Chapter 18 Prenatal Development and Diseases Associated with
Chapter 18 Prenatal Development and Diseases Associated with Pregnancy Learning Objectives (1 of 2) Explain process of fertilization; implantation; early development of ovum; origin of decidua, fetal membranes, and placenta Describe formation and elimination of amnionic fluid; conditions leading to abnormal levels
Explain causes and effects of spontaneous abortion and ectopic pregnancy Identify and explain problems following failure of contraceptive pills or intrauterine device Describe mechanism and clinical manifestations associated with abnormal attachment of placenta Learning Objectives (2 of 2) Differentiate: Identical vs. fraternal twins Describe determination of zygosity from
examination of placenta; disadvantages of a twin pregnancy Classify types of gestational trophoblast disease, methods of treatment Explain pathogenesis, clinical manifestations, diagnostic criteria, treatment for hemolytic disease of the newborn Fertilization Union of sperm and ovum occurs in fallopian tube
Sperm travel via own propulsion and by passive transported upward into the fallopian tubes by rhythmic contractions of uterine muscles Ovum is expelled from follicle at ovulation Fertilization is possible when sperm are present in fallopian tubes at the time egg is expelled at ovulation First cell division completed 30 hours after fertilization Only 1 sperm can enter egg
Sperm penetration causes zona pellucida to become impermeable to penetration by other sperm Normal sperm in vaginal secretions Mature ovum with adherent granulosa cells Early Development: Fertilized Ovum Fertilization occurs in fallopian tube
Sperm contain genetic material and enzymes for penetration Zygote develops into a small ball of cells Fluid accumulates to form blastocyst Inner cell mass: forms embryo Trophoblast: forms placenta and membranes Blastocyst begins to differentiate Implantation by end of 1st week
Blastocyst implants in endometrium Amnionic sac and yolk sac form Small germ disk and yolk sac project into chorionic cavity Organ systems begin to form; embryo becomes cylindrical by 4th week
In Vitro Fertilization and Embryo Transfer Some women ovulate normally but are infertile because fallopian tubes obstructed by scarring or removed due to previous ectopic pregnancies Patients follicle is aspirated by laparoscopy Ovum is fertilized and allowed to develop outside the body into 8- or 16-cell stage Fertilized ovum implanted into uterus
Low success rate Possibility of chromosomally abnormal embryos Abnormal embryos usually unable to survive and are aborted Stages of Prenatal Development Pre-embryonic period: First 3 weeks after fertilization Blastocyst becomes implanted and inner mass cell differentiates into 3 germ layers to eventually form
specific tissues within embryo Embryonic period: 3rd through 7th week Begins to assume a human shape All organ systems are formed Very critical period of development Fetal period: 8th week to term Fetus continues to grow No major changes in basic structure
Subcutaneous fat accumulates; fills body shortly before delivery Progressive changes in fetal size, 3.5 months, 4.5 months, and 5.5 months Fertilization and Early Development of Fertilized Ovum
Duration of Pregnancy Gestation: total duration of pregnancy from fertilization to delivery Dated from time of conception: 38 weeks Dated from first day of last menstrual period (date of ovulation unknown): 40 weeks First day of the calculation is two weeks before the date of conception
May be expressed as 280 days Also expressed as 10 lunar (28-day) months or 9 calendar (31-day) months; divided into 3 periods called trimesters Decidua, Fetal Membranes, Placenta Decidua: endometrium of pregnancy Decidua basalis: under chorionic vesicle Decidua capsularis: over chorionic vesicle
Decidua parietalis: lines rest of the uterus Chorion laeve: superficial smooth chorion Chorion frondosum: bushy chorion Amnionic sac: enclosed within chorion, forms a protective environment Yolk sac: forms intestinal tract Chorionic vesicle
Relation of Fetus to Decidua, Fetal Membranes, and Chorion Placenta Double circulation of blood Fetoplacental circulation: from fetus to villi Uteroplacental circulation: maternal blood circulates around villi No actual intermixing of maternal and fetal blood
Fetus connected to placenta by umbilical cord Functions of the placenta Provides O2 and nutrition for fetus Has endocrine function: synthesizes hormones (estrogen; progesterone; protein hormones) Human placental lactogen, HPL Human chorionic gonadotropin, HCG Amnionic Fluid (1 of 2) Produced by filtration and excretion
Filtration from maternal blood early in pregnancy Fetal urine later in pregnancy Fetus swallows fluid: Absorbed from fetal intestinal tract into fetal circulation Transferred across placenta into mothers circulation Excreted by mother in her urine Balance is maintained in secretion and excretion of amnionic fluid
Quantity varies with stage of pregnancy Amnionic Fluid (2 of 2) Polyhydramnios: increased volume of amniotic fluid Fetus unable to swallow and fluid accumulates (anencephaly) Fluid is swallowed but not absorbed due to congenital obstruction of fetal upper intestinal tract
Oligohydramnios: reduced volume of amniotic fluid Fetal kidneys failed to develop and no urine is formed Congenital obstruction of urethra does not allow urine to form amnionic fluid Gestational Diabetes Hyperglycemia: harmful to fetus Pregnancy hormones induce maternal insulin resistance Diabetes results from inability to increase insulin
secretion to compensate for increased insulin resistance Diagnosis: similar to non-gestational diabetes Diabetes usually relents following delivery Spontaneous Abortion 10-20% of all pregnancies Early abortion results from Chromosome abnormalities Defective implantation
Maldevelopment of fetus Late abortion results from Detachment of placenta Obstruction of blood supply through cord
Complication: Disseminated intravascular coagulation Cocaine abuse: disturbs blood flow to placenta and may cause placental abruption and intrauterine fetal death Small well-formed spontaneously aborted fetus near the end of the first trimester Fetus spontaneously aborted late in pregnancy because of interruption of blood supply through the umbilical cord
Ectopic Pregnancy Development of embryo outside the uterine cavity Most common site: fallopian tubes Predisposing factors Previous infection of fallopian tubes Failure of normal muscular contractions of tubal wall Both fallopian tunes predisposed Consequences
Rupture of fallopian tube Profuse bleeding from torn vessels Potentially life-threatening to mother Ectopic Pregnancy, fallopian tube with mass of placental tissue; embryo within intact amnionic sac Artificial Contraception Failure of oral contraceptives
Developing embryo exposed to synthetic estrogen and progestin compounds Exposure to estrogen and progestin compounds may induce congenital abnormalities in developing embryo Failure of an intrauterine device IUD predisposes pregnant uterus to infection Must be removed as soon as pregnancy is diagnosed
Abnormal Attachment of Umbilical Cord Velamentous insertion Cord attached to fetal membranes than placenta May tear or is compressed during labor May be fatal to infant No adverse effect on mother Velamentous insertion of
umbilical cord with vessels traversing fetal membranes Normal placenta Abnormal Attachment of Placenta Normally, placenta attaches high on the anterior or posterior uterine wall Placenta previa: placenta attached at lower part
of uterus; may cover cervix Central placenta previa: placenta covers entire cervix Partial placenta previa: margin of placenta covers cervix Causes episodes of bleeding late in pregnancy Hazardous to both mother and infant Requires delivery by cesarean section : Central Placenta Previa
B: Partial Placenta Previa Twins (1 of 3) Disadvantages of twinning Twins smaller than single infant at comparable stage of gestation Over-distention of uterus promotes premature onset of labor Delivery of premature infants
Reduced chance of survival Congenital malformations occur twice as often in twins Twins (2 of 3) Twin transfusion syndrome Vascular anastomoses connect placental circulations of identical twins One twin is polycythemic and one is anemic
Tolerated if minor disproportions in blood, if severe, may be fatal to both twins Vanishing twin: one of the twin dies and is resorbed Blighted twin: one of the twin dies and persists as degenerated fetus Twins (3 of 3) Fraternal twins: 2 separate ova fertilized
by 2 different sperm Identical twins: single fertilized ovum splits Conjoined twins: variable union between identical twins Stages at which formation of identical twins can occur, and types of placenta associated with each stage of twinning.
Partition between amnionic sacs in twin pregnancy A comparison of the formation of the placentas and fetal membranes in twins Placenta of identical twins with amnions removed revealing interconnecting blood vessels Identical twins exhibiting twin
transfusion syndrome Triplet placenta Conjoined twins exhibiting a large congenital defect in the abdominal wall X-ray of conjoined twins demonstrating extreme curvature of fetal spine
Gestational Trophoblast Disease (1 of 4) Trophoblastic cells covering villi continue to grow at excessive rate, producing higher HCG than in normal pregnancy Proliferating trophoblastic tissue may invade uterus, vagina, distant sites Hydatidiform mole (hydatid: fluid-filled vesicle; mole: shapeless structure) Occurs in 80% of affected patients
Complete mole Results from abnormal fertilization of an ovum lacking chromosomes and ovum fertilized by a single sperm bearing an X chromosome that is duplicated to form 46 Gestational Trophoblast Disease (2 of 4) Hydatidiform mole: complete mole Both X chromosomes come from the father No embryo develops
Chorionic villi become cystic structures resembling mass of grapes (complete mole) Hydatidiform mole: partial mole Normal ovum fertilized by 2 sperm, resulting in a fertilized ovum with 3 sets of chromosomes (69 chromosomes) Embryo forms but does not survive Less likely to exhibit aggressive behavior
Gestational Trophoblast Disease (3 of 4) Invasive mole Trophoblastic tissue invades deeply into uterine wall Occurs in 15% of affected patients Aggressive, destructive Gestational Trophoblast Disease (4 of 4) Choriocarcinoma
May arise following incomplete removal of invasive or incompletely removed mole Masses of proliferating trophoblast may extend into vagina Metastasizes to lungs and brain Treatment: curettage, periodic determination of HCG; hysterectomy; chemotherapy Erythroblastosis Fetalis (1 of 2)
Pathogenesis 1. Sensitization of mother to a blood group antigen in fetal RBCs 2. Mother forms antibodies that cross placenta 3. Maternal antibodies damage fetal RBCs 4. Fetus increases blood production to compensate for increased RBC destruction Variable severity Hydrops fetalis
Less intense hemolytic process Mild disease Erythroblastosis Fetalis (2 of 2) Hydrops fetalis Severe anemia causes heart failure and impaired hepatic plasma protein synthesis Results in edema Hemolytic process is extremely severe, causing death Infant dies in uterus during last trimester
Less intense hemolytic process Infant is born alive but moderately or severely anemic Mild disease Infant appears normal at birth then becomes anemic and jaundiced, develops edema Fetal Hydrops, stillborn with marked edema.
Swollen abdomen from enlarged liver and spleen and fluid accumulation in peritoneal cavity. Rh Hemolytic Disease (1 of 3) Most cases: Rh-negative mother and Rhpositive infant Consists of a series of allelic genes that determine multiple Rh antigens on red cells Rh-positive: red cells contain D (Rho) antigen
May be homozygous (genotype DD) May be heterozygous (genotype Dd) Rh-negative: red cells lack D (Rho) antigen Genotype dd Rh Hemolytic Disease (2 of 3) Mother sensitized to foreign antigen in infants cells and forms anti-D antibodies that cross placenta into infants blood
Rarely occurs in first pregnancy First Rh-positive infant born to Rh-negative mother is normal Rh antibodies not yet formed Treatment Exchange transfusion Fluorescent light therapy for hyperbilirubinemia Intrauterine fetal transfusion
Rh Hemolytic Disease (3 of 3) Prevention Rh immune globulin administered to mother Contains gamma globulin with Rh antibody Given within 72 hours after delivery of Rh-positive infant Rh antibody coats Rh antigen sites on surface of fetal red cells in maternal circulation to reduce sensitization Not 100% effective: 1.5% still form antibodies Some physicians recommend injections late in
pregnancy and after delivery to reduce incidence of sensitization Dual circulation of blood in the placenta Discussion A 30-year old woman prematurely delivered normal, well-formed female twins at 36 weeks of gestation. However, on examination of the placenta following
delivery, a third amnionic sac was noted with a degenerated fetus measuring 13 centimeters in length A. Vanishing twin B. Twin transfusion syndrome C. Blighted twin D. Conjoined twins E. Placenta previa Transfer of fetal Rh-positive red cells into
maternal circulation during postpartum placental separation ABO Hemolytic Disease (1 of 2) Pathogenesis Mother is type 0 (has anti-A and anti-B antibodies in her serum) while infant is type A or type B Maternal anti-A and anti-B antibodies attach to fetal red cells
Can occur in first ABO-incompatible pregnancy due to pre-existing anti-A and anti-B antibodies Manifestations Milder disease than Rh hemolytic disease because fetal A and B antigens are not as well developed unlike in adult cells; antibodies do not attach as firmly to fetal cells ABO Hemolytic Disease (2 of 2)
Manifestations A and B antigens also present in other fetal tissues, absorbing some of the antibodies that would otherwise attach to fetal cells Complications: anemia; hyperbilirubinemia; kernicterus Excess unconjugated bilirubin from red cell breakdown Treatment
Control hyperbilirubinemia by fluorescent light therapy Exchange transfusion not usually required Discussion The following are true of hemolytic disease of the newborn EXCEPT: A. Mother forms antibodies that cross the placenta and attack fetal red cells B. Infants red cells are protected by the mothers
antibodies C. Infant suffers edema from heart failure and impaired protein synthesis D. Infant compensates by increasing red blood cell production E. Infant may suffer severe hemolytic anemia and edema
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