reproductive system development Flashcards
Female anatomy:
External genitalia
Reproductive tract
Ovaries
- Vulva: labia majora/minora and clitoris
- vagina, uterus, cervix, fallopian tubes with fimbriae
- folliclles at various stages of development
Genetic disorders related to sex determination
-errors in separation of chromosome pairs during meiosis –> gametes get 2 or no copies of chromosomes from a parent –> if abnormal gamete is fertilized, makes weird chromosome combos
X = Turner's syndroms (f) XXY = Kleinfelter syndrome (m) XXX = Triple X (f) Y = not viable
Turner’s syndrome
1:2000 female births don't develop ovaries --> infertile short stature, webbed neck, low-set ears broad chest, widely spaced nipples arms turn out at elbows swollen hands and feet increased risk of heart defects learning disabilities
Kleinfelter syndrome
1:600 live male births
sterile bc small testes and low testosterone
-Bones: tall and osteoporosis
-underdeveloped external genitalia
-decreased secondary sex characteristics (low muscle mass, less facial/body hair, gynecomastia
-learning disabilities
-metabolic disorders (diabetes, hypertension)
-mental disorders (depression, anxiety, autism)
Triple X Syndrome
1: 1000 female births
- variable symptoms and severity
- tall; usually no other weird physical features
- normal sexual development
- disabilities associated with learning/speech
- motor skills difficulties
- mental disorders (anxiety, depression, autism)
Undifferentiated state (bipotential)
- no commitment in development of m vs f internal or external reproductive structures
- gonadal development: genital ridges differentiate into bipotential gonads with cortex and medulla
- Undifferentiated accessory ducts: Mullerian ducts (f) and Wolffian ducts (m) –> both connect to cloaca (future bladder)
Gonadal differentiation
-earlier in males (6-7 weeks) vs females (8-9 weeks)
SRY gene = sex determining region of the Y chromosome –> makes SRY protein
SRY and other proteins trigger the development of testis and the production of testosterone –> w/o SRY, ovaries develop
Ovarian development
Cortex:
- primordial gem cells migrate to cortex and become oogonia
- ovary containing oogonia: mitosis of oogonia makes millions, but most degenerate. Some go thru 1st meiotic division and are surrounded by layer of granulosa cells, becoming primoridal follicles (400,000 at birth)
Medulla: degenerates
All this is due to absence of SRY gene
Differentiation of genital ducts
-fetal testicular androgens (testosterone) and MDIF (Mullerian duct inhibiting factor) determine which ducts develop
Wolffian ducts: progressive development in males; regression in females –> epididymis, vas deferens, seminal vesicles, ejaculatory duct
Mullerian ducts: regression in males; development in females –> oviducts, uterus, cervix, upper 1/3 of vagina
cascade effect of SRY gene
SRY gene produces testis-determining SRY protein –> initiates production of proteins which cause gonad medulla to differentiae into a testis which has:
- Leydig cells that secrete testosterone which causes the development of Wolffian ducts and the development of male external genetalia via DHT
- Sertoll cells which secrete Anti-Mullerian hormone which causes the regression of the mullerian duct
differentiation of external genitalia
-genital tubercle - 8 weeks
Testosterone is converted to DHT (dihydrotestosterone) by 5-alpha reductase
- DHT acts on androgen-dependent tissues and stimulates the development of penis, scrotum, prostate, bulbourethral glands
- If no DHT, genital tubercle develops into clitoris, mons pubis, labia majora/minora
Differentiation of hypothalamus
Androgens = male = non-cyclic hypothalamus
No androgens = female = cyclic release of gonadotropins
Set point for sex steroid feedback is increased in both sexes
Set point pre puberty vs during and after puberty
Prepuberty = low set point
- low levels of gonadotropins
- low levels of sex hormones from gonads (e + p)
Puberty: increased set point
- less sensitive to inhibition from sex hormones
- increased secretion of gonadotropins
- increase in sex hormones from gonads
- new homeostasis for gonadotropin inhibition by sex hormones is established
Development of positive feedback of estrogen in adult females
- hypothalamus becomes desensitized to high levels of gonadal steroids
- surge of LH and FSH = ovulation
- hypothalamus also integrates information regarding nutritional and emotional status and sleep-wake cycles to determine if conditions are ok for ovulation
Sex differences: genetic or hormonal determinants?
Both
Presence/absence of a hormone causes changes in brain structures: testosterone, DHT, Estrogen
Activation of a hormone is required for a difference in brain function
different gene expressions
Neonatal behavior
-genetics, hormones, and treatment
Girls:
- more advanced in skeletal development
- more advanced neurologically: sensitive to tactile, oral, and visual stimuli; responsive to certain tastes; more interested in human faces
Childhood behavior
Brain development differs
Girls:
- earlier development of “right brain” - language skills
- nurturing bahavior
- preferences evident in play activities
Adult behavior
-no dif in intelligence or brain weight (once normalized)
Cerebral lateralization: girls have less definitive R and L brain differences (more connections bt sides) –> use dif brain areas in cognition –> greater verbal fluency
Evidence points to inherited sex differences with nurturing influences
Puberty
- ages 9-15
- Sexual maturation to obtain full reproductive capacity
- variable when it starts and how fast it goes
- High estrogen = positive feedback effect on LH and FSH secretion
Typical sequence of events during puberty
- growth spurt, initial increase in height, fat deposition on hips and breast
- initial breast development, pelvis widens, pubic hair
- maturation/growth of reproductive organs, external genitalia, and pigmented areola
- filling in of breasts, menarche, axillary hair
- ovulation occurs, skeletal growth rate declines, breast maturation complete, sweat and sebaceous oil gland development (acne)
- voice deepens slightly
- adult stature reached
Important hormones for puberty
Estrogen
- Sources: developing follicles and fat tissue
- breast maturation
- skeletal changes: pelvis widens and height increases
Androgens
- sources: adrenal gland
- pubic/axillary hair, voice changes, increased skin gland activity, long bone growth, sex drive (libido)
Growth hormone
Thyroid hormone
Why is age of puberty onset decreasing? (briefly)
nutrition day length stress environmental pollutants climate and altitude
Nutrition
- improved nutrition lowers puberty age
- poor results in delayed puberty: anorexia, ballet dancers, big fams, poor people, rural
Critical body fat hypothesis: obese girls reach puberty earlier –> leptin from fat inhibits appetite and might increase GnRH –> androgens in adrenal gland are converted into estrogen in fat tissue
day length
possible connections with melatonin and inhibition of GnRH
- increased day/light decreases melatonin secretion
- decreased melatonin removes its potential inhibition of GnRH
- GnRH stimulates FSH/LH
- increased estrogen levels
- early onset of puberty
Stress- physical or emotional
-increased secretion of cortisol from adrenal gland could inhibit reproductive function or trigger early onset of puberty
Early psychological stress (1st 5-7 years) leads to early puberty
environmental pollutants
some chems act like estrogen (xenoestrogens)
-early onset of puberty
*tend to delay puberty in boys
climate and altitude
warmer weather tends to cause earlier onset of puberty than colder weather
high altitude might delay puberty due to hypoxia
Adult stage: gametogenesis
oocytes
- oogonia - mitosis for gem cell proliferation
- primary oocytes –> meiosis –> secondary oocyte + 1st polar body –> secondary oocyte finishes meiosis at fertilization –> zygote and 2nd polar body
adult hormone production
brain:
- hypothalamus releases GnRH
- anterior pituitary releases FSH and LH
- posterior pituitary releases oxytocin
Gonads release e, p, and inhibin
Hormonal control of reproduction
-pulsatile release of GnRH stimulates release of LH and FSH
-FSH stimulates gametogenesis
LH stimulates sex hormone production
-negative feedback mechanisms to inhibit gonadotropins release (exception: sustained elevated estrogen stimulates gonadotropin release in FEMALES only)
Reproductive decline with age
- decline in fertility
- Perimenopause = fewer, erratic menstrual cycles –> start of menopause symptoms
Menopause (age 50)
- loss of ovarian function (no more menstrual cycles)
- follicular exhaustion
- stroma hypertrophy, primordial follicles disappear
- plasma gonadotropins increase because of follicular estrogen decline
- decrease in estrogen
Menopause symptoms: hot flashes
- no period or PMS
- Hot flashes: vasodilation of blood vessels in skin –> red, flushed face with sweating –> can spread across whole boy –> coincide with rapid heart rate
- lasts about 7 years
- variation in severity
- often interferes with sleeping
Menopause symptoms: the rest
- atrophy of external genitalia, breast and uterus
- vaginal lining changes: dryness (less lubrication) and increase in pH (more risk of infection)
- urinary incotinence: lose elasticity in urethra
- abdominal weight gain
- hair on chin and upper lip
- behavioral changes: irritability, fatigue, insomnia
Menopause: bones and heart
Osteoporosis:
- decreased bone mass causes increased risk of fracture –> also you might shrink because osteoporosis in vertebra
- caused by low estrogen
Cardiovascular disease:
- increased plaque formation
- hypertension
correlation between # of ovulations and menopause age
More ovulations = earlier menopause
-nulliparous (no births) and few children
Fewer ovulations = later menopause
- oral contraceptives that inhibit ovulation
- lots of kids
NOTE: low body weight causes earlier menopause, but for different reasons
Pros and Cons of HRT
HRT = hormone replacement therapy ERT = estrogen only, not progesterone
E+P
-decreases severity or eliminates menopausal symptoms (hot flashes, sleep disturbances, vaginal dryness, frequent urination, osteoporosis)
No cardiovascular disease protection though –> in fact, increased risk by 29% and increase stroke risk by 41%
Risk of cancers with ERT
Increased risk of breast cancer with ERT
- risk is related to how long you take ERT
- 5+ yrs = 54-71% increase
- no increase if <5 yrs
- HRT is riskier for breast cancer than ERT
- increased risk goes away 5 yrs after stopping therapy
Increased risk of endometrial cancer with ERT –> ERT is riskier than HRT
Increased risk of ovarian cancer with ERT
- 6-11 years: 40-70% greater risk
- unknown risk for HRT
Lifestyle changes to combat symptoms
Osteoporosis:
- weight bearing exercise
- medications to minimize bone breakdown
- increase calcium intake and Vit D3 and calcium supplements
- soy and wild yam are good too
