Lec 12 - Puberty Flashcards
what is puberty
when immature individual acquires the physical and behavioural attributes which will allow them to reproduce
what released from hypothal to trigger gonadotrophin release from apg
gonadotrophin releasing hormone (GnRH)
the 2 gonadotropins
Luteinising Hormone (LH)
Follicle Stimulating Hormone (FSH)
what do gonadotropins do to the gonads
stimulate gonads to:
1. produce/mature gametes
2. sex steroids release
what are male sex steroids
mainly androgens
e.g. testosterone
what are female sex steroids
mainly oestrogen and progesterone
what do sex steroids do
play a role on gonads themselves,
also have endocrine role:
- accessory reproductive organs
- secondary sexual characteristics
what happens during juvenile pause
- CNS dampens the GnRH pulse generator in the hypothalamus
- So = low gnhr activity
And low gonadotrophin production - also sensitive negative feedback from sex steroids
where is the GnRH pulse generator likely to be
hypothalamus = probably in arcuate nucleus
how is puberty initiated
inhbition from CNS released (mechanism unknown)
low level pulses of GnRH begin
and the sensitivity to negative feedback decreases
what kind of rhythm is gonadotropin released in
early on in puberty, has diurnal release (at night)
later on the dirunal release is lost
what is adrenarche
contribution of adrenal gland to puberty
= start of production of androgens
what are the androgens produced by adrenal gland
androstenedione
DHEA
what does androstenedione and DHEA get converted to
- testerone
- DHT = potent version of testosterone
(is converted in peripheral tissues)
what is the trigger for adrenarche
not sure of the trigger:
- independent of ACTH and cortisol
- may be indicated to IGF1 and growth hormone
- But people you have Addison’s disease (no adrenal function) STILL go into puberty, so not essential
first sign of puberty in males
Growth of testes usually first sign
- increasing mass of seminiferous tubules
- controlled by testosterone
Pubic hair development
what system used to assess puberty in males and females
Tanner grading system
progression of puberty in males
- No pubic hair; testes < 2.5cm
- Hair at base of penis; testes > 2.5cm
- Hair spread & coarser; testes & penis growth
- More hair but no spread to thighs; further
enlargement of testes & penis - adult appearance achieved
male secondary sexual characteristics
Other secondary sexual characteristics
increased laryngeal size
deepening of the voice
increased bone mass
increased mass & strength of skeletal muscle
thickened skin
increased & thickened hair on trunk, axillae & face
(last characteristic to appear – fully mature at age 25)
first sign of puberty in females
Breast development usually first sign
controlled by estrogen
= maybe asymmetrical
Pubic hair development
- controlled by testosterone
puberty in females developmetn
Preadolescent
Breast bud
Enlargement of breast & areola
Protruding 2º mound of areola
Adult size; recession of areola
other secondary sexual characteristics in females
keratization of vaginal mucosa
enlargement of labia minora and majora
uterine enlargement
increased fat deposition in hips & thighs
average age of menarche
12.8 +or- 1.2 in Caucasian girls
usually at tanner stag 4
what sex hormone increases GH secretion
estrogen
(in males, androgens would get aromatised to estrogen)
how do sex steroids directly afffect height
affect epiphysial plate
AR and ER expressed in all zones
what 2 things account fo the diff in male and female height
- 2 years earlier in girls (so males get 2 extra years of growth at childhood rate)
- girls have slower rate of growth during spurt
how has age of menarche changed over time
decreased from avg age of ~17 in 1800s to about 12-13 now (in developed countries)
what might the decrease in age of menarche be caused by
improved socioeconomic stability and nutrition
- possibly need particular body weight for puberty to occur
what is delayed/advanced puberty associated with
malnutriotion
elite athletes
= delayed
moderate obesity
= advanced
evidence that estrogen is locally produced in growth plate
transplant of growth plate from one animal to another
= found that closure of growth plate depended on donor and not recipient
= indicating locally produced estrogen
how come leptin was indicated as a possible hormone that triggered onset of puberty after certain weight reached
- expressed in adipose tissue
- levels increase at start of puberty
- k/o mice have low Gn levels & underdeveloped gonads
- similar phenotype in humans with mutations in leptin or receptor
- abnormalities reversed by leptin therapy
why is leptin NOT directly the trigger
not expressed by GnRH neurones
what is kisspeptin produced by
CNS = infundibular neurones
Peripheray = gonads, GI tract, placenta
where does kisspeptin act
at GPR54 = which is expressed by GnRH neurones
and stimulates GnRH release
what are mutations in GPR54 linked to
delayed puberty
how might kisspeptin be regulated by leptin
leptin receptor exists in kiss1 neurones
what is consitutional delay in puberty
normal delayed puberty in comaprison ot peers
(late bloomers)
what can gonadotropin deficiency be caused by
e.g. tumour
what can gonadal failure lead to
low sex steroids = low negative feedback so can lead to high Gn
what can gonadal failure be caused by
chemotherapy
what is precocious puberty
too early
caused by premature activation of HPG axis
what can precocious puberty be caused by
brain damage e.g.
Tumour, meningitis, head trauma
