MCP 23: Implantation and Germ Layer Flashcards
trophoblast
11 cells on the outside of the morula that are in contact with the environment, differentiates into two tissues when contacts endometrium
implantation 5-9 days
1.) when blastocyst reaches endometrium, attached via the embryonic pole 2.) trophoblast cells begin to dissolve connections between endometrium cells and form syncytiotrophoblast 3.) endometrium grows around the embryo (decidual reaction) 4.) ICM develops into two layers (epiblast and hypoblast) 5.) epiblast amniotic cavity forms 6.) cells from hypoblast travel along cytotrophoblast to surround blastocel 6.) syncytiotrophoblast continues to invade endometrium 7.) tropoblastic lacuna form
abembryonic pole
pole opposite the ICM on the implanted embryo
decidual reaction
endometrium growns around embryo
cytotrophoblast
trophoblasts retrain their plasma membranes on the abembryonic pole, also a thin layer of cytotrophoblast between the syncytiotrophoblast and the derivatives of the inner cell mass
epiblast
layer closest to the syncytiotrophoblast (AKA the primative ectoderm), this portion of the ICM will form the embryo, all 3 germ layers
hypoblast
layer furthest from the syncytiotrophoblast, facing the blastocoel, will form the yolk sac, sometimes the hypoblast is called the primitive endoderm
bilaminar disk
epiblast and hypoblast together
amniotic cavity
second fluid-filled space formed by the epiblast
tropoblastic lacuna
fluid filled spaced in syncytiotrophoblast where mother’s blood washes embryo’s blood
implantation days 8-12
1.) embryo continues to grown 2.) hypoblast stops migrating 3.) Heuser’s membrane formed 4.) extraembryonic reticulum forms between blastocoel and cytotrophoblast 5.) trophoblastic reticulum begin to fill with mother’s blood 6.) cells in extraembryonic membrane signal cells in epiblast to migrate along path between cytotrophoblast and extra embryonic reticulum 7.) extraembryonic reticulum dissolves and replaced by chlorionic cavity 8.) chorionic cavity causes extrembryonic mesoderm to split primary yolk sac into two parts
Heuser’s membrane
thin layer of cells that hypoblast forms between blastocoel and cyctotrophoblast
extraembryonic reticulum
thick, gelatinous structure between cytotrophoblast and Heuser’s membrane, eventually replaced by chlorionic cavity after extraembryonic mesoderm separates it from cytotrophoblast and Heuser’s membrane
primary yolk sac
when Heuser’s member and extraembryonic reticulum have formed
extraembryonic mesoderm
cells from epiblast that migrate between cytotrophoblast and extraembryonic reticulum , NOT part of the embryo proper, eventually completely surround extraembryonic reticulum when migration has ceased
chorionic cavity
replaced extraembryonic reticulum after extraembryonic mesoderm forms, filled with saline
secondary yolk sac
AKA definitive yolk sac, yolk sac split by cholionic cavity growth that surrounds developing embryo, embryonic mesoderm that surrounds secondary yolk sac for first blood vessels in developing embryo
primary stem villus
syncytiotrophoblast has invaded mother’s endometrium, trophoblastic lacunae in syncytiotropholbasts that are pooled with mother’s blood, layer of thin cytotrophoblast underneath syncytiotrophoblast, then underneath that is exposed extraembryonic mesoderm
secondary stem villus
extraembryonic mesoderm and cytotrophoblast push down into syncytiotrophoblast, no tissue layers are broken
tertiary stem villus
when secondary stem villus have pushed down into the maternal endometrium, occurs 21 days after fertilization and is the start of the fetal circulatory system, creates blood barrier between fetus and mother
ectopic pregnancy
when embryo implants at the incorrect site, most common site is the ampulla region, other possible locations include isthmus of the uterine tube, abdomen, cervix, ovary and fimbrae, surgery usually required, symptoms include vaginal bleeding and pain
pre-eclampsia
caused by shallow implantation of the embryo, present in 5% of pregnancies and causes 20% of birthing complications\
hydatiform mole
cyst composed only of placental tissue, no fetus present and common in mothers under 25 y/o, symptoms include vaginal bleeding, hypertension, edema, and abnormally high levels of hCG
molecular mechanism of pre-eclampsia
VEGF stimulates blood vessel growth by binding to Flt-1 on the surface of endothelial cells. There is also a soluble form of the receptor, sFlt-1, that competes for VEGF. sFLT-1 is usually present in small amounts. During pregnancy PLGF (placental growth factor) also stimulates vessel growth by binding to Flt-1. Women have elevated sFLT-1 levels five weeks before showing symptoms of pre-eclmapsia, since sFLT-1 is soluble and travels all over the body sopping up VEGF and PLGF–causes inadequate vessel formation.
treatment for pre-eclampsia
flooding mother with PLGF to prevent sFLT-1 from sopping it up