| A | B |
|---|
| What does hCG do? | It Stimulates progesterone in CL during luteal phase; signals pregnancy |
| What happens to the uterine endo.? | It erodes so that maternal blood cell come in contact w/ invading trophoblast |
| What does a single layer of fetal chorionac tropoblast tissue? | the fetal capillary system and the maternal blood system |
| What happend to the implantation area? | cell proliferation and differentiation |
| What is hPL (human placental lactogen)? | simmilar to growth hormone & prolactin; indices growth of embryo & fetus & stimulates dev. of mother's breasts |
| Where and when is hPL produced? | in the placental tissues; increses during late gestation to prep for lactation |
| What is the placenta? | A mini hormone factory; a transient organ |
| Is the uterus an immunologically privilegded site? | No |
| what does the zona pellucida do in regards to immunosuppression? | Faciltaties immune acceptance (prior to hatching) |
| What does the outer trophoblast cell layer do in regards to immunosuppression? | Its covered by a protective coat which masks mane of the surface antigens form detection and attack |
| What do progesterone, hCG, and hPL (placental lactogen) do in regards to immunosuppression? | Blunt the immune response (ex. cancers produce hCG) |
| What do fetal cells do in regards to immunosuppression? | They provide tolerance of mother's immune systen towards fetus; shed cells circulate through body like allergy shots. |
| Day -2 | ovulation |
| Day 0 | fertilization, oocyte's second miotic division |
| Day 3-4 | blastcyst moves from fallopian tube to the uterus |
| Day 3-5 | Blasocyst begins to produce hCG (tripoblast / chorion) |
| Day 4-6 | hCG first detected in he periphial blood (clinical detection) |
| Day 5-6 | Shedding of the zona pellucidia followed by decidualization |
| Day 6-7 | Attachment to uterine endometrium |
| Day 7-9 | Implantation of embryo begins |
| Day 12-14 | hCG detected in uterus (home testable) |
| Day 28 | shift in the site of steriod production begins (from CL to placenta); Cl shuts down |
| Day 49 | Placenta is primary source for progesterone production (crit. for maintaining pregnancy) it begins to function as a nutritive organ |
| Size of placenta | 16 meters^2 |
| How does the futus get nutrition before placenta is fully established (7-8 weeks)? | trophoblastic digestion and absorption of nutrients from progesterone primed endomatrium |
| What does the placta do? | diffuse nutrients, 0^2, co^2 (hemoglobin), & heat exchange, rids of wastes, makes and stores nutrients, protects from immuno attack (some antibodies can cross) |
| Antibodies= | immunoglobins, large proteins produced by 'b lymphocytes' |
| IgG | good. 80% of antibodies, pass through placenta |
| IgE | bad. responsible for allergies. Do not cross placenta |
| IgA | found in milk after birth; lots of proteins but not necessary |
| allantoic membrane | gives rise to blood vessels that eventually form the umbilical cord. |
| Placenta as an endocrime organ: steriods | make many, but progesterone and estrogen are REALLy imp. for maintaining pregnancy |
| Placenta as an endocrime organ: hCg | early pregnancy maintenance; role in immunosuppression, can stimulate Leydig cell funtion in male fetuses |
| Placenta as an endocrime organ: GnRH | Produced by placenta to promote hCG and steriod production; increases during the first 24 weeks of gestation |
| Placenta as an endocrime organ: CRF (Corticotropin releasing factor) | stimulates fetal adrenal galnd to produce coritcal, present from 7 weeks of gestation and increases during the last 5 weeks, help time birth |
| Placenta as an endocrime organ: PL (placental lactogen) | A protein hormone that resembles prolactin and growth hormone, helps fetal growth and development, immunosuppression, and maternal milk production |
| Placenta as an endocrime organ: Endorphins | natural painkillers |
| Morning sickness | nausea dur to an unknown cause, can be treated with antihistamines, but unknown safety |
| breast development | b/c increased prolactin (from pituitary) and estrogen. Mainly 3rd trimester. for lactation |
| Cardiovascular effects | higher blood pressure b/c more blood. |
| Respiratory system | Increased demand during last trimester, up to 30% near end of term |
| Skin | more blood flow to skin, skin may actually darken |
| Maternal metabolism | starts to metabolize fat to ensure sufficient glucose; more eating, uses stored, better efficency, less work |
| weight | gains 20-25 pounds,( placnets 2 pounds, feuts 7-8) |
| Size maily dependant on | the amount of hormones |
| Fraternal Twiss | (dizygotic) from 2 diff. eggs (4-0.2%); have 2 placentas |
| Identical Twins | (monozygotic) 1st cleavage as totipotent or after trophoblast formed (splits too early); single placenta (0.25% of births) |
| TTTS | Twin-Twin Transfusion Syndorm; blood vessel connections btween ident. twins - fix w/ amniocentesis of laser surgery |
| Conjoined twins | Siamese, incomplete splt at day 12-14, many share vital organs and don't survive |
| Ectopic pregancies | 16.8 of 1000 live births. 4th major cause of preg. related deaths |
| Where is the ectopic preg? | 96% in fallopian tubes, sometimes cervic, ovary, abdomal cavity; hCG doesn't tell where |
| Ultrasounds & ectopic preg | Hard to find, but only miss 1:30,000 ectopic pregnancies |
| How to detetct ectopic pregancies | bleeding, spotting, abdominal/pevlic pain |
| Amenorrhea | Absence of menstration; can diagnose actopic pregancy |
| What can burst in an ectopic preg? | The amnionic sac or the fallopian tube. = bleeding, pain, and even death |
| % able to achieve an normal preg. later | 50% |
| ectopic death rate | 1-2% for mother |
| Reproductive failure | only 31% of fertilizations result in viable offspring |
| Spontaneous abortion | (miscarrage) loss of embryo/fetus before 20 weeks |
| Genetic defects | 42% of miscarages |
| polyspermi | 15% of conceptions |
| Luteal phase defects | (LPD) 33% of early abortion |
| Lack of maternal recognition | innsufficient hCC produced by blastocyct |
| immunilogical incompatibility | maternal antobodies against father |
| Immune attack against trophoblast | prevents implantation or causes poor placentation |
| Immunte attacks against specific fetal tissue | ex. fetal enemia (Rh- women's Rh antobodies destroy the red bood cells of the fetus. treatable in utero and post partum |
| Septic pregancy | bacterial infection of uterus; affects both mother and fetus. |
| Diabetes mellitis | (3-5%) gestational diabetes associated w/ higher miscarrage rate |
| Hydatiform Moles | (1/1000) implantation of trophoblast w/ no viable embryo. Makes lots og hCG |
| Preg. deaths U.S. | 14/100,000 |
| Preg. deaths 3rd world | 740/100,000 |
