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ENDOCRINE > Y2 ENDOCRINE REPRODUCTION > Flashcards

Y2 ENDOCRINE REPRODUCTION Flashcards

1
Q

mean duration of menstrual cycle

A

28 days

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2
Q

average duration of menses

A

3-8 days

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3
Q

normal estimated blood loss during menstruation

A

=30ml

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4
Q

when during the menstrual cycle does ovulation usually occur?

A

day 14

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5
Q

low oestrogen levels signal the anterior pituitary to produce?

A

FSH

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6
Q

what stimulates follicle maturation?

A

FSH

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7
Q

what triggers ovulation?

A

surge in LH at peak of follicular growth

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8
Q

what secretory phase begins following ovulation?

A

luteal phase

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9
Q

what are the granulosa cells called in the luteal phase?

A

corpus luteum

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10
Q

peak progesterone production occurs?

A

one week after ovulation

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11
Q

if pregnant, embryo releases hormones to preserve?

A

corpus luteum

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12
Q

what hormone drops if there is no embryo to initiate menstruation?

A

progesterone

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13
Q

what structure of the hypothalamus produces GnRH?

A

arcuate nucleus

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14
Q

the ovary attaches to the pelvic side wall by?

A

infundibulopelvic ligament

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15
Q

where are the follicles within the ovary?

A

cortex

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16
Q

endometrium is which layers of the uterus?

A

basal and superficial.

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17
Q

what thickens in the uterus in response to oestrogen?

A

endometrium

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18
Q

endometrium sloughs off in response to?

A

drop/absence of hCG and progesterone

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19
Q

GnRH is what type of hormone?

A

deca-peptide

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20
Q

GnRH is released in which manner?

A

pulsatile

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21
Q

half life of GnRH?

A

2-4 minutes

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22
Q

what is FSH?

A

a glycoprotein of 2 subunites

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23
Q

half life of FSH?

A

several hours

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24
Q
  • acts on theca cells to cause uptake of cholesterol, androgen production and conversion to oestrogen.
A

LH

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25
Q

acts synergistically with FSH and induces FSH and LH?

A

oestrogen

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26
Q

Local peptide in follicular fluid that acts by negative feedback on pituitary FSH secretion. Locally enhances LH-induced androstenedione production.

A

inhibin

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27
Q

Found in follicular fluid it stimulates FSH induced oestrogen production.

A

activin

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28
Q

tubular components of the testis?

A

sertoli cells and germ cells

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29
Q

interstitial components of the testis?

A

leydig cells and capillaries

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30
Q

what happens to the cervical mucous pre-fertilisation?

A

it becomes thin

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31
Q

sperm cannot fertilise an egg without?

A

capacitation

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32
Q

where does capacitation occur?

A

female genital tract

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33
Q

what follows capacitation?

A

acrosome reaction

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34
Q

what allows sperm to penetrate the egg?

A

acrosome reaction

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35
Q

what triggers the acrosomal reaction?

A

zona pellucida ZP3

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36
Q

what prevents polyspermy?

A

zona reaction

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37
Q

how many sperm are deposited at the cervical opening during ejaculation?

A

400-600 million

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38
Q

how many sperm reach the fertilisation site?

A

=200

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39
Q

what controls the development and maintenance of female sexual characteristics?

A

oestrogens

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40
Q

granulosa cells are stimulated by LH to produce?

A

pregnenolone

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41
Q

expression of aromatase and 17B-HSD is controlled by?

A

FSH stimulation

42
Q

aromatase is expressed where?

A

non-gonadal sites

43
Q

aromatase facilitates?

A

peripheral aromatisation of androgens to estrone e.g. fat and bone

44
Q

progesterone is synthesised from and where?

A

pregnenolone in the

  • corpus luteum
  • placenta during pregnancy
  • adrenal glands
45
Q

main product during follicular maturation?

A

oestradiol

46
Q

main product in luteal phase following ovulation?

A

progesterone.

47
Q

reduction in frequency of periods to less than 9/year.

A

oligomenorrhoea

48
Q

failure of menarche by the age of 16 years.

A

primary amenorrhoea

49
Q

cessation of periods for >6 months in an individual who has previously menstruated

A

secondary amenorrhoea

50
Q

what may cause physiological amenorrhoea?

A
  • pregnancy

- post-menopause

51
Q

what may cause primary amenorrhoea?

A
  • congenital problems e.g. Turner’s, Kallman’s.
52
Q

what may cause secondary amenorrhoea?

A
  • ovarian problems: PCOS, premature ovarian failure.
  • uterine problem: uterine adhesions.
  • hypothalamic dysfunction: weight loss, over exercise, stress, infiltrative.
  • pituitary: high PRL, hypopituitarism.
53
Q

female hypogonadism is identified by?

A

low oestrogen levels.

54
Q

what is primary hypogonadism in females?

A
  • ovary problems.

e. g. premature ovarian failure.

55
Q

what form of hypogonadism in females is ass. with high LH and FSH?

A

primary

56
Q

what form of hypogonadism in females is ass. with low LH and FSH?

A

secondary

57
Q

what is secondary hypogonadism in females?

A
  • hypothalamus or pituitary problems e.g. high PRL, hypopituitarism.
58
Q

what causes premature ovarian failure?

A
  • chromosome abnormalities e.g. Turner’s, Fragile X.
  • gene mutations (FSH or LH receptor).
  • autoimmune disease e.g. Addison’s thyroid, anti-phospholipid.
  • iatrogenic e.g. chemo or radiotherapy.
59
Q

amenorrhoea, oestrogen deficiency and elevated gonadotrophins occurring at <40 years of age due to loss of ovarian function.

A

premature ovarian failure

60
Q

how do you diagnose premature ovarian failure?

A

FSH >30 on 2 separate occasions >1 month apart

61
Q

genetic disorder causing loss of GnRH secretion + anosmia or hyposmia.

A

Kallman’s syndrome

62
Q

Kallman’s syndrome more commonly affects?

A

males 4x

63
Q

Kallman’s syndrome shows a normal MRI pituitary but absence of?

A

olfactory bulbs

64
Q

Rotterdam criteria used to diagnose?

A

PCOS

65
Q

what are the Rotterdam criteria?

A

2 of:

  • menstrual irregularity
  • hyperandrogenism (hirsutism or elevated free testosterone).
  • polycystic ovaries
66
Q

in PCOS, oestrogen levels are?

A

normal

67
Q

what causes hirsutism?

A

excess androgen at hair follicle

68
Q

management of PCOS?

A
  • oral contraceptive pill.
  • anti-androgens e.g. cyproterone acetate.
    can give dianette = OCP + cyproterone acetate.
  • local anti-androgens e.g. efflornithine cream (vaniqa).
  • cosmesis: electrolysis and laser phototherapy.
69
Q

clinical features of Turner’s syndrome?

A
  • short
  • webbed neck
  • shield chest with wide spaced nipples
  • cubitus valgus
70
Q

Turner’s syndrome manifests in the CVS as?

A
  • coarctation of the aorta
  • bicuspid aortic valve
  • hypoplastic left heart
71
Q

Turner’s syndrome manifests in the GI system as?

A
  • crohn’s or UC.

- bleed

72
Q

what conditions (not CVS or GI) are ass. with Turner’s syndrome?

A
  • lymphoedema
  • hypothyroidism
  • osteoporosis
  • scoliosis
  • otitis media
  • renal abnormalities
73
Q

most common congenital form of primary hypogonadism in males?

A

Klinefelter’s

74
Q

Klinefelter’s karyotype

A

XXY

75
Q

Turner’s karyotype

A

XO

76
Q

Klinefelter’s biochemical results?

A
  • low testosterone
  • high LH/FSH
  • elevated SHBG/oestradiol
77
Q

secondary male hypogonadism biochemical results?

A
  • low/normal FSH and LH.

- low 9am testosterone

78
Q

what causes secondary hypogonadism?

A

hypothalamic or pituitary dysfunction

  • Kallman’s, CAH.
  • exercise, weight change, stress, systemic illness etc.
79
Q

management of male hypogonadism?

A

if <50 - testosterone therapy.

will not restore fertility and may actually act as contraception

80
Q

benefits of testosterone replacement therapy?

A
  • improved sexual function
  • bone health
  • body composition/muscle strength
  • improved QoL and cognition
  • insulin sensitivity and diabetes
81
Q

what causes gynaecomastia?

A
  • increased oestrogen action on breast tissue
82
Q

investigation of gynaecomastia?

A
  • testosterone, LH and FSH
  • oestradiol, prolactin.
  • AFP, SHBG and hCG.
  • LFTs

breast, testicular and adrenal imaging.

83
Q

GnRH released by?

A

neurons in the hypothalamus in pulsatile release

84
Q

GnRH stimulates?

A

FSH and LH synthesis/release from anterior pituitary

85
Q

FSH in females?

A

stimulates follicular development and endometrium thickening

86
Q

FSH in males?

A

stimulates sertoli cells and spermatogenesis

87
Q

LH in females?

A

peak stimulates ovulation, corpus luteum development and endometrium thickening.

88
Q

LH in males?

A

stimulates leydig cells, testosterone secretion and spermatogenesis

89
Q

oestradiol peaks when in regards to ovulation?

A

before

90
Q

progesterone peaks when in regards to ovulation?

A

after

91
Q

which hormone is responsible for infertile thick cervical mucous?

A

progesterone

92
Q

what hormone increases basal body temperature?

A

progesterone

93
Q

management of PCOS?

A

weight loss.
stop smoking/alcohol.
- folic acid 400mcg/5mg a day.
- metformin (insulin resistance)

94
Q

symptoms of pelvic inflammatory disease?

A
  • abdo/pelvic pain
  • fever
  • vaginal discharge
  • dyspareunia (difficult/painful intercourse).
  • cervical exctiation
  • menorrhagia
  • dysmenorrhoea
  • infertility
  • ectopic pregnancy
95
Q

“chocolate cysts” on ovary.

A

endometriosis

96
Q

presence of endometrial glands outside uterine cavity

A

endometriosis

97
Q

how can you test tubal patency?

A
  • laparoscopy

- hysterosalpingiogram

98
Q

when is laparoscopy contra-indicated?

A
  • obesity, previous pelvic surgery, Crohn’s disease.
99
Q

when should hysteroscopy be performed?

A

only where suspected or known endometrial pathology e.g. septum, polyps, adhesion

100
Q

how do you manage hyperprolactinaemia?

A
  • dopamine antigonists.
    e. g. Cabergoline (long-acting) 2x a week.

stop when pregnancy occurs

ENDOCRINE (12 decks)

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