LECTURE 4: General Embryology IV (NYUCD)

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Maternal componentderived from the uterine endometriumFunction of the Placentao Protection o Nutrition o Respiration o Excretion o Hormone productionAs the fetus grow there is a(n):increase in nutrients demand to provide to growing organs > demand is meet by an increase in surface area between maternal and fetal components. Via development of: CHORIONIC VILIVilli are formingaround ENTIRE REGION OF CHORIONChorionic Viliincrease surface area (SA) between maternal + fetal component = facilitates exchange of nutrients/wasteFORMATION OF THE VILLUS- Embryo is anchored into the endometrium of the mother - The trophoblast = multinucleated tissue with no membrane to separatePRIMARY VILLUScytotrophblast & synchtrophoblastSECONDARY VILLUSwhen the extrembryonic mesoderm invaginates between the syncytophoplast > mesoderm coreTERTIARY VILLUSo Blood vessel form o Lacunae are forming (vacuoles) in which the mothers blood is dumping > remember blood vesselsRELATION OF FETAL MEMBRANES TO WALL OF THE UTERUS (2nd - 3rd month)- Decidua parietalis --> fuses with decidua basalis - Decidua capsularis --> degenerates - Decidual basalis (from mother) + chorion frondosum (from embryo) --> eventually form the placenta - Chorion frondosum --> region where chorion REMAINS (because embryo attached) - Chorion laeve --> chorion is GONE (embryo DID not attach)Birth defectcongenital malformation = congenital anomaly > structural, behavioral, functional, and metabolic disorders present at birth.Birth defects arethe leading cause of infant mortalityMajor anomaliesoccur in ~3% of live-born infants.Minor anomaliesoccur in ~15% of newborns.Genetic factorsaccount for approximately 28% of birth defectsEnvironmental factorsproduce approximately 3% to 4%of birth defects.Multifactorial inheritanceproduces 20% to 25% of birth defectsIn 40% to 45% of birth defectsthe cause is unknown. >> CRITICAL PERIOD SO THAT EVERYTHING IS HAPPENING RIGHT TO PREVENT RISK OF MALFORMATION LATERTYPES OF ABNORMALITIES- Disruptions - Deformations - SyndromesDisruptionsmorphological alterations of already formed structuresDeformationsresults from mechanical forces that mold a part of the fetus.Syndromeso A group of anomalies occurring together that have a common cause. o Multiple manifestions & pigmentsEnvironmental Factors- Infectious agents - Radiation - Chemical agents - Nutritional deficiencies - Maternal disease(1941) German measlesthat affected a mother during early pregnancy caused abnormalities (cataract & heart defects) in the embryo.(1961) thalidomide- First report linking limb defects to a sedative thalidomide - Evidence that drugs could also cross the placenta and produce birth defects --> absence of the long arms so that head is attached to shoulder = PHOCOMELIAPHOCOMELIAhead attached to shoulderThe structures more sensitive to others to birth defectBy study done in (2010) by CDC + National Birth Defects Prevention Network 1st common: CLEFT PALATE & CLEFT LIP! 2nd common: CARDIOVASCULAR SYSTEM DEFECTS --> tetralogy of Fallot 3rd common: GI TRACT DEFECTS (neural crest defects) 4th common: CHROMOSOMAL MUTATIONS ( trisomy 21) --> turners syndrome: (X0) patient is female but lacks one of the 2 X chromosomes, fertilityPrenatal diagnosisultrasound, maternal serum screening, amniocentesis, chorionic villus samplingULTRASONOGRAPHYo Noninvasive technique that uses high-frequency sound waves reflected from tissues to create images. o Transabdominal or transvaginal (higher image resolution) o Performed between 18 & 20 weeks o Assess overall growth & development, and birth defectsMATERNAL SERUM SCREENINGo Concentrations of serum a-fetoprotein (AFP). o AFP is produced normally by the fetal liver --> peaks at approximately 14 weeks, and pass into the maternal circulation via the placenta. o AFP concentrations increase in maternal serum during the second trimester and then begin a steady decline after 30 weeks of gestation. o Test is performed between 15 & 20 weeks of gestation. o AFP can be used in combination with other markers such as unconjugated estriol (uE3), human chorionic gonadotropin (hCG) and inhibin A.Increased AFPNEURAL CREST DEFECTDecreased AFPCHROMOSOMAL ABNORMALITYAMNIOCENTESIS[not enough cells, very long process] o Approximately 20 to 30 ml of fluid is withdrawn from the amniotic cavity. o Procedure is performed transabdominally, in the second trimester (15 & 20 weeks). o The fluid is analyzed for biochemical factors, such as AFP. o Fetal cells are recovered in the amniotic fluid --> a. Perform karyotyping (several weeks) OR b. Polymerase chain reaction can be performed to test for specific genetic diseases.CHORIONIC VILLUS SAMPLING[can be performed earlier] o Collection of approximately 5 to 30 mg of villus tissue. o Performed in a transabdominal or transcervical manner (between 10 & 12 weeks). o Detection of genetic disorders and chromosomal anomalies (results in few days). o Disadvantage: This method does not assess neural tube defects or other malformations. o Advantage: have sufficient amount of cells in culture & can detect disease in a few days (FASTER) vs. amnio where you cant get enough cells & it takes LONGER