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Science of Repro > Puberty > Flashcards

Puberty Flashcards

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1
Q

Puberty

Reproductive perspective:

Clinical Perspective:

A

Goal to produce mature gametes:

Testes –> spermatozoa
Ovaries –> oocyte

Females: Breast development in females

Male: Increased testicular volume in males

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2
Q

Two endocrine events of puberty

They both together in their efforts?

A

Adrenarche & Gonadarche

Independently regulated

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3
Q

Adrenarche produce __ to exhibit features such as:

A

produce Adrenal androgens
->
Growth of pubic hair, axillary hair
Growth in height

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4
Q

Gonadarche

A

LH/FSH

LH - steroid synthesis –> secondary sex characteristics

FSH - growth of testis (male)/steroid synthesis/folliculogenesis (female)

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5
Q

Adrenarche occurs at approximately which years?

A

~6-8 years

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6
Q

What is adenarche characterised by?

A

Characterised by (re-)instigation of adrenal androgen secretion
Dehydro-epiandrosterone (DHEA)
Dehydro-epiandrosterone sulphate (DHEA-S)

No change in cortisol/other adrenal hormones - not a global activation of HPA axis

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7
Q
A

No change in cortisol/other adrenal hormones - not a global activation of HPA axis

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8
Q

Androgen secretion is from which part of adrenal gland?

A

Zona reticularis

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9
Q

Remodelling of the adrenal cortex causes

A

secretion of the androgens (eventually)

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10
Q

adrenal gland contains two zones

A

Foetal and definitive zones

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11
Q

Developmental Stage

Foetus –> Neonate

What happens to adrenal glands. Is DHEA/S present?

A

Foetal zone - DHEA (YES)
—>
Involution (shrinkage) of FZ (DHEA YES but decreases)

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12
Q

Neonate
—>
Infant

What happens to adrenal glands. Is DHEA/S present?

A

Definitive zone expands into:
- zona glomerulosa
- zona fasiculata (outer layers of AC)

At this stage there is NO DHEA/S produced.

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13
Q

Infant –> ~3yrs

What happens to adrenal glands. Is DHEA/S present?

A

Zona reticularis focal island forms

At this stage there is NO DHEA/S produced.

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14
Q

~3yrs -> ~4-5 yrs

What happens to adrenal glands. Is DHEA/S present?

A

Zona reticularis focal island expands

At this stage there is NO DHEA/S produced.

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15
Q

~4-5 yrs –> ~6yrs

What happens to adrenal glands. Is DHEA/S present?

A

Funcitonal Zona Reticularis developed

There is now DHEA/S production

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16
Q

~6yrs –> 12-13yrs

What happens to adrenal glands. Is DHEA/S present?

A

Zona Reticularis expansion

There is DHEA/S production

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17
Q

Cholesterol ———> DHEA–>DHEA/S?

Cholesterol –>_____–> ____—> DHEA—-> DHEA/s

Enzymes involved?

A

CYP17 - 2 types

SULT2A1

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18
Q

3𝛽HSD —-> Glucocorticoids?

A
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19
Q

In adrenarche, there is an increase in _______ in the ZR.

A

SULT2A1

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20
Q

This side of (3𝛽HSD —-> Glucocorticoids?) is switched off or expressed less due to what reason?

A

To prevent cholesterol and pregninalone going sideways pathway but committed to making DHEA and DHEAS

21
Q

DHEA/S goes to blood stream to which tissue to get converted?

What features would this then exhibit?

A

Converted to DHT in peripheral tissue metabolism

exhibit pubic hair, axillary hair, prostate, genital skin

22
Q

As an instigator, how is ACTH thought to instigate Adrenarche?

A
  • Dexamethasone suppresses adrenal androgen production
  • Children with ACTH receptor mutations fail to undergo adrenarche.

But, NO change in ACTH/cortisol during adrenarche

23
Q

As an instigator, how is POMC thought to instigate Adrenarche?

A

Proximal 18 AA region that positively regulated adrenal androgen production.

In vitro studies did not substantiate this

24
Q

As an instigator, how is POMC-related peptides thought to instigate Adrenarche?

A

b-lipotrophin and b-endorphin plasma levels correlate with increased DHEA/S at adrenarche

25
Q

What are the other factors ruled out for instigation of adrenarche?

Are there any conclusive mechanism for control ofadrenarche?

A

Other factors ruled out include prolactin, IGF-1 and insulin.

No conclusive mechanism for control ofadrenarche.

26
Q

Gonadarche in simple terms

A

(Re-)Activation of HPG axis.

27
Q

When does Gonadarche happen

A

Several years after adrenarche (typically ~11 yrs of age).

28
Q

What is Gonadarche driven by?

A

Driven by hypothalamic GnRH & pituitary gonadotrophins.

29
Q

HPG axis and puberty summarised

A
30
Q

Is the HPG activated at the 16th gestational week?

A

Yes

31
Q

Is the HPG activated before birth?

A

No HPG axis is not activated.

To make room for placental hormones.

32
Q

Is the HPG activated after birth

A

Post-natal 1-2 years, HPG axis is activated.

33
Q

At early puberty there is a nocturnal rise in?

A

Nocturnal rise in GnRH (LH)

34
Q

Tanner stages and consonance

A

series of physical changes occuring puberty 1-5.

Consonance is the progression through each stage.

35
Q

Every person has the same progression in the tanner stages, but what can differ?

A
  • time spent in each stage
  • time it takes to move from one stage to the other
36
Q

What controls the onset of puberty? Generally speaking:

A

Dialogue between our individual genetics and environmental factors

All impinge at different points of the HPG axis

37
Q

Why the fuss about precocious puberty? What conditions diseases?

A
  • cardiovascular disease
    • metabolic disease
    • obesity
    • diabetes
    • disordered behaviour
    • decreased adult height
    • decreased life expectancy
38
Q

What controls the onset of puberty? All the theories

A
  • Inherent maturation of CNS
  • Body fat/nutrition – Leptin and Ghrelin
  • Hypothalamic hormones - Kisspeptin, other factors?
  • Latest theories - Epigenetics?
39
Q

Epigenetics - what is that?

A

Changes in phenotype however no change in structure of sequence

e.g lifestyle + diet of parents had epigenetic effects on genes passed on to us

40
Q

Nutrition and body fat’s impact on onset of puberty:

3 observances + 1 observance (another card)

A

Extremes of energy excess (body fat mass) impact the timing of puberty in both sexes - particularly females

Under- and over-nutrition in foetal and/or neonates alters the timing of puberty in rodents and humans

Morbid obesity (females) can cause precocious puberty

critical fat mass” hypothesis

41
Q

“critical fat mass” hypothesis

A

Threshold % fat/body weight is required to attain (17%) and maintain female reproductive ability (22%)

42
Q

Leptin

tells brain you’re?

A

Sensor of energy sufficiency

Satiety factor - tells brain you’re full

Stimulates energy expenditure

Circulating levels directly proportional to amount of body fat

43
Q

Influence of leptin on reproductive system

A
  • hypogonadotrophic hypogonadism
  • Delayed/absent puberty
  • Can be reversed with leptin injection
  • Some leptin-deficient patients have normal menses/LH/oestradial levels- unknown why.
44
Q

Q. Is leptin the trigger to puberty?

A

Threshold of leptin required to be reached for puberty but not a DRIVER of puberty itself.

45
Q

Ghrelin

What does it sense?
What does it stimulate?

Other attribubes

A

Ghrelin senses the fasted state, to stimulate feeding and fat deposition.

A bolus of ghrelin stimulates the GH/IGF axis Via GHSR.

In ‘starvation’ (high ghrelin) decreased activity of the HPG axis.

Ghrelin decreases as puberty proceeds.

Ghrelin can decrease hypothalamic kiss1 expression in rat

46
Q

Low levels of leptin and high levels ghrelin

A

decreased LH.

47
Q

Mutations of Kisspeptin have been linked with..

A

Abnormal development of GnRH neurones hypogonadism

Failure to enter puberty

Hypothalamic hypogonadism

Activating mutations of GPR54 precocious puberty

Phenotype (mice):

Male: small testes and epididymis, delayed spermatogenesis infertility;

Female: small oviducts, folliculogenesis-no progression to ovulation, no oestrous cycles, infertility

48
Q

Integration of Kisspeptin-GnRH system with metabolic cues?

A

Reduced leptin in starvation, decreased GnRH secretion

Leptin directly excites Kiss1 neurones in ARC

Leptin deficiency »↓Kiss 1 mRNA in ARC

49
Q

?What switches on puberty?

A

An integration of central and peripheral inputs determined both by genetics and environment/nutrition

Science of Repro (15 decks)

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