Lect 3: Pregnancy, Parturition & Lactation Flashcards Preview

Unit 7 - Repro & Renal Physiology > Lect 3: Pregnancy, Parturition & Lactation > Flashcards

Flashcards in Lect 3: Pregnancy, Parturition & Lactation Deck (26)
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sperm binds zona pellucida; acrosomal reaction stimulated when sperm binds to one of the glycoproteins of the zona pellucida; calcium dependent process leads to fusion of the acrosome with the sperm plasma membrane (exocytosis). Hydrolytic enzymes released from acrosome penetrate the zp and the sperm oscillates to penetrate the oocyte. Cell membranes (of sperm and oocyte) fuse and the cytoplasmic portion of sperm head and tail enter the oocyte. Not the cell membrane


The oocyte undergoes the cortical reaction

triggered by rise in Ca/IP3-dependent process which prevents other sperm from fertilizing the oocyte. The oocyte completes the 2nd meiotic division and a 2nd polar body is expelled. The head of the sperm condenses to become the male pronucelus. Male and female pronuclei fuse to form a zygote. Zygote contains 46 chromosomes from two pairs of 23 chromosomes. CORTICAL REACTION prevents polyspermy.
Both acrosomal and cortical are calcium- dependent


During the female menstrual cycle changes take place in the ovaries and uterus, under the control of the hypothalamus and the ant. pit. During the follicular phase, several primary follicles undergo further development in responses to FSH ad synthesize androgens, which are converted to estradiol under the influence of LH.

Ultimately, one follicle fully matures and the others regress. The uterine endometrium proliferates in response to estradiol. Near midcycle, estradiol rises to a level that initiates positive feedback and thus a surge in LH and FSH release which results in ovulation. During the ensuing luteal phase, the mature follicle becomes the corpus luteum (Gr and Theca cells) which secretes progesterone and estradiol. The uterus undergoes further proliferative and secretory changes 6-7 days. The follicular phase is the late follicular phase and high levels of beta estradiol at this time primes the uterus by increasing the number of progesterone receptors to convert proliferate to secretory uterus…lots of glandular: mucus, juicy uterus. Not acceptable for implantation. This happens over 6-7 days. It becomes more secretory in response to progesterone. Unless pregnancy occurs, endometrial sloughing and menstruation, marking the beginning of a new cycle. Image shows 14-day fixed phase, luteal phase.


At the beginning of fertilization

your placenta is not well developed and cannot sustain blastocyst. Need corpus luteum first 8 weeks. LH luteinizes cells to produces estrogens, progesterone (high). Something has to come in keep the LH/corpus luteum around until the blastocyst can be supported by the placenta. hCG Is that something


Time course of Fertilization and Implantation

o Fertilization occurs in the fallopian tubes (typically)-takes 3-5 days for the blastocyst to make its way to the uterus and another 1-2 days for it to implant into the uterus. The synctiotrophoblasts of the blastocyst makes hCG (early on)…basis of home pregnancy test.
hCG stays high for sustainance of In addition to the flagella beating to cause motility of the sperm, uterine and cervical contractions facilitate sperm transport. At this early stage of pregnancy, the corpus luteum continues to produce steroids to maintain pregnancy as the placenta develops from trophoblasts and adjacent cells



o Is produced in the synctiotrophoblasts of the blastocyst. Looks and acts like LH
o Sustains the corpus luteum in the face of declining levels of maternal LH. This keeps up and increases sex steroid production. Highest during the 8th to the 13 weeks of pregnancy/ reason for morning sickness.
o Immunosuppressant, promotes growth and placental development.
o (In males hCG stimulates the testes of the male fetus to produce testosterone, leading to male organ development. Measured in urine after blastocyst implants)
o Image: hCG is good fr the first trimester but is limited in capacity to make steroids. Need the placenta. Need P-M-F unit. While hCG is high the corpus luteum is making steroids, they are not that high. Midway all the estrogens and progesterone are taking over.


The fetus derives nutrition from

the endometrial decidua (1st trimester) until the food can diffuse thru the placenta.


The placenta:

o Synthesizes 1.steroid hormone, 2. hCG and 3. somatomamotropins are related to growth hormomes promoting fuel economy and mammary gland development in mom


What happens to maternal levels of progesterone and estrogens

Maternal levels progesterone and estrogens rise and remain elevated during pregnancy. Progesterone spikes near -4 & -8 weeks


What's significant about estriol?

Estriol reflects adequate development of the placenta around 8 weeks.


Mom and fetus cooperate to produce pregnancy hormones:

o After about 8 weeks of gestation, the coorodinated activity of maternal-placental-fetal unit maintains high levels of estrogens & progesterone
o The placenta needs both mother and fetus to produce steroid hormones, unlike the self-sufficient corpus luteum. It lacks three enzymes: 17-alpha-hydroxylase, 17,20-desmolase and 16-alpha-hydroxylase enzymes.
o The fetus lacks 3-beta-hydroxysteroid dehydrogenase and aromatase activity. It doesn’t make steroids
o The mama supplies cholesterol in the form of LDL, which the placenta uses to make progesterone for export to the mother to maintain pregnancy.
o The fetal adrenal gland and liver supply the three enzymes (estrogens) lacking in the placenta.
o The fetus lacks the enzymes that catalyze the final steps in estrogen synthesis. If the fetus alone were to generate estrogens, it would be exposed to dangerous levels of hormones needed by mom.


How does mom's body respond to preganncy?

o Increased blood volume-hypertrophied uterus has more demands
o MAP decreases or is normal maybe due to vasodilation
o Increased cardiac output usually first trimester, due to SV
o Increased alveolar ventilation
o Increased demand for dietary protein, iron, folic acid
o Increased uterus and breasts
o Weight gain 25-35 lbs
o BMR increases especially in the latter half of pregnancy
o Adaptive change in cardiovascular and respiratory systems, fluid volume, metabolism and nutrition



o Uterus is quiescent throughout the pregnancy due to progesterone and relaxin.
o Last month of pregnancy has irregular braxton hicks contractions until the regular labor contractions occur
o Parturition may be triggered by an increase in fetal cortisol which increases the estrogen/progesterone ratio and thus the uterus’s contractile stimuli
o Prostaglandins initiate contractions of the uterine smooth muscle. These are sustained by oxytocin and more prostaglandins


Parturition and prostaglandins

The uterus, fetal membranes and placenta produce prostaglandins which act by paracrine mech to stimulate uterine smooth muscle cells, promote formation of gap junctions betw smooth muscles WHICH POTENTIATES their response to oxytocin to cause softening/thinning/dilation or effacement of the cervix. Oxy doesn’t initiate contractions. Ratio of estrogen/progesterone might
o During pregnancy, estrogen increases the number of oxytocin receptors on myometrial tissue in the uterus. Maternal oxytocin is released in bursts with increasing frequency during labor. This occurs in response to distension of the cervix


Positive feedback loops

sustain production of prostaglandins and oxytocin as labor progresses



is produced by the corpus luteum placenta and decidua. Increased production during labor may help to soften/dilate the cervix.


Involution of the uterus

Involution of the uterus occurs after delivery in response to the changed endocrine milieu
Baby’s head stretches cervix→cervical stretch excites fundic contraction→ fundic contraction pushes baby down & stretches cervix more→cycle repeats. During “uterine awakening” or initiation of parturition there is an increase in the # of gap junctions b/w myometrial cells. During “active labor” complete cervical dilation to deliver the newborn



o Oxytocin promotes milk let-down & uterine contractility
o Prolactin promotes milk synthesis after birth
o Both hormones released in response to suckling


Breasts respond to hormones even after pregnancy.

Mammogenic hormones

promote cell proliferation. Progesterone acts synergistically with estrogen to cause additional growth of breast lobules, with alveoli budding and secretory characteristics


Lactogenic hormones

promote milk production; Prolactin



promotes milk let-down; Oxytocin



maintains milk production Prolactin and *cortisol



The functional secretory unit of the breast. It is organized into lobules, which drain into a ductile.15-20 ducts drain into a duct that leads to the outside. There are myoepithelial cells surrounding each alveolus which promotes milk let down in response to oxytocin. Secretory epithelial cells comprise the alveolus and secrete milk in response to prolactin and cortisol



provides concentrated low-volume form of nutrition for the neonate’s immature GI tract during the first few days of life.
o It does not contain much fat as compared to human milk. Has lots of antibodies


*Estrogen and progesterone prevent actual secretion of milk.

The sudden loss of these steroids after deliver allows prolactin to exert its lactogenic effect. Upon suckling, prolactin levels spike



1. Stimulates sensory nerves which carry the signal from the breast to the spinal cord where they synapse with neurons that carry the signal to the brain
2. In the arcuate nucleus of the hypothalamus, the afferent input from the nipple inhibits neurons that release dopamine. Dopamine inhibits prolactin so with dopamine inhibited, prolactin can flow.
3. In the supraoptic and paraventricular nuclei of the hypothalamus, the afferent input from the nipple triggers the production and release of oxytocin from the post pit.
4. In the preoptic area and arcuate nucleus, the afferent input from the nipple inhibits GnRH release. GnRH promotes release of FSH and LH from the ant pit. With GnRH inhibited, LH & FSH are inhibited and thus the ovarian cycle is inhibited in lactating females/cannot be pregnant.