Lecture 26: Puberty Flashcards

1
Q
A
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2
Q

What’s the definition of normal puberty?

A
  • Central Activation of the H-P gonadal axis
  • Progressive sequential changes
  • Appropriate rate (over 3-4yrs)

All these things occur “in tempo”!!

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3
Q

Whats the first signs of puberty for boys and girls?

A

Girls (1st sign) :

  1. Breast development because eostrogen is the trigger ~10.5 yr
  2. Then Growth spurt
  3. Period 2-3 years later ~13-14yr

Boys (1st sign) :

  1. Increased testicular enlargment ~11-12yr
  2. >4ml (orchidometer)
  3. Growth spurt later testosterone > eostrogen 2-3 yrs later ~13-14yr
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4
Q

How many puberties do you have?

A

3 Puberties of life!!!!

All related back to LH, FSH and sexsteriods

  1. Pre-natal: We have a huge amount of sex steroids, LH and FSH, (how else would little boys be born with a fallace?)
  2. Infancy: another little puberty. Biys penile length increases, girls may have a little pubic hair or best budding
    • ​​Different to withdrawal bleeding/ baby period which is due to removal from mums high estrogen environment
    • Everything goes to sleep
  3. Adolescent: big, well-known puberty.
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5
Q

What inhibits puberty throughout childhood?

A

The Gonadostat.

  • An area of the brain that actively inhibits puberty
    • ​not able to find if you cut the brain up
  • Tonically inhibits throughout childhoduntil at some point it starts to loss that inhibition → 3rd puberty takes off.
  • Any damage to this area →early puberty
    • if you’re in a car accident and hit your head, or kids wiht meningitis
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6
Q

What do these terms mean?

Thelarche

Pubarche

Gonadarche

Menarche

Gynaecomastia

A

Thelarche: Breast development (breast budding in a girl)

Pubarche: Pubic hair development

Gonadarche: Gonadal development > makes a bit of eostrogen

Menarche: first menstrual period

Gynaecomastia: breast development in boys

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7
Q

What’s the impact off insulin on ovarian androgen production?

A

PCOS: Insulin resistant state

High levels of insulin intefere with their androgen production from thecal cells. Why they have male virilised symptoms.

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8
Q

Describe the LH and FSH release during puberty?

A

Early Puberty LH could be measured at 0 during the day

  • Tonic phase increases
  • Night Pulses begin

Mid Puberty

  • Greater increase in tonic phase
  • High amplitude night pulses

Late puberty Measure LH anytime and get a reading

  • Day and night pulses

If on COCP, LH level will be 0, as cycle is switched off!

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9
Q

A women who is having extremely irregular periods (~1yr) and we measured her LH levels and found them at 60 (extremely high)

What does this mean?

A

Tells us the ovaries have shut down = ovarian failure
Eg; women with Turners Syndrome

Nothing to do with brain as it is trying to compensate by increasing LH levels

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10
Q

Describe the Childhood to puberty transition

A
  • Gonadostat turned OFF (loss of inhibitory signal)
  • Increased pulsatile GnRH → pulsatile LH/FSH
  • Increased Sex steroid production
  • Reduced sensitivity to negative feedback from sex steroids (in hypothalamus and pituitary)
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11
Q

Describe Kisspeptin!

A
  • Product of the KISS1 gene
    • ​Expressed where we think Gonadostat is
  • Naturally occuring ligand for GPR54 receptor
  • Also has a role as a metastasis suppressor gene
  • Kisspeptin expressing neurons are located in:
    • Arcuate nucleus
    • Periventricular nucleus
    • Preoptic nucleus
  • Therefore they project into GnRH producing areas
  • KP neurons send prjections into the preoptic nucleus (GnRH cell bodies)
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12
Q

What evidence supports Kisspeptin as a puberty trigger?

A
  • GPR54 inactivating mutations → don’t go into puberty
    • have to give them GnRH
  • If you give someone Kisspeptin → prepubertal get LH stimulation and ovulation
  • KISS1 and GPR54 expression is increased at the start of puberty
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13
Q

What stimulates inhibin and then what does it inhibit?

What is inhibin produced by?

A

Inhibin is stimulated by FSH, the acts as a negative feedback to the FSH secretion from Ant. pituitary.

Produced By:

  • Leydig Cells (m)
  • Granulosa cells (f)

Dimer, 2 chains a and B (variable)

A and B form with indenticle function

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14
Q

What is Adrenarche?

A
  • An increase in adrenal (weak) androgen production (DHEAS hormone)
    • Occurs in late childhood (8-10yrs) → pongy smell
  • Temporal association with puberty, NOT AN ACTUAL SIGN/stage OF PUBERTY
  • Produces pubarche (pubic hair development)
  • Trigger is unknown

Big cause of anxiety for kids

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15
Q

DHEAS is produced from?

What can we measure from the adrenal steroid?

A

DHEA gets sulphated → DHEAS

We can measure Aldosterone, cortisol, DHT, estradiol, DHEA, DHEAS

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16
Q

What does Leptin do in regards to Puberty?

A
  • Leptin: an adipostatic hormone (leptos = thin)
  • Increased Leptin → increased fat mass
  • Potentailly a facilitatory signal to influence timing of puberty?
  • Supported by the fact that obese children have earlier onset of puberty
  • 1kg weight gain → lowers age of menarche by 13 days
17
Q

What will Leptin Deficiency lead to?

A

Can be due to abnormal leptin hormone or Abnormal leptin receptor.

Sufferers are morbidly obese and don’t go through puberty (no trigger)

  • Inject with leptin, to trim down and go through puberty like normal
  • Very rare
18
Q

Leptin levels peak ___________ in boys

A

Leptin levels peak jsut prior to puberty in boys

19
Q

What is the current Age of Menarche and what is this dependent on?

A
  • The average age is getting younger, due to increasing weights
  • Directly correlated with body fatness

There’s a wide racial variation (body fatness)

  • 11.5yrs US black (thicker women> taller, stronger)
  • 12.3yrs US white
  • 12.8yrs UK

Fallen in US by 0.34 in the past 25yrs

20
Q

How does body composition change inpuberty for males and females?

A

Prepubertal male and female are the same in terms of lean, skeletal and fat mass

Puberty:

  • Lean and skeletal mass; Males 1.5x more then females
  • Fat mass; Females 2x more then males
  • Fat
    • Males: truncal
    • Females: generalised
  • There’s increased bone mineral density in both with peak bone mass achieved in early 20’s