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YR2 LCRS Endocrinology > 9. Endocrine infertility > Flashcards

9. Endocrine infertility Flashcards

1
Q

what secretes gonadotrophin releasing hormone?

A

the hypothalamus

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2
Q

what does the secretion of GnRH stimulate?

A

the release of gonadotrophins (LH&FSH) from the anterior pituitary which (in men) stimulates testosterone release from the testes

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3
Q

what are the 3 phases of menstruation?

A
  1. follicular phase
  2. ovulation
  3. luteal phase
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4
Q

describe the follicular phase of menstruation

A
  • stimulation of oestradiol release from ovaries (via LH&FSH)
  • as oestradiol levels rise, it induces +ve feedback at the hypothalamus
  • increase in GnRH and a big LH surge (vital for ovulation)
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5
Q

describe the luteal phase of menstruation

A
  • if implantation does not occur the endometrium is shed (energy consuming)
  • menstrual shedding needs to occur otherwise the excessive growth of the endometrium could cause cancer
  • if implantation does occur -> pregnancy
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6
Q

what is infertility defined as and what proportion of couples is it a problem for?

A

inability to conceive after 1yr of regular unprotected sex

1:6 couples

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7
Q

what is primary gonadal failure?

A

when the ovaries and testes are not working

  • if testes aren’t working there is low testosterone -> less -ve feedback -> increased LH/FSH
  • if ovaries aren’t working there is less oestradiol -> increased LH/FSH
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8
Q

what is secondary gonadal failure?

A

when the hypothalamus or pituitary gland isnt working

  • problem with the hypothalamus/pituitary -> LH&FSH will be low
  • testosterone and oestradiol will be low
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9
Q

what does high FSH&LH but low testosterone/oestradiol suggest?

A

primary gonadal failure

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10
Q

what does low FSH&LH and low testosterone/oestradiol suggest?

A

secondary gonadal failure

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11
Q

what are the clinical features of male hypogonadism?

A
  • loss of libido (sexual interest)
  • impotence
  • small testes
  • decreased muscle bulk (testosterone is often used in anabolic steroids)
  • osteoporosis (testosterone is involved in bone strength)
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12
Q

what are the 4 main causes of male hypogonadism?

A
  1. hypothalamic-pituitary disease
    - hypopituitarism
    - kallman’s syndrome
    - illness/underweight
  2. primary gonadal disease
    - congential: klinefelter’s syndrome (XXY)
    - acquired: testicular torsion, chemotherapy
  3. hyperprolactinaemia
  4. androgen receptor deficiency
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13
Q

describe kallman’s syndrome

A

GnRH neurones don’t migrate and develop properly -> no GnRH released so patient can’t undergo puberty

anosmia (lack of smell)

undescended testes

low-normal stature

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14
Q

what causes anosmia in Kallman’s syndrome?

A

GnRH neurones and olfactory neurones migrate together in embryogenesis from the base of the brain upwards

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15
Q

how can male hypogonadism be investigated?

A
  • check LH, FSH and testosterone (if all low suggests secondary failure) -> MRI pituitary
  • check prolactin (high prolactin switches off gonadal axis)
  • check sperm count:
    azoospermia - 0 sperm
    oligospermia - less sperm
  • check appearance and motility of sperm
  • chromosomal analysis (e.g. for klinefelter’s)
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16
Q

how is male hypogonadism treated?

A
  • replacement testosterone (tablets, injections) to increase muscle bulk and protect against osteoporosis
  • subcutaneous gonadotrophin injections to induce spermatogenesis for fertility
  • dopamine agonist if the patient suffers from hyperprolactinaemia
17
Q

what are the endogenous sites of androgen production?

A
  • interstitial leydig cells of the testes
  • adrenal cortex
  • ovaries
  • placenta
  • tumours
18
Q

what are the main actions of testosterone?

A
  • development of the male genital tract
  • maintain fertility in adulthood
  • control of secondary sexual characteristics
  • anabolic effects (muscle, bone)
19
Q

what are the 2 enzymes involved in the conversion of testosterone and what do they convert testosterone to?

A

5𝛼-reductase converts testosterone into the active form dihydrotestosterone (DHT) which binds to androgen receptors

aromatase (found in brain and adipose tissue) converts testosterone to 17𝛽-oestradiol which binds to oestrogen receptors

20
Q

what will testosterone increase in adulthood?

A
  • lean body mass
  • muscle size and strength
  • bone formation and bone mass
  • libido and potency
21
Q

what are the 3 disorders in the female?

A
  1. amenorrhoea
  2. polycystic ovarian syndrome (PCOS)
  3. hyperprolactinaemia
22
Q

what are the different types of amenorrhoea?

A

primary amenorrhoea - failure to develop spontaneous menstruation by 16yo

secondary amenorrhoea - absence of menstruation for 3 months in a women who previously had cycles

oligomenorrhoea - irregular long cycles

23
Q

what are the causes of amenorrhoea?

A
  • pregnancy
  • lactation (high prolactin stops menstruation)
  • ovarian failure: early menopause, ovariectomy, chemotherapy, ovarian dysgenesis (turner’s syndrome)
  • gonadotrophin failure: hypothalamic/pituitary disease, kallman’s syndrome, low BMI, post-pill amenorrhoea, hyperprolactinaemia, androgen XS
24
Q

what are the signs of turner’s syndrome

A
  • short stature
  • cubitis valgus (forearm angled away from body)
  • gonadal dysgenesis (defective development)
25
Q

how can amenorrhoea be investigated?

A
  • pregnancy test
  • LH, FSH and oestradiol blood measurements
  • day 21 progesterone (to show ovulation)
  • prolactin measurement
  • thyroid function test
  • androgens
  • chromosomal analysis (e.g. for turner’s syndrome)
  • ultrasound scan ovaries/uterus
26
Q

how is amenorrhoea treated?

A
  • treat the cause (e.g. low weight)
  • if primary ovarian failure give HRT to increase fertility and to protect against osteoporosis
  • give gonadotrophins (LH&FSH) as part of IVF treatment
27
Q

what is polycystic ovarian syndrome associated with?

A
  • increased cardiovascular risk

- insulin resistance (diabetes)

28
Q

what is the criteria to diagnose PCOS?

A

2 of the following:

  • polycystic ovaries on the ultrasound scan
  • oligoovulation/anovulation
  • clinical/biochemical androgen excess
29
Q

what are the clinical features of PCOS?

A
  • hirsutism (XS hair growth in a male pattern)
  • menstrual cycle disturbance
  • increased BMI
30
Q

how is PCOS treated?

A

metformin - insulin sensitiser used in type 2 diabetes to prevent onset

clomiphene - anti-oestrogenic effect on the hypothalamo-pituitary axis by binding to oestrogen receptors in the hypothalamus and blocking -ve feedback. this increases GnRH and gonadotrophin secretion to kickstart HPG axis (5 day course)

gonadotrophin therapy as part of IVF treatment - super-stimulating follicles with IVF (however overstimulation can lead to ovarian hyper-stimulation syndrome)

31
Q

what does excess prolactin do?

A

switchs off GnRH pulsatility (-> infertility) and stops LH acting on ovaries and testes

32
Q

what are the causes of hyperprolactinaemia?

A
  • dopamine antagonist drugs
  • > anti-sickness tablets
  • > anti-psychotics
  • prolactinoma
  • stalk compression due to pituitary adenoma (mass blocks the secretion of dopamine so prolactin secretion is not inhibited)
  • PCOS
  • hypothyroidism (primary hypothyroidism increases TRH which stimulates prolactin)
  • oestrogens, pregnancy, lactation
  • idiopathic
33
Q

what are the clinical features of hyperprolactinaemia?

A
  • galactorrhoea
  • reduced GnRH secretion/LH action -> hypogonadism
  • prolactinoma (headaches and visual field defects)
34
Q

how can hyperprolactinaemia be treated?

A
  • treat the cause: stop drugs
  • dopamine agonist (bromocriptine, cabergoline)
  • prolactinoma treatment (pituitary surgery)

YR2 LCRS Endocrinology (18 decks)

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