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brs (phase 1b) > (endo) reproductive treatments > Flashcards

(endo) reproductive treatments Flashcards

1
Q

what are the symptoms are testosterone deficiency?

A
  • low libido
  • loss of early morning erections
  • decreased energy
  • reduced frequency dhaving
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2
Q

how is testosterone deficiency diagnosed?

A

at least two low measurements of morning fasting testosterone (i.e. before 11am)

then investigate the cause

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3
Q

how is testosterone replaced in deficient patients who do not desire fertility?

A

first treat symptoms then replace testosterone with:

1) daily gel (careful not to cross-contaminate parter)
2) 3-weekly IM injection
3) 3-monthly IM injection
4) implants, oral preparations

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4
Q

what TWO safety considerations must be taken into account when replacing testosterone?

A

replacing testosterone will:

1) increase haematocrit (risk of hyperviscosity + stroke)
2) increase PSA levels (can stimulate growth of prostate cancers)

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5
Q

how is primary hypogonadism treated?

A

difficult to treat

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6
Q

how is secondary hypogonadism treated if fertility is desired?

A

(deficiency of gonadotrophins - i.e. hypogonadotrophic hypogonadism)

treat with gonadotrophins (i.e. LH + FSH) to induce spermatogenesis

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7
Q

why is secondary hypogonadism treated with gonadotrophins?

A

(when fertility is desired)

give LH = to stimulate Leydig cells to increase intratesticular testosterone

give FSH = to stimulate seminiferous tubule development and spermatogenesis

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8
Q

what treatment would you recommend in the following scenario?

35yr old man with hypogonadism due to opioid abuse

1) LH 3, FSH 5 iU/L
2) low morning testosterone 7 nmol/L (normal 9-30 nmol/L)
3) fatigue and reduced shaving frequency
4) trying to conceive with his partner for 2 years with no success
5) sperm sample: low sperm count ie ‘male factor’ infertility

A

opiates suppress GnRH (and therefore LH, FSH and T)

so, as patient desires fertility

1) do NOT give testosterone
2) give hCG injections (which will act on LH receptors)
3) if no response to hCG injections after 6 months, give FSH injections

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9
Q

for a male patient with hypogonadism that desires fertility, why is testosterone NOT given?

A

giving T will via the negative feedback system, reduce LH + FSH further

= further reducing spermatogenesis, leading to infertility

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10
Q

for a male patient with hypogonadism that desires fertility, why are hCG injections given?

A

1) the hCG injections will act on the LH receptors to stimulate Leydig cells to produce androgens
2) if no response after 6 months, add FSH injections (to stimulate Sertoli cells)

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11
Q

what is the diagnosis in the following scenario?

  • 30 year old woman
  • unsuccessfully trying to conceive for 3 years
  • lack of periods (amenorrhoea)
  • hyperandrogenism (hirsutism and acne)
  • ultrasound scan = polycystic ovarian (PCO) morphology
  • LH 8.0 iU/L, FSH 4.5 iU/L
A

polycystic ovary syndrome (PCOS)

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12
Q

what are the symptoms of polycystic ovary syndrome (PCOS)?

A

1) hyperandrogenism (clinical/biochemical)
2) PCO morphology (on ultrasound)
3) oligomenorrhoea OR anovulation

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13
Q

what are the possible causes of hypothalamic amenorrhoea?

A

1) low body weight (BMI)
2) excessive exercise
3) stress
4) genetic susceptibilty

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14
Q

what is the most common cause of irregular periods/infertility?

A

PCOS

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15
Q

what is the purpose of ovulation induction in women experiencing infertility?

A
  • aim to develop one ovarian follicle by giving a low dose of FSH (injections)
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16
Q

why is a LOW dose of FSH given to women experiencing infertility during ovulation induction?

A

low dose to ensure only one follicle develops as

= > 1 follicle developing risks a multiple pregnancy = risks for mother + baby

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17
Q
  • PCOS is the commonest cause of anovulation -

in this scenario, how is ovulation restored?

A

1) lifestyle changes, weight loss, metformin
2) letrozole (aromatase inhibitor)
3) clomiphine (oestradiol receptor modulator)
4) FSH stimulation

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18
Q

what is letrozole?

A

first line medication to treat anovulation/infertility in women

= aromatase inhibitor

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19
Q

what is clomiphine?

A

medication to treat anovulation/infertility in women (second line after letrozole)

= oestradiol receptor modulator

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20
Q

why are FSH injections given to women experiencing infertility?

A

to stimulate the development of one follicle

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21
Q

explain the mechanism of action of letrozole

A

aromatase inhibitor

1) inhibits aromatase and so prevents the conversion or testosterone to oestradiol
2) less oestradiol results in less negative feedback to the hypothalamus + APG
3) less negative feedbakc stimulates more hypothalamic GnRH secretion and more pituitary LH/FSH secretion
4) results in more systemic LH + FSH = follicular development for ovulation

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22
Q

what effect does oestradiol normally have on the HPG axis?

A

via negative feedback, reduces hypothalamic GnRH and pituitary LH/FSH secretion

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23
Q

explain the mechanism of action of clomiphine

A

oestradiol receptor modulator

1) binds to the oestradiol receptor and antagonises it
2) blocks the oestradiol receptor and so less oestradiol activates the negative feedback system
3) decreased negative feedback causes increased hypothalamic GnRH and pituitary LH/FSH secretion
4) increased systemic FSH causes follicular development for ovulation

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24
Q

summarise the steps of IVF

A

IVF = in vitro fertilisation

1) give a large dose of FSH to stimulate many follicles to grow
2) oocyte retrieval from ovary
3) fertilisation in vitro = either IVF or ICSI
4) embryo incubation
5) embryo transfer (of strongest embryo and wait for implantation)

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25
Q

when is ICSI used over IVF?

A

in cases of male factor infertility

  • low sperm count
  • abnormally-shaped sperm
  • low sperm motility
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26
Q

what essential step must be done prior to oocyte retrieval in IVF?

A

must give a large, pharmacological dose of FSH

= to stimulate multiple follicles to grow (i.e. superovulation)

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27
Q

what must be done following administration of the FSH injection in IVF?

A

after FSH injection-induced superovulation, must give a hormone that prevents the LH surge

= to prevent ovulation from actually taking place

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28
Q

why is the premature ovulation prevented in IVF?

A

give hormone to prevent the LH surge that stimulates ovulation

= so the oocyte is not lost from the follicle when it is retrieved

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29
Q

what are two possible ways by which premature ovulation is prevented in IVF?

A

prevent the LH surge either by

1) SHORT protocol (GnRH antagonist)
2) LONG protocol (GnRH agonist)

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30
Q

what is the GnRH SHORT protocol?

A

give a GnRH antagonist
= inhibits GnRH secretion and therefore LH/FSH secretion, preventing the LH surge

  • start FSH from day 2. give GnRH antagonist from day 6
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31
Q

what is the GnRH LONG protocol?

A

give a GnRH agonist
= inhibits GnRH secretion and therefore LH/FSH secretion, preventing the LH surge

  • give GnRH agonist from before the end of the last cycle and then FSH from day 2 of next cycle
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32
Q

compare how the SHORT protocol compares to the LONG protocol to prevent premature ovulation

A

1) SHORT = give FSH from day 2 and GnRH antagonist from day 6
2) LONG = give GnRH agonist from end of last cycle and then FSH from day 2 of next cycle

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33
Q

explain how the GnRH SHORT protocol works

A

give a GnRH antagonist

= inhibits GnRH secretion
= inhibits LH/FSH secretion
= prevents LH surge

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34
Q

explain how the GnRH LONG protocol works

A

give a GnRH agonist

= continuous administration of GnRH desensitises the GnRH receptor
= so excess GnRH inhibits LH secretion from gonadotrophs

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35
Q

what is the function of the GnRH receptor and where is it found?

A

found on the surface membrane of gonadotrophs of the anterior pituitary gland

= GnRH binds to the GnRH receptors and stimulates gonadotrophin secretion

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36
Q

why is continuous administration of GnRH agonist an effective step in IVF?

A

continuous administration of GnRH agonist
= act on the the GnRH receptors, desensitising them eventually
= inhibiting LH (and FSH) secretion
= preventing LH surge, and therefore premature ovulation

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37
Q

what is the difference between pulsatile and non-pulsatile GnRH administration in IVF?

A

pulsatile = normal LH stimulation

non-pulsatile (i.e. continuous) = initial LH flare as receptors are stimulated, but eventually they become desensitised (so inhibit LH secretion)

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38
Q

when is pulsatile GnRH administration used as treatment?

A

in hypothalamic amenorrhoea

= to restore hypothalamic (HPG) axis and normal LH/FSH levels

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39
Q

what is done after preventing premature ovulation in IVF?

A

next step = LH exposure to mature eggs (oocyte maturation)

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40
Q

why is oocyte maturation an important step of IVF?

A

need mature oocytes so they can be fertilised (!!)

  • after preventing premature ovulation, need the oocyte to mature from metaphase 1 (diploid) TO metaphase 2 (haploid)

= maturation requires LH exposure

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41
Q

what are two ways in which oocyte maturation can take place in IVF?

A

1) hCG is normally given that acts on the LH receptors
= acts as an LH surge
= to induce oocyte maturation

2) GnRH agonist (in a pulsatile manner) can also be given to initially stimulate LH surge

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42
Q

how are oocytes converted from immature ones to mature ones in IVF?

A

immature oocytes = metaphase 1 (diploid)

LH exposure via GnRHa OR hCG

mature oocytes = metaphase 2 (haploidi)

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43
Q

why do oocytes need to be mature in IVF?

A

after maturation, achieve competence for fertilisation

= i.e. have half the genetic information (haploid) so can NOW, receive the other half of genetic material from the sperm

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44
Q

what three steps must be taken before oocyte retrieval in IVF?

A

1) FSH administration for superovulation
2) prevention of premature ovulation
3) LH exposure to mature oocytes

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45
Q

what steps follow oocyte retrieval in IVF?

A

1) oocyte retrieval
2) fertilisation
3) embryo incubation (3-5 days)
4) embryo transfer
5) pregnancy test/US scan

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46
Q

how long do you wait before doing a pregnancy test after transferring an IVF embryo to the endometrium?

A

approx 11 days

47
Q

name possible methods of contraception

A

1) barriers = male/female condoms, diaphragm, cap w spermicide
2) combined oral contraceptive pill (OCP)
3) progesterone-only pill (POP)
4) long-acting reversible contraceptive (LARC)
5) emergency contraception
6) vasectomy, female sterilisation

48
Q

name the two permanent methods of contraception

A

1) vasectomy

2) female sterilisation

49
Q

name possible barrier methods of contraception

A

1) male/female condom
2) diaphragm
3) cap w spermicide

50
Q

list the pros and cons of condoms as a form of contraception

A

pros

  • protect against STIs
  • easy to obtain (no need to see HCP)

cons

  • can interrupt sex/ erections
  • can reduce sensation
  • require some skill to use
51
Q

explain the mechanism of action of the oral contraceptive pill

A
  • OCP contains oestrogen + progesterone
  • increased O+P increases hypothalamic + pituitary negative feedback
  • reduced hypothalamic GnRH and pituitary LH/FSH secretion

three effects:

1) anovulation
2) thickens the cervical mucus
3) thins the endometrial lining

52
Q

why is anovulation caused when taking the OCP?

A

OCP increases oestrogen and progesterone

= increased -ve feedback
= reduced hypothalamic GnRH + pituitary LH/FSH secretion
= anovulation

53
Q

why does the cervical mucus thicken when taking the OCP?

A

progesterone thickens the cervical mucus to prevent sperm entry into the uterus

54
Q

why does the endometrial lining thin when taking the OCP?

A

oestrogen = causes proliferation + growth of the endometrial lining

progesterone = prevents endometrial hyperplasia by opposing the effects of oestrogen

= overall, thinning of the endometrial lining occurs
= reduces the risk of implantation

55
Q

list the pros and cons of the OCP as a form of contraception

A

pros

  • easy to take, effective
  • does not interrupt sex
  • can take several packets back to back to avoid withdrawal bleeds
  • reduce risk of endometrial + ovarian cancer

cons

  • difficult to remember
  • no protection against STIs
  • possible interactions w other medication
  • side effects possible (spotting, nausea, mood/libido changes, DVT/PE)
56
Q

what are the three common non-contraceptive uses of the OCP?

A

1) menorrhagia = reduces period pain + makes periods lighter
2) endometriosis = making periods less painful + lighter reduces endometriosis symptoms
3) PCOS = reduces LH secretion and therefore, reduces overactivation of androgen production in theca cell, reducing hyperandrogenism

57
Q

why can the OCP not be prescribed for a women with PCOS desiring fertility?

A

OCP = reduces LH/FSH secretion and causes anovulation so patient is not fertile

    • in this situation, treatment is either
      1) letrozole, clomiphine, IVF for infertility
      2) laser, waxing, creams for hyperandrogenism
      3) metformin + lifestyle changes for impaired glucose tolerance
      4) progesterone courses for risk of endometrial cancer –
58
Q

how does the OCP help with menorrhagia and endometriosis?

A 
OCP
= contains oestrogen + progesterone
= inhibits LH/FSH secretion
= anovulation (+ thins endometrial lining)
= makes periods lighter and less painful
(reducing symptoms of endometriosis)
59
Q

how does the OCP help with PCOS?

A

a symptom of PCOS is hyperandrogenism

= OCP inhibits LH secretion and therefore inhibits theca cell androgen production

60
Q

explain the mechanism of action of the progesterone-only pill

A

1) inhibit LH/FSH secretion and therefore inhibit ovulation

2) thicken the cervical mucus to prevent sperm penetration

61
Q

list the pros and cons of the progesterone-only pill (POP)

A

pros

  • suitable if patient cannot take oestrogen
  • easy to take
  • doesn’t interrupt sex
  • useful in menorrhagia

cons

  • difficult to remember
  • no protection against STIs
  • side effects (spotting, mood/libido changes)
  • SHORTER-ACTING (needs to be taken at the same time each day)
62
Q

why is the OCP preferred in some cases to the POP?

A

POP has to be taken at the same time every day to ensure efficacy
= shorter-acting (!!) compared to OCPwho

63
Q

which is more suitable for women who are breastfeeding: OCP, or POP?

A

POP - can be used when breastfeeding

64
Q

give examples of the most common long-acting reversible contraceptives (LARCs)

A

1) intra-uterine devices (i.e. copper coils)
2) intra-uterine systems
3) progesterone-only injectables or subdermal implants

65
Q

which is the most suitable contraceptive for nulliparous (no previous children) women and why?

A

copper coil

  • prevent implantation
  • rarely cause ectopic pregnancy
  • good emergency contraception
66
Q

what must be done before copper coil insertion?

A

exclude STIs and do a cervical screening test

67
Q

explain how an IUD (intra-uterine device) works

A

i.e. Copper coil

= works by mechanically preventing implantation + decreasing sperm & egg survival

68
Q

how long do IUDs last and what are the implications of it?

A

last approx 5-10 years

implications

  • can cause heavy periods
  • can come out in the first three months w periods (5%)
69
Q

explain how IUS (inttra-uterine systems) work

A

e.g. Mirena coil

= secrete progesterone that will

1) thin the uterine lining
2) thicken the cervical mucus

(can also help w heavy periods)

70
Q

how long do IUS last and when can they also be used, apart from contraception?

A

last 3-5 years (fewer years compared to IUDs)

can also be used to treat heavy periods (as IUS secrete progesterone)

71
Q

what is the most effective form of emergency contraception and how?

A

copper coil (i.e. intra-uterine device - IUD)

  • can be fitted up to 5 days after unprotected sex
72
Q

what two emergency contraceptive pills are available?

A

1) ulipristal acetate 30mg

2) levonorgestrel 1.5mg

73
Q

how does ulipristal acetate work as an emergency contraceptive?

A

30mg tablet

  • must be taken within FIVE days of unprotected sex
  • stops progesterone from working normally and prevents ovulation
74
Q

how does levonorgestrel work as an emergency contraceptive?

A

1.5 mg tablet

  • must be taken within THREE days of unprotected sex
  • synthetic progesterone that prevents ovulation
75
Q

which is less effective: ulipristal acetate or levonorgestrel?

A

levonorgestrel 1.5mg

= least effective (esp if BMI > 27kg/m2)

76
Q

what are the side effects of emergency contraceptive pills?

A

abdominal pain, nausea, headache

other medication an interfere w this

77
Q

what factors must be considered when choosing a form of contraception?

A

1) risk of VTE/stroke/CVD
2) comorbidities
3) other conditions that may benefit form contraception choice (menorrhagia, endometriosis, PCOS)
4) need to prevent STIs
5) concurrent medication (interactions, teratogenic drugs)

78
Q

in which scenarios are OCPs avoided?

A
  • stroke/CVD history
  • heavy smokers
  • diabetes w complications
  • liver cirrhosis
79
Q

what are the symptoms of menopause?

A

hot flushes

sweating

disturbed sleep + mood

low libido

vaginal dryness

joint & muscle aches

absent/irregular periods

80
Q

define peri-menopausal

A

within 12 months of last menstrual period (LMP)

81
Q

define post-menopausal

A

after 12 months of LMP

82
Q

summarise the main risks of hormone-replacement therapy

A

1) risk of VTE
2) hormone-related cancers (breast, endometrial, ovarian)
3) risk of CVD
4) risk of stroke

83
Q

what can HRT increase the risk of in terms of VTE?

A

1) DVT (deep vein thrombosis)

2) PE (pulmonary embolism)

84
Q

in which two forms can oestrogen HRT be taken?

A

oral or transdermal

85
Q

for patients at an increased risk of VTE, are oral or trasndermal oestrogens better and why?

A

oral = oestrogen ingested + undergoes first pass metabolism in the liver

transdermal = delivered directly into circulation

so transdermal > oral, as latter interferes w clotting factors in the liver and so increases the risk of vte

86
Q

what do oral oestrogens increase and when should they be avoided in particular?

A

increase SHBG (binds to oestrogen inactivating it), triglycerides and CRP

= should be avoided in patients w BMI > 30kg/m2

87
Q

does HRT increase the risk of breast cancer?

explain

A
  • combined HRT increases risks more than oestrogen only
  • continuous administration worse than sequential doses

(risk related to duration of treatment and reduces after stopping)

assess risk in each individual before prescribing

88
Q

does HRT increase the risk of ovarian cancer?

A

small increase in risk after long-term use

89
Q

does HRT increase the risk of CVD?

A
  • no increased risk if started before the age of 60 years

- only increased risk if started 10 years after menopause

90
Q

does HRT increase the risk of stroke?

A

only small increase in risk when

1) oral oestrogen > trajsdermal oestrogen
2) combined HRT > oestrogen HRT

91
Q

what are progestogens

A

any substance that will successfully bind to and interact with the progesterone receptors in the body including:

1) the natural hormone, progesterone
2) synthetic progestins

92
Q

what precautions must be taken to reduce the risk of endometrial cancer and why?

A

if oestrogen is prescribed (HRT)
= causes growth and proliferation of the endometrium
= can lead to endometrial hyperplasia and endometrial cancer

to prevent this, must prescribe PROGESTOGENS (!!)
= will act to oppose the proliferative actions of oestrogen and thin the endometrial lining, reducing endometrial hyperplasia

93
Q

how often does HRT safety need to be assessed?

A

assess HRT safety + efficacy at 3 months and then annually

94
Q

is bleeding normal in patients on HRT?

A
  • unscheduled bleeding is common in the first 3 months

- post-menopausal bleeding could indicate endometrial cancer

95
Q

what are the benefits of HRT in menopause?

A

1) relieve the symptoms of low oestrogen (i.e. disturbed sleep/mood, hot flushes, sweating, decreased libido)
2) less osteoporosis-related fractures

96
Q

define cisgender

A

same sex and gender (both align)

97
Q

define gender non-conforming

A

when sex and gender do not both align

when this causes stress = gender dysphoria

98
Q

define non-binary

A

gender does not match to traditional binary gender understanding
= includes agender, bigender, pangender, gender fluid

99
Q

define transgender

A

transitioning physical appearance from one gender to another

100
Q

define transgender man

A

female sex at birth, but male gender now

101
Q

what is more common: transgender men or transgender women?

A

transgender women x3 more common than transgender men

102
Q

how are prepubertal young people wanting to transition gender managed?

A

1) GnRH agonist (continuous administration) for pubertal suppression

THEN

2) administration of sex steroids

THEN (after hormonal therapy for 1-2 years)

3) gender reassignment surgery

103
Q

how are hormones masculinised for trasngender men?

A

1) testosterone injection + gels (but SIDE EFFECTS: OSA, low HDL, polycythaemia)
2) progesterone to suppress menstrual bleeding if required

104
Q

how do patients respond to hormone masculinisation for transgender men?

A
  • balding
  • deeper voice
  • acne
  • coarser, more facial + body hair
  • changes in the distribution of body fat
  • menstrual cycle stops
  • increased muscle mass + strength
  • enlargement of the clitoris
105
Q

how are hormones feminised for trasngender women?

A

1) oestrogen (transdermal, oral, IM)

2) reduce testosterone (GnRH agonists, anti-androgen medication)

106
Q

how is oestrogen given when feminising hormones for transgender women?

A

high dose oestrogen e.g. 4-5mg per day to aim for oestradiol levels of 734 pmol/L

107
Q

what are the side effects of giving oestrogen when feminising hormones for transgender women?

A

risk of

  • VTE
  • stroke
  • CVD
  • high triglycerides
  • hormone-sensitive cancers (breast, ovarian, endometrial)
108
Q

how is testosterone reduced when feminising hormones for transgender women?

A

either

1) GnRH agonist (to desensitise the HPG axis and inhibit LH/FSH secretion)

OR

2) anti-androgen medication (spironolactone)

109
Q

how do patients respond to hormone feminisation for transgender women?

A

** height, voice and Adam’s apple don’t change **

  • softer skin
  • changes in body fat distribution
  • breast development
  • decrease in testicular size
  • hair may become softer and finer
110
Q

how is oocyte count tested for?

A

test AMH (anti-Mullerian hormone)

= fewer eggs, fewer follicles, lower AMH levels

111
Q

how can non-endocrine causes of infertility be investigated in women?

A

hysterosalpingogram

= X-ray scan to look at the uterus and fallopian tubes

112
Q

explain the link between weight gain and androgen production

A

weight gain
= increased adipose tissue
= increased insulin resistance
= increased compensatory insulin secretion
= hyperinsulinaemia
= causes excess testosterone production in the ovaries

113
Q

explain the link between weight gain and androgen production

A

weight gain
= increased adipose tissue
= increased insulin resistance (can lead to further weight gain)
= increased compensatory insulin secretion
= hyperinsulinaemia
= causes excess testosterone production in the ovaries

brs (phase 1b) (71 decks)

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