Week 8 Lecture Content (Sex & Gender II) Flashcards

1
Q

Detail the hypothalamus-pituitary-gonad (HPG) axis and explain its role in Developmental Mechanisms

Be specific with brain regions, hormones, and downstream effects. How/where do kisspeptin and oxytocin fit into the HPG axis?

Lecture 24 on activational mechanisms, and the role of kisspeptin and oxytocin

A
  • HPG axis suppression during childhood; circhoral (hourly) rhythm of GnRH secretion initiates puberty.
  • Puberty triggers GnRH release from hypothalamus, leading to LH & FSH release from the anterior pituitary.
  • LH & FSH stimulate gonads to produce sex hormones (testosterone, oestrogen) and gametes (sperm, eggs), enabling sexual maturation and secondary sex characteristic development.
  • Kisspeptin acts as a permissive factor for puberty initiation. It stimulates GnRH-producing neurons and modulates HPG axis function.
  • Oxytocin promotes pair bonding and sexual behaviours through modulation of the HPG axis and limbic system.
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2
Q

Detail the hypothalamus-pituitary-gonad (HPG) axis and explain its role in Activational Mechanisms

Be specific with brain regions, hormones, and downstream effects. How/where do kisspeptin and oxytocin fit into the HPG axis?

Lecture 24 on activational mechanisms, and the role of kisspeptin and oxytocin

A

In adulthood, HPG axis activation facilitates reproductive readiness:
- Secondary sex characteristics develop to attract mates.
- Libido activation encourages sexual behaviour.
- Pair bonding promotes successful reproduction and care of offspring.

Oxytocin also aids in pair bonding by increasing feelings of trust and attachment in intimate relationships.

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3
Q

Puberty triggers ____ release from hypothalamus, leading to ___ & ___ release from the anterior pituitary.

A

GnRH, LH & FSH

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4
Q

Puberty triggers GnRH release from ___________, leading to LH & FSH release from the __________ _________.

A

hypothalamus, anterior pituitary

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5
Q

___ & ___ stimulate gonads to produce sex hormones (testosterone, oestrogen) and gametes (sperm, eggs), enabling sexual maturation and secondary sex characteristic development.

A

LH & FSH

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6
Q

LH & FSH stimulate _______ to produce sex hormones (testosterone, oestrogen) and _______ (sperm, eggs), enabling sexual maturation and secondary sex characteristic development.

A

gonads, gametes

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7
Q

_______ acts as a permissive factor for puberty initiation. It stimulates _____-producing neurons and modulates HPG axis function.

A

Kisspeptin, GnRH

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8
Q

________ promotes pair bonding and sexual behaviours through modulation of the HPG axis and limbic system.

A

Oxytocin

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9
Q

In adulthood, HPG axis activation facilitates reproductive readiness:
- _________ _____ ________ develop to attract mates.
- Libido activation encourages sexual behaviour.
- _____ ________ promotes successful reproduction and care of offspring.

A

Secondary sex characteristics, Pair bonding

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10
Q

_______ also aids in pair bonding by increasing feelings of trust and attachment in intimate relationships.

A

Oxytocin

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11
Q

Explain the main stages of gender transitioning, including the phases of hormone therapy.

Lecture 22 notes on gender transitioning

A

Stage 1: Life experience & psychological assessment
- 2+ years of living in the preferred gender identity without hormone or surgical interventions.
- Psychological evaluations and behavioural changes (pronouns, dressing, etc.) improve mental well-being.

Stage 2: Gender Affirming Hormone Therapy (GAHT)
- Involves oestrogen-based (E-GAHT) or testosterone-based (T-GAHT) hormone therapy.
- Requires diagnosis of Gender Dysphoria and involves careful monitoring.
- Hormone initiation is slow and requires long-term follow-up with adjustments over time.

Stage 3: Surgical intervention
- Available only after 1+ year of continuous GAHT.
- Can include gonad removal, genital alterations, and breast augmentation.

Stage 4: Long-term follow-up
- Lifelong hormone therapy and psychological support required.

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12
Q

Explain Stage 1 of gender transitioning

A

Stage 1: Life experience & psychological assessment
- 2+ years of living in the preferred gender identity without hormone or surgical interventions.
- Psychological evaluations and behavioural changes (pronouns, dressing, etc.) improve mental well-being.

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13
Q

Explain Stage 2 of gender transitioning

A

Stage 2: Gender Affirming Hormone Therapy (GAHT)
- Involves oestrogen-based (E-GAHT) or testosterone-based (T-GAHT) hormone therapy.
- Requires diagnosis of Gender Dysphoria and involves careful monitoring.
- Hormone initiation is slow and requires long-term follow-up with adjustments over time.

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14
Q

Explain Stage 3 of gender transitioning

A

Stage 3: Surgical intervention
- Available only after 1+ year of continuous GAHT.
- Can include gonad removal, genital alterations, and breast augmentation.

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15
Q

Explain Stage 4 of gender transitioning

A

Stage 4: Long-term follow-up
- Lifelong hormone therapy and psychological support required.

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16
Q

Stage 1 of gender transitioning:
_____ _________ & __________ __________
- __ years of living in the preferred gender identity without ______ or _______ interventions.
- ________ _________ and behavioural changes (pronouns, dressing, etc.) improve mental well-being.

A

Stage 1 of gender transitioning:
Life experience & psychological assessment
- 2+ years of living in the preferred gender identity without hormone or surgical interventions.
- Psychological evaluations and behavioural changes (pronouns, dressing, etc.) improve mental well-being.

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17
Q

Stage 2 of gender transitioning:
_______ _______ _______ _______
- Involves ________-based or ________-based hormone therapy.
- Requires diagnosis of ______ ______ and involves careful monitoring.
- Hormone initiation is slow and requires long-term follow-up with adjustments over time.

A

Gender Affirming Hormone Therapy (GAHT)
oestrogen-based (E-GAHT) or testosterone-(T-GAHT)
Gender Dysphoria

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18
Q

Stage 3 of gender transitioning:
_________ ________
- Available only after ___ year of continuous GAHT.
- Can include _____ removal, _____ alterations, and _______ augmentation.

A

Stage 3 of gender transitioning:
Surgical intervention
- Available only after 1+ year of continuous GAHT.
- Can include gonad removal, genital alterations, and breast augmentation.

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19
Q

Stage 4 of gender transitioning:
__________ _________
- ________ hormone therapy and psychological support required.

A

Stage 4 of gender transitioning:
Long-term follow-up
- Lifelong hormone therapy and psychological support required.

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20
Q

What are ‘puberty blockers’ and why/when would they be used? Why do they work?

A

Puberty blockers:
- GnRH analogs that suppress the HPG axis, halting the release of LH/FSH and preventing the production of testosterone/oestrogen.
- Used to delay puberty, especially in transgender youth, to give them time to explore gender identity without developing secondary sex characteristics.

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21
Q

Be able to describe histrelin’s (Supprelin’s™) mechanism of action, mode of action, and route of administration.

A

Histrelin (Supprelin™):
- Mechanism: Continuous activation of GnRH receptors leads to their desensitisation, thus stopping the HPG cascade.
- Mode: Administered via subcutaneous implant (usually in the upper arm), releasing over 12 months.
- Effects: Blocks development of unwanted features like breast growth or voice deepening.

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22
Q

Puberty blockers are _____ analogs that suppress the HPG axis, halting the release of ___/____ and preventing the production of testosterone/oestrogen.

A

GnRH, LH/FSH

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23
Q

Puberty blockers are GnRH analogs that suppress the ____ ____, halting the release of LH/FSH and preventing the production of _________/_________.

A

HPG axis, testosterone/oestrogen

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24
Q

Histrelin (Supprelin™) enables continuous activation of _____ receptors, leading to their desensitisation, thus stopping the ____ cascade.

A

GnRH, HPG

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25
Q

____________ enables continuous activation of GnRH receptors, leading to their desensitisation, thus stopping the HBG cascade.

A

Histrelin (Supprelin™)

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26
Q

Histrelin (Supprelin™) is administered via __________ ________, releasing over ___ months.

A

subcutaneous implant (usually in the upper arm), 12 months

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27
Q

From the lecture and video clip that was shown, what are the pros associated with puberty blockers and GAHT?

A
  • Can be life-saving by preventing distress from gender-incongruent puberty.
  • Claimed to be reversible and provide time for decision-making regarding GAHT or surgical options.
  • Reduces suicidal ideation in transgender youth.
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28
Q

From the lecture and video clip that was shown, what are the cons associated with puberty blockers and GAHT?

A
  • Unclear long-term effects, especially on bone health and brain development.
  • 95% of individuals on puberty blockers proceed to GAHT, suggesting it may not be a true “pause.”
  • Concerns about informed consent, especially for children under 18.
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29
Q

What is the evidence on Gender Identity and Transition Regret?

A
  • Studies show a low rate of transition regret (0.5-8%), with detransition often due to external pressures rather than internal dissatisfaction.
  • Debate about how persistent gender identity is in adolescence.
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30
Q

What was the “Cass Review”?

A
  • Independent review of gender services for youth in the UK.
  • Found weak evidence supporting puberty blockers, leading to their restriction except in clinical trials (as of June 2024).
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31
Q

__% of individuals on puberty blockers proceed to GAHT, suggesting it may not be a true “pause.”

A

95%

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32
Q

Studies show a ___ rate of transition regret (___-___%), with detransition often due to external pressures rather than internal dissatisfaction.

A

low, 0.5-8%

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33
Q

The ____ Review:
- Independent review of gender services for youth in the UK.
- Found weak evidence supporting puberty blockers, leading to their restriction except in clinical trials (as of June 2024).

A

Cass

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34
Q

Describe the 1st activation that occurs to prepare sexual behaviours in maturity.

Lecture 24 on activational mechanisms

A

Activation 1: Sexual maturation & secondary sex characteristics
- Driven by the HPG axis, the release of testosterone and oestrogen results in the development of secondary sexual characteristics like breast development, voice deepening, and muscle mass.
- These physical changes enhance mate attraction and reproductive readiness.

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35
Q

Describe the 2nd activation that occurs to prepare sexual behaviours in maturity.

Lecture 24 on activational mechanisms

A

Activation 2: Libido activation (Sexual desire)
- Sex hormones, particularly testosterone, stimulate the areas of the brain associated with libido and sexual motivation.
- Kisspeptin plays a role in stimulating the HPG axis and indirectly promotes sexual desire.

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36
Q

Describe the 3rd activation that occurs to prepare sexual behaviours in maturity.

Lecture 24 on activational mechanisms

A

Activation 3: Pair bonding and social behaviour
- Oxytocin and vasopressin are crucial for pair bonding, promoting attachment and social bonding between partners.
- These hormones influence areas of the brain like the limbic system, which is linked to emotional regulation and attachment behaviours.

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37
Q

Name the 3 main ‘activations’ that occur to prepare sexual behaviours in maturity.

  • Activation 1:
  • Activation 2:
  • Activation 3:

Lecture 24 on activational mechanisms

A
  • Activation 1: Sexual maturation & secondary sex characteristics
  • Activation 2: Libido activation (Sexual desire)
  • Activation 3: Pair bonding and social behaviour
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38
Q

Activation 1: Sexual maturation & secondary sex characteristics
- Driven by the ____ ____, the release of __________ and ________ results in the development of _________ sexual characteristics like breast development, voice deepening, and muscle mass.
- These physical changes enhance mate attraction and reproductive readiness.

A

Activation 1: Sexual maturation & secondary sex characteristics
- Driven by the HPG axis, the release of testosterone and oestrogen results in the development of secondary sexual characteristics like breast development, voice deepening, and muscle mass.
- These physical changes enhance mate attraction and reproductive readiness.

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39
Q

Activation 2: Libido activation (Sexual desire)
- Sex __________, particularly _______, stimulate the areas of the brain associated with libido and sexual motivation.
- ________ plays a role in stimulating the _____ _____ and indirectly promotes sexual desire.

A

Activation 2: Libido activation (Sexual desire)
- Sex hormones, particularly testosterone, stimulate the areas of the brain associated with libido and sexual motivation.
- Kisspeptin plays a role in stimulating the HPG axis and indirectly promotes sexual desire.

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40
Q

Activation 3: Pair bonding and social behaviour
- ________ and ________ are crucial for pair bonding, promoting attachment and social bonding between partners.
- These hormones influence areas of the brain like the _______ _______, which is linked to emotional regulation and attachment behaviours.

A

Activation 3: Pair bonding and social behaviour
- Oxytocin and vasopressin are crucial for pair bonding, promoting attachment and social bonding between partners.
- These hormones influence areas of the brain like the limbic system, which is linked to emotional regulation and attachment behaviours.

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41
Q

In theory, how would a GnRH analogue influence the HPG axis and subsequently fertility? Assume that it comes in an effective oral ROA, taken daily.

A

Mimics GnRH and leads to continuous activation, which desensitises GnRH receptors and suppresses LH/FSH release, halting gonadal function and fertility.

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42
Q

In theory, how would a testosterone analogue influence the HPG axis and subsequently fertility? Assume that it comes in an effective oral ROA, taken daily.

A

Exogenous testosterone provides negative feedback to the hypothalamus and pituitary, reducing GnRH, LH, and FSH, thereby lowering sperm production and fertility.

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43
Q

In theory, how would an oestrogen-progestogen combination pill influence the HPG axis and subsequently fertility? Assume that it comes in an effective oral ROA, taken daily.

A

Works similarly to female contraceptives, suppressing the HPG axis through negative feedback, preventing ovulation in females or reducing spermatogenesis in males.

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44
Q

In theory, how would a kisspeptin receptor antagonist influence the HPG axis and subsequently fertility? Assume that it comes in an effective oral ROA, taken daily.

A

Blocks kisspeptin from activating GnRH-producing neurons, reducing the release of GnRH, and subsequently lowering fertility by decreasing LH/FSH.

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45
Q

In theory, how would a combination pill containing FSH+LH receptor antagonists influence the HPG axis and subsequently fertility? Assume that it comes in an effective oral ROA, taken daily.

A

Directly block the effects of LH and FSH at the gonads, preventing spermatogenesis in males and ovulation in females.

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46
Q

In theory, how would an oxytocin receptor agonist influence the HPG axis and subsequently fertility? Assume that it comes in an effective oral ROA, taken daily.

A

Primarily affects social bonding and pair-bonding behaviours rather than direct reproductive functions, with minimal impact on fertility.

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47
Q

In theory, how would a PDE5 inhibitor influence the HPG axis and subsequently fertility? Assume that it comes in an effective oral ROA, taken daily.

A

Works by enhancing blood flow and does not affect the HPG axis or fertility directly. It facilitates erections but has no effect on hormonal regulation. (E.g. Viagra)

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48
Q

GnRH __________ mimics GnRH and leads to continuous activation, which desensitises GnRH receptors and suppresses LH/FSH release, halting gonadal function and fertility.

A

GnRH analogue mimics GnRH and leads to continuous activation, which desensitises GnRH receptors and suppresses LH/FSH release, halting gonadal function and fertility.

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49
Q

GnRH analogue ________ GnRH and leads to _________ activation, which __________ GnRH receptors and __________ LH/FSH release, __________ gonadal function and fertility.

A

GnRH analogue mimics GnRH and leads to continuous activation, which desensitises GnRH receptors and suppresses LH/FSH release, halting gonadal function and fertility.

50
Q

GnRH analogue mimics GnRH and leads to continuous activation, which desensitises GnRH _________ and suppresses ___/___ release, halting __________ function and fertility.

A

GnRH analogue mimics GnRH and leads to continuous activation, which desensitises GnRH receptors and suppresses LH/FSH release, halting gonadal function and fertility.

51
Q

_____ analogue mimics _____ and leads to continuous activation, which desensitises _____ receptors and suppresses LH/FSH release, halting gonadal function and fertility.

A

GnRH analogue mimics GnRH and leads to continuous activation, which desensitises GnRH receptors and suppresses LH/FSH release, halting gonadal function and fertility.

52
Q

___________ ________ provides negative feedback to the hypothalamus and pituitary, reducing GnRH, LH, and FSH, thereby lowering sperm production and fertility.

A

Exogenous testosterone/testosterone analogue provides negative feedback to the hypothalamus and pituitary, reducing GnRH, LH, and FSH, thereby lowering sperm production and fertility.

53
Q

Exogenous testosterone/testosterone analogue provides ________ feedback to the hypothalamus and pituitary, ________ GnRH, LH, and FSH, thereby _______ sperm production and fertility.

A

Exogenous testosterone/testosterone analogue provides negative feedback to the hypothalamus and pituitary, reducing GnRH, LH, and FSH, thereby lowering sperm production and fertility.

54
Q

Exogenous testosterone/testosterone analogue provides negative feedback to the _____________ and ________, reducing _____, ____, and ____, thereby lowering sperm production and fertility.

A

Exogenous testosterone/testosterone analogue provides negative feedback to the hypothalamus and pituitary, reducing GnRH, LH, and FSH, thereby lowering sperm production and fertility.

55
Q

___________-__________ combination pill works similarly to female contraceptives, suppressing the HPG axis through negative feedback, preventing ovulation in females or reducing spermatogenesis in males.

A

Oestrogen-progestogen combination pill works similarly to female contraceptives, suppressing the HPG axis through negative feedback, preventing ovulation in females or reducing spermatogenesis in males.

56
Q

Oestrogen-progestogen combination pill works similarly to female contraceptives, suppressing the ____ _____ through negative feedback, preventing ________ in females or reducing ___________ in males.

A

Oestrogen-progestogen combination pill works similarly to female contraceptives, suppressing the HPG axis through negative feedback, preventing ovulation in females or reducing spermatogenesis in males.

57
Q

Oestrogen-progestogen combination pill works similarly to female contraceptives, ___________ the HPG axis through __________ feedback, ___________ ovulation in females or ____________ spermatogenesis in males.

A

suppressing; negative; reducing

58
Q

Kisspeptin receptor ___________ blocks kisspeptin from activating GnRH-producing neurons, reducing the release of GnRH, and subsequently lowering fertility by decreasing LH/FSH.

A

Kisspeptin receptor antagonist blocks kisspeptin from activating GnRH-producing neurons, reducing the release of GnRH, and subsequently lowering fertility by decreasing LH/FSH.

59
Q

Kisspeptin receptor antagonist ________ kisspeptin activating GnRH-producing neurons, __________ the release of GnRH, and subsequently _________ fertility by __________ LH/FSH.

A

Kisspeptin receptor antagonist blocks kisspeptin from activating GnRH-producing neurons, reducing the release of GnRH, and subsequently lowering fertility by decreasing LH/FSH.

60
Q

___________ receptor antagonist blocks _________ from activating GnRH-producing neurons, reducing the release of GnRH, and subsequently lowering fertility by decreasing LH/FSH.

A

Kisspeptin receptor antagonist blocks kisspeptin from activating GnRH-producing neurons, reducing the release of GnRH, and subsequently lowering fertility by decreasing LH/FSH.

61
Q

Kisspeptin receptor antagonist blocks kisspeptin from activating _____-producing neurons, reducing the release of _____, and subsequently lowering fertility by decreasing __/___.

A

Kisspeptin receptor antagonist blocks kisspeptin from activating GnRH-producing neurons, reducing the release of GnRH, and subsequently lowering fertility by decreasing LH/FSH.

62
Q

_____and ____ receptor antagonists directly block the effects of ___ and ___ at the gonads, preventing spermatogenesis in males and ovulation in females.

A

FSH and LH receptor antagonists directly block the effects of LH and FSH at the gonads, preventing spermatogenesis in males and ovulation in females.

63
Q

FSH + LH receptor ___________ directly block the effects of LH and FSH at the gonads, preventing spermatogenesis in males and ovulation in females.

A

FSH + LH receptor antagonists directly block the effects of LH and FSH at the gonads, preventing spermatogenesis in males and ovulation in females.

64
Q

FSH + LH receptor antagonists directly _______ the effects of LH and FSH at the gonads, __________ spermatogenesis in males and ovulation in females.

A

FSH + LH receptor antagonists directly block the effects of LH and FSH at the gonads, preventing spermatogenesis in males and ovulation in females.

65
Q

FSH + LH receptor antagonists directly block the effects of LH and FSH at the ________, preventing _________ in males and __________ in females.

A

FSH + LH receptor antagonists directly block the effects of LH and FSH at the gonads, preventing spermatogenesis in males and ovulation in females.

66
Q

Oxytocin receptor _________ primarily affects social bonding and pair-bonding behaviours rather than direct reproductive functions, with minimal impact on fertility.

A

agonist

67
Q

________ receptor agonist primarily affects social bonding and pair-bonding behaviours rather than direct reproductive functions, with minimal impact on fertility.

A

Oxytocin receptor agonist primarily affects social bonding and pair-bonding behaviours rather than direct reproductive functions, with minimal impact on fertility.

68
Q

Oxytocin receptor agonist primarily affects _________ ________ and ______ ________ behaviours rather than direct _________ functions, with minimal impact on _______.

A

Oxytocin receptor agonist primarily affects social bonding and pair-bonding behaviours rather than direct reproductive functions, with minimal impact on fertility.

69
Q

_______ ________ (e.g., Viagra) works by enhancing blood flow and does not affect the HPG axis or fertility directly. It facilitates erections but has no effect on hormonal regulation.

A

PDE5 inhibitor (e.g., Viagra) works by enhancing blood flow and does not affect the HPG axis or fertility directly. It facilitates erections but has no effect on hormonal regulation.

70
Q

PDE5 inhibitor (e.g., _______) works by enhancing blood flow and does not affect the HPG axis or fertility directly. It facilitates erections but has no effect on hormonal regulation.

A

PDE5 inhibitor (e.g., Viagra) works by enhancing blood flow and does not affect the HPG axis or fertility directly. It facilitates erections but has no effect on hormonal regulation.

71
Q

PDE5 inhibitor (e.g., Viagra) works by enhancing blood flow and does not affect the _____ ______ or _________ directly. It facilitates _________ but has no effect on __________ regulation.

A

PDE5 inhibitor (e.g., Viagra) works by enhancing blood flow and does not affect the HPG axis or fertility directly. It facilitates erections but has no effect on hormonal regulation.

72
Q

In male rats castration reduces libido and copulatory behaviours. ______________ supplementation restores sexual behaviours, but increasing ___________ further does not result in increased libido beyond the baseline.

A

In male rats castration reduces libido and copulatory behaviours. Testosterone supplementation restores sexual behaviours, but increasing testosterone further does not result in increased libido beyond the baseline.

73
Q

Do higher testosterone levels correlate with higher sex drive?

A

No

74
Q

In female rats ovary removal reduces ________ and ________ sexual behaviours. Estradiol supplementation restores sexual behaviour, indicating that oestrogen plays a role in promoting female sexual behaviour.

A

In female rats ovary removal reduces proceptive and receptive sexual behaviours. Estradiol supplementation restores sexual behaviour, indicating that oestrogen plays a role in promoting female sexual behaviour.

75
Q

In female rats ovary removal reduces proceptive and receptive sexual behaviours. _______ supplementation restores sexual behaviour, indicating that _________ plays a role in promoting female sexual behaviour.

A

In female rats ovary removal reduces proceptive and receptive sexual behaviours. Estradiol supplementation restores sexual behaviour, indicating that oestrogen plays a role in promoting female sexual behaviour.

76
Q

Menopause or ovary removal affects libido variably, and __________ _________ _________ with oestrogen and progesterone can help restore it.

A

Menopause or ovary removal affects libido variably, and hormone replacement therapy (HRT) with oestrogen and progesterone can help restore it.

77
Q

_________ supplementation in women has shown mixed results, with no consistent evidence that it boosts libido significantly.

A

Testosterone supplementation in women has shown mixed results, with no consistent evidence that it boosts libido significantly.

78
Q

Testosterone supplementation in women has shown ______ results, with ________ evidence that it boosts libido significantly.

A

Testosterone supplementation in women has shown mixed results, with no consistent evidence that it boosts libido significantly.

79
Q

What is the mechanism and mode of action of Viagra?

A
  • Mechanism of action: PDE5 inhibitor, which increases nitric oxide and enhances blood flow to the penis, facilitating erections.
  • Mode of action: Vasodilation, primarily effective for erectile dysfunction; does not influence libido directly.
    Use for libido: Not useful as a libido booster, as it only enhances physical capability, not sexual desire.
80
Q

What is the mechanism and mode of action of Addyi?

A
  • Mechanism of action: Affects serotonin receptors by decreasing serotonin and increasing dopamine and norepinephrine levels.
  • Mode of action: Targets the brain’s reward system, aiming to increase sexual desire in females with Female Sexual Interest/Arousal Disorder (FSIAD).
81
Q

Would Viagra be useful as a libido-boosting treatment?

A

Not useful as a libido booster, as it only enhances physical capability, not sexual desire.

82
Q

Would Addyi be useful as a libido-boosting treatment?

A

Mixed efficacy; may slightly increase libido, but its effects are often comparable to placebo.

83
Q

Viagra (sildenafil):
- Mechanism of action: _____ inhibitor, which increases nitric oxide and enhances blood flow to the penis, facilitating erections.
- Mode of action: ________, primarily effective for erectile dysfunction; does not influence libido directly.

A

PDE5; Vasodilation

84
Q

Viagra (sildenafil):
- Mechanism of action: PDE5 _________, which increases ______ ______ and enhances blood flow to the penis, facilitating erections.
- Mode of action: Vasodilation, primarily effective for erectile dysfunction; does not influence libido directly.

A

Viagra (sildenafil):
- Mechanism of action: PDE5 inhibitor, which increases nitric oxide and enhances blood flow to the penis, facilitating erections.
- Mode of action: Vasodilation, primarily effective for erectile dysfunction; does not influence libido directly.

85
Q

Addyi (flibanserin):
- Mechanism of action: Affects ________ receptors by decreasing ________ and increasing __________ and _____________ levels.

A

serotonin; serotonin; dopamine; norepinephrine.

86
Q

Addyi (flibanserin):
Mode of action: Targets the brain’s reward system, aiming to increase sexual desire in females with __________________________________________.

A

Female Sexual Interest/Arousal Disorder (FSIAD).

87
Q

Addyi (flibanserin):
Mode of action: Targets the ______ ______ ______, aiming to increase sexual desire in females with Female Sexual Interest/Arousal Disorder (FSIAD).

A

Addyi (flibanserin):
Mode of action: Targets the brain’s reward system, aiming to increase sexual desire in females with Female Sexual Interest/Arousal Disorder (FSIAD).

88
Q

The HPG axis starts with the release of ______ from the hypothalamus, which triggers the pituitary to release ______ and ______.

A

GnRH, LH, FSH

89
Q

During puberty, the HPG axis initiates the development of ______ sex characteristics and the production of ______ in males and ______ in females.

A

secondary, testosterone, estrogen

90
Q

Kisspeptin is a peptide hormone that activates ______ neurons, triggering the release of ______ and starting puberty.

A

GnRH, GnRH

91
Q

Oxytocin promotes pair bonding and attachment by acting on the ______ system and modulating the ______ axis.

A

limbic, HPG

92
Q

The first stage of transitioning involves living as the preferred gender identity for at least ______ years, which is associated with improved ______ _____.

A

two, mental well-being

93
Q

GAHT stands for ______, and the two primary forms are ______-GAHT and ______-GAHT.

A

Gender Affirming Hormone Therapy, E, T

94
Q

Surgical intervention is typically only available after ______ year(s) of continuous hormone therapy and includes procedures like ______ removal.

A

one, gonad

95
Q

Transitioning requires long-term follow-up that includes both ______ and ______ specialists.

A

psychiatric, endocrinological

96
Q

Puberty blockers work by mimicking ______, which leads to desensitisation of ______ receptors and halts puberty.

A

GnRH, GnRH

97
Q

The main effect of puberty blockers is to prevent the release of ______ and ______, stopping the development of secondary sex characteristics.

A

testosterone, estrogen

98
Q

Histrelin (Supprelin™) is typically administered via a subcutaneous ______, which lasts about ______ months.

A

Histrelin (Supprelin™) is typically administered via a subcutaneous ______, which lasts about ______ months.

99
Q

One key ethical concern with puberty blockers is the issue of ______ ______, especially for children under ______ years old.

A

informed consent, 18

100
Q

One of the main arguments in favor of puberty blockers is that they are claimed to be ______, though this is debated.

A

reversible

101
Q

Long-term effects of puberty blockers, particularly on ______ health, are not well understood.

A

bone

102
Q

The evidence shows that ______ percent of individuals who take puberty blockers go on to receive GAHT.

A

95%

103
Q

The Cass Review concluded that the evidence base for puberty blockers is ______, leading to their restriction to ______ in the UK.

A

weak, clinical trials

104
Q

In an experiment on puberty blockers, one outcome measure to assess would be the effect on ______ health over a period of ______ years.

A

bone, 5-10

105
Q

A key method to assess brain changes in youth taking puberty blockers could involve ______ imaging.

A

neuro

106
Q

The first activation for sexual behavior is the development of ______ sex characteristics, which helps facilitate ______ _______.

A

secondary, mate attraction

107
Q

Libido activation is driven largely by the sex hormone ______, which stimulates sexual motivation in both males and females.

A

testosterone

108
Q

______ and ______ are hormones that promote pair bonding, facilitating emotional and social attachment between partners.

A

Oxytocin, vasopressin

109
Q

A GnRH analogue would lead to continuous stimulation of GnRH receptors, causing the ______ ______ to shut down and reducing fertility.

A

HPG axis

110
Q

A testosterone analogue would inhibit the release of ______ and ______ by providing negative feedback to the hypothalamus and pituitary.

A

GnRH, LH

111
Q

A kisspeptin receptor antagonist would reduce activation of ______ neurons and lower the secretion of ______, which is essential for initiating puberty.

A

GnRH, GnRH

112
Q

A PDE5 inhibitor like Viagra primarily affects ______ and does not directly influence ______ or fertility.

A

blood flow, libido

113
Q

In male rats, castration leads to a decrease in ______ behavior, which can be restored by ______ supplementation.

A

sexual, testosterone

114
Q

Human studies have shown that blood _________ levels do not correlate well with increased sexual behavior.

A

Testosterone

115
Q

In female rodents, the removal of ovaries reduces ______ behaviors, but these can be restored with injections of ______

A

proceptive/receptive, estradiol

116
Q

Human females show ______ responses to HRT, with mixed evidence on whether testosterone improves ______.

A

variable, libido

117
Q

Viagra (sildenafil) is a ______ inhibitor that increases ______ _____ to facilitate erections, but does not influence sexual desire.

A

PDE5, blood flow

118
Q

Addyi (flibanserin) works by affecting ______ receptors, increasing ______ and ______ levels, which may enhance libido in women.

A

serotonin, dopamine, norepinephrine

119
Q

While Viagra is useful for ______ dysfunction, Addyi is aimed at treating low ______ in women with Female Sexual Interest/Arousal Disorder (FSIAD).

A

erectile, libido

120
Q

While _______ is useful for erectile dysfunction, ______ is aimed at treating low libido in women with Female Sexual Interest/Arousal Disorder (FSIAD).

A

Viagra, Addyi