wk 13, lec 2 Flashcards
theca cell vs granulosa cell
Theca:
-respond to LH
-make progesterone and androgens from cholesterol
-dont make estrogen (no aromatase enzyme)
the androgens diffuse across cell
granulosa:
-respond to FSH
-dont make androgens, take them from theca cell and turn them into estrogens
-later in cycle respond to LH and make progesterone
spiral arteries in the uterus are sensitive to
progesterone
Progesterone withdrawal
at the end of the cycle →
constriction and ischemia
of the functional layer of
the endometrium
when is the period of endometrial receptivity for implantation of the embryo? (6-10 days after fertilization of oocyte)
fertilize at day 14
implant day 20-24
endometrial factors that aid implantation
pinopods (protrusion near gland openings to absorb fluid, depend on elevated progesterone in midluteal)
secretion of ECM proteins for attachment/implantation (laminin, fibronectin, glycoproteins)
secrete proteases to help blastocysts to hatch out of zona pellucida
pinopods need which homrone and what is their function
progesterone; absorb fluidsecretion of ECM proteins for attachment/implantation (laminin, fibronectin, glycoproteins)
secretion of ECM proteins for attachment/implantation - what are they
laminin, fibronectin, glycoproteins
predicualization
changes to stromal cells in endometrium in response to progesterone
happens 3-5days after ovulation
changes in predicidualization
enlarge stromal cells
develop eosinophilic cytoplasm to secrete glycogen
develop prominent Golgi and ER
stromal cells differentiate into decidual cells and then function?
- secrete laminin, fibronectin, heparin sulfate, and type IV collagen
- Store glycogen to nourish the blastocyst
- Form a dense layer called the zona compacta
blastocysts secrete something to complete process of decidualization
increased by integrins and fibronectins –> contact each other –> implantation
capacitation of sperm
after sperm are ejaculate in fallopian tubes; sperm mature; then can fertilize oocyte
increased membrane fluidity
Surface glycoproteins removed from the head of the sperm cell,
increased motility, and increased cholesterol is inserted into the
plasma membrane → increased membrane fluidity
what increases membrane fluidity of sperm for capacitation
Surface glycoproteins removed from the head of the sperm cell,
increased motility, and increased cholesterol is inserted into the
plasma membrane → increased membrane fluidity
sperm getting to ampulla of fallopian tube?
many lost from acidic pH of vagina
muscular contraction help propel them there and so does ciliary movement and peristalsis
steps of fertilization
- sperm bind zona pellucida
- acrosome rxn
- sperm penetrates zona pellucida
- fusion of egg and sperm membranes
- egg cortical rxn triggered by entry of sperm nucleus
- female pronucleus
- male pronucleus
fertilize egg from ampulla –> implanted in uterus endometrium
usually 8 days; day 20-24
lots of fluid; pinopods absorb to bring embryo and endometrium closer
decidualization
storage of glycogen in endometrial cells to feed the blastocyst
(get ready for implantation)
increase integrals and fibronectins –> implantation in endometrium
implantation (embryo invades the endometrium)
when?
what does blastocyst become?
blastocysts forms and attaches to uterine lining at day 5 after fertilization
hatches out of ZP
trophoblast –> cytotrophoblast –> synctiotrophoblast when adhesion occurs
invasion of blastocyst (synctiotrophoblast) completes decidualization
when does blastocyst bind to adhere to endometrium
CAM
what does blastocyst turn into when binds endometrium
trophoblast differentiates into the
syncytiotrophoblast and cytotrophoblast.
then can invade uterine stroma
implantation: syncytiotrophoblast becomes ?
multinuclear cell mass
invades endometrial stroma
forms villi; via proteinases and adhesion molecules
what does syncytiotrophoblast secrete when implantation occurs
human chorionic gonadotropin
(hCG)
hCG function
prevents the shedding of the endometrium (and loss of the embryo) by
maintaining ovarian secretion of steroid hormones (i.e. progesterone)
Why is fetal Hb able to
obtain oxygen from
maternal Hb?
fHb has higher oxygen affinity than adult Hb
left shift to oxygen dissociation curve
what can cross mother fetal placental barrier
IgG
otherssss i.e. oxygen, carbs, hormones, drugs, viruses
what does fetal hemoglobin have lower affinity for (compared to adult hemoglobin)
2,3-diphosphoglycerate (2,3-DPG)
((is a molecule that binds to hemoglobin
and reduces its affinity for oxygen))
so fHb is less effected by 2,3DPG
structural different in fetal vs adult hemoglobin
- Fetal hemoglobin is composed of two α-globin chains and two γ-globin
chains - Adult hemoglobin (HbA) is composed of two α-globin chains and two β-
globin chains
what is hCG secreted by
and its function
synctiotrophoblasts
to maintain corpus luteum (so it can secrete progesterone and prevent spasm of spiral arteries, death of endometrial lining and uterine contractions)
hCG binds TSH receptor weakly to cause what in mom
mild hyperthyroid
Human placental lactogen (hPL) function?
what is it the antagonist of?
promotes development of?
Helps the fetus take up glucose and store/convert it into fatty acids and ketones
▪ Antagonizes insulin – may contribute to gestational diabetes
▪ Promotes development of mammary glands
after wk 8 what is the major site of progesterone and estrogen production in mom
trophoblast cells in the placenta
how do placental trophoblast cells make progesterone
from maternal LDL cholesterol
The placenta lacks 17α-hydroxylase and, therefore, cannot convert
progesterone to androgen
progesterone from placenta goes to maternal circulation and some is converted into
and then goes back into placenta as what
DHEAS (sulphation to reduce biological activity) by maternal adrenal gland
DHEAS reenters placenta, gets de-sulfated to DHEA and then converted into androstenedione and testosterone
placenta has what enzyme to turn testosterone into estradiol and estrone
aromatase
for the estrogens to go back into maternal circulation and help with pregnancy
path for hormones between mom and baby
placenta trophoblast makes progesterone from LDL (no 17a hydroxyls to turn it into androgen)
progesterone goes into mom and becomes DHEAS
DHEAS back into baby –> DHEA –> androstenedione and testosterone –> estradiol and estrone (via aromatase) –> back to maternal circualtion
fetus converts pregnenlonone and progesterone to
cortisol
–> goes into placenta and becomes corticosterone (seperate from moms cortisol)
((progesterone could also could go back to move become DHEAS then back to baby and become androgens then estrogen))
estrogens impact in pregnnacy
increase uteroplacental blood flow
enhance LDL receptor expression in synctiotrophoblast (makes progesterone)
induce things for parturition (prostaglandins, oxytocin receptors)
help breast growth
relaxin impacts in pregnancy
▪ Prevents contraction of myometrium to prevent premature labour
▪ During labour, however, it may soften the cervix
▪ Produced by corpus luteum, decidua, and later the placenta
cardiovascular changes in pregnancy
increase blood volume
increase stroke volume, HR, cardiac output
decrease peripheral resisntacen
increase erythropoeisis (which eats up iron and could cause anemia) but blood volume increases more so ‘dilutional’ anemia
what causes increase blood volume and decreased peripheral resistnace in pregnancy
increase BV: estrogen and aldosterone
decrease PR: vasodilate via estrogen and progesterone
pulmonary changes in pregnancy
bronchodilation and increased tidal volume –> increased ventilation (progesterone increase, drop in pCO2, mild respiratory alkalosis)
expand uterus –> compress diaphragm (minor decrease in FRC and RV)
renal changes in prengnacy
increase GFR
increase aldosterone –> increase H20 and Na+ retention –> edema
no increase in K+
what hormones/ things make labour happen
prostaglandins= smooth muscle contractions (soften, thin and dilate cervix)
estrogen increases oxytocin receptors
oxytocine cause uterine contractions; positive feedback
stages of labout
frist stage
-latent phase: infrequent and irregular contraction; slow cervical dilation
-active phase: cervical fully dilated, painful regular contractions
second stage
-full dilation to deliver of baby
-urge to bear down w contractions
third stage
-seperate and expulsion of placenta
fourth stage
-1st postpartum hour
during pregnancy how do mammary glands develop
estrogen causes ductile system
progesterone stimulates alveolar glands
placental lactogen develops breasts
prolactin made throughout pregnancy but inhibited by progesterone and placental lactogen
what happens to mammary glands after childbirth
placental hormonal [ ] decline and no longer inhibit prolactin
breast produce milk
mechanical stimulate (suckle) to release oxytocin from posterior pituitary
stimulate milk release
nipple needs to be stimulated regularly to keep making milk
mammogenesis
lactogenesis
galactokinesis
galactopoiesis
mammogenesis= breast development
–> estrogen, IGF1, cortsiol, prolactin
lactogenesis= milk prodcution
–> prolactin, hPL, cortsiol, IGF1, thyroid
galactokineses= milk ejection/ letdown reflex (via myopethelial contraction)
–> OT, AVP
galactopoeises= maintain milk production
–> prolactin, cortsiol
prolactin important for which stage of lactation
▪ Mammogenic, lactogenic, and galactopoeitic
▪ Primary hormone for maintaining milk production once
it is initiated (galactopoeisis)
prolactin suppresses
GnRH
most women breastfeeding are anovulatory
strongest stimuli for prolactin release
suckling
also estrogen and TRH
oxytocin for which part of lactation
galactokinesis (milk ejection/letdown reflex)
Initiates contraction of not only uterine muscle, but
myoepithelial cells surrounding the alveoli
oxytocin is stimulated by
suckling
psychogenic associated with suckling (i.e. hear infant cry)
suppressed by stress and anger
steps in milk!
- suckling stimuli –> hypothalamus
- inhibit dopamine (which usually inhibits lactotrophs in anterior pituitary) –> prolactin release
- release oxytocin
- inhibit GnRH
ectopic pregnancy sites
Ampullary (70%)»_space;
isthmal (12%) > fimbrial
(11%) > ovarian (3%) >
interstitial (2%) >
abdominal (1%)
fallopian tube most commone
risk factors for ectopic pregnancy
PID, previous ectopic, tubal
damage, endometriosis, IVF,
smoking (dose dependent- affects
tubal motility and function)
signs and sx of ectopic prgnnacy
amenorrhea (missed period)
vaginal bleeding/ spotting
ab pain
breast tender, nausea
syncope
diagnose and treat ectopic pregnancy
dx: beta-hCG, ultrasound
if severe ab pain then treat surgically or medically via high dose methotrexate
placenta previa
placenta over or near the cervix (lower part of uterus)
frequent (1/200) esp if have fibroids/leiomyomas and multiple pregnancies
may resolve by itself
possible c section
sx of placenta previa
painless vaginl bleeding after wk 30
dx and therapy for placenta previa
dx: ultrasound
if too much bleeding do transfusion
deliver via c section
placental abruption
premature detachment of placenta from uterus
idiopathic but predisposed byL: cocaine, hypertension, trauma, chorioamnionitis
usually in 3rd trimester
sx of placental abruption
vaginal bleeding with crampy ab and back pain, ab tender
hypertensive disorders of pregnancy
eclampsia and pre-eclampsia
ecampsia vs pre-elcampsia
pre eclampsia: hypertension, edema, proteinuria
(after 20 weeks gestation)
eclampsia: pre-eclampsia plus convulsions (seizures)
complications of exlampsia
DIC, renal failure, hypercoagulability, pulmonary edema
HELLP – hemolysis, elevated liver enzymes, low platelets
(complication of pre-eclampsia)
pre eclampsia
decidual blood vessels remain constricted and narrowed
placenta is ishemic
secrete anti-angiogenic factors than impair vasodilation, cause decreased PGI2 and hypercoagulatbility
sx of pre-eclampsia
headaches, visual disturbances
(blurred vision, scotomas), hyper-reflexia
- more severe cases involve edema, changes in urine colour (indicating hematuria), abdominal pain
impacts on baby of hypertesnion (eclampsia) in pregnancy
IUGR (intrauterine growth restriction), placental abruption,
premature delivery
gestational diabetes
oral glucose tolerance test in late 2nd trimester
treat w insulin
complication: hypertesnion, pre-eclampsia, ketoacidosis, retinopathy, pyelonephritis, macrosomnia, congenital anomalies, preterm labour, hypoglycemia etccc
Gestational Trophoblastic Disease
abnormal growth on placenta
benign (molar) or malignant
hydatidiform mole (gestational trophoblastic disease)
abrnomal grrwoth
- Trophoblastic proliferation and degeneration of chorionic villi
- Complete mole – fetus is not identified; partial mole – has
some fetal parts attached
from abnormal fertilization (all chromosomes are paternal; 2 sperm fertilize 1 egg)
could become malignant if placenta not removed
no baby
choriocarcinoma (gestational trophoblastic disease)
malignant cancer from placenta cells
usually from molar pregnancy
post partum hemorrhage
Loss of > 500 mL of blood with vaginal delivery or > 1000 mL
with C-section
from: trauma (i.e uterine rupture), coagulopathy, tissue (ie. gestatonal trophoblastic neoplasia), tone (fibroids) etcccc
