placenta Flashcards
structure of placenta
humans have a villous hemochorial placenta- maternal blood comes in direct contact with fetal trophoblasts (but not fetal blood). It is discoid in shape and has chorioallantoic vasculature. Placental structure is not highly conserved among species
· Explain the different functions of the placenta.
Support the growth and development of the fetus, Transport Nutrients, O2, Waste, CO2, Endocrine- Steroid and peptide hormones
describ prelacunar stage
Days 6-8. Outer layer of trophoectoderm forms non-miotic multinucleated syncytiotrophoblast. Inner layer remains as single cells called cytotrophoblasts. The cytotrophoblast cells proliferate providing for the developing syncytium that invades the adjacent maternal tissue
Lacunar stage
aka trabecular stage. Days 9-12. Vacuoles appear within the syncytiotrophoblasts and fuse to form lacunae (lakes). syncytiotrophoblasts form pillars called trabeculae. The lacunae make contact with the endometrial capillaries and some maternal erythrocytes may be observed within the lacunae. This is the region that will develop into the intervillous space. Implantation is complete at this point.
Villous stage
Days 13-18. development (in three stages) of chorionic villi. The cytotrophoblasts proliferate and begin to invade up the trabeculae.
Describe a primary, secondary and tertiary villous
Primary: consists of a cytotrophoblast core surrounded by synctytiotrophoblast. Secondary: extraembryonic mesoderm grows into the cytotrophoblast. Tertiary: Eventually, the mesenchymal cells differentiate into blood vessels resulting in the formation of an arteriocapillary network within the villous
floating villi/ anchoring villi
anchoring: attachment to uterus. Site for invasive cytotrophoblast deployment. Floating: majority of placental mass. Site of nutrient and waste exchange
types of trophoblast invasion
Interstitial invasion: cytotrophoblasts invade the entire endometrium and the first third of the myometrium. Endovascular invasion: cytotrophoblasts invade the uterine spiral arterioles through their superficial myometrial segments. Only the termini of veins are breached
maternal fetal blood separation
No direct mixing. Fetal blood in the capillaries of the tertiary villi are separated from maternal blood surrounding the villous by a “placental membrane” composed of the capillary endothelium, mesenchyme, cytotrophoblast, and syncytrophoblast.
Maternal fetal circulation
the two umbilical arteries carry deoxygenated blood from the fetus to the placenta, branching into arterioles following the course of the villous tree forming a capillary network within the chorionic villi. Maternal blood in the intervillous space provides oxygen to the fetal blood in the villi. The chorionic villi capillaries then form venules that ultimately connect to the umbilical vein, which carries oxygenated blood back to the fetus
Third trimester placenta divisions
The maternal surface is divided by septa into cotyledons. Each cotyledon contains several main stem villi with many branching villi.
Placental terminal villi
Grape-like structures located on tertiary villi that have many capillaries and highly dilated sinusoids. Terminal villi are the locations where most of the villous growth and transplacental transport takes place. This arrangement minimizes the transit distance between the fetal and maternal circulations
amniotic fluid function
vital factor for fetal growth and development and provides mechanical protection for the fetus. Amniotic fluid volume ranges from 250 ml at 18 weeks to 1,000 ml at 34 weeks, with decreasing volume thereafter
Amniotic fluid production
Early in pregnancy, amniotic fluid is simply an ultrafiltrate of maternal plasma. Once the fetal kidneys start working (12 weeks), fetal urine becomes the major source; and in late pregnancy amniotic fluid is primarily fetal urine, with a small contribution from fetal lung secretions
Oligohydramnios
a subnormal volume of amniotic fluid. Can be caused by rupture of membranes, poor placental perfusion due to pre-gestational diabetes, hypertension, preeclampsia, or twin-twin transfusion. Also nephrotoxic drugs like prostaglandin synthase inhibitors and ACEI interfere with normal fetal renal function