endocrine fertility Flashcards

1
Q

axis in males

A

GnRH= FSH/LH= testes produces testosterone (inhibin - feedback to hypothalamus and pituitary)

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2
Q

axis in follicular phase for females

A

GnRH= LH/FSH= ovary produces oestradiol+ progesterone (inhibin - feedback)

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3
Q

axis in ovulation for females

A

ovary produces more oestradiol, which causes more GnRH, leading to an LH surge= ovulation

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4
Q

luteal phase

A

endometrium shed if implantation occurs

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5
Q

define infertility, how common and cause

A

not able to get pregnant after 1 yr on regular unprotected sex

happens to 1 in 6 couples, caused by abnormalities in males or females

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6
Q

what occurs in primary gonadal failure

A

low testosterone/ovary= high GnRH and LH/FSH

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7
Q

what occurs in hypo/pituitary disease

A

low FSH/LH and low GnRH (GnRH can’t be measured), so low testosterone/oestradiol

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8
Q

clinical features of male hypgonadism

A

low libido, impotence (no erection), small testes, less muscle and osteoporosis

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9
Q

causes of male hypogonadism

A

hypo/pituitary disease- either pituitary disease or kallmans syndrome (low GnRH, often combined with lack of smell aka anosmia) or illness/underweight (due to low leptin- less reproductive hormones secreted

primary gonadal disease- either inherited (klinefelters) or acquired (testicular torsion+ chemotherapy)

hyperprolactinaemia (not common in men)

rarely androgen receptor deficiency

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10
Q

investigating male hypogonadism

A

measure LH, FSH and testosterone- if low, MRI of pituitary needed

measure prolactin

measure sperm count- azospermia means NO sperm during ejaculation, oligospermia means less

analyse chromosomes for klinefelters

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11
Q

treatment of male hypogonadism

A

replacement testosterone for all- if they want fertility, not possible for primary gonadal disease, but possible for hypo/pit disease with LH+ FSH mimicking injections (Hcg given)- testosterone alone won’t produce sperm

dopamine agonist for hyperprolactinaemia

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12
Q

where testosterone produced

A

leydig cells, adrenal cortex, ovaries, placenta and tumours

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13
Q

actions of testosterone

A

develops male genital tract

supports fertility as adult

secondary sexual features

anabolic effects (including bone)

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14
Q

testosterone conversions

A

testosterone converted into dihydrotestosterone (DHT- active form) via 5alpha-reductase, or oestradiol via aromatase, which act on androgen and oestrogen receptor respectively (nuclear receptors)

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15
Q

define amenorrhoea and types

A

absence of periods

primary- never had period before (often congenital)

secondary- someone whos had period before hasn’t had one for 3 months (ie cycle was working perfectly at one point, so rarely congenital)

oligomenorrhae- irregular periods

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16
Q

causes of amenorrhoea

A

pregnancy/breastfeedin (hgih prolactin)

ovarian failure- can be premature ovarian failure (menopause by 40 rather than normal 51), ovariectomy/chemotherapy (toxic to ovaries) or turners (X chromosome missing)

gonadotrophin failure- hypo/pit disease, kallmanns syndrome, low BMI (due to low leptin) and the pill (switches off axis, so stop taking it every 4 years)

hyperprolactinaema

gonadal tumour= excess androgens

17
Q

investigating amenorrhea

A

pregancy test- MOST IMPORTANT

LH, FSH+ oestradiol- cycles are variable so won’t be very useful, but if all low, could indicate hypo/pituitary disease

day 21 progesterone- should have a rise if person has ovulated

prolactin/thyroid tests (high or low TSH can cause problems)

androgens (if high, can switch off axis)

chromosome analysis for turners

ultrasound scan of ovaries

18
Q

treatment of amenorrhoea

A

treat cause eg if low weight, make them eat

primary ovarian failure- become infertile, so give HRT: important as in premature failure, females have not received full dose of oestrogen= osteoporosis, so HRT vital

hypo/pit disease- HRT to replace oestrogen, and LH/FSH if fertility desired via IVF (like men)

19
Q

polycystic ovarian syndrome- incidence and effects

A

occurs in 1/12 women, and can lead to increased CVD and diabetes

20
Q

diagnosing PCOS

A

need 2 of the following- lots of cysts in ovaries on ultrasound, oligo/anovulation (lack of ovulation), and excess androgens

21
Q

features of PCOS

A

hirsutism (excess hair), problems with periods, and increased BMI

22
Q

treatment of PCOS

A

metformin- for insulin resistance

clomiphene- binds to oestrogen receptor, preventing -feedback, so axis vamped up

FSH/LH via IVF for fertility

23
Q

control of prolactin

A

TRH stimulates prolactin a bit, but main control is the inhibitory dopamine

24
Q

actions of prolactin

A

causes lactation, and reduces LH actions and GnRH pulsatility (released at regular intervals)

25
Q

causes of hyperprolacinaemia

A

dopamine-antagonists like anti-psychotics

prolactinoma

pituitary adenoma compressing stalk- prevents dopamine reaching pituitary

PCOS

hypothyroidism (high TRH)

oestrogen/pregnancy/ lactation

26
Q

features of hyperprolactinaema

A

galactorrhoea- lactation

lower GnRH/LH= hypogonadism

prolactinoma- causes head ache/visual problems

27
Q

treatment of hyperprolactinaema

A

treat cause eg drugs

dopamine agonists eg cabergoline (can help with prolactinoma)

pituitar surgery