronic ITP. Even with a reduction or discontinuation of corticosteroid treatment, remission can be maintained.Anti-D immunoglobulin, administered intravenously, may be an effective treatment for Rh-positive children or adults diagnosed with acute or chronic ITP. Anti-D immunoglobulin forms red blood cell complexes that block the destruction of platelets. This treatment cannot be used for patients who are Rh-negative or who have undergone a splenectomy. When a patient is refractory to the above treatments, other treatment possibilities include thrombopoietic drugs to stimulate the megakaryoblast or Rituximab, a treatment that targets CD 20-positive B-cells.Splenectomy may be a last resort treatment for chronic ITP sufferers if their platelet counts are below 30 x 109/ L or if symptoms warrant it. In ITP, antibodies develop that coat the platelets. The spleen produces macrophages whose Fc receptors recognize and destroy these antibody-coated platelets. Removing the spleen would decrease platelet destruction, but it is a last resort since the immunologic function of the spleen would also be lost.
|Which of the following set of conditions would preclude HDN as a result of Rh incompatibility:||View Page|
|The incidence of HDFN due to anti-D varies significantly according to race and ethnicity.||View Page|
|Factors That Affect Production of Anti-D|
Exposure to D+ red cells: Anti-D is red cell immune. The usual route of exposure to the D antigen is during pregnancy. Fetal bleeds into the mother occur more commonly at delivery but some may occur antenatally due to small lesions in the placenta or due to placenta previa, amniocentesis, abdominal trauma, abortion, ectopic pregnancy, etc. Transfusion is a relatively rare route of exposure since Rh-negative individuals normally receive only Rh-negative donor red cells. However, Rh-negative transfusion recipients may be exposed to small volumes of D-positive red cells in Rh-positive platelet concentrates. Also, there are rare reports of fresh frozen plasma, not normally matched for Rh(D), causing anti-D production.Volume of fetal bleed: In general, the larger the fetal bleed, the more likely the mother is to produce anti-D. Approximately 1 pregnancy in 400 result in a fetomaternal hemorrhage (FMH) of 30 mL or greater. ABO incompatibility between mother and fetus: If fetal red cells are ABO incompatible with the mother, maternal anti-A or anti-B will rapidly remove fetal cells from the circulation before anti-D can be produced. This protection decreases the chance of anti-D being produced but does not eliminate it entirely.
|The appropriate dosage of Rh immune globulin (RhIg) to administer post-delivery to an Rh-negative mother delivering an Rh-positive child is calculated based on the estimated volume of fetal bleed.What is the value of x in the formula given below that is used to calculate RhIg dosage?Number of vials of 300 µg RhIg = volume of fetal bleed/x mLEnter the number in the box below that is represented by x in the formula; do not spell out the number.(e.g., use "5" and not "five").||View Page|
These are the results of the crossmatch that was being performed in the transfusion service laboratory while the patient was receiving the two units of O Rh-negative RBCs. Cells Gel IAT* Donor I** 2+ Donor 2** 2+ Donor 3 3+ Donor 4 3+ Donor 5 2+ Donor 6 3+ * IAT = indirect antiglobulin test ** O Rh-negative RBC (Donors 3 - 6 are O Rh-positive)
|Antigen phenotyping results|
The patient's pretransfusion red cells and all donor red cells involved in the case (two group O Rh-negative RBC and four group O Rh-positive red cells initially crossmatched) were phenotyped for Jka.As expected, the patient typed as Jk(a-). The six donor RBC that were incompatible in the initial crossmatch were Jk(a+).The frequency of the Jka gene in Caucasians is ~77%, with most Caucasian red cells (50%) typing as Jk(a+b+).