Pregnancy and placenta Flashcards
1
Q
Mechanisms and conditions that facilitate implantation 1
A
- Zona pellucida prevents implantation (i.e. ectopic), embryo must “hatch” out of zona pellucida to implant
- Around day 6/7 (post fertilization) the endometrium is in secretory phase: glands are secreting, venous lakes have formed, storm is loose and edematous
- Blastocyst (no zona pellucida) arrives at uterus and attaches to endometrium via integrins
- It infiltrates the endometrium: trophoblasts (outer cell lining) secrete proteases that degrade ECM
2
Q
Mechanisms and conditions that facilitate implantation 2
A
- The trophoblast proliferates and divides into 2 layers: cytotrophoblast (stem cell like) and syncytiotrophoblast (terminally differentiated)
- The syncytiotrophoblast forms the invasive outer layer that surrounds the blastocyst
- The cytotrophoblast cells are contained w/in the syncytiotrophoblast and will slowly be incorporated into syncytiotrophoblast layer during placenta development
- Both layers begin producing hCG
3
Q
Functions of hCG, hCS, E and P and their changes throughout pregnancy 1
A
- When the embryo reaches the endometrium and begins to implant (day 7-9) it has roughly 1 wk to release hCG, which is the signal to keep the corpus luteum (hCG acts like LH on CL)
- If hCG is not released by the end of the cycle the corpus luteum will degrade, E/P will not be continually made by CL, and the endometrium will be sloughed (undergo menses)
- The embryo relies on E+P production from corpus luteum until the end of the first trimester, when the placenta is fully formed and makes its own E+P
- hCS, P, and E all begin rising around week 12 (about end of first trimester- pregnancy is usually 38 wks, or 40 wks since last menstrual period), which coincides w/ a fall in hCG levels
- hCG, hCS, and P are made by trophoblast cells, E is made by fetal cells and trophoblast cells working together
4
Q
Functions of hCG, hCS, E, P, relaxin and their changes throughout pregnancy 2
A
- hCS (human chorionic somatommamotropin): helps prepare mammary glands for lactation, reduces maternal glc utilization so more glc is available for fetus
- E: stimulates growth of myometrium for parturition (increases oxytocin receptor numbers in myometrium), helps prepare mammary glands for lactation
- P: suppresses uterine contractions to provide quiet environment for fetus, promotes formation of cervical mucous plug, helps prepare mammary glands for lactation
- P also acts on placenta as an immunosuppressant to block fetal rejection
- Relaxin: similar to IGF, its concentration is highest during first trimester (prevents uterus contractions) to do the job progesterone would do (but progesterone is low during first trimester)
- Relaxin also softens cervix, relaxes pubic ligaments for delivery
5
Q
Chorionic villus 1
A
- Syncitiotrophoblasts expand and create a network forming cavities (lacunae) filled w/ endometrial (maternal) blood
- Only syncytiotrophoblasts ever contact maternal cells, and the cytotrophoblasts proliferate w/in the syncytiotrophoblast layer
- The primary villi (pillars of placenta) consist of only syncytiotrophoblasts on the outside (lining the lacunae) and cytotrophoblasts on the inside
- Lacunae are filled w/ maternal blood (not in vessels), and fetal blood is always contained w/in vessels of the villi (starting at tertiary villus)
6
Q
Chorionic villus 2
A
- As the placenta develops the cytotrophoblasts develop a basal lamina beneath them, and inside the basal lamina a CT core (which blood vessels will eventually grow from)
- A secondary villus contains the CT core w/ a basal lamina lining, and the cytotrophoblasts and syncytiotrophoblasts outside of the basal lamina
- The syncytiotrophoblast and cytotrophoblasts (under LM) look like one dark purple staining layer (can’t tell the two cell types apart @ low mag)
- At the junction of the endometrium and lacunar spaces there are dark pink patches of eosinophilic non-cellular material (fibrinoid)
7
Q
Chorionic villus 3
A
- Around 3 months the villi are tertiary villi: now are branches of the villus stem into lacunae to increase surface area
- A tertiary villus contains fetal capillaries (endothelial cells) w/in the CT core, surrounded by a basal lamina, surrounded by the syncytiotrophoblast (w/ some remaining cytotrophoblasts) layer
- Thus there are 3 layers btwn fetal blood and maternal blood
- There are resident macs w/in fetal capillaries/CT core: hofbauer cells
8
Q
LM of cytotrophoblasts and syncytiotrophoblasts
A
- At high enough mag, the darkly staining cells that are at the periphery of the villi are syncytiotrophoblasts
- The pale cells are cytotrophoblasts, they also reside at the periphery of the villi
9
Q
Synthesis of steroid hormones during pregnancy 1
A
- Progesterone is made only in placenta (marker for placenta status), but estrogens are made in both placenta and fetus (marker for fetus status)
- Mother donates LDL cholesterol to placenta, where it is converted into P by trophoblast cells (doesn’t require gonadotropic hormone stimulation)
10
Q
Synthesis of steroid hormones during pregnancy 2
A
- In the placenta LDL is also converted into androgen precursors, which are sent to the fetal adrenals then liver to be made into weak androgens
- The weak androgens are brought back to the placenta, which has a large amount of aromatase activity
- The androgens are thus converted into 3 estrogens (estradiol, estrone, estriol) in the placenta
- Thus the placenta can make estrogens but only from androgens, and only the fetus can make the androgens from LDL
11
Q
Decidua
A
- Decidua basalis is equivalent to stratum functionalis in a non-pregnant women (both layers will be shed)
- The stratum functionalis turns into the placenta + decide basalis, both layers are still above the stratum basalis and myometrium (both are kept at delivery)
- The decidua basalis is the layer of endometrial tissue below the placenta and above the stratum basalis (will be shed along w/ placenta)
- Spiral arteries pierce the myometrium, stratum basalis, and decidua basalis to reach the placental lacunae
- Decidua basalis contains enlarged glands secreting glycogen/lipids and venous networks
12
Q
Parturition
A
- Initiation is not understood, but once contractions begin there is a positive feedback loop that causes parturition
- Fetal brain is thought to be largely responsible for onset of contractions
- Parturition is initiated by an increase in oxytocin (causes contractions) and a decrease in progesterone (inhibits contractions)
- The reasons for these changes are not known
- Once myometrium begins contracting there is a positive feedback loop that further increases oxytocin, leading to more contractions (by increasing SmM Ca and PG levels-> increase Ca)
- Estrogens increase oxytocin receptors in myometrium throughout pregnancy so myometrium is prepared for partuirtion
13
Q
3 stages of labor
A
- First stage is cervix dilation and effacement: there must be dilation (to 10cm) and thinning (effacement) of cervix for vaginal delivery
- 10cm dilation indicates second stage (active/pushing stage)
- Third stage is placenta release
14
Q
Tocolytics 1
A
- Tocolytics reduce smooth muscle contractions and attempt to delay preterm labor
- These usually only give 1-2 days extra in womb, but long enough to give CCS to let fetal lungs develop more
- Goal of these drugs is to inactivate myosin light chain kinase, the activity of which depends on Ca levels (no myosin light chain kinase = no phosphorylation of myosin light chain = no interaction w/ actin = no contractions)
15
Q
Tocolytics 2
A
- The most widely used drugs are B2 adrenergic agonists (ritodrine, terbutaline) which activate AC and increase cAMP leading to a decreased intracellular Ca
- Other mechanisms/drugs: COX inhibitors decrease PG synthesis (PGs increase contractions by increasing Ca levels in SmM), magnesium sulfate (blocks V-gated Ca channels and inhibits Ca action), L-type Ca channel blockers (nifedipine)
- COX inhibitor indomethacin usually used in pts w/ dysmenorrhea, it can cause oligohydramnios when used as a tocolytic
