Adolescent Gynaecology Flashcards

1
Q

Puberty

A
  • Usual onset between 8-14 years
  • Secondary sexual characteristics <8 years = Precocious puberty or Menarche <9 years
  • Nil secondary sexual characteristics > 14 years =delayed puberty
  • Primary amenorrhoea = nil menarche by age 16 years despite normal Secondary sexual characteristics
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2
Q

Progression of puberty

A

Telarche (Breast development) - Adrenarche (Hair development: Independant of HPO axis and usually follows telearche by few months) - Menarche ( Onset of menstruation, Usually 2-3 years post telarche)

Breast and Hair development assessed using Tanner staging system from stage 1 (Nil) to stage v ( adult pattern)

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3
Q

Delayed Puberty

A
  • Hypergonadotrophic Hypogonadism: gonadal failure
    Normal Karyotype: POF, Chemo, radiation, autoimmune, galactosaemia
    Abnormal Karyotype: Turners 45X0 or Swyers 46XY with abnormality SRY gene
  • Hypogonadotrophic Hypogonadism
    Reversible: Familial/constitutional, Intracranial tumour (Pituitary adenoma, craniopharyngioma), weight loss/anorexia/excessive exercise, Primary Hypothyroidism
    Irreversible:
    Chronic illness
  • Diabetes
  • Renal impairment
  • Cystic fibrosis
  • Crohn’s disease
  • Coeliac disease
    Kallman’s syndrome
  • 1:7500
  • X-linked mutation of Kal-1 gene
  • Dysgenesis of olfactory bulbs and GnRH neurones
  • Causes delayed puberty associated with anosmia
    Sheehan’s syndrome
    Panhypopituitarism
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4
Q

Management Delayed Puberty

A

Hypo/Hypo:
- Treat underlying cause if known/possible
-Pulsatile gonadotrophins via subcutaneous pump or puberty induction as described below
- Consider ceasing treatment intermittently if cause unknown to see if spontaneous menstruation occurs
- Fertility – can have ovulation induction
Hyper/Hypo:
Puberty induction
Low-dose oral oestrogen (ie 2mcg EE)
Increase dose every 6 months
Once breakthrough bleeding occurs and breast development complete add progesterone
* Cyclical HRT or cOCP
o Fertility
Requires oocyte donation for fertility

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5
Q

Precocious puberty

A
  • Central precocious puberty (gonadotrophin dependent) 80%
    o ‘True’ precocious puberty, usually idiopathic
    o Rarely due to brain tumours/CNS malformations
    o Elevated FSH/LH
  • Peripheral precocious puberty (gonadotrophin independent)
    o Pseudopuberty, always pathological
    o Hormone-producing ovarian tumours – ie granulosa cell tumour
    o Exogenous oestrogen exposure
    o Congenital adrenal hyperplasia
    o McCune-Albright Syndrome
  • Genetic mutation
  • Polyostotic fibrous dysplasia and café-au-lait spots
    o Hypothyroidism (elevated TSH stimulating FSH receptors)
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6
Q

Management Precocious puberty

A
  • Treat cause if known
  • Aim: Slow growth to achieve maximal adult height, attenuate and diminish established precocious characteristics, achieve maximal adult health, facilitate avoidance of abuse
  • Central causes
    o Continuous GnRH agonist administration
    o Downregulates pituitary GnRH receptors and suppresses LH/FSH production
  • Peripheral causes
    o Treat underlying cause
    Minimal treatment options available for McCune Albright
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