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(endo) sex hormones during life Flashcards

1
Q

what is puberty?

A

attaining the capability to reproduce:

  • maturation of reproductive organs + development of secondary sexual characteristics
  • production of sex steroids (e.g. oestradiol, testosterone)
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2
Q

how are adolescents undergoing puberty staged?

A

using Tanner staging from I-V, where I is pre-pubertal and V is adult

1) in girls = thelarche (breast development)
2) in boys = testicular volume
3) both = pubarche (pubic hair)

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3
Q

how is testicular volume determined in males?

A

using a prader orchidometer

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4
Q

define gonadarche

A

activation of gonads by HPG axis

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5
Q

define thelarche

A

breast development in females

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6
Q

define menarche

A

menstrual cycles

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7
Q

define spermarche

A

spermatogenesis

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8
Q

define adrenarche

A

adrenal androgen production

starts approx two year before gonadarche

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9
Q

define pubarche

A

pubic hair development

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10
Q

what are the female secondary sexual characteristics?

A
  • breast development
  • hair growth (pubic, axillary)
  • sweat gland composition (skin oiliness, acne)
  • changes to external genitalia
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11
Q

what are the male secondary sexual characteristics?

A
  • deepening of voice
  • hair growth (pubic then axillary + facial)
  • sweat gland composition (skin oiliness, acne)
  • changes to external genitalia
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12
Q

which hormone causes the development of secondary sexual characteristics in males?

A

testosterone

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13
Q

which hormone causes the development of secondary sexual characteristics in females?

A

oestradiol

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14
Q

what age does puberty occur in girls?

A

onset = 8-13 years

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15
Q

what age does puberty occur in boys?

A

onset = 9-14 years

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16
Q

what is usually the first sign of puberty in girls?

A

thelarche (e.g. breast development)

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17
Q

what is the expected testicular size in prepubertal boys?

A

< 4ml

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18
Q

what is the expected testicular size in adult men?

A

> 15ml

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19
Q

what is GnRH secretion like in childhood?

A

quiescence of HPG axis during childhood

i.e. inactivity, dormancy

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20
Q

what is GnRH secretion like in puberty?

A

increased nocturnal GnRH pulsatility

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21
Q

what is GnRH secretion like in adulthood?

A

normal pulsatile GnRH secretion

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22
Q

what is ‘mini-puberty’ in in males?

A

when GnRH/LH/FSH/oestradiol/T increase in the foetus but falls during infancy to the quiescent phase of childhood

= testicular descent, penile length, Sertoli cell maturation, behavioural effects

(neonatal/foetal activation of the HPG axis)

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23
Q

what is precocious puberty?

A

when puberty commences before the age of 8

more common in girls > boys

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24
Q

what is delayed puberty?

A

when puberty commences after the age of 14

more common in boys > girls

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25
Q

when does menarche occur?

A

mean age = 12.7 years
(soon after peak height velocity)

approx 2 years after thelarche (breast development)

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26
Q

define primary amenorrhoea

A

absence of menses at age 15 years in the presence of normal growth and secondary sexual characteristics

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27
Q

define secondary amenorrhoea

A

when a woman who already menstruates does not get her period for at least 3-6 months

(but common for periods to be anovulatory/irregular for first 18 months)

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28
Q

what is the commonest physiological cause of secondary amenorrhoea in women?

A

pregnancy (!)

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29
Q

how long is the menstrual cycle on average?

A

approx 28 days

can be 24-35 days, +/- 2 days each month

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30
Q

define amenorrhoea

A

1) absence of periods for at least 3-6 months
OR
2) up to 3 periods in total in a year

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31
Q

define oligomenorrhoea

A

irregular/infrequent periods

1) >35 day cycles
2) 4-9 cycles per year

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32
Q

differentiate between amenorrhoea and oligomenorrhoea

A

amenorrhoea = absence of periods

oligomenorrhoea = few periods

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33
Q

what happens in the follicular phase of the menstrual cycle?

A

1) increased FSH production
2) stimulates follicular development
3) FSH stimulates the inner granulosa cells of the follicles to start producing E2 and inhibin
4) via negative feedback from E2, FSH levels fall
5) restrict the FSH window and non-dominant follicles, with no FSH, undergo atresia

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34
Q

what does reduced FSH secretion in the follicular phase of the menstrual cycle cause?

A

negative feedback due to increased E2 production
= reduced FSH
= follicular atresia of the non-dominant follicles

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35
Q

what happens in the pre-ovulatory phase of the menstrual cycle?

A

1) the most E2 secretion happens from the dominant/Graafian follicle
2) the increase in E2 causes a switch to a positive feedback w the gonadotrophins
3) an LH surge results (and to a lesser extent, an FSH surge)
4) the LH surge causes ovulation

36
Q

which hormone is secreted primarily in the luteal phase of the menstrual cycle?

A

progesterone

37
Q

which blood test is done to see if ovulation has taken place?

A

midluteal D21 progesterone

38
Q

which hormone dominates the proliferative phase of the uterine cycle?

A

oestradiol

39
Q

which hormone dominates the secretory phase of the uterine cycle?

A

progesterone

40
Q

what happens in the proliferative phase of he uterine cycle?

A

endometrial lining regrows

41
Q

what happens in the secretory phase of he uterine cycle?

A

transformation of the endometrial lining to be receptive for implantation

42
Q

what is the impact of continuous, non-pulsatile GnRH secretion?

A

decreased LH/FSH secretion

43
Q

what is GnRH pulsatility like during the menstrual cycle?

A

follicular phase = 90-120 mins

luteal phase = 180-240 mins

44
Q

define hypogonadism

A

in men = reduced testosterone

in women = reduced oestrogen

45
Q

what is primary hypogonadism?

A

reduced/no sex steroid production due to damaged gonads

= low E2/T but high LH + FSH

46
Q

what are the possible causes of hypogonadism in men?

A

infection, trauma or cancer of the testes

47
Q

what is the commonest physiological cause of primary hypogonadism in women?

48
Q

what is secondary hypogonadism?

A

reduced/no sex steroid production NOT due to damaged gonads BUT due to a secondary/pituitary cause

= low E2/T and low LH + FSH

49
Q

what are some causes of secondary hypogonadism?

A

high prolactin

pituitary tumour

50
Q

what is secondary hypogonadism also called?

A

hypogonadotrophic hypogonadism

51
Q

what hormone levels are expected in primary hypogonadism in women (e.g. menopause)?

A

low E2/T

high LH + FSH

low inhibin

52
Q

why are inhibin levels low in menopausal women?

A

due to their follicular pool being very small, they have very little inhibin

(this + low E2 causes increased FSH)

53
Q

what are the symptoms of menopause?

A
  • skin dryness
  • hair thinning
  • hot flushes
  • mood disturbance
  • osteoporosis
  • sexual dysfunction
  • weight gain
  • amenorrhoea
  • cessation of fertility
  • climateric periods
54
Q

why is osteoporosis a symptom of menopause?

A

decreased bone mineral density
= as E2 is required to stimulate osteoblast activity

(so in menopause, with little/no E2, osteoblasts cannot function to stimulate bone formation)

55
Q

what are perimenopausal women compared to postmenopausal women?

A

perimenopausal = within 1 year of the last menstrual period (LMP)

postemenopausal = after 1 year of the LMP

56
Q

why is menopause said to be climateric?

A

irregular periods in years close to menopause

57
Q

how is menopause treated?

A

hormone replacement therapy = oestrogen replacement

must also add progeterone! if endometrium is intact

58
Q

why are oestrogen and progesterone both given to treat menopause in women w an endometrium?

A

giving just oestrogen = stimulates the endometrium so MUST ADD PROGESTERONE to prevent the risk of endometrial hyperplasia/cancer

59
Q

when do AMH levels peak in women?

A

in early adult life

60
Q

what is the average age menopause occurs?

A

45-55 years

very few = <1% undergo premature menopause before 40 years

61
Q

what are the symptoms of early menopause?

A

same symptoms as early menopause

62
Q

what is early menopause also known as?

A

premature ovarian insufficiency

conception can still happen in 20% of the cases

63
Q

how is early menopause diagnosed?

A

high FSH (>25 iU/L)

= x2 at least 4 weeks apart

64
Q

what are the main causes of early menopause?

A

autoimmune

genetic (fragile X syndrome, Turner’s syndrome)

cancer therapy

65
Q

how is the total testosterone in circulation found?

A

60% = SHBG-bound testosterone (strongly bound = unavailable)

38% = albumin-bound (weakly bound = bioavailable)

2% = free testosterone (active)

66
Q

what can testosterone in circulation bind to and how does each differ?

A

1) SHBG = strongly bound to this and so is unavailable

2) albumin = weakly bound to this so is bioavailable

67
Q

in late-onset hypogonadism, why does free testosterone fall?

A

usually, SHBG increases w age and so more binds to the free testosterone

= reduces free testosterone levels bc SHBG-bound version is unavailable

68
Q

when is the optimal time to measure testosterone?

A

1) highest in the morning, so should measure it before 11am

2) measure it fasting as presence of glucose can cause T levels to fall by 20%

69
Q

why is testosterone best measured fasting?

A

as presence of glucose can cause testosterone levels to fall by 20%, affecting final results

70
Q

what are the symptoms of testosterone deficiency?

A
  • sexual dysfunction (low libido, erectile dysfunction)
  • low energy levels
  • mood disturbance
  • increased fat + reduced muscle mass
  • gynaecomastia
  • reduced spermatogenesis
  • reduced bone health
71
Q

why do some males with low/borderline testosterone levels have normal sperm production?

A

(testosterone is required for spermatogenesis)

  • testosterone is usually higher in the testes than elsewhere in the blood and so if there are low blood levels of T, the intratesticular levels are usually sufficient enough for spermatogenesis
72
Q

which enzyme catalyses the conversion of testosterone into oestrogen?

73
Q

which enzyme catalyses the conversion of testosterone into dihydrotestosterone?

A

5-alpha-reductase

74
Q

where is testosterone normally converted into oestrogen?

A
  • ovaries = granulosa cells
  • testes = Sertoli cells
  • brain
  • bone
  • skin
  • adrenal gland
  • adipose tissue
75
Q

where is testosterone normally converted into dihydrotestosterone?

A

testes (seminal vesicle, epididymis)

prostate

liver

76
Q

why is DHT (dihydrotestosterone) produced?

A

more potent ligand for androgen receptor

77
Q

which oestrogen is testosterone converted into?

A

17B-oestradiol

78
Q

which oestrogen is androstenedione converted into?

79
Q

name an aromatase inhibitor and its use

A

anostrazole

e.g. breast cancer

80
Q

name a 5-alpha-reductase inhibitor and its use

A

finasteride

e.g. prostate cacer

81
Q

what stimulates aromatase action?

A 
age
obesity
insulin
gonadotrophins
alcohol
82
Q

differentiate between primary and secondary hypogonadism

A

primary = problem w the ovaries or testes

secondary = problem w the hypothalamus or pituitary gland

83
Q

why is testosterone important to men?

A

hair growth, sexual function, muscle, voice

84
Q

why is oestrogen important to women?

A

bone health, skin, hair, sexual function

85
Q

why is progesterone important to women?

A

endometrial preparation for implantation

86
Q

what is the male equivalent to POI?

A

POI = premature ovarian insufficiency i.e. menopause before 40

in men = late-onset hypogonadism

brs (phase 1a) (7 decks)

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