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Year 1 - BRS > 4.12 - Sex Hormones During Life > Flashcards

4.12 - Sex Hormones During Life Flashcards

1
Q

What is the definition of puberty?

A
  • maturation of reproductive organs
  • production of sex steroids e.g. oestradiol/testosterone
  • develop secondary sexual characteristics
  • attain capability to reproduce
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2
Q

How do we assess puberty development in boys and girls?

A
  • Tanner staging (has 5 stages)
  • in girls - thelarche (breast development)
  • in boys - genitalia (testicular volume)
  • we also assess pubarche (pubic hair development) in both
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3
Q

What is the Tanner staging for thelarche (breast development)?

A
  • 1 (prepubertal) - elevation of papilla only
  • 2 - breast bud with elevation of breast and papilla and enlargement of areola
  • 3 - further enlargement of breast and papilla with no separation of their contours
  • 4 - projection of areola and papilla to form a secondary mound
  • 5 (adult) - mature breast, projection of papilla only as areola conforms to breast contour
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4
Q

What is the Tanner staging for genitalia (testicular volume)?

A
  • 1 (prepubertal) - testes, penis and scrotum same size as early childhood
  • 2 - early enlargement of testes 2-6cm3; scrotal skin reddens and changes in texture
  • 3 - penis lengthens; testes enlarge 6-12cm3; growth of scrotum
  • 4 - further penile and scrotal growth; testes 12-15cm3
  • 5 - genitalia adult in size and shape; testes >15cm3
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5
Q

What is the Tanner staging for pubarche (pubic hair development)?

A
  • 1 (prepubertal) - vellus hair no different form abdominal hair
  • 2 - slightly pigmented, downy hair
  • 3 - darker, coarser, more curled hair
  • 4 - adult pubic hair that does not reach thighs (axillary hair)
  • 5 - adult hair now on thighs
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6
Q

What does ‘-arche’ mean and what types are there?

A
  • -arche = onset of
  • gonadarche - activation of gonads by HPG axis
  • thelarche - breast development
  • menarche - menstrual cycles
  • spermarche - spermatogenesis
  • adrenarche - adrenal androgen production e.g. DHEAS and DHEA (starts two years before gonadarche) - more important in girls as androgens are produced from adrenal gland so is more responsible for pubarche, whereas in boys they are produced in the testes
  • pubarche - pubic hair
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7
Q

What are secondary sexual characteristics in girls?

A
  • effects of oestradiol
  • breast development
  • hair growth - pubic, axillary
  • sweat gland composition - skin oiliness/acne
  • changes to external genitalia
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8
Q

What are secondary sexual characteristics in boys?

A
  • effects of testosterone
  • deepening voice
  • hair growth - pubic then axillary, facial
  • sweat gland composition - skin oiliness/acne
  • changes to external genitalia
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9
Q

What are the first and late signs of puberty in girls?

A
  • first - thelarche
  • late - menarche
  • onset 8-13 years
  • breast bud –> onset pubic hair –> peak height velocity –> menarche –> adult pubic hair –> adult breast
  • adrenarche: 6-9 years
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10
Q

What are the prepubertal and adult testicle sizes?

A
  • prepubertal < 4 mls
  • adult size > 15mls
  • testicular volume measured using a Prader orchidometer
  • testicular volume >2ml –> onset pubic hair –> onset penis growth –> peak height velocity –> adult genitals –> adult pubic hair
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11
Q

When does adrenarche happen in boys?

A

7-10 years

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12
Q

What is the term for starting puberty below 8 years?

A
  • precocious
  • more common in girls
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13
Q

What is the term for starting puberty after 14 years?

A
  • delayed
  • more common in boys
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14
Q

How do DHEAS/DHEA levels change during adrenarche in boys and girls?

A

DHEAS/DHEA increases in both boys and girls

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15
Q

How do LH, FSH, testosterone and oestradiol levels change during gonadarche in boys and girls?

A
  • LH and FSH go up in both
  • testosterone increases a lot in boys, and a little in girls
  • oestradiol increases a tiny bit in boys and a lot in girls
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16
Q

What is normal GnRH secretion like in HPG axis?

A
  • pulsatile
  • if secretion was continuous non-pulsatile, rather than stimulation of pituitary you would get decrease in LH+FSH production and therefore hypogonadism
  • useful in treating prostate cancer - we give non-pulsatile GnRH which causes castration by reducing FSH+LH, which reduces testosterone levels
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17
Q

How does GnRH pulsatility change during the menstrual cycle?

A
  • in follicular phase, there are pulses every 2 hours
  • in luteal phase this goes up to 4 hours
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18
Q

How does GnRH secretion change from foetus to adult?

A
  • increases foetal
  • peaks and decreases to infant
  • smaller peak at infant
  • decreases during childhood until puberty - quiescence of HPG axis
  • increases during puberty - increased nocturnal GnRH pulsatility
  • stable during adult - normal pulsatile GnRH secretion
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19
Q

When does menarche start?

A
  • 2.3 years after thelarche
  • soon after peak height velocity (PHV) when girl grows most
  • mean age is 12.7 years (range 10.7-16.1)
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20
Q

How long are menstrual cycles?

A
  • 28 day cycle (24-35 days range)
  • +/- 2 days each month
21
Q

What is amenorrhoea?

A
  • no periods for at least 3-6 months
  • or up to three periods a year
22
Q

What is primary amenorrhoea?

A

Starting periods later than 16 years is regarded as abnormal

23
Q

What is secondary amenorrhoea?

A
  • common for periods to be irregular/anovulatory for first 18 months
  • periods start then stop for at least 3-6 months
  • commonest physiological cause is pregnancy
24
Q

What is oligomenorrhoea?

A
  • irregular or infrequent periods >35 day cycles
  • or 4-9 cycles per year
25
Q

What are the main phases of the ovarian cycle?

A
  • follicular phase
  • ovulation
  • luteal phase
26
Q

What are the steps of the follicular (pre-ovulatory) phase of the ovarian cycle?

A
  1. FSH rises
  2. 2-3 follicles start to grow
  3. produce E2 (oestradiol) and inhibin B, which reduce FSH by negative feedback on pituitary
  4. these restrict ‘FSH window’ and non-dominant follicles undergo atresia (as there are more FSH dependent than dominant ones)
  5. a dominant ‘Graafian’ follicle emerges
  6. E2 continues to rise
  7. there is a switch to positive feedback on hypothalamus and pituitary by high E2 (from -ve feedback at low E2)
  8. induces a mid-cycle LH surge
  9. causes ovulation
27
Q

What happens during the ovulation phase of the ovarian cycle?

A

The positive feedback from release of oestradiol induces a mid-cycle LH surge which causes ovulation

28
Q

What happens during the luteal phase of the ovarian cycle?

A
  1. empty follicle becomes corpus luteum, which releases progesterone and oestradiol
  • progesterone highest in midluteal (day 21, 3/4 through cycle) phase - gives evidence of ovulation
29
Q

Describe the steps of the uterine cycle?

A
  1. menstrual phase (shedding of endometrium)
  2. proliferative phase (action of oestradiol) - endometrial lining regrows with growth of new epithelial cells, gland proliferation and 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
30
Q

What happens if sperm meets egg and embryo implants in endometrium?

A
  • embryo starts producing beta-hCG which acts on LH receptors on corpus luteum which maintains production of progesterone and oestradiol through first part of pregnancy
  • if there is no fertilisation, no embryo formed = no hCG = no stimulation of corpus luteum = it dies = no more progesterone and oestradiol to maintain endometrium lining
31
Q

What is hypogonadism?

A
  • decreased oestrogen in a woman
  • decreased testosterone in a man
32
Q

What is primary hypogonadism?

A
  • something directly affecting gonads leading to low E2 and testosterone
  • but high LH and FSH due to reduced negative feedback
  • causes in men are infection / trauma / cancer of testes
  • causes in women is menopause - also causes low inhibin which partly leads to high FSH
33
Q

What is secondary (or hypogonadotrophic) hypogonadism?

A
  • problem in pituitary gland or hypothalamus leading to low (or normal) FSH/LH and low E2/testosterone
  • causes include pituitary tumour, high prolactin
34
Q

What are the symptoms of menopause? (Due to a lack of oestradiol)

A
  • skin dryness / hair thinning
  • hot flushes / sweating / sleep disturbance
  • mood disturbance
  • osteoporosis - decreased bone mineral density (BMD) as E2 stimulates osteoblasts, joint pain
  • sexual dysfunction - vaginal dryness, decreased libido
  • genito-urinary disturbance
  • weight gain
  • amenorrhoea - perimenopausal if you are within one year of last menstrual period and postmenopausal if you are after one year of last menstrual period
  • cessation of fertility
  • climacteric - irregular periods in years close to menopause
35
Q

What are the treatments for menopause?

A
  • oestrogen replacement through MHT (menopausal hormone therapy), previously known as HRT (hormone replacement therapy)
  • oestrogen stimulates endometrium to proliferate
  • add progesterone too to prevent risk of endometrial hyperplasia/cancer if endometrium is intact
36
Q

What is ovarian reserve and give an example of a marker and how it changes throughout a woman’s life?

A
  • ovarian reserve is how many eggs are in the ovaries before you reach menopause
  • Anti-Mullerian Hormone (AMH) produced by granulosa cells in ovaries is an ovarian reserve marker that peaks in early adult life and is very low at menopause
37
Q

What is the range and median age of menopause, and what is premature menopause?

A
  • range 45-55 years
  • median 51 years
  • only 1% of women undergo menopause below 40 years old and they are premature
38
Q

What is premature ovarian insufficiency (POI)?

A
  • same symptoms as menopause
  • previously called ‘premature ovarian failure (POF)’
  • difference is that conception can still happen in 20% of cases
  • diagnosis: high FSH > 25 iU/L on at least two occasions, four weeks apart
  • early menopause
39
Q

What causes premature ovarian insufficiency (POI)?

A
  • autoimmune
  • genetic e.g. fragile X syndrome / Turner’s syndrome (XO)
  • previous cancer therapy e.g. radio/chemotherapy
40
Q

Is there an andropause?

A
  • after age 40, male testosterone decreases by 1% every year
  • however free testosterone decreases more steeply which can be associated with hypogonadism symptoms like erectile dysfunction, low libido - late onset hypogonadism (age-related decreased testosterone)
41
Q

What is the ‘free hormone’ hypothesis with testosterone?

A
  • this is the binding of total testosterone in circulation
  • 60% strongly bound to SHBG (sex hormone binding globulin) = unavailable for tissues
  • 38% weakly bound to albumin = still bioactive
  • 2% free testosterone = active
42
Q

With age, how do SHBG and free testosterone levels change?

A

Total testosterone is unchanged, but SHBG is increased and free testosterone is reduced

43
Q

What kind of rhythm does testosterone have and under what conditions should it be measured?

A
  • diurnal rhythm
  • testosterone is higher in the morning = measure before 11am
  • can fall around 20% with sugar = ideally measure it fasting
44
Q

What are symptoms of testosterone deficiency?

A
  • sexual dysfunction - reduced libido
  • erectile dysfunction + loss of early morning erections
  • hair growth - frequency of shaving decreases
  • energy levels decrease - fatigue
  • mood disturbance
  • body composition - increased fat and reduced muscle mass
  • gynaecomastia - breast enlargement in men
  • spermatogenesis - decreases as high levels of intratesticular testosterone needed
  • bone health - can lead to osteoporosis as testosterone usually converted to oestrogen which is needed for good bone health
45
Q

How is testosterone converted into DHT and what is DHT?

A
  • through 5-alpha-reductase to di-hydro-testosterone (DHT)
  • 5-alpha-reductase found in testes (seminal vesicle, epididymis), prostate, skin of scalp, liver
  • DHT is a more potent ligand for androgen receptor (AR) than testosterone - binds to receptors more effectively
46
Q

How can 5-alpha-reductase activity be reduced?

A
  • using 5-alpha-reductase inhibitors
  • e.g. finasteride to treat prostate cancer as we want less of the potent DHT in them
47
Q

How is testosterone converted to oestrogens?

A
  • through aromatase
  • e.g. androstenedione converted to oestrone, testosterone converted to 17B-oestradiol
  • aromatase found in adipose tissue, adrenal glands, ovaries (granulosa cells), testes (Sertoli cells), brain, bone, skin
48
Q

What factors increase aromatase function?

A
  • age
  • obesity
  • insulin
  • gonadotrophins
  • alcohol
49
Q

How can aromatase activity be reduced and when is this needed?

A
  • by aromatase inhibitors
  • e.g. anastrozole used in breast cancer to reduce testosterone being converted to oestrogens as we want less oestrogen in them

Year 1 - BRS (73 decks)

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