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1B reproductive treatments Flashcards

1
Q

What are the symptoms for low T?

A
  • Loss of early morning erections
  • Lower libido
  • Decreased energy
  • Lower frequency of shaving
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2
Q

How do we diagnose low T?

A
  • at least 2 low measurements of serum T before 11am (when it’s meant to be high)
  • Investigate the cause of low T
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3
Q

What different types of T replacement treatments are there?

A
  • Daily- gel (e.g. Tostran)- care not to contaminate partner
  • 3 weekly intramuscular injections (e.g. Sustanon)
  • 3 monthly intramuscular injections (e.g. Nebido)
  • Less common (implants, oral preparations)
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4
Q

What do we need to monitor for safety in testosterone replacement?

A
  • increased haematocrit (risk of hyperviscosity and stroke)
  • Prostate (Prostate specific antigen (PSA) levels)
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5
Q

How do we treat primary and secondary hypogonadism?

A
  • Primary- hard to treat
  • Secondary (deficiency of gonadotrophins i.e. hypogonadotrophic hypogoandism)- treat with gonadotrophins (i.e. LH and FSH) to induce spermatogenesis
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6
Q

What would LH and FSH do to testes?

A
  • LH stimulates Leydig cells to increase intratesticular T to much higher levels than in circulation (x100)
  • FSH stimulates seminiferous tubule development and spermatogenesis
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7
Q

Why do we avoid giving T to men desiring fertility?

A

For secondary hypogonadism (low sperm and T levels) in men desiring fertility, giving T would lower LH and FSH further and further reduce spermatogenesis

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8
Q

What do we give instead of T to men desiring fertility?

A
  • hCG injections (which act on LH receptors)
  • If no response after 6 months, add FSH injections
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9
Q

What is hypothalamic amenorrhoea?

A

When you have insufficient energy for fertility from decrease in hypothalamus function

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10
Q

What are the causes of hypothalamic amenorrhoea?

A
  • Low body weight
  • Excessive exercise
  • Stress
  • Genetic susceptibility
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11
Q

What is the aim of ovulation induction?

A
  • To develop 1 ovarian follicle
  • If >1 follicle develops, there’s risk of multiple pregnancy (twins/triplets) which has risks for mother and baby during pregnancy
  • Ovulation induction aims to cause small increase in FSH
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12
Q

What are different methods to restore ovulation?

A
  • Lifestyle/weight loss/metformin
  • FSH stimulation by injection
  • Letrozole (aromatase inhibitor)
  • Clomiphene
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13
Q

How does letrozole work?

A
  • Inhibits aromatase which converts T to E2
  • E2 usually causes negative feedback on hypothalamus and pituitary gland to reduce LH and FSH production
  • There’s decreased negative feedback now however due to low E2 so there’s increased FSH which stimulates follicle growth
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14
Q

How does clomiphene work?

A
  • It’s called a modulator since it acts like an agonist/antagonist depending on tissue its in
  • We’re interested in it being an E2 receptor antagonist- works in same way as letrozole
  • Decreased negative feedback since E2 receptors are blocked → less negative feedback → more FSH → stimulation of follicle growth
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15
Q

What are the steps to IVF?

A

1) Induce growth of multiple follicles through giving large FSH dose

2) Collect eggs directly from ovary

3) Fertilise eggs in vitro by either:

  • putting it in dish with sperm and naturally letting sperm fertilise egg
  • ICSI (intracytoplasmic sperm injection)- take a single sperm and inject it directly into egg- usually done when there’s problem in sperm (male factor infertility)

4) Eggs grown in incubator for few days

5) After 3-5 days, we choose strongest embryo and transfer it back into endometrium of woman

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16
Q

What is premature ovulation?

A

Release of egg from follicle before we collect eggs for IVF

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17
Q

How do we prevent premature ovulation?

A

We give a hormone that suppresses LH surge. There are 2 ways of doing it:

  • GnRH antagonist protocol (short protocol)
  • GnRH agonist protocol (long protocol)
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18
Q

How does GnRH antagonist protocol work?

A
  • Start FSH from day 2 of menstrual cycle
  • At day 6 we start GnRH antagonist- will prevent LH surge
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19
Q

How does GnRH agonist protocol work?

A
  • Start GnRH agonist from day 21 of previous cycle (day -7 of current cycle)
  • Start FSH like usual on day 2
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20
Q

How can both a GnRH agonist and antagonist be used to block an LH surge?

A
  • GnRH needs to be given in pulsatile manner to stimulate LH
  • Agonist: If we give non-pulsatile continuous GnRH, we get desensitisation of GnRH receptor- causing initial flare of LH, but then LH inhibition
  • So giving GnRH agonist can act like an antagonist and be used to induce LH inhibition

Antagonist is more self-explanatory- it’s preferred in cases where an immediate effect is needed

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21
Q

How do we mature the egg after preventing premature ovulation?

A
  • We give LH exposure to induce oocyte maturation
  • When eggs are immature, they’re at metaphase 1 and are diploid
  • After being exposed to LH, they go into metaphase 2 and become haploid (can now be fertilised by sperm)
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22
Q

Which hormones do we give commonly to induce oocyte maturation?

A
  • hCG- acts on LH receptors but is much longer acting than LH
  • GnRH agonist is second most common
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23
Q

How many pregnancies are unplanned?

A

19-30%

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24
Q

What are the advantages of condoms?

A
  • Protect against STIs
  • Easy to obtain- free from clinics/no need to see a healthcare professional
  • No contra-indications as with some hormonal methods
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25
Q

What are the disadvantages of condoms?

A
  • Can interrupt sex
  • Can reduce sensation
  • Can interfere with erections
  • Some skill to use e.g. correct fit
  • 2 aren’t better than 1
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26
Q

How does the oral contraceptive pill work?

A
  • HPG axis negative feedback:1) Pill has oestrogen and progesterone2) This has negative feedback on hypothalamus and pituitary3) This decreases LH and FSH leading to anovulation
  • Thickening of cervical mucus
  • Thinning of endometrial lining to reduce implantation
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27
Q

What are the advantages to the oral contraceptive pill?

A
  • Easy to take- 1 pill a day at any time
  • Effective
  • Doesn’t interrupt sex
  • Can take several packets back to back and can avoid withdrawal bleeds through this
  • Reduces endometrial and ovarian cancer
  • Weight neutral in 80% of people (10% gain weight and 10% lose- usually progesterone leads to this)
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28
Q

What are the disadvantages of the oral contraceptive pill?

A
  • Can be difficult to remember to take
  • No protection against STIs
  • P450 enzyme inducers may reduce efficacy (if you’re on other medication that affects liver enzymes since that’s also where OCP is metabolised)
  • Not the best choice during breastfeeding
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29
Q

What are possible side effects to the oral contraceptive pill?

A

Try different OCPs to see which suits best

  • Spotting (bleeding in between periods)
  • Nausea
  • Sore breasts
  • Changed in mood or libido
  • Feeling more hungry
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30
Q

What is an extremely rare side effect of the oral contraceptive pill?

A

Blood clots in the legs or lungs (2 in 10,000)

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31
Q

What are non-contraceptive uses of the pill?

A
  • Helps make periods lighter and less painful (e.g. endometriosis or period pain or menorrhagia)
  • Withdrawal bleeds will usually be very regular
  • PCOS: help reduce LH and hyperandrogenism
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32
Q

What are the advantages of the progesterone only pill (POP) aka minipill?

A
  • Works same as OCP but less reliably inhibits ovulation
  • Often suitable if you can’t take oestrogen
  • Easy to take- 1 pill a day every day
  • Doesn’t interrupt sex
  • Can help heavy or painful periods
  • Periods may stop (temporarily)
  • Can be used when breastfeeding
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33
Q

What are the disadvantages of the progesterone only pill (POP) aka minipill?

A
  • Can be difficult to remember
  • No protection against STIs
  • Shorter acting- needs to be taken at the same time each day
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34
Q

What are the side effects of the progesterone only pill (POP) aka minipill?

A
  • Irregular bleeding
  • Headaches
  • Sore breasts
  • Changes in mood
  • Changes in sex drive
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35
Q

What are coils suitable for and what do they do overall?

A
  • Suitable for most women including nulliparous women (no previous children)
  • Prevent implantation of conceptus- important consideration for some religions
  • Can be used as emergency contraception
36
Q

What do we need to check before insertion and what is a rare thing that can happen with coils?

A
  • Exclude STIs and cervical screening up to the day before insertion
  • Rarely can cause an ectopic pregnancy where embryo may implant in fallopian tube
37
Q

What are the 2 types of coil?

A
  • Intra-uterine device (IUD) i.e. copper coil
  • Intra-uterine systems (IUS) e.g. Mirena coil
38
Q

What does the IUD do?

A
  • mechanically prevent implantation
  • decrease sperm egg survival
39
Q

How long does an IUD last?

A

5-10 years

40
Q

What are the side effects to an IUD?

A
  • Can cause heavy periods
  • 5% can come out especially during first 3 months with periods
41
Q

What does the IUS do?

A
  • Secretes progesterone to thin the lining of womb and thicken cervical mucus
  • Can be used to help with heavy bleeding
42
Q

How long does an IUS last for?

A

3-5 years

43
Q

What is the 3rd type of LARC?

A

Progesterone-only injectable contraceptives or subdermal implants

44
Q

When can an IUD be used?

A
  • It’s the most effective
  • Can be fitted up to 5 days after unprotected sex (<1% chance of pregnancy)
45
Q

What are the 2 morning after pills?

A
  • Ulipristal acetate 30mg (ellaOne)
  • Levonorgestrel 1.5mg (Levonelle)
46
Q

How does ulipristal acetate work?

A
  • Stops progesterone working normally and prevents ovulation
  • Must be taken within 5 days of unprotected sex (earlier the better)
47
Q

How does levonorgestrel work?

A
  • Least effective esp if BMI is more than 27 kg/m^2
  • Synthetic progesterone prevents ovulation (doesn’t cause abortion)
  • Must be taken within 3 days of unprotected sex
48
Q

What are the side effects of the morning after pills?

A
  • Headache
  • Abdominal pain
  • Nausea

If you vomit within 2/3 hours of taking it, you have to take another.

49
Q

What can make the morning after pill less effective?

A

Liver P450 enzyme inducer medications

50
Q

What factors matter for choice of contraception?

A
  • Risk of venous thromboembolism (VTE)/CVD/stroke
  • When they have other conditions that may benefit from OCP
  • Are they taking concurrent drugs that will affect contraceptives?
  • If there’s a need for STIs (barrier contraception would help)
51
Q

When should women avoid OCP?

A

If they have:

  • Smoking (>15 a day) and age >35 years
  • Diabetes with complications e.g. retinopathy/nephropathy/neuropathy
  • Migraine with aura (risk of stroke)
  • Stroke or CVD history
  • Current breast cancer
  • Liver cirrhosis
52
Q

What conditions can benefit from OCP?

A
  • Menorrhagia
  • Endometriosis
  • Fibroids
53
Q

What concurrent drugs can affect contraceptives?

A
  • P450 liver enzyme inducing drugs (e.g. anti epileptics, some antibiotics)
  • Teratogenic drugs (e.g. lithium or warfarin)- more effective methods of contraception needed (e.g. progesterone only implant, or intrauterine contraception)
54
Q

Describe the efficacy of different types of contraception

A

User dependent: dependent on users remembering to take it, etc

55
Q

What are the risks of HRT?

A
  • Venous thrombo-embolism: DVT or pulmonary embolism
  • Risk of stroke
  • Hormone sensitive cancers
  • Risk of cardiovascular disease
56
Q

How is HRT a risk of venous thrombo-embolism?

A

Oral oestrogens undergo first pass metabolism in liver where they can increase SHBG, triglycerides, CRP and increase chance of clots

57
Q

How can we reduce the chance of VTE?

A
  • Transdermal oestrogens are safer for VTE risk than oral because the drug goes straight into bloodstream
  • Avoid oral oestrogens in BMI >30 kg/m^2
58
Q

How is stroke a risk of HRT?

A
  • Small increased risk
  • Oral is better than transdermal oestrogen in terms of risk
  • Combined is better than oestrogen only in terms of risk
59
Q

What hormone sensitive cancers are a risk of HRT?

A
  • Breast cancer
  • Ovarian cancer
  • Endometrial cancer
60
Q

How is breast cancer a risk of HRT?

A
  • slight increase in only women on combined HRT (both oestrogen and progesterone)
  • Risk related to duration of treatment and reduces after stopping
  • Continuous combined HRT worse than sequential (e.g. oestrogen first then progesterone)
  • Assess risk in each individual before prescribing
61
Q

How is ovarian cancer a risk of HRT?

A

Small increase in risk after long term use

62
Q

How can we reduce the chance of endometrial cancer?

A
  • Must prescribe progestogens in all women with an endometrium to decrease risk of endometrial cancer
  • Assess HRT safety/efficacy at 3 months and then annually
  • Unscheduled bleeding is common within first 3 months
63
Q

What are progestogens?

A

Synthetic progestins and the natural hormone progesterone

64
Q

What can indicate endometrial cancer?

A

Post-menopausal bleeding

65
Q

At what age does cardiovascular disease become a risk of HRT?

A
  • No increased risk if started before age 60 years
  • Increased risk if started 10 years after menopause
66
Q

To which group can oestrogen supplements be beneficial?

A

Possible benefits in young women e.g. premature ovarian insufficiency (POI)

67
Q

What are the benefits of HRT?

A
  • Relief of symptoms of low oestrogen e.g. flushing, disturbed sleep, decreased libido, low mood
  • Less osteoporosis related fractures- decreased by one third
68
Q

What is the definition of gender?

A

A social construct- how you see yourself as male, female or non-binary

69
Q

What is the definition of sex?

A

Biologically defined e.g. male, female or intersex

70
Q

What is the definition of cisgender?

A

Same sex and gender

71
Q

What is the definition of gender non-conforming?

A

Gender doesn’t match assigned sex

72
Q

What does gender dysphoria mean?

A

When sex and gender don’t align and it causes distress

73
Q

What does non-binary mean?

A

Gender doesn’t match to traditional binary gender understanding.

Includes agender, bigender, pangender, gender fluid

74
Q

What does transgender mean?

A

Transitioning or planning to transition physical appearance from one gender to another

75
Q

What is the definition of a transgender man?

A

Female sex at birth, but male gender (FtM no longer used)

76
Q

How do prepubertal young people transition?

A
  • GnRH agonist for pubertal suppression and then sex steroids
  • Post treatment regret is 1-2%
  • Gender reassignment surgery after 1-2 years of hormonal treatment
77
Q

What are the masculinising hormones for transgender men?

A
  • Testosterone (injections, gels)
  • Progesterone to suppress menstrual bleeding if needed (endometrial hyperplasia is 15%)
78
Q

What are the side effects of T?

A
  • Polycythaemia
  • Lower HDL
  • Obstructive sleep apnoea (OSA)
  • No increase in CVD
79
Q

What happens in 1-6 months of taking masculinising hormones for transgender men?

A
  • Balding (depending on age and family pattern)
  • deeper voice/acne/increased and coarser facial and body hair
  • Change in distribution of body fat
  • Enlargement of clitoris
  • Menstrual cycle stops
  • Increased muscle mass and strength
80
Q

What are the feminising hormones for transgender women?

A
  • Oestrogen (transdermal, oral, intramuscular)
  • Reduce testosterone
81
Q

How much oestrogen is taken for transgender women?

A

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

82
Q

What are the side effects of taking oestrogen for transgender women?

A
  • VTE dose related at 2.6%
  • cardiovascular disease
  • hormone sensitive cancers e.g. breast cancer, abnormal liver function tests 3%
  • High bp
  • high triglycerides
83
Q

How is testosterone reduced?

A
  • GnRH agonists (induce desensitisation of HPG axis)
  • Anti-androgen medications (e.g. cyproterone acetate, spironolactone)
  • Height, voice and Adam’s apple won’t change
  • Consider sperm banking before starting hormone therapy
84
Q

What happens in 1-3 months of taking feminising hormones?

A

Decrease in sexual desire/function (including erections)/ baldness slows or may reverse

85
Q

What happens in 3-6 months of taking feminising hormones?

A

Softer skin/ change in body fat distribution/ decrease in testicular size/ breast development/ tenderness

86
Q

What happens in 3-6 months of taking feminising hormones?

A

Hair may become softer and finer

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