Sex Hormones Flashcards
Puberty
Maturation of reproductive organs
Production of sec steroids
Attain reproductive capability
Develop secondary sexual characteristics
How do we assess puberty development in boys and girls
Tanner staging (has 5 stages)
In girls telarche breast development measured
In boy’s testicular volume measured using orchidometer
Pubarche measured in both
Arche types
- Gonadarche - Activation of gonads by HPG axis, the earliest gonadal
changes ofpuberty - Thelarche - Onset of breast development (occurs before menarche)
- Pubarche - Onset of pubic hair (occurs before menarche)
- Menarche - Onset of first menstrual cycle
- Spermache- spermatogenesis
- Adrenarche- activation of adrenal androgen production like DHEAS and DHEA (starts 2 years before gonadarche)- in girls, androgens are produced from adrenal gland so is more responsible for pubarche than in boys (where androgens (testosterone) are produced in testes)
Adrenarche is pre pubertal
Secondary sexual characteristics in girls
Effects of oestradiol
Breast development
Hair growth pubic
Sweat gland composition
Changes to genitalia
Secondary characteristics boys
Deepening of voice
Hair growth
Sweat gland composition
Changes to genetalia
Puberty onset’s
8-13 in girls where first sign is thelarche and last is menarche
9-14 in boys where prepubertal testicles are less than 4mls and adult is greater than 15
What does gonadarche activate
HPG axis
Increase in LH and Fsh
How do androgens FSH LH and testosterone change in puberty
Adrenarche-DHEAS/DHEA increase in both
Gonadarche-LH and FSH increase in both. Testosterone increases a lot in boys and little in girls. Oestradiol increases a lot in girls and a little in boys
What would happen if GnRH was non pulsatile
Cause decrease in LH and FSH production thus hypogonadism
Can treat prostate cancer due to decrease reducing testosterone
GnRH pulsatility
In follicular phase there’s pulses every two hours
In literal phase this is every 4 hours
Primary hypogonadism
Something directly affecting gonads causing low E2 and testosterone however high LH and FSH due to reduced negative feedback
In woman it’s caused by menopause and causes low inhibin
In men it’s caused by infection trauma or cancer of testes
Secondary hypogonadism
Problem in pituitary gland or hypothalamus leading to low FSH or LH and low e2 and testosterone
Caused by high prolactin or pituitary tumour
Primary vs secondary amenorrhea
Primary is where they have never menstruated and start period later than 16
Secondary is irregular periods which start and stop for 3-6 months
Most common physiological cause is pregnancy
Oligomenorrhoea
Irregular or infrequent periods
Greater than 35days or 4-9 cycles per hear
Ovarian cycle
Follicular phase
1) FSH rises
2) 2-3 follicles start to grow
3) Produce low level of E2 (oestradiol) and produces Inhibin B which reduces FSH by negative feedback on pituitary
4) These restrict ‘FSH window’ and non-dominant follicles undergo atresia as they are more FSH dependent than dominant
5) Dominant Graafian follicle emerges (which produce more E2)
6) Oestrodiol (E2) continues to increase
7) There is a switch to positive feedback on hypothalamus + pituitary by high E2 (from -ve feedback at low E2), so high E2 leads to LH (& FSH, but mainly LH)
Ovulation
8) This +ve feedback induces a mid-cycle LH surge which causes ovulation (release of egg from follicle) **
Luteal phase
9) Empty follicle becomes corpus luteum which releases progesterone and oestradiol → progesterone is highest in midluteal (day 21) phase- gives evidence of ovulation
- Corpus luteum development through LH secretion
- Corpus luteum degrades due to absent HCG stimulation → Shedding of endometrium lining → Menstrual cycle restarts.
Why does corpus luteum secrete progesterone
To maintain endometrium
Uterine cycle
1) Menstrual phase (shedding of endometrium)
2) Proliferative phase- action of oestradiol- endometrial lining regrows with
- growth of new epithelial cells
- gland proliferation
- increase in stroma/arterioles
3) Secretory phase- action of progesterone (from corpus luteum)- changes endometrium to be receptive for implantation by
- increasing volume of stromal cells leading to thick spongy lining
- cork-screw shaped glands secreting glycogen
- coiling and lengthening of spiral arteries
What happens when embryo implants into endometrium
Embryo produces beta hcg which acts in LH receptors in corpus luteum in order to maintain progesterone production
If no implantation then no hcg made so corpus luteum died
Menopause
Due to lack of Oestradiol
Dory skin
Hair thinning
Hot flushes or sweating
Mood disturbances
Osteoporosis
Sexual dysfunction
Weight gain
Infertility
Treated by oestrogen replacement through HRT which stimulates endometrium to grow
Must add progesterone to prevent risk of endometrial hyperplasia or cancer
Ovarian reserve
How many eggs are in ovaries be for reaching menopause
Anti mullerian hormone is a reserve marker secreted by granulosa cells leaking in early adult life
Primary ovarian insufficiency
Same symptoms as menopause
Conception can still happen in 20% of cases
Diagnosis is high serum FSH
Caused by autoimmune genetic and cancer therapy
Andropause
Free testosterone decreases rapidly which can be associated with hypogonadism
What is most testosterone strongly bound to
Sex hormone binding globulins
What is the free hormone hypothesis with testosterone
Binding of total testosterone in circulation
Most bound to SHBG then albumin
Rest is free
Rhythm of testosterone
Diurnal rhythm so measure when fasting before 11am
Symptoms of testosterone deficiency
Sexual dysfunction
Erectioe dyfunctiin
Hair growth
Energy levels decrease
Mood disturbance
Body composition
Gynaecomastia
How is testosterone converted to DHT
Through 5 alpha reductase which is found in testes,prostate,skin of scalp,liver
Can reduce 5 alpha reductase inhibitors by finasteride which treats prostate cancer
How can aromataste activity be reduced
Anastrozole used in breast cancer
