Chapter 10 - Reproductive Physiology Flashcards

1
Q

Things that can define sex

A

Chromosomal Sex, Gonadal Sex, Phenotypic Sex, and Gender Identity

Chromosomal Sex - presence of Y chromosome is considered male, absence of Y chromosome is considered female

Gonadal Sex - presence of ovaries is designated female, presence of testes is designated male

Phenotypic Sex - appearance of external genitalia (most commonly used for definition of sex), newborn with penis is considered boy newborn with vagina is considered girl (this is typically consistent with gonadal sex in normal sexual differentiation AKA vagina + ovaries and penis + testes)

Gender identity - basic sense of being male or female, independent of any other definition of sex, regulated by brain development

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2
Q

Complete Androgen Insensitivity Syndrome (CAIS)

A

CAIS patients do not have androgen receptors for cells to respond to the male reproductive hormone (testosterone) released by the testes - exhibit male gonadal sex (have testes) but female phenotypic sex (have a vagina)

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3
Q

General Principle of Fetal Sexual Differentiation

A

Sex-determining region of the Y chromosome (SRY) gene directs the differentiation of fetal undifferentiated gonads into testes (it encodes the transcription factor that is necessary for development of testes)

In absence of SRY gene, the default for fetal sexual differentiation is female

In addition to SRY gene, sex hormones and receptors are necessary for the profession of male sexual differentiation from testes to male genitalia (genetic deficiencies in sex hormone-regulating enzymes (such as 5-alpha-reductase) and sex hormone receptors (such as androgen receptors) can result in abnormal male phenotypic sex despite normal male chromosomal sex)

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4
Q

Klinefelter and Turner Syndromes

A

Klinefelter - XXY individuals, develop as males because of presence of SRY gene

Turner - XO individuals, develop as female because no SRY gene

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5
Q

Male Fetal Sexual Differentiation

A

In fetuses with XY chromosomes, SRY gene enables undifferentiated gonads to develop into testes

Two hormones produced by fetal testes (anti-Mullerian hormone, AMH, and testosterone) are essential for development of male genitalia - AMH causes the regression of the Mullerian ducts in the male fetus and testosterone (produced by Leydig cells in the testes) enables development of Wolffian ducts into vas deferens, epididymis, and seminal vesicles

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6
Q

Female Exposure to Testosterone

A

Exposure of females to testosterone in utero can lead to abnormal differentiation toward the male phenotype

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7
Q

Female Fetal Sexual Differentiation

A

Absence of Y chromosome (and SRY gene) leads to female differentiation - undifferentiated gonads become ovaries

In the absence of testosterone, the Wolffian duct system regresses and Mullein duct system develops into the oviduct (fallopian tubule) and uterus and in the absence of DHT the external genitalia develop into a vagina

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8
Q

Meiosis

A

The basic cellular process for production of sperms in males and ova in females - begins with DNA replication (forming two sister chromatids per chromosome), during interphase prior to meiosis I, crossover between homologous chromosomes can lead to formation of recombinant chromatids from the two parent chromosomes (this is important for creating genetic diversity of sperms and eggs)

During human meiosis I, homologous chromosomes segregate from each other to form two daughter cells having 23 chromosomes, with two chromatids per chromosome

During human meiosis II, the two chromatids of each chromosome separate from each other to form two daughter cells each having 23 chromosomes with one chromatid per chromosome

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9
Q

Spermatogenesis by Meiosis

A

Start with a primary spermatocyte that has 23 pairs of homologous chromosomes with two chromatids per chromosome (before meiosis I is interphase and there is crossover between homologous chromosomes)

Then form two secondary spermatocytes after Meiosis I, each contains 23 chromosomes with two chromatids per chromosome

Then form four spermatids after Meiosis II, each contains 23 chromosomes with one chromatid per chromosome

Then differentiate into fully differentiated spermatozoa

Primary Spermatocyte (46 Chromosomes, 2 chromatids) –> Secondary Spermatocyte (23 chromosomes, 2 chromatids) –> Spermatid (23 chromosomes, 1 chromatid) –> Spermatozoa

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10
Q

Male Reproductive System Anatomy

A

Consists of penis, accessory glands (seminal vesicles, prostate gland), a pair of vas deferens, and two testes (organs of spermatogenesis)

The descent of testes out of the abdominal cavity through the inguinal canal during fetal development is essential for male fertility because spermatogenesis requires a temperature that is 2-4 degrees below core body temperature

Seminiferous tubules produce sperm, epididymus stores sperm, and vas deferens transports sperm to the penis

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11
Q

Spermatogenesis

A

Undifferentiated spermatogonium are nurtured to the differentiated spermatozoa by Sertoli cells in the seminiferous tubules of testes

The blood-testes barrier separates the Sertoli cell-formed seminiferous epithelium into the outer basal and inner adluminal compartments - the outer basal compartment is the location of spermatogonial renewal and differentiation and the inner adluminal compartment is the location of the production of secondary spermatocytes from primary spermatocytes by meiosis I and II and differentiation of spermatocytes into spermatid

The blood-testis berries is dynamic and allows for crossing of spermatocytes from the basal compartment to the adluminal compartment

A fully differentiated sperm has a head, mid-piece, tail and end piece:
The head holds the nucleus and acrosome, nucleus holds genetic material and acrosome contains enzymes that facilitate that entry of a sperm into the ovum during fertilization
Mid piece contains mitochondria for energy metabolism
Tail contains motor proteins for sperm motility

Semen ejaculated during intercourse is usually 10% sperm and 90% seminal plasma (secretions from seminal vesicles and prostate glands)

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12
Q

Male Reproductive Hormonal System

A

2 distinct branches: regulation of spermatogenesis and secretion of testosterone

Hypothalamus secretes GnRH which stimulates anterior pituitary to release FSH and LH

FSH stimulates spermatogenesis as nurtured by Sertoli cells in the testes and by negative feedback to the anterior pituitary, Sertoli cells secreting an inhibitory peptide inhibin which inhibits FSH secretion from anterior pituitary (negative feedback)

LH stimulates the secretion of testosterone by Leydig cells in the testis and testosterone inhibits the secretion of GnRH (at the hypothalamus) and LH (at the anterior pituitary) via negative feedback

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13
Q

Effects of Testosterone

A
  1. Maintenance of accessory reproductive organs
  2. Maintenance of secondary sex characteristics (growth of testes and penis)
  3. Increase sex drive
  4. Increase protein synthesis is skeletal muscle
  5. Bone growth in adolescence
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14
Q

5-alpha-reductase

A

5-alpha-reductase catalyzes the conversion of testosterone to DHT, a hormone necessary for the development of the penis

If males are exposed to 5-alpha-reductase inhibitors in utero it can lead to underdevelopment of the penis

Testosterone –> DHT happens in many organs (prostate, testis, hair follicles, liver, skin, brain) and in adults it is the major androgen in the prostate gland, excessive amounts can cause prostate enlargement and obstruction of urinary tract, treated with pharmacological inhibitors of 5-alpha-reductase

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15
Q

Erectile Function Basics

A

Penile erection is a complex spinal reflect that can be initiated by mechanical, visual and mental stimuli - erectile tissue is the vascular tissue (known as corpora cavernosa) that consists of vascular sinusoids lined with endothelial and vascular smooth muscle cells, when the corpora cavernosa is filled with blood, the penis becomes erect

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16
Q

Synthesis of NO in Penis

A

Nitric Oxide (NO) released by neurons (nonadrenergic and noncholenergic) and endothelial cells and prostaglandin E1 released by cells within the penis are the major mediators of cavernosal smooth muscle relaxation during penile erection, NO is synthesized from L-arginine by neuronal nitric oxide synthase in neurons and endothelial NO synthase in endothelial cells - both syntheses are stimulated by intracellular calcium concentration

Increase in intracellular [Ca2+] –> Activation of nNOS or eNOS –> Synthesis of NO from L-arginine

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17
Q

Vascular Steps for Penile Erection

A
  1. Dilation of cavernosal arterioles and arteries increases inflow of blood to corpora cavernosa
  2. Relaxation of cavernosal smooth muscle cells increases compliance of corporal cavernosa for filling of blood (corporal tissue swells with blood, erecting penis)
  3. Compression of cavernosal veins by the erectile tissue reduces the outflow of blood from corpora cavernosa and maintains the rigidity of the penis
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18
Q

Cascade to Penile Erection

A
  1. Electrical stimulation leads to increase in intracellular [Ca2+] in nonadrenergic, noncholinergic neurons and parasympathetic stimulation via muscarinic ACh receptors lead to increase in intracellular [Ca2+] in endothelial cells
  2. lipid soluble NO diffuses into cavernosal smooth muscle cells to induce muscle relaxation via
  3. NO activates guanylyl cyclase
  4. Guanylyl cyclase catalyzes the formation of cGMP from GTP (PDE5 catalyzes the degradation of cGMP to CMP so the guanylyl cyclase to PDE5 ratio is a major determinant of [cGMP] and strength of penile erection)
  5. cGMP activates cGMP-dependent protein kinase (cGK)
  6. cGK stimulates Ca2+ uptake by the SR, inhibits calcium channels and activates potassium channels on the cell membrane
  7. Decrease in intracellular [Ca2+] in cavernosal muscle cells
  8. Relaxation of cavernosal smooth muscle cells
  9. Penile erection

cGMP is the intracellular messenger for penile erection

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19
Q

Erectile Dysfunction

A

Inhibitors of PDE5 can treat erectile dysfunction by enhancing intracellular [cGMP] in cavernosal smooth muscle cells

PGE1 injection and pharmacological inhibitors of PDE2,3,4 have also been developed for treating erectile dysfunction

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20
Q

Prostaglandin E1 (PGE1)

A

Mediator of penile erection - PGE1 is released by cells in the penis and induces cavernosal smooth muscle relaxation by activating a GCPR on the cell membrane and triggering this cascade:

  1. Activation of adenylyl cyclase
  2. Conversion of ATP to cAMP (cAMP is degraded to AMP by PDE 2,3,4)
  3. Activation of cAMP-dependent protein kinase (PKA)
  4. PKA-mediated stimulation of Ca2+ uptake from SR, inhibition of calcium channels, and activation of K+ channels on cell membrane
  5. Decrease in intracellular [Ca2+]
  6. Cavernosal smooth muscle contraction
  7. Penile erection
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21
Q

Female Reproductive Anatomy

A

Consists of clitoris, labium minus and labium magus, vagina, cervix, uterus, uterine (fallopian) tubes, and ovaries

The clitoris, the main organ of orgasm in females, is similar to the penis in being developed from the same embryonic structure and having cavernous erectile tissue

The vagina is the entrance and exit from the female reproductive tract and vaginal mucosa is responsive to female reproductive hormones and undergoes changes in thickness during a menstrual cycle (in non-pregnant females it reaches its peak thickness at the middle of the cycle)

The uterus is the site of embryo implantation and placental formation as well as fetal development

Uterine (fallopian) tubes are conduits for the transport of ova from ovaries toward the uterus for fertilization with a sperm, which typically occurs inside the fallopian tube

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22
Q

Oogenesis

A

Similar to spermatogenesis bc utilizes meiosis for production of ovum

By the time of birth, all oogonia have developed into primary oocytes (therefore an oocyte released at the time of ovulation is as old as the ovulating person, and errors in meiosis tend to increase with age to maternal age is a risk factor for developing chromosomal abnormalities in the ovum)

Typically only one primary oocyte becomes dominant for development into a mature ovum during each menstrual cycle (approx 28 days)

23
Q

Asymmetric oogenesis process

A

Oogenesis is an asymmetric process (spermatogenesis produces 4 sperms from one primary spermatocyte whereas oogenesis produces only one ovum from a primary oocyte) and in Meiosis I the secondary oocyte captures the majority of the cytoplasm:
primary oocyte, undergoes maturation with DNA duplication giving 46 chromosomes with 2 chromatids per chromosome –> secondary oocyte (released from ovary into fallopian tube via ovulation for fertilization by sperm, if fertilization does not occur then it will not continue and will be expelled by the uterus during the menstrual cycle, if it does occur it will undergo Meiosis II and continue) + 1 polar body (contains very little cytoplasm and undergoes extrusion and degeneration) –> Mature ovum, contains 23 chromosomes with one chromatid per chromosome (fuses with sperm to form zygote) + 3 polar bodies (extruded)

Ovulation —> First Polar Body + Secondary Oocyte (if fertilized) –> Meiosis II –> Secondary Polar Body + Mature Ovum

Mature Ovum + Sperm –> Zygote

24
Q

Female Reproductive Hormone System Fluctuations and Estrogen Production

A

Reproductive hormones in human females undergo significant oscillations during a menstrual cycle (bc female reproductive endocrine cells and oocyte are part of the ovarian follicle that undergo development and degeneration during a menstrual cycle), ovarian follicle undergoes development and degeneration during a menstrual cycle (and theca cells and granulose cells also undergo development and degeneration during the cycle, causing the fluctuations in hormone levels), endometrial layer of uterus also undergoes growth and degeneration during a menstrual cycle because endometrial growth is dependent on reproductive hormones

25
Q

Ovarian Follicle Structure and Functions (generation of estrogen)

A

An ovarian follicle consists of an oocyte and follicular fluid in the center, with outer layers of granulose and theca cells - granulose serve two functions (nurturing of ovarian follicular development and conversion of androgens to estrogens)

Theca cells are endocrine cells that secrete androgens (androstenedione and testosterone) which are then converted by the enzyme aromatase in granulose cells to estrogens (estrone and estradiol)

Theca cells –> Androgens –> Granulosa Cells –> Estrogens

26
Q

Female Reproductive System Hormones

A

GnRH also known as LHRH (released from hypothalamus) and same anterior pituitary hormones (FSH and LH)

FSH stimulates granulosa cells to secrete factors that are essential for ovarian follicular development and stimulates granulosa cells to convert androgens to estrogens for secretion (by negative feedback, granulosa cells respond to FSH with the secretion of the inhibitory peptide inhibit which inhibits FSH secretion from anterior pituitary gland)

LH stimulates theca cells to secrete androgens, which are converted by granulosa cells to estrogens (by negative feedback, estrogens and progesterones inhibit the secretion of GnRH by hypothalamus and LH by anterior pituitary)

27
Q

Postovulatory Ovarian Follicle

A

Following ovulation, the follicle is transformed into corpus letup, an endocrine gland that secretes estrogen and progesterone in response to stimulation by LH

Progesterone secreted by the corpus lute is essential for maintaining the uterine endometrium for implantation of the embryo during early stage of pregnancy

28
Q

The Menstrual Cycle (and phases)

A

Refers to cyclical changes in the female reproductive system

Duration: ~28 days

Follicular Development and Degeneration –> Fluctuations in the secretion of Reproductive Hormones —> Uterine Endometrial Growth and Degeneration

Begins with Menstruation (overlaps with beginning of follicular phase), follicular phase lasts until ovulation, then luteal phase until next menstruation

29
Q

Uterine Endometrial Degeneration

A

Causes menstrual bleeding, is the first day of the cycle (beginning of endometrial degeneration, when levels of estrogen and progesterone have failed to their lowest levels after degeneration of the corpus letup), degenerated endometrium is expelled by the uterus as menstrual blood

30
Q

Follicular Phase

A

Characterized by follicular development, increases in plasma concentration of FSH, LH, estrogens and androgen, and uterine endometrial development

Development of ovarian follicle from the first day of the menstrual cycle to the day before ovulation, body temperature during this phase is 1 degree lower than body temperature after ovulation (change in body temperature can help determine time of ovulation and fertile window for conception)

Plasma concentrations of FSH and LH increase during the follicular phase because GnRH secreting cells in the hypothalamus and FSH and LH secreting cells in the anterior pituitary become active in the absence of feedback inhibition by estrogen and inhibit, FSH and LH together stimulate development of the oocyte, theca cells, and granulosa cells in the ovarian follicle (theca cells secrete androgens which are converted to estrogens by granulosa cells), plasma concentration of androgens and estrogen increases during the follicular phase and peaks just before ovulation

In response to rising level of estrogen, uterine endometrium begins to develop around the 8th day of the menstrual cycle

31
Q

Ovulation

A

The process of releasing an ovum from an ovarian follicle (typically occurs in middle of cycle AKA day 14), happens by positive feedback from estrogen-induced LH surge that triggers ovulation (LH is a stimulant of estrogen secretion, so both are amplified to very high levels):

High plasma [estrogen] –> GnRH surge –> LH surge –> Ovulation (release of a secondary oocyte from the ovarian follicle, captured by fallopian tube and transported by ciliated cells along the tube toward the uterus)

Unfertilized secondary oocyte typically survives in Fallopian tube for up to two days, this is the “fertile window” for conception

After ovulation, the postovulatory ovarian follicle begins to evolve into a different reproductive endocrine gland, the corpus lute, and the menstrual cycle enters the luteal phase

32
Q

Luteal Phase

A

Development of the corpus lute - an endocrine gland evolved from the postovulatory ovarian follicle (“yellow body”), it functions to secrete progesterone and estrogen (essential for supporting the growth of the uterine endometrium for embryo implantation)

If the secondary oocyte is not fertilized by sperm, the corpus lute will spontaneously undergo degeneration resulting in the fall in plasma concentration of estrogen and progesterone, degeneration of uterine endometrium, and menstrual bleeding

If the secondary oocyte is fertilized by a sperm and the embryo is implanted into the uterine endometrium, the placenta-forming cells will secrete human chorionic gonadotropin (hCG) that rescues the corpus luteum from degeneration and the corpus lute will continue to secrete progesterone for 4-5 weeks after implantation of embryo, by which point the placenta becomes the major source of estrogen and progesterone for sustaining pregnancy

33
Q

Timeline/Puberty in Males and Females

A
  1. Around age 8, hypothalamus increases production of GnRH
  2. GnRH triggers LH and FSH release from anterior pituitary
  3. LH and FSH trigger testosterone production in testes and estrogen production in ovaries
  4. Spermatogenesis and penis and scrotum grow, facial hair grows, larynx elongates (lowering voice), shoulders broaden, body armpit and public hair grow, musculature increases across the body
    Folliculogenesis, breasts develop and mature, hips broaden, public hair grows
  5. Before puberty, hypothalamus and pituitary are very sensitive to negative feedback signals from testosterone and estrogen, during puberty this sensitivity decreases to levels usually seen in adults in order to allow increase in these hormones for development of secondary sex characteristics
34
Q

Side Effects of Anabolic Steroid Use

A

Increases muscle mass but:

  1. increase BP
  2. acne, male pattern baldness, liver disease
  3. Jaundiced eyes with liver disease
  4. Chest tenderness and breast growth in men
  5. RUQ tenderness, liver disease
  6. Testicular atrophy and prostatic hypertrophy in men
  7. Generalized muscle hypertrophy with disproportionately large upper body mass (esp. neck, shoulders, arms, and chest)
  8. Oedema due to water retention
35
Q

Penile Erection Contractor Contributors and Relaxation Contributors

A

Contraction: NE, Epinephrine, angiotensin II, serotonin, tumor necrosis factor, prostanoids

Relaxation: ACh, DA, ATP, adenosine, VIP, prostanoids, endocannabinoids, adrenomedullin

36
Q

Sperm Fertilization (until zygote)

A

Sperm motility is necessary to fertilize egg in the fallopian tube (1-2 days after ovulation), fertilized egg (zygote) then undergoes cell divisions and migrates down the fallopian tube toward the uterus for implantation into the uterine endometrium, implantation at blastocyst stage is 8-9 days after fertilization

Sperm undergoes capacitation during its migration through the female reproductive tract to become competent for fertilization - sperm capacitation consists of releasing cholesterol, glycoprotein, and other molecules from the surface of the sperm to enable the acrosome of the head to undergo necessary acrosomal reaction for entering the oocyte

A sperm penetrates the matrix of cumulus cells and undergoes the acrosomal reaction in which acrosomal enzymes are released by exocytosis and the sperm then binds to the zone pellucid of the ovum and it travels through into the perivitelline space and the sperm fuses with the oocyte membrane via specific oocyte membrane surface proteins, fertilization of the oocyte triggers meiosis with the formation of a mature ovum and the secondary polar body and this fusion leads to the formation of a zygote

37
Q

Blastocyst Implantation

A

Fusion of sperm and egg led to zygote which then undergoes cell division to form an embryo (polyspermy is blocked by fertilized ovum releasing cortical granules from cortex by exocytosis which causes the zone pellucid to become non-receptive to binding of other sperms)

At time of implantation a blastocyst consists of an inner cell mass (embryo blast), cavity (blastocoele) and the surrounding trophoblast - contact between the blastocyst and the uterine endometrium stimulate endometrial and trophoblast cells to undergo proliferation and differentiation for the formation of placenta

  1. The blastocyst digests the uterine mucosa when it initially implants in the endometrium
  2. Eventually the endometrium grows over and surrounds the embryo, fully securing it to the uterine lining
  3. Implanted embryo continues to grow within the endometrium
38
Q

Placenta and Hormones

A

The placenta functions as an interface for diffusional transport of nutrients and waste between maternal and fetal circulation (the chorionic villi, fingerlike structure within the placenta, are formed by the invasion of trophoblast cells from the embryo and are perfused by umbilical vessels of the fetus whereas the intervillous space of the placenta is perfused by maternal blood vessels)

The placenta also functions as an important endocrine gland - during embryo implantation it secretes hCG important for rescuing the corpus lute from degeneration (this hormone can be found in maternal blood as early as 48 hours after implantation and it is an indicator of pregnancy)

Secretion of progesterone by corpus luteum is essential for maintaining the uterine endometrium for placental development during early pregnancy and after the 6-10th week of pregnancy, the placenta becomes the major source of progesterone and estrogen

Progesterone is important for maintaining quiescence of the myometrium for fetal growth during pregnancy and estrogen is important for supporting the development of uterine myometrial contractility near term, breast development during pregnancy, and cervical ripening during labor

39
Q

Time-Dependent Changes for Parturition (Labor)

A

Complex, regulated by hormones, inflammatory cytokines and local mediators

Time-dependent changes in uterine contractility and cervical openings are essential for successful pregnancy and labor, uterine smooth muscle cells are quiescent during pregnancy for accommodating fetal growth but become contractile near term for expelling the baby and the cervix is closed and rigid during pregnancy for bearing the weight of the fetus but it becomes soften and ripened (loss of tissue compliance) near term for allowing the baby to exit th uterus during labor

Progesterone/estrogen activity ratio appears to be an important determinant of uterine smooth muscle contractility and cervical opening during pregnancy, a high ratio during pregnancy inhibits uterine smooth muscle contractility and cervical ripening to accommodate and hold the fetus (progesterone inhibits uterine contractility in part by suppressing the expression of oxytocin receptors in uterine smooth muscle cells), a reversal of the ratio (progesterone withdrawal) near terms causes smooth muscle contractility and cervical ripening (treatment with progesterone has been used to prevent pre-term birth)

40
Q

Oxytocin and Prostaglandins

A

Oxytocin stimulates uterine smooth muscle contractility during parturition - in a positive feedback mechanism, the contracting uterus sends neural signals to the brain to stimulate secretion of oxytocin by the posterior pituitary gland (maximizes oxytocin release and uterine contractions to expel baby from uterus)

Placenta also produces large amount of oxytocin during pregnancy but its contribution during labor is unclear

Prostaglandins within the uterus stimulate uterine smooth muscle contractions near term and stimulate the degradation and reorganization of the extracellular matrix (for example, collagen in the cervix) to cause cervical softening and ripening for the baby to exit the uterus

Oxytocin and Prostaglandins E1 and E1 are sometimes used to induce labor

41
Q

Oral Contraceptives

A

Estrogen and Progestin

Estrogen prevents release of FSH and keeps ovaries inactive

Progestin increases the thickness of the cervical mucus, decreases sperm motility, slows movement of ovum, suppresses ovulation (sometimes), inhibits development of uterine lining, suppresses mid cycle peaks of LH and FSH, and may reduce cilia activity in the fallopian tube

42
Q

Age-Dependent Changes in FSH and Inhibin Levels and Hot Flashes

A

At 12 inhibin is much higher than FSH, decreases so they are equal around 25, at 36 FSH is higher and by 45 it is very high

Estrogen withdrawal causes increase NE which increases activation of alpha receptors in hypothalamus, causing reduction in thermoregulatory neutral zone, giving autonomic reactions to cool the body, leading to a hot flash (also sweating threshold decreases post-menopause)

43
Q

Pulmonary Fetal Circulation

A

Lungs in the fetus are not ventilated with air so the placenta functions as the gas exchanger between maternal circulation and fetal circulation - umbilical arteries carry deoxygenated blood away from the fetal systemic arterial system to the placenta for oxygenation and the umbilical vein carries oxygenated blood from the placenta to the fetal systemic venous system via the ductus venosus (total pulmonary blood flow is less than total systemic blood flow)

Due to the presence of high vascular resistance in the fetal pulmonary circulation and two low-resistance shunts between the right and left fetal hearts, a significant amount of systemic venous return to the right heart flows directly into the fetal systemic arterial system bypassing the pulmonary circulation

The foramen ovale is an opening between the right and left atrium in the fetal heart that allows a significant amount of systemic venous return to the right atrium to flow into the left atrium (instead of the right ventricle) to reduce the amount of blood flow into the pulmonary circulation:

Right Atrium –> Foramen Ovale –> Left Atrium

The ductus arterioles is a low-resistance vascular conduit between the main pulmonary artery and aorta in the fetal heart which allows a substantial amount of pulmonary arterial blood to flow into the aorta (reducing the amount of blood flow into pulmonary circulation)

Pulmonary Artery –> Ductus Arteriosus –> Aorta

44
Q

Stimulation of Milk Production

A

During pregnancy, estrogen, progesterone, and prolactin stimulate breast development and maturation by stimulating the development of alveoli in the breast for milk secretion and storage and the ductal system for carrying milk to the nipple

Prolactin is the major hormone for stimulating milk synthesis by alveolar epithelial cells. The increase in plasma concentration of prolactin during pregnancy is largely due to stimulation by estrogen (progesterone stimulates breast development but inhibits milk synthesis but plasma progesterone levels fall after expulsion of the placenta, thereby removing the inhibitory effect of progesterone on milk synthesis), milk synthesis begins at 2-3 days after birth but mature milk production occurs 2-3 weeks after birth

Suckling of breast by an infant or pump stimulates secretion of prolactin from the anterior pituitary (removing inhibitory effect of dopamine on prolactin-secreting cells) and stimulates release of oxytocin which stimulates the contraction of myoepithelial cells surrounding the alveoli resulting in milk ejection (oxytocin also stimulates the uterine smooth muscle contractions, facilitating the return of the uterus to the pre-pregnancy size)

45
Q

Breast Milk Makeup

A

Immediately after birth the breast produces colostrum, a fluid containing low concentration of milk protein and high concentration go immunoglobulin and other biological factors that stimulate the development of the GI tract and immune system in the newborn

46
Q

Weaning (Cessation of Lactation)

A

Weaning (cessation of breast-feeding) includes the loss of alveoli and return of the breast to the non-lactating state, relaxation is the process of restarting lactation after a period of weaning by mechanical stimulation of the breast with a breast pump and/or nursing child, this mechanical stimulation appears to be sufficient to stimulate the release of prolactin and induce lactation because it is possible to induce lactation in non-pregnant women via mechanical stimulation using a breast pump

47
Q

Lactation Induction

A

Dopamine receptor antagonists can induce lactation by blocking the inhibitory effect of dopamine on prolactin secretion

48
Q

Lactation and Menstruation

A

The process of lactation suppressed the release of GnRH from the hypothalamus, thereby delaying the onset of menstrual cycles in breast-feeding women (lactation has been proposed as a natural method of contraception)

49
Q

Fetal Circulation

A
  1. Blood arrives via the umbilical vein
  2. The ductus venous shunts oxygenated blood from the placenta away from the semi functional liver and toward the heart
  3. Oxygenated blood from placenta enters right atrium via inferior vena cava
  4. The foramen oval allows oxygenated blood in the right atrium to reach the left atrium
  5. The ductus arteriosus connects the aorta with the pulmonary artery, further shunting blood away from the lungs and into the aorta
  6. Mixed blood travels to the head and body and back to the placenta via the aorta
50
Q

Neonatal Circulation

A

Immediately after birth: the ductus arteriosus constricts, allowing all blood leaving the right ventricle to travel to the lungs via the pulmonary arteries and the foramen ovale closes, leaving a small depression called the fossa ovals which isolates deoxygenated and oxygenated blood within the heart

51
Q

Can have negative effects on child

A

Sparse environment, genetic and epigenetic inheritances, obesity during pregnancy, excessive gestational weight gain, high dietary sugar and fat, diabetes during pregnancy

Excess glucose, ketone bodies, FAs and AAs can lead to inflammation, adiposity and hyperinsulinemia

52
Q

Stages of Labor

A

Stage 1 - Dilation of cervix
Stage 2 - Birth
1. Presentation of head
2. Rotation and delivery of anterior shoulder
3. Delivery of posterior shoulder
4. Delivery of lower body and umbilical cord
Stage 3 - Afterbirth Delivery - placenta detaches and exits through vagina

53
Q

Cycle for Uterine Contraction

A

Brain stimulates pituitary gland to secrete oxytocin –> oxytocin carried in bloodstream to uterus –> oxytocin stimulates uterine contractions and pushes baby toward cervix –> head of baby pushes up against cervix –> nerve impulses from cervix transmitted to brain –> brain stimulates pituitary gland to secrete oxytocin