Placental and Maternal Phys Flashcards
1
Q
How long does the fertilized egg stay in the fallopian tubes? When does it arrive in the uterus?
A
- for the first 3 days
- day 4
2
Q
Outer and inner layer of the zona pellucida?
A
- outer layer= trophoblast = placenta and fetal membranes
- inner layer = cell mass to become embryo and fluid
3
Q
When does the trophoblast implant into the endometrium?
A
- day 6-7
4
Q
How does implantation of the blastocyst occur?
A
- in response to 17-OH progesterone from the corpus luteum, the endometrium glands are filled with glycogen, mucus, and rich blood supply (the secretory endometrium)
- implantation takes several days
- the conceptus is genetically diff from the mother
- genetically foreign cells usually rejected by immune system - this doesn’t occur during normal pregnancy - due to modifications of mother’s immune system
5
Q
Progenitor cytotrophoblast cells differentiate into what 2 layers?
A
- extravillous cytotrophoblast (inner)
- villous cytotrophoblast (outer)
6
Q
What is the importance of the extravillous cytotrophoblast?
A
- invasive into the decidua and myometrium
- invasive into spiral arteries which are remodeled into wide uteroplacental arteries (which anastomose with endometrial veins to form a lacunar system of low resistance)
- form core of villi (covered in synctiotrophoblast)
7
Q
Impt of villous cytotrophoblast?
A
- able to become syncytiotrophoblast
- forms placental villi with base of cytotrophoblast cells (Langhans layer) with overlying syncytiotrophoblast on surface
- specialized epithelium w/o distinct cell boundaries covering villous tree: transport of gases, nutrient and wastes as well as synthesis of peptide and steroid hormones that influence placental, fetal and maternal systems
- also forms 2 umbilical arteries and 1 vein
8
Q
What is the decidua influenced by? What do the decidual cells form?
A
- influenced by progesterone and later with invasion of trophoblasts (implantation), the stromal cells of secretory endometrium become decidual cells
- decidual cells directly under implantation site form basal plate of placenta (decidua basalis) and a factor limiting myometrial invasion
9
Q
What always separates the embyronic circulation from maternal blood and decidua?
A
- layer of trophoblast cells
10
Q
What is nitabuch’s layer?
A
- a layer of fibrin b/t the boundary zone of compact endometrium and cytotrophoblastic shell in the placenta
- possible role in preventing host/graft rejection
- allows for separation of placenta after delivery
11
Q
Why is the placenta considered an extra brain?
A
b/c:
- interface b/t mother and fetus
- prevents rejection of fetal allograft
- enables respiratory gas exchange
- transports nutrients
- eliminates fetal waste products
- secretes peptide and steroid hormones
12
Q
What are the metabolic fxns of the placenta?
A
- glycogen synthesis: uptake of glucose from maternal circulation, glycogen as an energy reserve
- cholesterol synthesis: as precursor for production of progesterone and estrogen
- removal of lactate: a waste product of placental metabolism is transferred to maternal circulation
- protein metabolism
13
Q
What are the placental peptide hormones?
A
- hCG: maintains corpus luteum production of progesterone until placenta takes over at 6-8 wks, regulates placental steroid production
- hPL: antagonizes maternal secretion of insulin to increase fetal glucose supply
- placental CRH: stimulates fetal ACTH resulting in fetal adrenal making DHEA-S as precursor to placental estrogen, in latter gestation, fetal cortisol stimulates CRH release which stimulates fetal ACTH that acts as an endocrine mediator of onset of labor
- IGF: regulates fetal growth
- VEGF
- placental growth factor
14
Q
What are the placental steroid hormones? Fxns?
A
- progesterone: maintains a non-contractile uterus, also anti-inflammatory and immunosuppressive to protect fetus
- estrogens: stim by placental HCG, also maternal and fetal blood supply DHEAS as substrate for additional estrogens (mostly from fetal adrenal)
15
Q
Role of enzymes that degrade maternal glucocorticoids?
A
- placenta regulates exposure of fetus to glucocortiocoids
- this has an impt role in regulating fetal organ development and maturation
16
Q
What materials are being transfered across the placenta? Where is this occurring?
A
- occurs at syncytiotrophoblast layer
- CO2 and O2 exchange
- glucose
- amino acid: fetus dependent on these for protein synthesis
- fatty acids from breakdown of maternal TGs
- immunoglobulin G (maternal abs)
- drugs (high MW least likely)
17
Q
Role of estrogen in pregnancy?
A
- enlargement of uterus
- breast enlargement and growth of ductal structure
- enlargement of external genitalia
- relaxation of pelvic ligaments
- affects many aspects of fetal development
18
Q
Role of progesterone in pregnancy?
A
- induces endometrial secretory cells to decidual cells
- contributes to development of conceptus b/f implantation, affects cell cleavage in developing embryo
- inhibits myometrial contractions
- may be involved with immune tolerance of fetus
- influences breasts for lactation
- helps develop thick mucous plug of cervix (helps prevent infection)
- along with estrogen changes cervix, vagina, vulva to allow for sufficient stretching to allow delivery
19
Q
What ophthalmic changes occur in pregnancy?
A
- cornea thickens: may cause problems for contact lens wearers, may cause blurred vision. Pregnancy is CI for refractory surgery
- decrease in IOP
- visual field changes or double visions are abnormal
- diabetic retinopathy may worsen dramatically during pregnancy
- with toxemia of pregnancy, choroidal vascular insufficiency causes secondary retinal detachments
20
Q
Dental changes in pregnancy?
A
- gingivitis: hormonal changes soften the tissues in the mouth contributing to bleeding or inflammation
- epulis of pregnancy: hyperplastic, grandulomatous lesion. Composed mainly of capillary vessels and endothelial proliferation, referred to as “pregnancy tumor”.
similar lesions seen in non-preg individuals with dilantin therapy
21
Q
GI changes in pregnancy?
A
Mostly due to progesterone (relaxation of smooth muscle)
- relaxation of esophageal sphincter - increased GERD
- decreased PUD due to increased mucus and decreased gastric secretion
- gallbladder empties incompletely in response to meals during pregnancy (results in increased risk of gall stones)
- delayed gastric emptying, slowed small bowel transit and decreased large bowel peristalsis - constipation, impaction
- increased portal venous pressure (but not central venous pressure)
- N/V (nausea gravidarum: 4-16 wks tx with Vit B6 (pyridoxine) 50-100 mg daily
- hyperemesis gravidarum: persistent and severe N/V = wt loss, dehydrayion, elect. imbalances, caused by rapid rising serum levels of hCG and estrogen: more comon in mult reg tx with IV fluids, antiemetics
22
Q
Renal and urinary changes in pregnancy?
A
- progesterone relaxes bladder wall and reduces ureteral tone and peristalsis, effect may persist 12-16 wk postpartum
- physiological hydroureter of pregnancy: can hold 200-300 ml of urine: enlarging uterus can compress ureter at pelvic brim (R more than L)
- hydronephrosis is common (R more than L)
- changes predispose preg women to UTIs and pyelonephritis
