Reproductive System
Table of Contents
Female Reproductive System 1
Anatomy & Physiology 1
Oxytocin & Prolactin 5
Menstrual Cycle 7
Pregnancy 8
Labor 11
Breastfeeding 16
Menopause 18
Estrogen & Progesterone 19
Sexual Development 27
Development of the Reproductive System
27
Puberty & Tanner Staging 31
NOTES
INTERNAL ORGANS
Ovaries (female gonads)
• Epithelial, follicular, granulosa, theca, oocyte
cells
• Secrete estrogen, progesterone Figure 8.1 External organs of the female
• Located superior, lateral to uterus reproductive system.
• Held in place by ovarian, broad, suspensory
ligaments
O Suspensory ligaments contain ovarian l~[Link]
artery, vein, nerve plexus
• Made up of outer cortex, inner medulla OVARIES
(FEMALE GONADS)
° Cortex contains ovarian follicles (oocytes
surrounded by granulosa cells); medulla
contains blood vessels, nerves
Vagina
• Extends from uterus, opens into vulva
(covered by hymen in childhood)
• Outer muscular wall containing rugae; inner
mucous membrane of stratified squamous
epithelium
• Fornix (superior, domed area) connects to
sides of cervix
Figure 8.4 Outer cortex of ovary containing
follicles and inner medulla containing blood
vessels, nerves.
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ANTERIOR VIEW LATERAL VIEW
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surrounding structures.
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FOLLICULAR DEVELOPMENT
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Figure 8.8 Stages of follicular development. Stage one: primordial follicles ----> primary follicles,
meaning that the follicular cells surrounding the primary oocyte develop into granulosa cells.
Stage two: primary follicles----> secondary follicles----> teritary (Graafian) follicles. This stage
results in a few fast-growing Graafian follicles. Stage three: dominant follicle is established.
Ovulation: dominant follicle ruptures, releases secondary oocyte into fallopian tube. The
secondary oocyte stops in meta phase of meiosis II. Luteal phase: weeks 3 to 4 of menstrual
cycle. The remains of the follicle turn into the corpus luteum. If fertilization occurs, the corpus
luteum keeps making progesterone until the placenta forms. If not, the corpus luteum stops
making hormones after about ten days, becomes fibrotlc-o corpus albicans.
OXYTOCIN PROLACTIN(PL)
• Essential for progression of labor, control • Synthesized by lactotrophs in anterior
of postpartum bleeding, return of uterus to pituitary----> target tissue (breasts)
pre-pregnancy state (involution) • Synthesis inhibited by dopamine during
• Synthesized, secreted by hypothalamus ----> non-pregnant/non-breastfeeding state
travels down axons to posterior pituitary
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NEUROENOOCRINE REFLEX
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Figure 8.11 Illustration of the neuroendocrine reflex. In response to the suckling of a baby,
oxytocin released from the posterior pituitary stimulates ejection of milk, and prolactin released
from the anterior pituitary increases milk production.
6
FUNCTIONS DURING & AFTER O Positive feedback loop: t uterine
LABOR contractions=- fetal head pushes
• Oxytocin (powerful uterine muscle against cervix -e neural signal travels
stimulant) produced during pregnancy, to spinal cord ---'> hvpothalamus e- j
does not stimulate uterine contractions due oxytocin release from posterior pituitary
to ---'> I uterine contractions ---'> cycle
O Rapid degradation by placental continues until delivery (baby, placenta)
oxytocinase • After labor, milder contractions continue
O Progesterone-induced inhibition of n Clamp down on placental arteries at
oxytocin receptors on myometrium placental attachment slte e- ! bleeding
• Estrogen-induced oxytocin receptor O Gradually I size of uterus (involution)
expression+ j myometrial sensitivity to O Additional oxytocin released during
oxytocin promotes uterine contractions breastfeeding ---'> speeds involution
during labor
MENSTRUAL CYCLE
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• Menstruation (menses): shedding of uterine Day 1
functional endometrium • Hypothalamus releases gonadotropin-
• Occurs approx. every 28 days releasing hormone (GnRH)---'> anterior
pituitary releases FSH, LH ---'> one oocyte
domtnates=- develops within primary
follicle
• Primary (primordial) follicle: oocyte
surrounded by single layer of granulosa
cells (nourish oocyte)
Days 1-13
• Granulosa cells proliferate---'> follicle grows
---'> develops outer layer of cells (theca layer)
---'> respond to LH by producing estrogen ---'>
mature follicle
O Estrogen acts on uterine endometrium
to prepare for fertilized egg ---'>
Figure 8.12 The uterine endometrium
initiates uterine proliferative phase -
consists of a thin base layer and a functional
endometrial lining grows
layer. The functional layer is subject to the
O Estrogen also feeds back to
changes (thickening and shedding) that occur
hypothalamus, pituitary---'> turns off
during the menstrual cycle.
GnRH, FSH, LH
Day 14
FOLLICULAR PHASE • Brief LH surge stimulates ovulation ---'>
• Ovulation (days 1-14): maturing follicles, follicle ruptures---'> oocyte ejected out of
proliferation of uterine mucosa, dominated follicle
by estrogen
7
LUTEAL PHASE Day25
• After ovulation, empty follicle collapses • If fertilization does not occur - corpus
- turns into corpus luteum - produces luteum undergoes apoptosis -
progesterone (approx. 14 days) progesterone levels fall
O Endometrium becomes highly • If fertilization does occur - embryonic
vascularized, glycogen-filled tissue tissue secretes human chorionic
(secretory phase) gonadotropin (hCG) - signals corpus
luteum to continue production of estrogen,
Days 15-24 progesterone to support pregnancy
• Egg travels through fallopian tube
PREGNANCY
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• Obstetric history (GTPAL) activity (6-8 weeks)
O G (gravidaJ: number of pregnancies,
regardless of duration (including current ESTIMATED DATE OF DELIVERY
pregnancy) (EDD)
O T: number of term infants born • Calculated from last menstrual period (LMP)
O P: number of preterm infants born to estimated date of delivery (EDD)
O A: number of spontaneous/induced • Naegele's rule: add 7 days to 1st day of
abortions LMP, subtract 3 months, add 7 days, add 1
O L: number of currently living children year
O Example: G3P1202 (3 pregnancies, 1 • Ultrasonic examination
term birth, 2 preterm births, 0 abortions, , Measurement of crown-to-rump length
2 living children) in first trimester
• Pregnancy lasts approx. 280 days (40 • Measurement of fundal height estimates
weeks); divided into three trimesters pregnancy progression
O Symphysis: 12-14 weeks
SIGNS & SYMPTOMS O Umbilicus: 20 weeks
O Rises above umbilicus 1 cm/week until
Presumptive
36weeks
• Amenorrhea; breast fullness, tenderness;
nausea/vomiting ("morning sickness");
urinary frequency; fatigue; fetal movement PHYSIOLOGICAL CHANGES IN THE
(16-20 weeks of gestation) REPRODUCTIVE SYSTEM
Probable Uterus
• Uterine enlargement; softening of uterine • l size, capacity due to hypertrophy,
isthmus (Hegar sign); vaginal, cervical hyperplasia, mechanical stretching
purplish-blue discoloration (Chadwick sign); • 20 times larger
positive urine/serum hCG • l strength, distensibility,
contractile
proteins, number of mitochondria
Positive
• l volume capacity (10 ml-5 L)
• Auscultation of fetal heart tones (7-8
• Softening of uterine isthmus (Hegar's sign)
weeks of gestation); "quickening" (fetal
movements); fetal sac visualized by
ultrasound (5-6 weeks); fetal cardiac
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• Hyperpigmentation (due to estrogen, j
melanocyte activity) ---'> melasma (chloasma)
Figure 8.15 Pregnancy is a high volume brownish "mask of pregnancy"; linea
state. Plasma volume l > RBC volume j ---'> ! nigra formation on abdomen; darkening of
hematocrit (physiologic anemia).
10
nipples, areolae, vulva • "Diabetogenic state" of pregnancy
• j cutaneous blood flow - I heat O j need for glucose, insulin production -
dissipation - pregnancy "glow" hypertrophy, hyperplasia of pancreatic
• ! connective tissue strength secondary to beta cells
j adrenal steroid levels - stretch marks • ! thyroid-stimulating hormone (TSH);
(striae gravidarum) in breasts, abdomen, thyroid gland enlarges; t total T3, T 4
thighs, inguinal area • Reproductive hormones
• Estrogen-induced vascular permeability - O hCG from placenta; estrogen,
spider nevi, angiomas, pal mar erythema progesterone from corpus luteum (first,
second trimesters). placenta (second,
Musculoskeletal
third trimesters)
• Abdominal distension + shift in center of O Suppressed FSH, LH due to feedback
gravity - lordosis from estrogen, progesterone, inhibin
• Enlarging uterus - separation of 0 ! oxytocin levels throughout pregnancy
abdominal rectus muscles (diastasis recti)
- l labor onset - Tl second stage of
• j progesterone, relaxin - j joint mobility, labor
"waddling" gait
O Widening of symphysis pubis
NUTRITIONAL NEEDS
° Facilitates accommodation of fetus into
• Recommendation of additional 300 kcal/
pelvis
day, weight gain of 25-35 pounds (11.5-
• High bone turnover, remodeling
16 kg)
Endocrine 0 11 lb (5 kg): placenta, amniotic fluid,
• j size of pituitary gland; mostly due to fetus
proliferation of lactotroph cells 0 2 lb (0.9 kg): uterus
O I intrasellar pressure - j risk of 0 4 lb (1.8 kg): j blood volume
postpartum infarction (Sheehan 0 3 lb (1.4 kg): breast tissue
syndrome) in setting of postpartum 0 5-10 lb (2.3-4.5 kg): maternal reserves
hemorrhage • 600 mcg folic acid/day - RBC synthesis,
• t parathyroid hormone (meets calcium placental/fetal growth, ! risk of neural tube
need of developing fetal skeleton) defects
• Physiologic hypercortisolism • 1,000-1,300 mg calcium/day supports
O l need for estrogen, cortisol - t pregnancy, lactation
glucocorticoids from adrenal glands - • 60g protein daily supports tissue growth
supports fetal somatic, reproductive • 27 mg iron/day supports j RBCs
growth
LABOR
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• Labor (parturition): uterine contractions PREMONITORY SIGNS
- cervical changes - delivery of baby, • Cervical changes
placenta O Remodeling of cervix by enzymatic
• Begins at term (37-42 weeks of gestation) collagen dissolution, j water content -
• Duration of three stages varies with softening. t distensibility
gravidity (nulliparas typically longer than • Cervical softening - expulsion of mucus
multi paras) plug - "bloody show" (pink-tinged mucus)
11
• Spontaneous rupture of amniotic Transition phase
membranes (ROM) • 30 minutes-2 hours
• Intense contractions every 1.5-2 minutes
False labor
• Duration 60-90 seconds
• AKA Braxton-Hicks contractions
• Cervical dilation 7-lOcm
• True labor: regular, increase in frequency,
duration, intensity; produce cervical • Effacement 100%
changes (e.g. dilation/opening up,
effacement/getting thinner); pain begins SECOND STAGE
in lower back. radiates to abdomen, not
• AKA pushing stage
relieved by ambulation
• Begins with full dilation
• False labor: irregular, intermittent
• Navigation through maternal pelvis dictated
contractions; no cervical changes; pain in
by 3 Ps
abdomen; walking may decrease pain
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Passenger O Gynecoid: rounded pelvic inlet,
• Fetal size midpelvis, outlet capacity adequate;
° Fetal head most critical; cephalopelvic optimal for vaginal delivery
disproportion - labor dystocia (difficult/ O Android: heart-shaped pelvic inlet; !
obstructed) midpelvis diameters, outlet capacity;
O Macrosomia (birth weiqht z 90th associated with labor dystocia
percentile for gestational age/> 4500 g) O Anthropoid: oval-shaped pelvic inlet;
associated with shoulder dystocia (fetal midpelvis diameters, outlet capacity
shoulder unable to pass below maternal adequate; favorable for vaginal delivery
pubic symphysis), birth injuries O Platypelloid: oval-shaped pelvic inlet,
• Fetal attitude: relationship of fetal parts to ! midpelvis diameters, outlet capacity
one another adequate; not favorable for vaginal
° Full flexion (chin on chest; rounded delivery
back with flexed arms, legs); smallest • Cardinal movements (mechanisms of labor)
diameter of head (suboccipitobregmatic O Descent:: presenting part reaches pelvic
diameter) presents at pelvic inlet inlet (engagement) before onset of labor
• Fetal lie: relationship of fetal cephalocaudal - degree of descent (fetal station),
axis (spinal column) to maternal relationship of presenting part to
cephalocaudal axis maternal ischial spines - fetus moves
O Longitudinal (ideal): fetal spine lies from pelvic inlet (-5 station) down to
along maternal ischial spines (0 station) to pelvic outlet
(+4 station) to crowning at vaginal
O Transverse: fetal spine perpendicular to
opening (+5 station)
maternal
° Flexion: fetal chin presses against chest,
O Oblique: fetus at slight angle
head meets resistance from pelvic floor
• Fetal presentation: fetal/presenting part O Internal rotation: fetal shoulders
enters pelvic inlet first
internally rotate 45°; widest part of
• Cephalic: head first shoulders in line with widest part of
O Vertex (most common): optimal for pelvic inlet
easy delivery; head completely flexed O Extension: fetal head passes under
onto chest - occiput (part of fetal skull symphysis pubis (+4 station). moves (+5
covered by occipital bone) is presenting station), emerges from vagina
O Brow: fetal head partially extended; O Restitution (external rotation): head
sinciput (part of fetal skull covered externally rotates as shoulders pass
by frontal bone, anterior fontanelle to through pelvic outlet, under symphysis
orbital ridge) presenting part pubis, turns to align with back
° Face: fetal head hyperextended; fetal O Expulsion: anterior shoulder slips under
face from forehead to chin presenting symphysis pubis, followed by posterior
part shoulder, rest of the body; marks end of
• Breech: head up; bottom. feet. knees second stage
present first
° Frank breech: hips flexed, knees
THIRD STAGE
extended; bottom presents
• Delivery of placenta, umbilical cord, fetal
° Complete breech: hips, knees flexed;
membranes; uterus contracts firmly,
bottom presents
placenta begins to separate from uterine
O Incomplete breech: one/both hips not wall
completely flexed; feet present
O Shoulder: transverse lie; shoulders
present first FOURTH STAGE
• Physiological adaptation to blood loss.
Passage initiation of uterine involution
• Route through bony pelvis
• Size. type of pelvis
13
FtTAL ATTlllJOE.
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FETAL P~[Link]
Figure 8.17 Fetal attitude, lie, and presentation are all critical factors in determining the fetus'
ease of passage through the maternal pelvis.
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formed in fetal gastrointestinal tract • Presentation: firm, tender breast; may have
• Helps establish healthy gut microbiome l vascular markings
• Treatment: empty breasts (t breastfeeding,
Transitional milk pumping); warm shower/compresses
• Produced 7-10 days postpartum; thinner before feeding (enhances let-down), cool
than colostrum; light yellow color compresses after feeding; nonsteroidal
anti-inflammatory drugs (NSAIDs);
Mature milk application of cool green cabbage leaves
• Produces 2 weeks postpartum • Prevention: frequent feedings, good latch
• Watery, slight bluish color; fat content to ensure emptying breast
increases during feeding
• Biologically complex Sore, cracked nipples
O Protein, fat, sugars (e.g. lactose, • Cause: improper latch, positioning
oligosaccharides), vitamins, minerals, • Presentation: pain; blister/bleb on nipple if
immunoglobulins, antibodies (esp. pores plugged
secretory lgA), immune cells (e.g. • Treatment: cool/warm compresses; apply
macrophages, neutrophils), immune- expressed breast milk to nipple; mild
modulating factors (e.g. lactoferrin, analgesics (e.g. acetaminophen)
lysozyme, lactoperoxidase) • Prevention: good breastfeeding technique
• Low in vitamin D; supplementation often
recommended Mastitis
• Continues to be produced until lactation • Cause: bacterial infection
ceases • Presentation: usually unilateral, localized
• Healthy maternal diet supports breast milk warmth, tenderness/pain, edema,
production erythema, firmness; acute onset of flu-like
symptoms (e.g. fever, fatigue)
• Treatment: continued breastfeeding,
CONTRAINDICATIONS & CAUTIONS NSAIDs, antibiotics
TO BREASTFEEDING
• Prevention: good hygiene
Contraindications
Yeast infections
• Certain maternal medications (e.g.
chemotherapy), illicit drugs (e.g. cannabis, • Cause: Candida albicans; history of infant
heroin) oral/diaper candidal infection/maternal
vaginal candidal infection
• HIV infection (in high-income settings)
• Presentation: infant may have white
• Herpes zoster, herpes simplex
plaques in oral area; mother may
O If lesions on breast experience pain, red/sore nipples
• Tuberculosis • Treatment: for mother, topical antifungal
O Until approx. 2 weeks of maternal applied after feeding; infant, nystatin
pharmacotherapy solution swabbed into oral mucosa after
feeding
Cautions
• Prevention: good hygiene; avoid excessive
• Smoking discouraged (l risk of SIDS,
moisture by keeping breasts dry between
respiratory problems) feedings
• Minimize alcohol; if consumed, wait two
hours before breastfeeding
• Limit caffeine
BREASTFEEDING PROBLEMS
Engorgement
• Cause: milk accumulation in breast tissue,
vascular congestion, resulting in pain
17
MENOPAUSE
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• Diagnosed when menstrual cycles have Others
stopped for entire year, no identified • Urinary tract dysfunction ----. dysuria, urinary
pathological cause urgency
• Caused by natural effects of ovarian • Mood lnstabllltv -e depression, anxiety
follicular depletion during aging process • Decline in cognitive function, difficulty
• Usually begins age 50 concentrating
• Preceded by perimenopause • ! collagen content in skin ----. t skin
0 4 years before final menstrual period; wrinkling
missed/irregular menstrual cycles, • ! lean body mass
changes in bleeding patterns (heavy, • Individualized approach for menopausal
prolonged, light) hormone therapy (MHT)
, Estrogen/estrogen+ progestin helpful in
HORMONAL CHANGES some cases
• ! estrogen, progesterone ----. ! hypothalamic
inhibiticn=-s j bursts of GnRH----. l FSH,
LH
PHYSIOLOGICAL EFFECTS OF
ESTROGEN WITHDRAWAL
Hot flashes
• Caused by hypothalamus-associated
thermoregulatory dysfunction ----. vasomotor
instability
• Sensation of heat (centered on chest, face
----. generalized). diaphoresis, palpitations,
anxiety
• Night sweats
O Hot flashes occur at night----. trouble
sleeping
• Avoid triggers (e.g. hot drinks, spicy foods);
maintain cool ambient temperature; dress
in lighter clothing
• Stops within few years of onset
Vulvovaginal atrophy
• Vaginal dryness. loss of vaginal rugae----.
dyspareunia
• Vaginal estrogen creams. lubricants helpful Figure 8.19 Hormone activity in a regular
menstrual cycle. Estrogen and progesterone
! protective effects from estrogen levels ! during menopause because the
• j risk of cardiovascular disease ovaries run out of functional follicles ----. no
theca or granulosa cells to produce more
• ! bone marrow density ----. l risk of
hormones. So ! estrogen, progesterone ----. !
osteoporosis. bone fractures
hypothalamic inhibition ----. t bursts of GnRH
O l vitamin D. calcium (diet, supplements) ----. l FSH, LH.
helpful
18
ESTROGEN & PROGESTERONE
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• Female steroid hormones, produced mainly estrogen, progesterone
by ovaries
O Some estrogen produced in adrenal EFFECTS OF ESTROGEN
cortex, adipose tissue; secreted by
• Maturation of female reproductive organs
placenta during pregnancy
(e.g. uterus, fallopian tubes, vagina)
° Corpus luteum secretes estrogen,
• Secondary sexual characteristics (e.g.
progesterone
breast growth, fat distribution)
• Three types
• I estrogen (pre-ovulation) - prepares
O Estradiol (most biologically active), uterine epithelium for implantation
estrone, estriol (endometrial proliferation); endometrial
secretion in collaboration with progesterone
SYNTHESIS • Dominant hormone during the follicular
• Cholesterol - theca cells - converted to phase of ovarian cycle; follicle maturation;
pregnenolone via cholesterol desmolase - initiates ovulation via FSH, LH surge
pregnenolone converted into progesterone
Pregnancy
via 3-beta-hydroxysteroid dehydrogenase
(HSD) - released into blood - binds • Secreted by placenta to support uterus;
to plasma proteins (e.g. albumin) - stimulates development of myometrium
transported to target tissues • f melanin-stimulating hormones -
• Remainder of pregnenolone converted to hyperpigmentation
17-hydroxypregnenolone - converted • f vascularityof upper respiratory tract;
into dehydroepiandrosterone (DHEA) - hypersecretion of mucus
finally converted into androstenedione • Preparation for labor
(testosterone precursor) by 3-beta-HSD O Stimulates development of myometrial
• Androstenedione diffuses to nearby gap junctions, promotes coordinated
granulosa cells - androstenedione contractions
converted to testosterone by 17 -beta- O Promotes cervical ripening
hydroxysteroid - testosterone converted O j uterine responsiveness to oxytocin
to 17-beta-estradiol dehydrogenase
(l oxytocin receptors), triggering
aromatase (most biologically active type of
parturition
estrogen during reproductive period)
• Breasts
• 17-beta-estradiol released into blood -
O Stimulates growth of duct cells
binds to sex hormone-binding globulin
(SHBG) Systemic
O Plasma protein, carries 17-beta- • Required for closure of epiphyseal plates
estradiol to target tissues (e.g. uterus, (both sexes)
vagina, bones)
• Anabolic effect on bones
• ! low-density lipoprotein (LDL), f high-
SECRETION density lipoproteins (HDL)
• Regulated by hypothalamic-pituitary- • Maintains flexibility of blood vessels
ovarian axis through feedback loops • Promotes skin elasticity, fat deposition
• At puberty, pulsatile release of GnRH from • ! estrogen during perimenopausal/
hypothalamus - anterior pituitary secretes menopausal years - f risk of
FSH, LH - ovarian follicles differentiate cardiovascular morbidity, osteoporosis,
into thees, granulosa cells - secrete sexual dysfunction
19
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EFFECTS OF PROGESTERONE • Breasts: t alveolar-lobular development,
• Dominant hormone during luteal phase of prevents milk production during pregnancy
ovarian cycle (inhibits prolactin)
• j progesterone (secretory phase of • Respiratory:: j sensitivity to C02, mild
menstrual cycle) - forms decidual tissue hyperventilation, ! airway resistance
for implantation • l vasodilation
Pregnancy Systemic
• Maintains pregnancy: ! irritability of • Works with estrogen to promote bone
myometrium - ! risk of spontaneous remodeling - f bone density
abortion • Promotes skin elasticity
• Cervis: forms mucus plug
Figure 8.20 The steps of progesterone synthesis. LH stimulates proliferation of theca cells -
cholesterol desmolase converts more cholesterol into pregnenolone.
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the next steps to synthesize 17-beta-estradiol.
20
i
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Figure 8.22 Synthesis of 17-beta-estradiol from androstenedione. FSH increases the activity of
aromatase. Some target tissues for 17-beta-estradiol include the uterus and vagina, bones, and
blood vessels.
21
NOTES
• Seminiferous tubules
O Surrounded by epithelial lining.
22
capillaries, Leydig cells • Spermatogonium (diploid cell)
O Spermatogonia (primordial sperm cells) undergoes mitosis - two daughter cells
- spermatocytes (towards lumen) - (spermatogonia)
spermatids - sperm (most central); , One spermatogonia cycled back to
Sertoli cells (extend from margin to serve as spermatogonium
lumen; provide nutrients; establish , Second spermatogonia continues on to
blood-testis barrier) produce sperm
O Tubules combine - rete testis (in • Spermatogonia (diploid cell) undergoes
mediastinum testis) - efferent ducts - mitosis - primary spermatocyte
epididymis • Primary spermatocyte undergoes meiosis I
- secondary spermatocytes (haploid cells)
INTERNALORGANS emerge
• Ducts for sperm, accessory glands (seminal • Secondary spermatocytes undergo meiosis
vesicles, prostate gland. bulbourethral II - spermatids (haploid)
glands) • Spermatids enter lumen - cellular
Sperm
• Acrosome: enzymes to penetrate oocyte
(female gamete)
• Neck (midpieceJ: mitochondria for energy
• Tail: helps sperm swim
• Mature, swim in epididymis head; move
through seminiferous tubules, rete testis by
peristalsis
Spermatogenesis
• Begins at puberty
• Hypothalamus secretes gonadotropin- Figure 65.4 Sperm anatomy.
releasing hormone (GnRH) - pituitary
secretes luteinizing hormone (LH), follicle-
stimulating hormone (FSH)
HYPOTHALAMUS
O LH binds to Leydig cells - stimulates
testosterone production OG11RH
FSH binds to Sertoli cells - produces
) ~r
°
LOBULE
SEMINIFEROUS
SEMINIFEROUS TUBULE
TUBULE
Figure 65.5 Hypothalamus secretes GnRH,
stimulates pituitary release of FSH. LH
(important to testosterone production).
Figure 65.3 Testes anatomy.
23
differentiation ---'> acquire tail ---'> mature sperm
• Regulation via feedback loops [Link] ,f~ [Link]
O Sertoli cells secrete inhibin ---'> negative
feedback to pituitary---'> ! FSH @ 1(5\
\::::J PRIMARY
[Link]
O Leydig cells secrete testosterone e-
negative feedback to pituitary---'> I LH
"'
@)
Ejaculation
• Mature sperm exit through tail of
epididymis ---'> vas deferens ---'> secretions
I "=EIOSIS I
x y
from seminal vesicle at ampulla ---'> SECONDARY 1(5\ 1(5\
ejaculatory ducts ---'> secretions from [Link] \:::I \::::::,,
prostate gland ---'> secretions from
bulbourethral glands---'> empty into urethra
I\ I\ MEIOSIS II
• Accessory glands secrete fluids into urethra
~ ~ ~ ~
O Seminal: seminal fluid (contains fructose
I
O
O
for energy, prostaglandins for transport)
Prostate: prostatic fluid (alkaline---'>
neutralizes acidic vaginal secretions)
Bulbourethral: lubricant
• Semen (seminal fluid): final mixture of all
SPERMA-:;!
lJl
Figure 8.6 Spermatogenesis.
fluids with spermatozoa
• During ejaculation, bladder sphincter
contracts (prevents urine from mixing with
semen)
!LADDER
@VAS DEFERENS
@SEMINAl:
VESICLE
@PROSTATE
@ !VL!OVRETHRAL
GLAND
CD EPIDIDYMIS
Figure 65.7 Once produced. the mature sperm exit the tail of the epididymis (1) and travel
through the vas deferens (2) where they are combined with secretions of the seminal vesicles
(3) at the ampulla. The mature sperm then pass through the ejaculatory ducts and secretions of
the prostate gland (4). Finally, the bulbourethral gland (5) secretions are added and the semen is
ejaculated through the urethra.
24
TESTOSTERONE
osmsJI:/ -l:es-1:os-l:eTone
WHAT IS TESTOSTERONE? NEGATIVE FEEDBACk
• Main androgenic hormone REGULATION
• Produced, released by Leydig cells of testes • High testosterone levels - inhibits
• Synthesized from cholesterol in series of hypothalamus from secreting GnRH,
steps involving multiple enzymes pituitary gland from secreting LH
• Sertoli cells in testes secrete glycoprotein
• Inactivated in liver - eliminated in urine,
bile called inhibin - inhibits pituitary gland
secreting FSH
• Active locally on Sertoli cells (paracrine
action)
O Sertoli cells produce androgen-binding
.-~- RISING.....---
protein (ABP) - keep testosterone
TESTOSTERONE
levels high
Testosterone reinforces follicle-
Jy-=rr;STOSTERONE
FALLING
O
a)-
• Active in rest of body (endocrine action)
Circulation in bloodstream
• Approx. 98% bound to proteins (albumin, GnRH LEYOIG
sex-hormone binding globulin) SECRETION CELLS
~ci~T-3
ONot biologically active when bound to
protein
° Functions as reservoir of free
testosterone
O Production regulated by androgens,
Figure 65.8 Testosterone production is
estrogens
regulated through a negative feedback
• Approximately 2% free, biologically active loop by the hormones released by the
hypothalamus and the Leydig cells.
PRODUCTION
Regulated by hypothalamic-pituitary axis MECHANISM OF ACTION
• Low testosterone - hypothalamic arcuate • Binding on androgen receptor in cell of
nuclei secrete GnRH into hypothalamic- target tissue - androgen-receptor complex
hypophyseal portal blood - GnRH moves into nucleus - gene transcription -
arrives to anterior lobe of pituitary gland generation of new proteins - physiological
- pituitary gland secretes FSH, LH (AKA effects
gonadotropins)
O LH - Leydig cells produce testosterone EFFECTS OF ANDROGENIC
by increasing cholesterol conversion into
HORMONES TESTOSTERONE &
pregnenolone (first step of testosterone DIHYDROTESTOSTERONE
production)
° FSH - spermatogenesis, Sertoli cell Testosterone
function • Masculinizes internal genital tract in male
fetus; promotes descent of testes before
birth
25
• Puberty: muscle mass increases;
epiphyseal plates close; penis, seminal
vesicles grow; spermatogenesis; rise of
libido; secondary sexual characteristics
(thickens vocal cords, deepening voice,
male pattern of hair growth)
• Adulthood: maintains reproductive tract;
anabolic effect on proteins
Oihydrotestosterone (DHT)
• Produced from testosterone by 5 alpha-
reductase in target tissues
• Determines
° Fetal maturation of external male
genitalia (penis, scrotum, prostate)
O Hair distribution (baldness)
O Sebaceous gland activity
• 5 alpha-reductase inhibitors
block testosterone conversion in
dihydrotestosterone ---> treats male pattern
baldness, benign prostatic hypertrophy
O Propecia (finasteride)
26
NOTES
DEVELOPMENT OF THE
REPRODUCTIVE SYSTEM
osms.i"l/reprodue-live-s14s-lem-dev
SEXUAL DIFFERENTIATION MALE DEVELOPMENT
• Series of events begins at conception,
Male gonadal development
ends with sexual characteristics acquisition
(designated biologically male/female) • Embryo genetically male - gene
expression in Sex-determining Region in Y
• During first five gestational weeks
chromosome (SRY) promoted
O Gonadal ridge develops, later becomes
, SRY-region genes promote testis-
differentiated gonads
determining factor production -
• Week 6 testis-determining factor acts on
O Primordial germ cells start migrating undifferentiated gonads - gonadal
from yolk sac towards gonadal ridge transformation into testes
• Week 7 , Gonadal ridge becomes seminiferous
O Primordial germ cells promote tubules, rete testis, straight tubules
gene expression contained in sex • Testes contain three functional cell types
chromosomes
, Germ cells: produce spermatogonia -
• Wolffian, Mullerian ducts: structures that produce male gametes in puberty
will develop into rest of reproductive tract;
, Serto/i cells: synthesize anti-Mullerian
remain undifferentiated until week 8
hormone
, Leydig cells: synthesize testosterone
(~OtJ~\>AI.)
-~ e:_ttJITAL ----
iu>~t.
r
(-
vo'-""~A,
VITtL.\.1...,f. Oll'-T
2~~;;) Plll~[Link]
[Link]"I [Link]
• t-\1C.,.llPIT6•
?
Figure 66.1 Illustration of the migration of primordial germ cells to the gonadal ridge in week 6.
At this point, the gonad is undifferentiated, meaning that it can develop into ovaries or testes.
27
Male internal reproductive organ , Promotes Wolffian/mesonephric-duct
development growth, differentiation
• Wolffian ducts give rise to male internal • Urogenital sinus: develops into external
genitalia reproductive organs; undifferentiated until
O AKA mesonephric duct/mesonephros gestational week 9
O Meso = middle, in between; nephros = , Urethral tolds-« urethra (both)
kidney , Labioscrotal swellings---> scrotum
O Two functions: connects primitive , Primordial phallus---> penis
kidney to cloaca; develops into male
genitalia Male external reproductive organ
development
O Growth, differentiation stimulated by
testosterone • Male external genitalia differentiation from
urogenital sinus depends on testosterone
• Male internal reproductive organ
presence
development depends on Sertoli cells,
Leydig cells, urogenital sinus , 5 alpha reductase in target tissues
converts testosterone ---> more potent
• Sertoli cells: synthesize, secrete anti-
dihyd rotestosterone
Mullerian hormone; AKA Mullerian
inhibiting substance , Dihydrotestosterone: responsible for
masculinizing external genitalia
O Promotes Mulleriarvparamesonephrfc-
duct atrophy
• Leydig cells: synthesize, secrete
testosterone ---> become internal male
genitalia
WU.I< l
SUTOI.I
---),. ~i,,1u.11F,aovs ceus
1118\ILE.S
Figure 66.2 Biologically male sexual differentiation, week 7: genes in Sex-determining Region
of Y chromosome (SRY) code for testis-determining factor (which initiates development of
testes). Primitive sex cords=- medullary cords that carry primitive germ cells deeper into
mesoderm. The surface epithelial layer of each gonad thins out=- tunica albuginea. Later,
medullary cords=- seminiferous tubules, straight tubules, rete testis. The primordial germ
cells settle in seminiferous tubules mature into dormant spermatogonia. During puberty,
spermatogonia start dividing---> sperm (male gametes). During week 8, some cells in the
seminiferous tubule walls differentiate into Sertoli cells, and cells between the seminiferous
tubules differentiate into Leydig cells.
28
FEMALE DEVELOPMENT , Lack of testosterone induces Wolffian
duct degeneration
Female gonadal development
, Lack of antl-Mullerian hormone
• Without functional SRY gene promotes Mullerian ducts persistence
O Week 9: ovaries begin developing - develop into fallopian tubes, uterus,
O Week 10: ovarian cortex, inner medulla upper Ya of vaginal canal
distinguishable , Rest of female reproductive organs arise
• Ovaries contain three functional cell types from urogenital sinus
O Germ cells: produce oogonia; located in
Female external reproductive organ
ovarian cortex (oogonia-haploid cells
development
that remain arrested in prophase 1 of
meiosis until ovulation) • Urogenital sinus develops into external
reproductive organs; undifferentiated until
O Granulosa cells: synthesize estradiol
gestational week 9
O Theca cells: synthesize progesterone
, Urethral folds - urethra (both 1), labia
• Ovarian follicle: oogonium surrounded by minora
granulosa cells, connective tissue
, Labioscrotal swellings - labia majora,
Female internal reproductive organ mons pubis
development , Primordial phallus - clitoris
• Mullerian duct - female genitalia • Female external genitalia differentiation
O AKA paramesonephric duct/ , Androgen absence-dependent
paramesonephros (testosterone, dihyd rotestosterone)
O Para = on the side of; meso = middle, in • Phenotypic differentiation complete at
between; nephros = kidney week 12 - earliest ultrasound-based sex-
• Female internal reproductive organ determination date
development primarily depends on testes
absence
29
LATERAL ANTERIOR
WOLFFIAN DUC.1
4 l''ll~Lc. llUp.()1)'1(.TIVE
$'(5TclV\
Figure 66.4 The genital ducts are initially undifferentiated, tubular structures that run down the
embryo's back inside the two nephrogenic cords on either side of the embryo. The Wolffian and
Mullerian ducts start in the thoracic and upper lumbar region and continue down the embryo's
back until they open into the part of the cloaca called the urogenital sinus.
[Link] l)U<.TUI.(S
£PIOIO'ft-\l)
Figure 66.5 Male internal reproductive organ differentiation and descent of gonads.
WOU'flAfJ l>U<.T
t>t<>t ,,uu,,u (
MVLLtlUAIJ l)<J(.f _)
P£11-SISTS
VTU!OIIACallllllL
Pl!III\Olll>IVM
Figure 66.6 Female internal reproductive organ differentiation and descent of gonads.
30
SEX VS. GENDER Internal, external reproductive organ
• Gender structure
O Socially-constructed characteristics/ • Male genitalia
behaviors associated with biologically , Internal: prostate, seminal vesicles, vas
male/female people deferens, epididymis
O E.g. norms, roles, relationships between , External: penis, scrotum
individuals • Female genitalia
• Genetic sex , Internal: fallopian tubes, uterus, upper%
O Individual's chromosomal composition vaginal canal
oXY: males , External: clitoris, labia majora, labia
o XX: females minora, lower% vaginal canal
O Established by oocyte, sperm cell fusion
• Gonadal sex
O Individual's reproductive organs
O Male: testes
° Female: ovaries
• Phenotypic sex
UNDIFFERENTIATED
-
EXTERNAL SEX ORGANS
., ...... -
LASIOSC..IZOTAL SW£[Link]\
Caf.~ITAL TulWlCU
l
P!llMOROIA(.
PHAU.11~
MALES FEMALES
~
~ A8~£>Jef. 05 TESTOSnflo~~
MO,JS PUIJIS
l.~Bll\ [Link]
[Link] LABIA .-,A'loiA
ScllOTU""
Figure 66.7 Male and female external sex organs. Phenotypical differentiation is complete at
week 12.
31
PUBERTY & TANNER STAGING
osmsJl/pu\>[Link]
PUBERTY Adrenarche
• Sexual maturation process involving • f adrenal androgen production by adrenal
endocrine, physical changes; controlled by cortex
hypothalamic-pituitary-gonadal axis
Thelarche
• Begins between ages 10-14 in females;
between age 12-16 in males • Breast tissue appears
, Ovarian estradiol-guided
GnRH secretion
• Pulses from hypothalamus regulate Menarche
luteinizing hormone (LH), follicle- • First menstruation occurs
stimulating hormone (FSH) secretion from , Ovarian estradiol-guided
anterior pituitary - development of sexual , First menstrual cycles tend to be
characteristics anovulatory
= Primary sex characteristics: genitals
(organs directly involved in sexual Spermarche
reproduction) • First sperm production occurs
= Secondary sex characteristics: , FSH, LH, testosterone-guided
sex-specific physical characteristic , Nocturnal sperm emissions, sperm
not necessary involved in sexual appears in urine
reproduction (e.g. pubic hair-both
sexes, voice changes-males, breast Pubarche
development-females) • Pubic hair appears
, Adrenal androgens-guided
Gamete production
, Association: body hair; acne; apocrine
• Oocytes (females); sperm (males)
sweat glands activation
• Males: LH acts on Leydig cells - produces
testosterone; FSH acts on Sertoli cells -
produces sperm
AMOVIIIT OF HO!tMOl\lt.
• Females: LH acts on ovarian follicles - VARll~ OlllR UF~TIMf>
produces progesterone, androstenedione
(converted into estrogen)
, Estrogen, progesterone levels vary
according to menstrual cycle phases f$H>LH
32
TANNER STAGING Stage 3
• System for describing predictable steps • 1 Pubic hair becomes coarser
during sexual maturation • 0 Penis begins to enlarge in size, length
• Centers on two, independent criteria • <j> Breast mounds form
O Appearance: pubic hair in males,
females Stage 4
O Genital development: j testicular • 1 Pubic hair begins to cover pubic area
volume, penile growth (males); breast • o Penis begins to widen
development (females) Breast enlargement forms "mound-on-
• <j>
mound" breast contour
FIVE CATEGORIES OF TANNER Stage 5: adult
STAGING • 1 Pubic hair extends to inner thigh
Stage 1: pre-pubertal • 0 Penis, testes enlarged to adult size
• 1 No pubic hair present in either sex • <j> Breast takes on adult contour
Stage 2
• 1 Soft pubic hair appears
• o Measurable testes enlargement
• <j> Breast buds appear
33









