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endocrine infertility Flashcards

1
Q

describe the normal male reproductive axis

A

hypothalamus produces pulisitile GnRH

stimulate pit to produce LH and FSH

stimulate testis to produce testosterone, also inhibin whihc acts -ve feedback on hyp and pit

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2
Q

what are the 3 phases of the normal menstrual cycle

A

follicular

ovulation

luteal

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3
Q

describe the axis in the follicular phase

A

hyp produce pulsitile GnRH

pit produce LH and FSH

ovaries produce oestradiol and progesterone, inhibin provides -ve feedback

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4
Q

describe the female axis in ovulation

A

high levels of oestragen cause +ve feedback on hyp and pit = LH surge - matures eggs

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5
Q

summarise the luteal phase

A

if implantation occurs - preg

if not - endometrium is shed - menstruation

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6
Q

what is the definition of infertility, how common is it

A

inability to concieve after 1 yr of regular unprotected sex - sometimes 2 yrs because IVF expensive

1:6 couples

problems in males, females or both

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7
Q

Explain the abnormalities in the hypothalamo-pituitary gonadal axis that cause primary hypogonadism *

A

ovary or teste failure = low sex hormone = low -ve feedback = high GnRH and LH FSH

LH and FSH are what are measured in circulation

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8
Q

Explain the abnormalities in the hypothalamo-pituitary gonadal axis that cause secondary hypogonadism *

A

failure of hypothalamus/pituitary

low LH FSH - less trophic action on sex organs = less sex hormone

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9
Q

clinical features of male hypogonadism *

A

clinical features are because of a reduction in testosterone:

loss of libido

impotence

small testes

decrease muscle bulk

osteoporosis - testosterone is trophic to bones

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10
Q

causes of male hypogonadism *

A

hypopituitarism - pit tumour, inflammation (hypophysitis)

kallman’s syndrome - anosmia and low GnRH

illness

underweight - less leptin which is produced by white adipoise tissue and is permissive of reproductive pathways

primary gonadal disease - congenital (Klinefelter’s XXY), acquired (testicular torsion- ischemia, chemo)

hyperprolactinaemia

androgen receptor deficiency - rare

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11
Q

describe Kallman’s syndrome *

A

failure of GnRH secretion

also lack smell (anosmia) because migration of the GnRH neuron and olfactory neurons happen together

no puberty

stature - low normal

lack of secondary sex characteristics

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12
Q

describe the investigations for male hypogonadism *

A

hormones - LH FSH testosterone - if all low need to do MRI pit

prolactin - ig high block reproduction

sperm count - azoospermia = absence of sperm in ejaculate. oligosermia = reduced number of sperm in ejaculate. motility of sperm is also important

chromosomal analysis - test for klinefelters XXY

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13
Q

describe the treatment for male hypogonadism *

A

replacement testosterone - wont make sperm, but fell good and good for bones

if primary hypogonadism- infertile

for fertility if secondary hypogonadism - subcutaneous gonadotrophins (LH (as HCG) recombinant FSH) - stim spermogenesis

dopamine agonist for hyperprolactinaemia - lower prolactin and cause a rise in testosterone

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14
Q

what are the endogenous sites of production of androgens

A

interstitial leidig cells of the testes

adrenal cortex

ovaries

tumour - if v androgenic and have weight loss

placenta

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15
Q

what are the main actions of testosterone

A

development of the male genital tract

maintains fertility in adulthood

control of secondary sex characteristics

anabolic effects - muscle and bone

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16
Q

describe the mechanism of action of testosterone *

A

98% protein bound

5a reductase converts it to dihydrotestosterone (active form) acts via androgen receptor

aromatase in fat tissue converts it to 17B oestradial (E2) - therefore obese people have a problem with fertility - act via oestrogen receptor

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17
Q

clinical uses of testosterone *

A

increase:

lean body mass

muscle size and strength

bone formation and bone strength in young men,

libido and potency

treat primary testicular failure/primary hypogonadism

treat secondary hypogonadism

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18
Q

side effect of testosterone therapy *

A

testes get small - switch of endogenous axis by -ve feedback cause infertility long term

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19
Q

define amenorrhoea *

A

absence of periods

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20
Q

define primary amenorrhoea *

A

failure to begin sponataneous mutation by 16yrs of age

congenital

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21
Q

describe secondary amenorrhoea *

A

absence of menstruation for 3 months in a women who has previously had cycles- iue axis was working at one point

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22
Q

define oligomenorrhoea *

A

irregular long cycles

normal cycles between 25-35 days

23
Q

causes of amenorrhoea *

A

preg

lactation - high prolactin

ovary filure: primary ovarian insufficiency (- early menopause because all eggs have apoptosed - people come in with irregular period high LH adn FSH, low oestradiol), ovariectomy, chemo

ovarian dysgenesis (Turners 45 XO) - lacking one chromosome - ovaries dont grow

gonadotrophin failure: hypo/pit disease, Kallmann’s syndrome, low BMI, post pill amenorrhoea

hyperprolactinaemia

androgen excess - gonadal tumour - rare

24
Q

describe Turner’s syndrome *

A

short stature

cubitus valgus - wide carrying angle

gonadal dysgenesis

1:5000 live female births

25
describe post pill amenorrhoea \*
pituitary goes to sleep because of exogenous oestrogen and porgesterone have to stoo the pill every 4 years
26
describe teh investigations of amenorrhoea \*
preg test LH FSH Oestradioal measurement - tricky because of cycles, if fall very low = pit/hyp problem day 21 (18, 21, 24) progesterone - will be a peak if ovulating prolactin, thyroid function tests androgens (testosterone, androstenedione, DHEAS) - if high switch off periods chromosomal analysis for XO ultrasound scan of ovaries/uterus for PCOS
27
treatment of amenorrhoea \*
treat the cause primary ovarian insufficiency - infertile, hormone replacement therapy give back oestrogen otherwise you would get osteoporosis - no risk because body would be making it anyway hyp/pit disease - HRT, gonadotrophins as part of IVF for fertility
28
describe PCOS
incidence 1:12 women associated with increased CV risk
29
criteria to diagnose PCOS \*
need 2 of: polycystic ovaries on uterus oligo-/anovulation clinical/biochem androgen excess a lot of women get the diagnosis but if it means anything for the pt is different
30
clinical features of PCOS \*
hirsuitism menstrual cycle disturbance increased BMI
31
treatment of PCOS \*
metformin - for diabetes - insulin sensitiser, PCOS women have insulin resistance Clomiphene - for irregular periods - is anti-oestrogenic in hyp-pit axis - bind to oestrogen receptors in hypothalamus - blocking normal feedback = increase secretion of GnRG and gonadotrophins gonadotrophin therapy as part of IVF treatment reverse circadian prednisolone - take in morning and night suppress acth by -ve feedback so suppress androgen production. for hirsuitism - mechanical hair removal, oestrogen or reduce testosterone
32
summarise the control of prolactin secretion \*
stimulated by TRH inhibited by dopamine prolactin inhibuts GnRH pulsatility (infertile) and LH actions of ovary/testes - switch off period/reduce testosterone
33
causes of hyperprolactinaemia \*
dopamine antagonist drugs: anti-emetics (metoclopramide), antipsychotics (phenothiazines) prolactinoma - benign stalk compression due to pit adenoma - stop dopamine coming down stalk = increase in prolactin PCOS hypothyroidism - increase TRH oestrogens preg lactation idiopathic
34
clinical features of prolactinoma \*
galactorrhoea reduced GnRH secretion/LH action more than hypogonadism prolactinoma - headache, visual field defect
35
hyperprolactinoma treatnment \*
treat the cause dopamine agonist - bromocriptine, cabergoline (very potent, once or twice week) for prolactinoma - dopamine agonist therapy, pit surgery rarely needed
36
hyperprolactinoma investigations \*
Drug history Serum prolactin Pregnancy test Thyroid function tests Anterior pituitary function MRI pituitary Visual fields
37
PCOS investigations \*
Increased LH (LH/FSH ratio) - causes ovaries to make extra testosterone Testosterone may be high, low SHBG (sex hormone binding globulin) therefore increased free testosterone Prolactin – mildly raised Ovarian USS – multiple 3-5mm cysts
38
why can you concieve on cabergoline \*
it is a dopamine agonist - raise the action of dopamine - inhibit prolactin - high prolactin would ave been inhibiting the gnrh access by acting on kisspeptin neurons - therefore LH and FSH would return to normal so can ovulate
39
why would prolactin be raised \*
pregnancy marathon running dopamine antagonists sex chronic renal/epatic failure raised TRH so in hypothyroidism
40
describe a microprolactinoma \*
\<10mm in size press on optic chiasm = bitemporal hemianopia
41
wy would damage to the pituitary stalk cause high prolactin \*
stop dopamine coming from the hypothalamus which would inhibit prolactin
42
can you use cabergoline in pregnancy \*
yes stop if microprolactinoma unless near the optic chiasm, continue if macroprolactinoma worry about compressing the pituiatry stalk - do visual field tests if see visual field defects increase the dose or do transphenoidal surgery - in 2nd trimester stop near the end of pregnancy - can pass into breast milk
43
wat is a problem of radioactive therapy for pit adenomas \*
can knock off the other pituitary axis
44
what is oligomenorrhoea \*
periods \>35 days apart
45
why would a thin person have secondary amenorrheoa \*
low leptin doesnt stimulate the kisspeptic neurons so the gnrh axis is switched off
46
where does oestrogen act to inhibit LH and FSH \*
ERa receptors on kisspeptin neurons
47
what acts on kisspeptin neurons and what is the effect \*
too little leptin shuts off gnrh axis too much prolactin and oestrogen switches off axis
48
what causes hypothalamic amenorrhoea \*
negative energy balance - losing too much weight too much exercise psychological stress high prolactin
49
what tests would you perform on someone with oligomenorrhoea \*
LH and FSH test preg hCG AMH - antimalaria hormone that goes down near pregnancy, high in PCOS progesterone - if high indicate they have ovulated - comes from the corpus luteum oestrogen prolactin tsh and free T4
50
what is the condition if a pt hhas high oestrogen and low LH and FSH \*
pregnancy - oestrogen made by the corpus luteum and placenta - provides -ve feedback on LH adn FSH could be on exogenous oestrogen
51
what is the condition with low lh fsh and oestrogen \*
hypogonadotrophin ypogonadism -gonadotrophs arent working (low lh and fsh) which is what is causing low gonad hormone (oestrogen) it is a problem in hypothalamus or pit or genetic mutation eg kallmans syndrome (cant smell either and have no functional gnrh)
52
what is the condition with high LH and FSH and low oestrogen \*
hypergonadotrophic hypogonadism from ovarian failure (Menopause) - ovaries shrink = low oestrogen = high lh and fs via -ve feedback one of reading could by LH surge in ovulation - need to do readings couple of months apart (however would expect oestrogen to be high to in this case)
53
is someone with oligomenorrhoea likely to have low gonadotropins \*
no

endo - yr2 (24 decks)

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