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Placenta Information and Courses from MediaLab, Inc.

These are the MediaLab courses that cover Placenta and links to relevant pages within the course.

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Advances in Noninvasive Prenatal Testing For Down Syndrome and other Trisomies
Diagnostic Tests

Diagnostic tests for Down syndrome (Trisomy 21) are considered invasive testing procedures. Note: The American College of Obstetricians and Gynecologists (ACOG) recommends that pregnant women of all ages have the option of bypassing the screening test and choosing instead to have a diagnostic test for Down syndrome.Diagnostic tests may be offered for several reasons, including:Will be age 35 or older at deliveryAbnormal results obtained on screening tests or ultrasoundPrior child or pregnancy with a birth defect Diagnostic tests, which use a sample of fetal cells, include one or both of the following procedures:Chorionic villus sampling (CVS): CVS is usually done between 10 and 12 weeks of pregnancy. It is considered an invasive procedure since the procedure involves the collection of chorionic villus cell samples from the placenta, either via a needle insertion into the abdominal wall or a catheter in the vagina. Samples are analyzed for fetal chromosome abnormalities.Amniocentesis: Amniocentesis is performed between gestational weeks 16 and 20 and is also classified as an invasive procedure. A thin needle is placed into the abdominal wall and a sample of the amniotic fluid is collected. The sample is analyzed for fetal chromosome abnormalities. Both CVS and amniocentesis are highly accurate for diagnosing Down syndrome and/or ruling out the condition. However, because they are invasive procedures, there are risks, including miscarriage, preterm labor, infection, or injury to the fetus or mother.

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Screening Tests, continued: Maternal Serum Screening

Maternal serum screening tests may be performed during the first and second trimester of pregnancy. These serum tests involve the measurement of specific biomarkers in the maternal blood. These five biomarkers are typically used to assess the risk for Down syndrome: Maternal Serum Alpha-fetoprotein (MS-AFP) AFP is a fetal protein that is initially produced in the fetal yolk sac and liver; by the end of the first trimester of pregnancy, most if not all of the AFP is produced by the fetal liver. The concentration of AFP peaks in fetal serum at 10-13 weeks gestation. The fetal AFP normally diffuses across the placental barrier and into the maternal circulation so that MS-AFP rises throughout pregnancy to about 250 ng/mL at 32 weeks gestation. Lower MS-AFP values may be associated with increased risk for trisomy 21 (Down syndrome) or trisomy 18 (Edwards syndrome).Unconjugated estriol (uE3-estriol) Estriol is a female sex hormone that increases during pregnancy. It is produced by the placenta and passes into the maternal bloodstream during pregnancy. Its roles during pregnancy may be linked to the proper functioning of the uterus, softening of the cervix, and assistance in the lactation process. A biologically active form of estriol called uE3-estriol increases in the maternal circulation during pregnancy by the seventh to ninth weeks of gestation and continues to increase throughout pregnancy. uE3-estriol levels in maternal serum is typically decreased in the Down syndrome pregnancy. Human chorionic gonadotropin, total or free beta subunit (beta-hCG) HCG is a glycoprotein hormone produced by the placenta during pregnancy. It is present in blood and urine around 7-13 days following fertilization of the ovum. HCG has two subunit chains, alpha and beta. The beta subunit confers its specificity. A specific smaller part of the hormone, called free beta hCG may be used as a screening test during the first trimester of pregnancy. An increase in maternal serum free beta hCG (ie, greater concentration than in other pregnancies) may indicate an increased risk for Down syndrome. Total beta-hCG is tested as part of a triple or quad screen during the second trimester of pregnancy. An increase in total beta hCG in the maternal serum is also associated with increased risk of Down syndrome.Dimeric inhibin A (DIA) Inhibins are a family of glycoproteins mainly secreted by the ovaries and testicles. The beta subunits of the inhibins exist in two forms, the A and B forms. DIA is secreted by the ovaries and is designed to inhibit the production of the hormone FSH by the pituitary gland. The level of DIA is increased in the blood of mothers of fetuses with Down syndromePregnancy Associated Plasma Protein A (PAPP-A) PAPP-A is produced by the covering of the newly fertilized egg. It is thought to be involved in local proliferative processes such as wound healing and bone remodeling. Unexplained low levels of PAPP-A in the maternal serum during pregnancy may indicate increased chance for intrauterine growth restrictions, premature delivery, preeclampsia, and stillbirth. In the first trimester, low levels of this protein are seen in Down syndrome pregnancies.In the first trimester, serum screening is typically done in combination with an ultrasound to screen for nuchal translucency. Serum screening in the first trimester usually involves the measurement of two biomarkers in the maternal serum, free beta-hCG and PAPP-A. Combining the results of these two biomarkers with an ultrasound improves the screening process. In the second trimester during weeks 16-18, maternal serum assays for 3-4 levels of biomarkers are typically performed. The screening for these biomarkers has been established as a triple or quadruple (quad) screen, since the benefit of the screening lies in the combined use of the three to four biomarkers. The biomarkers used in the screening process may include MS-AFP, uE3-estriol, total beta HCG, and DIA. Increased serum levels of MS-hCG and DIA combined with decreased levels of UE3-estriol and MS-AFP suggests an increased risk of Down syndrome. Maternal age, family history, weight, race, and diabetic status are also used to determine a numeric risk for Down syndrome. It is important to understand that for women who have positive triple or quad screening results, only a very small number of them have babies who actually have a chromosomal abnormality.

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Antinuclear Antibody Testing: Methods and Pattern Interpretation
History of ANA Testing

Slide-based ANA testing using a cell substrate started in the 1950s and continues to be the gold standard method. In the early days of ANA testing, rodent tissue (stomach, liver and/or kidney) was commonly used as the substrate. Rodent tissue however had several drawbacks such as small cell size, a lack of dividing cells (mitotics) and poor antigen expression that made interpretation of ANA patterns difficult. In the 1980s, cultured cell lines were examined for utility as an ANA substrate and the human epithelial- like cell line HEp-2 gained popularity. HEp-2's advantages over rodent tissue are: A large nucleus Better antigen expression Abundant mitotic cells that assist in interpretation of the ANA pattern (if grown properly).More recently a cell line called HEp-2000® has become popular for ANA detection. HEp-2000® is a HEp-2 cell line that has been transfected with the cDNA for overexpression of the SSA/Ro antigen. This results in a substrate with all of the original advantages of HEp-2 plus an added advantage of increased sensitivity for detection of antibodies directed to the SSA/Ro antigen and the ability to identify these clinically significant antibodies during the screening process.(Ref4)It has also been demonstrated that antibodies to SSA/Ro develop early in the disease process.(Ref5) Perhaps most importantly, if a woman has anti-SSA/Ro antibodies and becomes pregnant there is a risk of the antibodies crossing the placenta, resulting in the fetus developing neonatal lupus and congenital heart block in utero.The advantage of using these transfected cells is documented in the current Clinical and Laboratory Standards Institute (CLSI) guidelines for ANA testing. Here they note the "dramatically increased" sensitivity of transfected cells for the detection of SS-A/Ro and the unaltered effect of transfection on other ANA patterns.(Ref6)

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Authentic and Spurious Causes of Thrombocytopenia
Thrombocytopenia in Neonates

Transplacental ITP may occur in newborn infants who are born to mothers with ITP. If the mother has had one baby born with thrombocytopenia, it is usually an indication that all subsequent infants will also be born with thrombocytopenia. A very small percentage of babies born with ITP will have severe thrombocytopenia. Neonatal alloimmune thrombocytopenia (NAIT) is caused by platelet destruction that is the result of alloantibodies stimulated by foreign antigens during pregnancy or blood transfusions. Platelet destruction by alloantibodies may occur in neonates if the mother lacks the platelet-specific antigen but the baby has inherited the antigen from its father. When maternal IgG antiplatelet antibodies cross the placenta, immune destruction of the neonate's platelets occurs. The major concern with both of these conditions is intracranial bleeding if the neonate's platelet count is less than 50 X 109/L. NAIT has a high mortality rate due to bleeding into the central nervous system. Prompt diagnosis of the condition and treatment is critical. The thrombocytopenia lasts on average 3 - 4 weeks postnatal until the maternal antibodies have cleared the newborn's system.

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Disseminated Intravascular Coagulation (DIC)

DIC is a condition that is usually secondary to an underlying disease or condition. Some of the activators of DIC are sepsis, placenta abruptio, snake bites, toxin, trauma, graft vs. host disease, and burns.The mechanisms that are involved in DIC include a hyperactivated coagulation system, a hyperactivated fibrinolytic system, or both simultaneously. In most cases the coagulation factors are consumed as soon as they are made and platelets are also consumed in the coagulation process. Clots are made rapidly and then rapidly destroyed as the fibrinolytic system is hyperactivated.

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Basic Tissue Orientation and Paraffin Embedding Technique
Placenta

Placental specimens submitted to histology may include:Membrane roll: Place on edge perpendicularly to the block face to show membrane layers.Placental disc sections: Embed these flat and centrally located in the block face.Umbilical cord segments: Embed these as other tubes, on end to show the lumen (vessel) openings in cross-section.

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Case Studies in Clinical Microbiology
Review 3

Rouquette C. Berche P. The pathogenesis of infection by Listeria monocytogenes Microbiologia. 12:245-58, 1996 Listeria monocytogenes is a Gram-positive bacterium responsible for severe infections in human and a large variety of animal species. It is a facultative intracellular pathogen which invades macrophages and most tissue cells of infected hosts where it can proliferate. The molecular basis of this intracellular parasitism has been to a large extent elucidated. The virulence factors, including internalin, listeriolysin O, phospholipases and a bacterial surface protein, ActA, are encoded by chromosomal genes organized in operons. Following internalisation into host cells, the bacteria escape from the phagosomal compartment and enter the cytoplasm. They then spread from cell to cell by a process involving actin polymerisation. In infected hosts, the bacteria cross the intestinal wall at Peyer's patches to invade the mesenteric lymph nodes and the blood. The main target organ is the liver, where the bacteria multiply inside hepatocytes. Early recruitment of polymorphonuclear cells lead to hepatocyte lysis, and thereby bacterial release This causes prolonged septicaemia, particularly in immunocompromised hosts, thus exposing the placenta and brain to infection. The prognosis of listeriosis depends on the severity of meningoencephalitis, due to the elective location of foci of infection in the brain stem (rhombencephalitis). Despite bactericidal antibiotic therapy, the overall mortality is still high (25 to 30%).

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Chemistry / Urinalysis Question Bank - Review Mode (no CE)
Serum alkaline phosphatase activity is derived from all of the following organs except:View Page
Estriol levels in conjunction with hCG and AFP can be obtained during pregnancy to:View Page
All of the following are sources of serum alkaline phosphatase except:View Page
Match the tissues on the left with the corresponding LDH isoenzyme peak on the right.View Page

Hemolytic Disease of the Fetus and Newborn
ABO HDFN - Etiology and Symptoms

ABO HDFN is the most common type of HDFN, in that anti-A is the antibody most often found bound to the red cells of a newborn. While the disease is usually so mild as to not require treatment, severe HDFN is possible. EtiologyABO HDFN is caused by maternal IgG anti-A or anti-B, which can be produced as a result of prior pregnancy or prior inoculation (some common inoculations contain A or B substances). In Caucasians, most often the mother is group O and the child is group A, although other combinations are possible. Group O people tend to produce IgG ABO antibodies more commonly than other blood groups.Just as in other types of HDFN, maternal IgG antibody crosses the placenta and destroys fetal red cells.SymptomsTypical symptoms of ABO HDFN include mild anemia and especially jaundice appearing in the first 24 hours. In rare severe cases the infant can have the more severe symptoms of Rh HDFN, except that prenatal death is unlikely. Rationales to explain the mild nature of ABO HDFN include Fewer A and B antigens on fetal cells Poorly developed fetal A and B antigens Presence of A and B antigens on cells and tissues other than red cells

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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.

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Use in Pregnancy

As applied to pregnancy, RhIg's purpose is to prevent immunization to the D antigen in the perinatal period and thus prevent HDFN due to anti-D. If the mother has already produced anti-D, RhIg is of no use in moderating the immune response.Accordingly, RhIg is routinely administered to Rh negative women not previously sensitized to the D antigen under the following circumstances:1, Antenatal. Antepartum prophylaxis of 300 µg (1500 IU) at about 28 weeks gestation in the USA and Canada, which could be weeks later, depending on how appointments are scheduled. To illustrate variation in antenatal international practice, in the UK, smaller doses of RhIg (e.g., 500 IU) may be given at 28 weeks and 34 weeks, although many UK facilities issue a 1500 IU dose at 28–30 weeks. With antenatal administration, the Rh of the fetus is usually unknown. Some transfusion services recommend a further antenatal dose if the infant is undelivered after 40 weeks.2. Postnatal. Prophylaxis of 300 µg (1500 IU) at delivery of an Rh positive or weak D infant within 72 hours of delivery whenever possible. If RhIg administration is delayed beyond 72 hours, laboratory policies differ as to when it would no longer be administered. The longer the delay, the more likely RhIg may fail to suppress production of anti-D, but it is still worth trying. Note: Because RhIg contains IgG anti-D, when given antenatally, it can cross the placenta and sensitize fetal D-positive red cells. Occasionally the fetus may be born with a weakly positive DAT, but significant hemolysis does not occur. For this reason some guidelines recommend that labs do NOT routinely perform DATs on infants whose mothers have received antenatal RhIg.

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Related Uses

RhIg is also indicated in these special circumstances: Antepartum fetal maternal hemorrhage (FMH), suspected or proven as a result of placenta previa, amniocentesis, chorionic villus sampling, cordocentesis, other obstetrical manipulative procedures (e.g., external version or abdominal trauma such as may occur in a car accident or fall); Therapeutic abortion; Vaginal bleeding during pregnancy; Loss, or threatened loss, of fetus at any gestational stage; Ectopic pregnancy. For these non-routine indications, depending on the level of medical care the pregnant woman receives or the awareness level of the risks involved, there is increased potential for RhIg to be administered inappropriately or not at all.

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When given during pregnancy, RhIg may cross the placenta and sensitize fetal D-positive RBCs.View Page

Introduction to the ABO Blood Group System
Immunoglobulin

The predominant immunoglobulin class for the B antibodies produced by individuals with group A phenotype and the A antibodies produced by individuals with group B phenotype is IgM. Small quantities of IgG and IgA may also be present.The ABO antibodies found in the serum of group O individuals include anti-A and anti-B. An antibody designated anti-A,B is also present. Anti-A,B in group O individuals tends to be predominantly IgG, although IgM and IgA components are also present.Infants of group O mothers are at higher risk for hemolytic disease of the fetus and newborn (HDFN) than those born to mothers with group A or B because IgG immunoglobulins readily cross the placenta. IgM molecules do not cross the placenta because of their larger size. However, the HDFN that results is usually mild and often subclinical. Infants generally survive with little or no intervention.It is important to note that immune antibodies are usually IgG. Both naturally occurring and immune ABO antibodies are critically important in transfusion since both sensitize, and usually hemolyze, red cells with the corresponding antigen.

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Parasitology Question Bank - Review Mode (no CE)
Contact with infected cat feces is responsible for the transmission of:View Page
Which parasite listed here is capable of crossing the placenta and causing serious harm to fetus?View Page

Rh negative female with anti-D at delivery: A case study
Use in Pregnancy

As applied to pregnancy, RhIg's purpose is to prevent immunization to the D antigen in the perinatal period and thus prevent HDFN due to anti-D. If the mother has already produced anti-D, RhIg is of no use.Accordingly, RhIg is routinely administered to Rh negative women* not previously sensitized to the D antigen under the following circumstances:1, Antenatal. Antepartum prophylaxis of 300 µg (1500 IU) at about 28 weeks gestation in the USA and Canada, which could be weeks later, depending on how physician appointments are scheduled. To illustrate variation in antenatal international practice, in the UK smaller doses of RhIg (e.g., 500 IU) may be given at 28 weeks and 34 weeks, although many UK facilities issue a 1500 IU dose at 28–30 weeks. With antenatal administration, the Rh of the fetus is usually unknown. Some transfusion services recommend a further antenatal dose if the infant is undelivered after 40 weeks.2. Postnatal. Prophylaxis of 300 µg (1500 IU) at delivery of an Rh positive or weak D infant, preferably within 72 hours of delivery but can be given up to 28 days later if administration is delayed. If RhIg administration is delayed beyond 72 hours, laboratory policies differ as to when it would no longer be administered.* Policies related to women who are weak D (formerly Du) are discussed later.Note: Because RhIg contains IgG anti-D, when given antenatally, it can cross the placenta and sensitize fetal D-positive red cells. Occasionally the fetus may be born with a weakly positive DAT, but significant hemolysis does not occur.

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Related Uses

RhIg is also indicated in these special circumstances: Antepartum fetal maternal hemorrhage (FMH), suspected or proven as a result of placenta previa, amniocentesis, chorionic villus sampling, cordocentesis, other obstetrical manipulative procedures (e.g., external version or abdominal trauma such as may occur in a car accident or fall); Therapeutic abortion; Vaginal bleeding during pregnancy; Loss or threatened loss of fetus at any gestational stage; Ectopic pregnancy. For these non-routine indications, depending on the level of medical care the pregnant woman receives or the awareness level of the risks involved, there is increased potential for RhIg to be administered inappropriately or not at all.

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When given during pregnancy, RhIg may cross the placenta and cause a positive DAT in the newborn.View Page


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