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Hannah's Reproductive > Sex Hormones and Disease > Flashcards

Sex Hormones and Disease Flashcards

1
Q

What is the pattern of GnRH release?

A

Pulsatile release

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2
Q

How is release of pituitary hormones stimulated by GnRH regulated?

A

Frequency of GnRH pulses controls relative release of pituitary hormones

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3
Q

How does oestrogen feed back on the HPG axis?

A

Inhibits release of GnRH and pituitary hormones

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4
Q

How does testosterone feed back on the HPG axis?

A

Inhibits release of GnRH and pituitary hormones

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5
Q

What enzyme is responsible for oestrogen synthesis?

A

Aromatase

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6
Q

What enzyme is responsible for DHT synthesis?

A

5a-reductase

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7
Q

What are the 3 oestrogens? Which is measured?

A

Oestriol
Oestrone
Oestradiol (17B-oestradiol is measured)

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8
Q

What are oestrogens used to treat?

A

Hypogonadism in young females
Primary amenorrhoea in adults (in combination with progestin)
Contraception (in combination with progestin)
Symptoms of menopause (in combination with progestin)

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9
Q

List 7 possible beneficial effects of HRT

A

Improved bone density
Relief from flushes, fatigue and vaginal dryness
Reverses atrophy of vulva, vagina, urethra
Improved sleep
Reduced incidence of colorectal cancers
Reduced incidence of coronary heart disease?
Reduced incidence/delayed onset of AD?

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10
Q

What are 3 adverse effects of HRT?

A

Breast tenderness
Nausea
Fluid retention

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11
Q

Give 2 examples of conditions for which there is an increased risk following HRT

A

Breast/uterine cancer

Risk of thromboembolism/stroke

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12
Q

What is the mechanism of action of oestrogen?

A

Binds to ER on the cell membrane or in the cytoplasm
Enters the nucleus
Dimerises or binds to TFs (e.g. AP1)
Binds DNA to influence gene transcription (activation or repression)

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13
Q

What is an additional possible mechanism of action of oestrogen?

A

May also bind non-ER membrane receptors (e.g. GPR30)

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14
Q

What are the 2 subtypes of ER hypothesised to be responsible for tissue-specific effects?

A

ER-a (predominantly)

ER-B (less well understood)

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15
Q

What is the role of oestrogen in breast cancer?

A

Acts on ER to promote growth

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16
Q

What is the role of progesterone in breast cancer?

A

Acts on PR to promote differentiation

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17
Q

What is 1 post-menopausal change proposed to account for the increased risk of breast cancer?

A

% of women who are ER and PR positive increases (60-65% pre-menopausal to 70-75% post-menopausal)
Oestrogen and progesterone together promote growth and differentiation of breast tissue which may increase the risk of neoplastic transformation

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18
Q

Give 4 examples of SERMs and their pharmacological classification

A

Agonist: oestradiol
Partial agonists: tamoxifen, raloxifene
Antagonist: fulvestrant

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19
Q

What is the advantage of raloxifene over tamoxifen in terms of the profile of risk?

A

Tamoxifen acts as an agonist on uterine endometrium and increases the risk of uterine cancer (raloxifene is an antagonist at uterine ER receptors)

20
Q

What is the advantage of ER partial agonists tamoxifen and raloxifene over antagonist fulvestrant?

A

Tamoxifen and raloxifene are agonists at bone and CV ERs, and are hypothesised to have protective health effects here

21
Q

What is tamoxifen used for clinically?

A

Palliative treatment of metastatic breast cancer

Adjuvant therapy after lumpectomy

22
Q

List 5 adverse effects of tamoxifen

A

Endometrial hyperplasia, polyps and cancer
Thromboembolic events
Thrombocytopaenia
Ocular toxicity
Menopausal symptoms (hot flushes, atrophic vaginitis)

23
Q

In what tissue is there high aromatase activity?

A

Breast adipose mesenchymal cells

24
Q

What is the hypothesised mechanism of action of oestradiol in post-menopausal women and men? What is 1 clinical repercussion of this activity?

A

Paracrine hormone

Can produce gynaecomastia in 2-5% of men

25
Q

What are the benefits of use of aromatase inhibitors in the treatment of breast cancer?

A

Improved disease free survival after tamoxifen
Reduced incidence of contralateral breast cancer
Reduced number of thromboembolic events
Reduced incidence of endometrial cancer

26
Q

List 4 possible risks and adverse effects of aromatase inhibitors

A

Increased bone loss and fracture risk
Increased arthralgia
Potential poorer lipid profile, hepatic steatosis and metabolic syndrome (with long term use; may be CV protective in short term)
Menopausal signs

27
Q

Where in males is DHT synthesised?

A

Prostate
Seminal vesicles
Epididymis
Skin

28
Q

What are the 4 main roles of testosterone?

A

Negative feedback influencing gonadotrophin release
Spermatogenesis
Sexual differentiation
Anabolic effects

29
Q

What are the 3 main roles of DHT?

A

Prostate development
External virilisation
Sexual maturation

30
Q

What is unique about the cellular action of testosterone?

A

Can bind to receptors in the cytoplasm or directly in the nucleus

31
Q

What is the mechanism of action of testosterone and DHT?

A

Testosterone enters the cytoplasm
Testosterone converted to DHT by 5a-reductase (depending on expression of enzyme in tissue)
DHT binds androgen receptor in cytoplasm
DHT-receptor complex dimerises in nucleus and binds DNA promoters, resulting in transcription of testosterone-dependent genes

32
Q

What are 5 therapeutic uses of androgens?

A

Hypogonadism
Senile osteoporosis
Increasing speed of recovery from surgery and chronic debilitating dieases
Pituitary dwarfism (promotes skeletal development)
Endometriosis (reduces pain and inflammation, restores hormonal balance and may promote some local oestrogen production)

33
Q

What effect do androgens have on CV health?

A

Increase LDL and decreased HDL

Increased risk of coronary heart disease

34
Q

What are 6 adverse effects of androgens in females?

A 
Acne
Facial hair
Deepening of voice
Male pattern baldness
Excessive muscle development
Menstrual irregularities
35
Q

What are 4 adverse effects of androgens in males?

A

Priapism
Impotence
Decreased spermatogenesis
Gynaecomastia

36
Q

What are 2 adverse effects of androgens in children?

A

Premature closure of epiphyseal plates

Abnormal sexual maturation

37
Q

What are 3 possible adverse effects of androgens in athletes?

A

Liver damage
Increased aggression
Psychotic episodes

38
Q

What are the 2 classes of anti-androgens?

A

Receptor antagonists

5a-reductase inhibitors

39
Q

What is the difference between cyproterone and flutamide?

A

Cyproterone is steroidal

Flutamide is non-steroidal (may be selective for prostate)

40
Q

What is cyproterone used to treat?

A

Prostate cancer

Androgenisation in females

41
Q

List 4 adverse effects of cyproterone

A

Cognitive changes
Fatigue
Anaemia
Decreased spermatogenesis

42
Q

What is flutamide used to treat?

A

Metastatic prostate cancer

43
Q

List 6 adverse effects of flutamide

A 
Diarrhoea
Anaemia
Hepatic injury
Oedema
Dizziness
Blurred vision
44
Q

What is finasteride and what is it used to treat?

A

5a-reductase inhibitor

Used to treat BPH and hair loss

45
Q

List 5 possible adverse effects of finasteride

A 
Impotence
Decreased libido
Ejaculation disorder
Breast enlargement and tenderness
Breast cancer (reported)
46
Q

What is the mechanism of breast enlargement caused by finasteride?

A

Prevents conversion of testosterone to DHT in breast tissue

Testosterone is converted to oestrogen instead, promotes breast growth

Hannah's Reproductive (5 decks)

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