Reproductive hormones

Leteinising hormone
Follicle stimulating hormone
- released by ant pituitary in response to pulsatile gonadotropin releasing hormone (GnRH)
- negative feedback of oestrogen or testosterone
females:
- growth of ovarian follicles and steroidogenesis
- mid-cycle surge LH triggers ovulation
- FSH increases during menopause
  - ovaries become less responsive to FSH
  - fluctuating ovarian activitiy means not reliable predictors of menopause
Males
- FSH -> sertoli cells
  - sprematogensis
- LH interstitial Leydig cells of testes to produce testosterone

dominant ovarian hormone
- secreted during luteal phase
- prepare uterus for implantation
- if hcg released from placenta and maintain s corpus luteum -> progesterone levels remain raised
at approx. 12wks placenta begins to produce progesterone in place of corpus luteum
decrease after delivery and during breast feeding
low in women after menopause
men - almost all converted to testosterone in teses
fertility investigation only indication for testing
- d20-23
- 0-6 ovulation unlikely
- 7-25 ovulation possible
- >25 ovulation likely

stimulates breasts to produce milk after oestrogen priming
inhibited by hypothalamic release of dopamine
hypothyroidism can also be associated with hyperprolactinaemia
- if TRH raised
prolactin-secreting tumours most common type of pituitary tumour
- small
  - microprolactinomas
    - anovulation or other menstrual disturbance
    - galactorrhoea
    - sexual dysfunction
- rarely large
  - macroprolactinoma
    - headaches
    - bitemporal hemianopia
diurnal variation in prolactin levels
- lowest 3hrs after waking
- best collected in afternoon
Stress and illness may elevate levels

primary androgen
- responsibel for development and maintenance of male sexual characteristics
- stimulates anabolic processes in non-sexual tissues
males
- LH —> Leydig cells in testes —> testosterone
females
- peripheral conversion of androgen precursor steroids to testosterone
- fluctuate with menstrual cycles
- increase in pregnancy
- stable during and after menopause
- PCOS = most common cause of hyperandrogensims
- Rarely
  - Cushing’s syndrome
  - congenital adrenal hyperplasia
  - androgen secreting tumours
free testosterone
- total and sex hormone binding globulin
  - rarely required
  - only when abnormal total
    - hyperthyroidism
    - anticonvulsant use
    - severe obestiy

structurally and functionally identical to LH apart from beta chain
- hence beta-hCG
released by tropoblast cells during pregnancy
outer layer of developing blastocyst following conception and embryonic implantation
stimulates progesterone production by corpus luteum
increases vascularity between trophoblast and uterus wall
detectable \~3d after implantation of embryo
- 6-12d after ovulation and fertilisation
during normal pregnancy
- double \~every 2 d
- begin to decrease at 8-10wk
- remain elevated throughout pregnancy
- twins = higher
  - not reliable to predict this
TV uss can be used after approx. 5wk gestation or hCG >1000-2000
non-viable pregnancy may be indicated by decrease or plateua in early pregnancy
following miscarriage may take 3-4wk to return to non pregnnat levels (\<5)
- may remain elevated in incomplete miscarriage
males:
- produced by some testicular tumours

reassuracne and watchful waiting
investigate:
- if no sign of breast development
  - first sign
  - 12-14yo
- or menstruation not begun by age 16yo
common causes:
- weightloss
- dieting
- excessive exercise
- pituitary/thyroid disease
- anatomical abnormalities
  - Mullerian agenesis
- Congenital abnormal
Investigations:
- FSH/LH
  - low
    - hypogonadotropic hypogonadism
      - Kallmann syndrome
      - Space occupying pituitary
  - high
    - hypergonadotropic hypogonadism
      - Turner’s syndrome
- oestradiol
  - can indicate whether absolutely no evidence of ovarian oestrogen activity
  - or have statrted to rise from pre-pubertal levels
  - low oestradiol associated with low LH suggestive of hypothalamic amenorrhoea
- prolactin
  - pituitary cause
- testosterone
  - PCOS
- TSH
- FT4
normal hormone levels but otherwise normal development may suggest anatomical abnormal
- imperforate hymen
- Mullerian agenesis
  - congential malformation = absent uterus and fallopian tubes

cessation of menstration who previously menstruating = secondary
consistently >35d - oligo
causes
- hypothalamic amenorrhoea
- PCOS
- premature ovarian failure
- rule out pregnancy
Investigations:
- FSH/LH
- oestradiol
FSH >20 and decrease oestradiol
- female \<40yo
- suggests premature ovarian failure
low LH and oestradiol = hypothalamic cause
- weight loss
- excessive exercise
- stress

2/3 of:
- hyperandrogenism
- oligomenorrhoea
- and/or anovulation and polycystic ovaries on USS
Testeosterone testing not necessarily required
- if total te stosterone >5 and hirsuit
- rule out late-onset congenital adrenal hyperplasia
- Cushing syndrome
- tumour
  - adrenal
  - ovarian

first sign - increase size of testes around 12yo

indicated imbalance between free oestrogen and androgens
distinguish between true gynacomastia
- concentric rubbery or firm mound of tissue around nipple
from accumulation of adipose tissue
common during mid-late pregnancy
- usually resolves within a couple of years
rises again in older males
- decrease in free testosterone
once eliminate medicines as causes
- anti-androgens
- TCA
- metronidazole
- spironolactone
- CCB
- cimetidine
- concurrent illness
  - cirrhosis
test:
- testosterone
  - followed by LH if low
- oestradiol
- hCG
  - in rare cases
    - testicallar tumour

clincial signs and symptoms
- reduced libido
- absent early morning erection
consider testosterone
- early morning levels
- if one within reference - no need to do more
- if low then confimratory test when well and LF
if LF low
- consider prolactin
FSH only if investigating infertility
Hi LH = primary hypogonadism