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MB2: Endocrinology > Reproductive endocrinology > Flashcards

Reproductive endocrinology Flashcards

1
Q

what hormone is produced at implantation

A

HCG

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2
Q

what does the corpus luteum produce

A

progesterone

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3
Q

describe how insulin resistance is produced in the pregnant mother

A

hPL and placental progesterone cause IR to direct nutrition to foetus
if the mother is already insulin resistant then diabetes can occur

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4
Q

when does foetal organogenesis begin

A

5 weeks, possibly earlier

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5
Q

managing gestational diabetes in mothers?

A 
good sugar control 
folic acid 5mg 
consider tablets to insulin 
regular eye checks
avoid ACEI/statin 
start aspirin 12 weeks
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6
Q

what should be given to a mother with gestational diabetes during labour

A

IV insulin

IV dextrose

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7
Q

blood sugar control in diabetic mother during pregnancy

A

pre meal - 4-4.5 mmol/L

2hr post meal - 6-6.5mmol/L

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8
Q

what drug modification should be made in T1DM

A

insulin increase

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9
Q

what drug modification should be made in T2DM

A

consider changing metformin to insulin

if on many drugs consider change to insulin pre pregnancy

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10
Q

what drug modification should be made in GDM

A

metformin, maybe insulin

lifestyle

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11
Q

how many with GDM develop T2DM post pregnancy

A

50% after 10-15y

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12
Q

true/false - GDM mothers should be monitored 6 weeks post natal either by OGTT or fasting to screen for T2DM

A

true

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13
Q

preventing diabetes after GDM

A 
keep weight as low as possible 
healthy diet 
aerobic exercise 
annual fasting glucose 
metformin/pioglitazone?
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14
Q

function of FSH?

A

males - spermatogenesis

females - growth of ovarian follicles and ovary secretes oestrogen

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15
Q

function of LH?

A

males - secretion of testosterone

females - ovulation and progesterone production by corpus luteum

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16
Q

describe the release of GnRH

A

released in a pulsatile manner

constant in males and cyclical in females

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17
Q

high/low frequency pulses drive LH and high/low frequency pulses drive FSH

A

high frequency - LH

low frequency - FSH

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18
Q

oestrogen/progesterone increases pulsatility frequency of GnRH and oestrogen/progesterone decreases pulsatility frequency of GnRH

A

oestrogen increases to cause the LH surge

progesterone decreases

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19
Q

describe the purpose of kisspeptin receptors

A

neurons in hypothalamus don’t have oestrogen/progesterone receptors to respond to changes and so the kisspeptin neurons adjacent to the hypothalamus respond to it §

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20
Q

how long is the female menstrual cycle

A

roughly 28 days
follicular phase 14±7
luteal is generally 14

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21
Q

describe the relationship of oestrogen to FSH/LH

A

rising FSH stimulates oestrogen, which exerts -ve feedback to FSH
oestrogen exerts +ve feedback to cause FSH rise and LH surge

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22
Q

how does progesterone influence LH secretion

A

LH stimulates corpus luteum to produce progesterone, acts by -ve feedback to alter GnRH pulsatility so less LH secreted

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23
Q

follicular growth - what do theca cells do in response to LH

A

convert cholesterol to androgen

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24
Q

follicular growth - what do granulosa cells do in response to FSH

A

convert androgen to oestrogen by aromatase

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25
Q

describe folliculogenesis and how one follicle is selected for ovulation

A

early growth is independent of gonadotrophins

once follicle reaches certain size it becomes gonad dependent and if this doesnt coincide with FSH rise it is lost

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26
Q

describe a possible evolutionary mechanism why follicles are so FSH dependent

A

rising oestrogen causes initial drop in FSH

only the follicle with most FSH receptors and best vascularity can survive this drop

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27
Q

when does LH surge occur in relation to ovulation

A

34-36 hours prior

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28
Q

what oestrogen threshold is required for an increase in GnRH pulsatility for the LH surge

A

200pg/ml

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29
Q

function of progesterone

A 
increased angiogenesis 
maintains endometrial thickness and increased secretion 
infertile thick mucus 
relaxation of myometrium
thermogenic 
inhibits LH
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30
Q

function of oestrogen

A

increased thickness of endometrium
regulates LH surge
reduced vaginal pH by lactic acid increase
decreased viscosity of cervical mucus

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31
Q

sperms ability to penetrate cervical canal mucus is dependent on

A

thickness of mucus
motility of sperm
interaction with mucins
interaction with ROS

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32
Q

where is sperm synthesised

A

seminiferous tubules of testes

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33
Q

describe how testosterone causes sperm production

A

released into circulation and taken up be sertoli cells
maintains integrity of blood testes barrier
release mature sperm from sertoli cells by influence of peritubular myoid cells

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34
Q

in males what does FSH do and how is it under -ve feedback

A

acts on sertoli cells for spermatogenesis

-ve feedback by inhibin on hypothalamus/pituitary

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35
Q

in males what does LH do and how is it under -ve feedback

A

LH acts on leydig cells to primary produce testosterone
also enhances spermatogenesis
free testosterone acts as -ve feedback on hypothalamus and pituitary

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36
Q

what is testosterone broken down to for cell effects and what enzyme breaks it down

A

broken down to dihydrotestosterone by 5-hydroreductase and oestradiol by aromatase

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37
Q

what is primary hypogonadism in males and how would it appear on bloods
what is affected by primary hypogonadism

A

decreased testosterone due to less functional testes so less -ve feedback
higher GnRH and FSH/LH
spermatogenesis is usually affected

38
Q

what is secondary hypogonadism in males, how would it appear on bloods
what is affected by hypogonadism

A

low testosterone due to hypothalamic/pituitary dysfunction
low testosterone despite low/normal FSH/LH
testosterone and spermatogenesis affected

39
Q

congenital causes primary hypogonadism

A

kleinefelter syndrome
cryptorchism
Y chromosome microdeletions

40
Q

acquired causes primary hypogonadism

A 
testicular trauma/torsion 
chemotherapy/radiation 
varicocele 
orchitis - mumps 
infiltrative disease - haemachromatosis 
medications - glucocorticoids, ketoconazole
41
Q

congenital causes secondary hypogonadism

A

kallmanns syndrome

prader willi syndrome

42
Q

acquired causes secondary hypogonadism

A 
pituitary tumour, infection, infiltrative disease, apoplexy, head trauma 
hyperprolactinaemia 
obesity, diabetes 
steroids, opiates 
acute systemic illness 
eating disorders
excess exercise
43
Q

what genetic pattern does kleinefelter syndrome have

A

47XXY or 46XY/47XXY mosaicism

44
Q

diagnosis of kleinefelter syndrome

A

karyotyping

45
Q

increased risks in kleinefelter syndrome?

A

breast cancer

non-hodgkins lymphoma

46
Q

what is kallmanns syndrome and what is it associated with

A 
deficiency of GnRH 
hyposmia or anosmia 
red-green colour blindness 
cleft lip/palate 
unilateral renal agenesis 
bimanual synkinesis
47
Q

pre pubertal signs hypogonadism men

A 
small male sexual organs, testes, penis, prostate 
decreased body hair 
high pitched voice 
low libido 
gynaecomastia 
decreased bone/muscle mass 
euchnoidal habitus 
symptoms as per cause
48
Q

post pubertal signs hypogonadism men

A

normal skeletal proportions and penis/prostate/voice
low libido, decreased spontaneous erections
decreased pubic, axillary hair and reduced shaving frequency
reduced testicle volume
gynaecomastia
decreased energy/motivation
decreased muscle/bone mass
symptoms per cause

49
Q

when is SHBG higher

A 
ageing 
hyperthyroidism 
high oestrogen 
liver disease
HIV
anti-epileptic drugs
50
Q

when is SHBG lower

A 
hypothyroidism 
low oestrogen 
obesity 
diabetes 
steroids 
nephrotic syndrome
51
Q

what should be performed if a male with suspected hypogonadism presents with infertility

A

semen analysis

52
Q

determining hypogonadism in men?

A

low AM testosterone x2
if FSH/LH high then primary and karyotype and iron studies
if FSH/LH low/normal then secondary and check medications, prolactin/pituitary hormones, MRI, iron study

53
Q

testosterone gel - mode of administration and frequency, benefits, disadvantages

A

transdermal and daily
fast onset and convenient
mimics circadian rhythm
can cause interpersonal transfer, compliance issues and irritation

54
Q

oral testosterone - mode of administration and frequency, benefits, disadvantages

A

once daily oral
convenient
nausea

55
Q

nebido (undecanoate) - mode of administration and frequency, benefits, disadvantages

A

IM 10-14 weeks
convenient and good compliance, steady level
hard to withdraw side effects, pain at site, cough, contraindicated in bleeding disorders

56
Q

sustanon (isocaproate) - mode of administration and frequency, benefits, disadvantages

A 
IM 2-3 weeks 
easy to withdraw, self administered
cough following injection 
local pain at site 
contraindicated in bleeding disorders
57
Q

contraindications to testosterone replacement therapy?

A

hormone responsive cancer
possible prostate cancer, raised PSA or suspicious prostate on DRE
haematocrit >50%
severe sleep apnoea or heart failure

58
Q

monitoring of TRT

A 
3-6 monthly bloods on start then annual 
general health/testosterone levels 
regular PSA, DRE
haematocrit 
signs sleep apnoea
59
Q

what is amenorrhoea

A

absent menstruation

60
Q

what is oligomenorrhoea

A

cycles >42 days or <8 periods per year

61
Q

what physiological concept is used in ovulation test kits and how accurate is it

A

LH surge as ovulation occurs around 36 hours later

97% accurate

62
Q

what is spinnbarkeit and what does it mean

A

cervical mucus in high oestrogen becomes thin, slippery and stretchy
signifies presence of ovulation

63
Q

during and post ovulation, how much does basal body temperature increase by, and when is it measured

A

0.2-0.4 degrees C

taken in morning before moving around

64
Q

true/false- if there are regular menstrual cycles then ovulation is highly likely

A

true

65
Q

how could you confirm that ovulation is occurring in a regular cycle

A

midluteal serum progesterone

>30nmol/L x 2

66
Q

true/false - midluteal progesterone can be done in someone who is anovulatory

A

false - it can be done, but it is hard in clinical practice to do as the patient has irregular/absent periods

67
Q

what blood tests would you do in a patient with irregular cycles

A

hormone evaluation

FSH, LH, oestradiol, testosterone, SHBG, prolactin

68
Q

in a patient with hypothalamic pituitary failure (type I), how would FSH/LH and oestradiol be

A

low with oestrogen deficiency

69
Q

patients with hypothalamic pituitary failure have oligomenorrhoea/amenorrhoea

A

amenorrhoea

70
Q

what challenge test can be done in patients with hypothalamic pituitary failure

A

progesterone challenge test
administration of progesterone to induce period a week later
if +ve then oestrogen levels are not low
if -ve then there is low oestrogen, uterine abnormality or cervical stenosis

71
Q

causes of hypothalamic pituitary failure

A 
anorexia nervosa 
excessive exercise 
stress
low BMI
brain/pituitary tumours 
head trauma 
kallmann's syndrome 
drugs - steroids/opiates
72
Q

pre treatment used for all women with suspected/confirmed ovulation disorders?

A 
stabilise weight 
rubella vaccination 
semen analysis of partner 
folic acid 
check DHx
patent fallopian tube 
modify lifestyle
73
Q

how would you possibly manage someone with hypothalamic pituitary failure

A

if hypogonadotrophic hypogonadism
pulsatile GnRH - administered 90mins as IV/s/c pump
gonadotrophin daily injection - risk multiple pregnancy
need to USS monitor responses

74
Q

what group of ovulation disorders in women are most common

A

group II - hypothalamic pituitary dysfunction

75
Q

biochemical features of hypothalamic pituitary dysfunction (group II)

A

normal gonadotrophins, excess LH

normal oestrogen

76
Q

diagnosis of PCOS

A

2/3
signs of hyperandrogenism - acne, hirsutism
oligo/amenorrhoea
polycystic ovaries from USS

77
Q

treu/false - most patients with PCOS have amenorrhoea

A

false - they have oligomenorrhoea

78
Q

how may ovaries appear polycystic on USS

A

12/more than 2-9mm follicles
increased ovarian volume >10mm
unilateral/bilateral appearance

79
Q

describe the formation of hyperandrogenism in PCOS

A

caused due to hyperinsulinaemia which lowers level of SHBG and increases levels of free testosterone

80
Q

describe the formation of insulin resistance in PCOS

A

diminished biological response to insulin level
normal pancreatic reserve leads to hyperinsulinaemia
can lead to diabetes in genetically predisposed or in obese

81
Q

management of PCOS

A 
clomifene citrate 
metformin may help with clomifene
gonadotrophin therapy 
laparoscopic ovarian diathermy 
IVF
82
Q

rule of 4 with laparoscopic ovarian diathermy and possible risk?

A

ovarian destruction

4 seconds, 40W, 4 punctures

83
Q

risks associated with ovulation induction?

A

ovarian hyperstimulation
multiple pregnancy
ovarian cancer theoretically

84
Q

risks to the mother with multiple pregnancy

A 
postnatal depression
pre-eclampsia 
gestational diabetes
hyperemesis 
anaemia 
hypertension 
operative delivery
85
Q

risks to child with multiple pregnancy

A

early/late miscarriage
stillbirth
low weight or prematurity
disability - CP, ADHD, speech issues, congenital heart disease

86
Q

biochemical features of ovarian failure

A

high FSH/LH

low oestrogen levels

87
Q

causes of ovarian failure

A 
turner's syndrome 
fragile X syndrome 
XX gonadal agenesis 
autoimmune ovarian faiure 
bilateral oophrectomy 
pelvic chemo/radiotherapy 
idiopathic
88
Q

management of ovarian failure

A

HRT
egg/embryo donation
ovary/egg/embryo cryopreservation when ovarian failure anticipated
counselling/support netwoek

89
Q

biochemical diagnosis hyperprolactinaemia causing amenorrhoea and galactorrhoea

A

low/normal FSH/LH
low oestrogen
raised prolactin on 2 occasions
normal TFT

90
Q

management of hyperprolactinaemia

A

cabergoline first line, stop once pregnancy occurs

MB2: Endocrinology (13 decks)

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