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BRS Term 2 > Sex hormones (18) > Flashcards

Sex hormones (18) Flashcards

1
Q

How do we define puberty?

A
  • maturation of reproductive organs
  • production of sex-steroids
  • develop 2y sexual characteristics
  • attain capability to reproduce
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2
Q

What is Tanner Staging/how is it used to describe development?

A

Thelarche= breast development in girls (1= pre pubertal…5= adult breasts)

Testicular volume in boys (1.5ml prepubertal…adult size testes >15mls)- assessed using orchidometer

Pubarche= pubic hair onset in both (1=prepubertal…5= adult hair)

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3
Q

What is gonadarche?

A

activation of gonads by HPG axis

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4
Q

What is menarche?

A

onset of menstrual cycles

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5
Q

What is spermarche?

A

onset of sperm production

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6
Q

What is adrenarche?

A

onset of androgen production by adrenal glands

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7
Q

What 2y sexual characteristics are caused by estradiol in girls?

A
  • breast development
  • hair growth: pubic and axillary
  • sweat gland changes: oily skin/ acne
  • changes to external genitalia
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8
Q

What 2y sexual characteristics are caused by testosterone in boys?

A
  • deepening of voice
  • hair growth: pubic then axillary, facial
  • sweat gland changes: oily skin/acne
  • changes to external genitalia
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9
Q

What age is the onset of puberty for girls?

A

8-13

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10
Q

What age is the onset of puberty for boys?

A

9-14

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11
Q

What is the difference in the stage at which peak height is obtained for girls/boys?

A

in girls: at around tanner stage 2-3

in boys: 3-4

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12
Q

What are hormonal changes like during puberty?

A

adrenarche: DHEA (adrenal androgen) gradually increase
gonadarche: LH + FSH inc.
testosterone inc. in boys
oestradiol inc. in girls

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13
Q

What is GnRH and how can we describe its secretion?

A

gonadotrophin releasing hormone

- pulsatile secretion

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14
Q

Why are LH and FSH called gonadotrophins?

A

they stimulate the gonads (testes/ovaries) to make testosterone/oestrogen

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15
Q

How does GnRH secretion vary with age?

A
  • in late foetal life and early neonatal life: activation of HPG axis (“mini puberty”)- important for early maturation of gonads
  • in childhood: quiescence (inactivity) of HPG axis
  • as puberty is approached: inc. nocturnal GnRH pulsatility
  • as puberty is established: normal pulsatile GnRH secretion
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16
Q

How do we classify delayed puberty?

A

doesn’t start by 14yrs

more common in boys

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17
Q

How do we classify precocious puberty?

A

starts before 8yrs

more common in girls

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18
Q

When does menarche usually occur?

A
  1. 3yrs after thelarche/ soon after peak height velocity

- mean age= 12.7yrs

19
Q

When do we classify primary amenorrhoea?

A

period starting later than 16yrs

20
Q

When do we classify secondary amenorrhoea?

A
  • periods start but then stop for at least 3-6 months

N.B. common for periods to be irregular/anovulatory

21
Q

How long is a normal menstrual cycle in an adult woman?

A 
28 days (24-35)
relatively stable from month to month
22
Q

When do we classify oligo-menorrhoea?

A
  • few periods over a year
  • irregular/infrequent periods >35 day cycles
  • or 4-9 cycles per year (less= amenorrhoea)
23
Q

What are the hormone levels during the follicular phase (pre-ovulatory)?

A
  1. FSH rises- follicle stimulating hormone
  2. 2-3 follicles start to grow
  3. produce E2 (estradiol) and inhibin B–> -ve feedback to reduce FSH
  4. smaller follicles die off bc lack FSH (atresia) during ‘FSH window’
  5. bigger follicle survives bc less dependent on FSH- Graafian follicle
  6. follicle produces E2–> levels inc.
  7. switch to +ve feedback
  8. induces LH surge- causes ovulation (release of egg from follicle)
24
Q

What are the hormone levels during the luteal phase?

A

(low FSH and LH)

corpus luteum produces progesterone (most important) and oestradiol

25
Q

What is the purpose of B-hCG in pregnancy?

A

maintains continual production of progesterone by corpus luteum
(emulates LH- binds to receptors)

26
Q

What would happen if GnRH was secreted in a non-pulsatile fashion?

A

continuous non-pulsatile administration of GnRH causes decreased LH/FSH secretion–> dec. testosterone/oestrogen

27
Q

What is hypogonadism?

A

reduced function of testes/ovaries- low testosterone/ oestrogen levels

28
Q

What is primary hypogonadism?

A

caused by direct damage to gonads

e. g. infection/trauma/testicular cancer/menopause
- ->dec. sex steroid levels
- -> reduced -ve feedback to hypothalamus and pituitary
- -> inc. LH+FSH

29
Q

What is secondary/hypogonadotrophic hypogonadism?

A

e.g. pituitary tumour, hyperprolactinaemia
–> dec./not inc. LH+FSH levels
–> dec. sex steroid levels
(N.B. despite dec. sex steroid and -ve feedback–> no inc. in LH/FSH from pituitary)

30
Q

What happens in menopause in terms of the HPG axis?

A 
example of 1y hypogonadism
ovaries reduced function
--> dec. oestrogen (E2)
--> reduced -ve feedback
--> inc. FSH(/LH) bc low inhibin
31
Q

What are symptoms of menopause?

A

lack of estradiol

  • dry skin/ thin hair
  • hot flushes/sleep disturbance
  • mood disturbance
  • osteoporosis (bc E2 stimulates osteoblasts)
  • sexual dysfunction- dryness, libido
  • amenorrhoea (no period for 1yr/ infertility)
  • climacteric- irregular periods in years approaching menopause
32
Q

How do we treat menopause?

A

hormone replacement therapy- oestrogen

N.B. adding progesterone prevents risk of endometrial hyperplasia and cancer bc otherwise lining would continue to grow + not shed

33
Q

*How can we assess ovarian reserve?

A

AMH (anti-mullerian hormone) levels- produced by Sertoli cells in ovaries- v. low at menopause

34
Q

What age does menopause occur?

A

median age= 51yrs
range= 45-55
<40yrs= premature

35
Q

What is premature ovarian insufficiency (POI)?

A
  • same symptoms as menopause but early
  • high FSH and low E2
  • 20% can get pregnant
36
Q

What are causes of POI?

A
  • autoimmune
  • genetic e.g. Fragile X syndrome, Turner’s
  • cancer therapy: previous radio/chemotherapy
37
Q

What is the binding of ‘total testosterone’ in circulation?

A
  • 60% SHBG bound testosterone–> unavailable
  • 38% albumin-bound testosterone–> bioavailable (bound weakly)
  • 2% free testosterone–> ACTIVE
38
Q

What causes ‘late onset hypogonadism’ in males?

A

SHGB increases, so more of total testosterone binds–> free testosterone reduced

39
Q

How do testosterone levels vary throughout the day?

A

high in morning (before 11am)- gradually reduces during day

ideally measured when fasting as sugar can dec.

40
Q

What are symptoms of testosterone deficiency?

A
  • sexual dysfunction: dec. libido, erectile dysfunction (esp. loss of morning erections)
  • hair growth- frequency of shaving change?
  • energy levels- wellbeing, fatigue
  • body composition- inc. fat? dec. muscle mass? gynaecomastia (male breast enlargement)
  • spermatogenesis reduced
  • bone health (inc. risk of osteoporosis bc conversion to oestradiol)
41
Q

What is the action of aromatase in fat tissue, ovaries/testes and bone?

A

converts testosterone–> 17B-oestradiol
and
androstenedione–> oestrone

N.B. low testosterone–> low oestradiol–> inc. risk of osteoporosis

42
Q

What factors increase the action of aromatase?

A

age, OBESITY, insulin, gonadotrophin, alcohol

43
Q

How would we treat breast cancer that is sensitive to oestrogen?

A

use aromatase inhibitor e.g. tamoxifen

to reduce prod. of oestradiol

44
Q

How would we treat prostate cancer where we don’t want DHT?

A

use 5-alpha reductase inhibitor e.g. finasteride

BRS Term 2 (36 decks)

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