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MBCHB3: Reproduction, Development and Ageing > Lecture 24: Puberty > Flashcards

Lecture 24: Puberty Flashcards

1
Q

What are the outcomes of puberty?

A
  • Secondary sex characteristics appear and mature
  • Adolescent growth spurt
  • fertility is achieved
  • Profound psychological changes
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2
Q

How are the outcomes of puberty achieved directly or indirectly?

A

These changes result directly or indirectly from:

  • Maturation of the Hypothalamic-pituitary Gonadotrophin unit
  • Stimulation of the sex organs
  • Secretion of sex steroids
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3
Q

What is the normal start and progression of puberty?

A

Normal puberty starts at a normal time and progresses at a normal rate (~4 years)

  • Central activation of the HP Gonodal axis
  • Progressive sequential changes
  • Appropriate rate 3-4 years
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4
Q

What are the first signs of puberty in girls?

A

Girls first signs

  • Breast development (Tanner stage 2)
  • Then growth spurt
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5
Q

What are the first signs of puberty in boys?

A
  • Increased testicular enlargement
  • > 3ml
  • Growth spurt later
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6
Q

What are the so called three puberties?

A

Fetal life: HPA axis turns on & sexual differentiation occurs

Infant: Minipuberty, HPA axis turns on a little and then turns off.

Teen: Regular puberty

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7
Q

Describe the pubertal onset and sequence in girls:

A

Insert slide 8

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8
Q

Describe the pubertal onset and sequence in boys:

A

Insert slide 9

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9
Q

Define:

  • Thelarche
  • Pubarche
  • Gonadarche
  • Menarche
  • Gynaecomastia
A
  • Thelarche : Breast development
  • Pubarche : Pubic hair development
  • Gonadarche : Gonadal development
  • Menarche : First menstural period
  • Gynaecomastia : Breast development in boys
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10
Q

Whats a better indicator of male development than pubic hair?

A

Testicular volume

+3ml = puberty, orchidometer

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11
Q

What happens to penile growth?

A

Stops between 5-10 and after 18

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12
Q

Write some notes on tanner stage breast development:

A

Stage 2: Elevation of breast, bud still attatched
Stage 3: Further elevation and areola but no separation or contour
Stage 4: Areola and papilla form a secondary mound above level of breast.
Stage 5: Areola recesses to the general contour of the breast

About shape and contour NOT SIZE

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13
Q

Slide 18

A

slide 18

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14
Q

Where in the Hypothalamus is GnRH released from?

A

GnRH : Median preoptic nucleus

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15
Q

Describe the negative feedback loop of GnRH in females and so on:

A

GnRH (Hypo) -> FSH and LH -> (FSH acts on GCs to produce aromatase and Inhibin) (LH acts on Theca cells to produce Androgens) [Aromatase converts Androgens to estrogens)

Estrogen i.e estradiol negatively feedbacks to H&P
Inhibin negatively feedsback to pituitary
Progesterone produced from the later CL negatively feeds back to the H&P

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16
Q

Describe the negative feedback loop of GnRH in males and so on:

A

GnRH (Hypo) -> FSH and LH -> (LH acts on leydig cells to produce testosterone) (FSH acts on sertoli cells to produce inhibin)

Testosterone feedsback negatively to the HYPOTHALAMUS

Inhibin feedsback negatively to the pituitary

17
Q

Describe the changes in LH and FSH secretion during puberty:

A

Early: Tonic phase increases, night pulses begins

Mid-puberty: Greater increase in tonic phase, Higher amplitude night pulses

Late puberty: Day and night pulses

18
Q

What is the gonadostat?

A
  • Intrinsic CNS inhibitory system (enhances HPG negative feedback loops)
  • Sex steroid dependent
  • GABA appears to be the potent inhibitor of GnRH secretion
19
Q

Insert slife 28

A

thanks

20
Q

Describe the childhood to puberty transition:

A
  • Gonadostat is turned off
  • Increased pulsatile GnRH and LH/FSH secretion
  • Increased sex steroid production
  • Reduced sensitivity to negative feedback from sexy steroids
21
Q

What is kisspeptin? Where does it send neurons?

A
  • Product of the kiss-1 gene
  • Natural occuring ligand for GPR54
  • Has neurons: Arcuate nucleus, periventricular nucleus, preoptic nucleus (GnRH cellbodies)
22
Q

Whats the evidence to suggest kisspeptin as a puberty trigger?

A

Evidence:

  • GPR54 inactivation mutations leads to a failure to go into puberty
  • Kisspeptin administration to prepubertal rats stimulates LH and ovulation
  • KISS1 and GPR54 expression increased at the start of puberty
  • The GPR54 receptor regulates GnRH secretion and or release from the hypothalamus
23
Q

What stimulates inhibin and what does it do?

A
  • Inhibin release stimulates by FSH
  • Negative feedback to FSH secretion

Produced by sertoli cells and GCs

24
Q

Whats the role of leptin in puberty?

A
  • May be a facilitatory signal to influence timing of puberty
  • Increased fat = increased leptin (adipostatic hormone) and obese children have earlier onset puberty
  • Leptin levels peak just prior to onset of puberty in boyus
  • Leptin deficient mice dont achieve puberty, but, administration of leptin induces puberty
25
Q

When does adrenarche occur? Whats its relation to puberty? What does it cause?

A
  • Occurs in late childhood (8-10)
  • Increased adrenal production of androgens i.e DHEA
  • Temporal association with puberty, not a sign
  • Induces Pubarche, adult body odour, acne, oily skin
26
Q

Whats the age of menarche?

A

… Getting younger

  • Directly correlated with body fatness
  • Wide racial variations (body fatness)
27
Q

How does body composition relate to puberty?

A

Prepubertal male = female in terms of lean, skeletal and fat mass

Puberty:

  • Lean mass, skeletal muscle mass (M 1.5x F)
  • Fat mass (F 2X M)
  • Fat: Males: Truncal, Females, generalised
  • Increased body mineral density in puberty with peak bone mass achieved in early 20s
28
Q

What are the pubertal growth factors?

A
  • Increased sex steroids
  • Increased growth hormone
  • Increased IGF-1
  • Increased insulin
29
Q

What categorizes someone into preocious puberty?

A

Boys:

  • < 8 y/o
  • Later growth spurt

Girls:

  • Growth spurt
  • Tanner stage 2 (i.e signs of puberty)

Both:

  • Indicates HPG turned on
  • FSH and LH measureable
  • Can do GnRH stimulation test
30
Q

What are possible pathologies of precocious puberty?

A
  • Might be no pathology esp. in girls
  • BUT common in children with neurological problems/brain injury i.e epilepsy or CP

Common pathologies

  • Hypothalamic hamartoma
  • CNS tumor

The younger the male is the more likely of pathology

31
Q

What is the treatment and further investigation of precocious puberty?

A
  • MRI (tumors)
    Meds
  • To preserve final height
  • Social indications

The meds are very long acting GnRH agonists. Shuts down axis because axis requires pulsatile GnRH secretion to be active

32
Q

What does early breast development indicate and what are some possible causes?

A

Indicates exposure to estrogen (not necessarily puberty)

Could be:

  • True central puberty (progressive, growth acc, bone age advances)
  • Benign premature thelarche (minimal development, not progressive)
  • Peripheral estrogen source i.e ovarian cyst or tumor
  • Exogenous estrogen (hormonal meds or essential oils)
33
Q

What does premature pubarche indicate and what are some causes?

A

Indicates androgen exposure

Girls:
- Premature adrenarche (no breast development)

Boys:

  • Premature adrenarche (<3ml testis)
  • True puberty (>3ml testis, testosterone elevated)

Or:

  • Abnormal secretion: Tumor, CAH
  • Exogenous: Meds, body building drugs
34
Q

What is late puberty?

A

> 13 in girls, >14 in boys

- Usually is just exaggerated constitutional delay of growth and development (normal)

35
Q

What are some causes of late puberty?

A

Hypogonadotrophic hypogonadism
- I.e pituitary malformation, pituitary damage, kallmann syndrome (cant smell)

Primary hypogonadism
- i.e turner syndrome, klinefelter syndrome, (LH and FSH will be high)

MBCHB3: Reproduction, Development and Ageing (24 decks)

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