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endo - yr2 > endocrine infertility > Flashcards

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
Q

describe post pill amenorrhoea *

A

pituitary goes to sleep because of exogenous oestrogen and porgesterone

have to stoo the pill every 4 years

26
Q

describe teh investigations of amenorrhoea *

A

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
Q

treatment of amenorrhoea *

A

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
Q

describe PCOS

A

incidence 1:12 women

associated with increased CV risk

29
Q

criteria to diagnose PCOS *

A

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
Q

clinical features of PCOS *

A

hirsuitism

menstrual cycle disturbance

increased BMI

31
Q

treatment of PCOS *

A

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
Q

summarise the control of prolactin secretion *

A

stimulated by TRH

inhibited by dopamine

prolactin inhibuts GnRH pulsatility (infertile) and LH actions of ovary/testes - switch off period/reduce testosterone

33
Q

causes of hyperprolactinaemia *

A

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
Q

clinical features of prolactinoma *

A

galactorrhoea

reduced GnRH secretion/LH action more than hypogonadism

prolactinoma - headache, visual field defect

35
Q

hyperprolactinoma treatnment *

A

treat the cause

dopamine agonist - bromocriptine, cabergoline (very potent, once or twice week)

for prolactinoma - dopamine agonist therapy, pit surgery rarely needed

36
Q

hyperprolactinoma investigations *

A

Drug history

Serum prolactin

Pregnancy test

Thyroid function tests

Anterior pituitary function

MRI pituitary

Visual fields

37
Q

PCOS investigations *

A

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
Q

why can you concieve on cabergoline *

A

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
Q

why would prolactin be raised *

A

pregnancy

marathon running

dopamine antagonists

sex

chronic renal/epatic failure

raised TRH so in hypothyroidism

40
Q

describe a microprolactinoma *

A

<10mm in size

press on optic chiasm = bitemporal hemianopia

41
Q

wy would damage to the pituitary stalk cause high prolactin *

A

stop dopamine coming from the hypothalamus which would inhibit prolactin

42
Q

can you use cabergoline in pregnancy *

A

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
Q

wat is a problem of radioactive therapy for pit adenomas *

A

can knock off the other pituitary axis

44
Q

what is oligomenorrhoea *

A

periods >35 days apart

45
Q

why would a thin person have secondary amenorrheoa *

A

low leptin

doesnt stimulate the kisspeptic neurons

so the gnrh axis is switched off

46
Q

where does oestrogen act to inhibit LH and FSH *

A

ERa receptors on kisspeptin neurons

47
Q

what acts on kisspeptin neurons and what is the effect *

A

too little leptin shuts off gnrh axis

too much prolactin and oestrogen switches off axis

48
Q

what causes hypothalamic amenorrhoea *

A

negative energy balance - losing too much weight

too much exercise

psychological stress

high prolactin

49
Q

what tests would you perform on someone with oligomenorrhoea *

A

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
Q

what is the condition if a pt hhas high oestrogen and low LH and FSH *

A

pregnancy - oestrogen made by the corpus luteum and placenta - provides -ve feedback on LH adn FSH

could be on exogenous oestrogen

51
Q

what is the condition with low lh fsh and oestrogen *

A

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
Q

what is the condition with high LH and FSH and low oestrogen *

A

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
Q

is someone with oligomenorrhoea likely to have low gonadotropins *

A

no

endo - yr2 (24 decks)

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