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Human development block > Puberty > Flashcards

Puberty Flashcards

1
Q

Which hormones control puberty?

A
  • GnRH
  • LH
  • FSH
  • Neuroendocrine hormones
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2
Q

Which female steroid hormones are involved in puberty

A
  • Oestradiol
  • Progesterone
  • Adrenal androgen precursors
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3
Q

Which male steroid hormones are involved in puberty?

A
  • Testosterone
  • Dihydrotestosterone( DHT)
  • Adrenal androgens
  • Oestradiol
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4
Q

What does testosterone get aromatised to?

A

Oestrogen—> This gives us our growth spurt( growth plates fuse together)

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5
Q

Define gonadarche

A

Activation of the gonads by the pituitary hormones FSH-LH

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6
Q

Define adrenarche

A

Increase in production of androgens by the adrenal cortex

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7
Q

Define Thelarche

A

Appearance of breast tissue—-> oestradiol(ovaries)

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8
Q

Define Menarche

A

First menstrual bleed-oestradiol on endometrial lining-non ovulatory

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9
Q

Define spermarche

A

First sperm production- nocturnal sperm emissions FSH,LH—> testosterone

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10
Q

Define pubarche

A
  • Appearance of pubic hair —> androgens from adrenal gland
  • First appearance of axillary hair, apocrine body odour& acne
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11
Q

What is estradiol responsible for?

A
  • Breast development
  • Growth acceleration
  • Skeletal maturation
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12
Q

What is estradiol together with progesterone responsible for?

A

-Menstruation

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13
Q

Outline the hypothalamic-pituitary-ovarian axis

A
  • Hypothalamus releases GnRH which stimulates the gonadotroph cell
  • The gonadotroph cell releases FSH&LH which stimulate folliculogenesis in the ovary
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14
Q

Which hormones inhibit the activity of the gonadotroph in females?

A
  • Inhibin
  • Progesterone
  • Estrogens ( primarily estradiol)
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15
Q

Outline the hypothalamic-pituitary-testicular axis

A
  • Hypothalamus releases GnRH which stimulates the gonadotroph cell
  • The gonadotroph cell releases FSH&LH which stimulate spermatogenesis in the testis
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16
Q

Which cells produce testosterone?

A

The Leydig cells of the testis

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17
Q

Which hormones inhibit the activity of the gonadotroph in males?

A

-Inhibin B

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18
Q

Which hormones inhibit the activity of the hypothalamus in females?

A
  • Progesterone

- Estogens (primarily estradiol)

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19
Q

Which hormones inhibit the activity of the hypothalamus in males?

A

-testosterone

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20
Q

Describe the pattern of testosterone conc on a graph

A
  • Spikes
  • As you go on in puberty, the spikes become higher& bigger and they become diurnal
  • Girls also get oestrogen which also spikes but not to the same extent
21
Q

Outline the tanner stages for genitalia

A
  1. ) Pre-pubertal
  2. ) Beginning of onset of puberty; testes enlarges from 3ml–>4ml
  3. ) darker colour-redness
  4. ) even darker and larger,scrotal sac comes down more
  5. ) darkest and largest
22
Q

Outline the tanner stages for pubic hair in boys

A
  • 5 stages
  • 5 has the most pubic hair
  • Pubic hair starts at the base of the penis
23
Q

Outline the mammary/breast tanner stages

A
  • 5 stages
  • gradual growth of breast tissue
  • areolar+ nipple increase in size
  • 5th stage: theres is a smooth contour of the breast; the growth is complete
24
Q

What is one of the first testicular difference in puberty for boys

A

Testicular stages increases from 3ml to 4ml

25
Q

Outline the tanner stages for pubic hair in females

A
  • 6 stages
  • gradual increase in amount of pubic hair
  • Starts along the labial line
  • If it starts elsewhere it isnt true puberty
26
Q

What pubertal tanner stages exist for boys?

A
  • (A) Axillary hair( A1-A3)
  • (P) Pubic hair (P1-P5)
  • (G) Genitalia (G1-G3)
27
Q

Which pubertal tanner stages exist for girls?

A
  • (A) Axillary hair (A1-A3)
  • (P) Pubic hair (P1-P6)
  • (B) Breast development (B1-B5)
  • (M) Monarche; menstrual, the onset of the menses (M1-M2)
28
Q

What determines pubertal timing ?

A
  • Genetics eg mum& daughter have their period around the same time
  • Environment eg insectides, pesticides, hormone disrupters, phytooestrogens found in soya milk
  • Nutritional status eg anorexia delays it
  • Health status eg immunocomprimisation
29
Q

What other changes apart from those outlined by the tanner stages, are associated with puberty?

A
  1. ) Anaemia
    - more likely in girls
  2. ) Gynecomastia
  3. ) Acne
    - caused by androgenic stimulation
    - Higher serum levels of dehydroepiandrosterone sulfate( DHEAS)
30
Q

What is precocious puberty?

A
  • 2 or 2.5 SD earlier than the population norms
  • May range from variants of normal development to pathologic conditions; may be genetics
  • BOYS: before 9yrs
  • GIRLS: before 8yrs
31
Q

What is true central precocious puberty (TCPP)?

A
  • Gonadotrophin dependent
  • Early maturation of the HPG axis
  • Sequential maturation
  • Pathologic 40-75% of boys
  • Pathologic in 10-20% of girls
  • Sexual characteristics are appropriate for the child’s gender
32
Q

What is peripheral precocity?

A
  • Gonadotrophin independent
  • Excess of secretion of sex hormones-gonads,adrenal glands, exogenous sources of sex steroids, ectopic production of gonadotropin from a germ cell tumor
  • Non sequential maturation
  • Isosexual or contrasexual
33
Q

What are benign pubertal variants?

A

-Premature thelarche
-Isolated androgen-mediated sexual characteristics
( precocious adrenarche)
-Can be a variant of normal puberty

34
Q

What are the characteristics of central precocious puberty

A
  • Accelerated linear growth
  • Advanced bone age
  • Pubertal levels of LH
  • Pubertal levels of FSH
35
Q

What causes TCPP

A
  1. )Idiopathic
  2. )CNS lesions- neurogenic TCPP
    - Hamartomas
    - other cns tumours: astrocytomas,ependyomas, pinealomas, optic& hypothalamic gliomas
    - CNS irradiation
    - other CNS lesions: hydrocephalus, cysts, trauma, CNS inflammatory disease, congenital midline defects
  3. ) Genetics
    - Gain of function mutation in the KISS1 &KISS1R
  4. ) Previous excess sex steroid exposure/miscellaneous
    - Priming from adrenarche
    - Mc cune albright
    - Extreme prematurity
  5. )Pituitary gonadotrophin-secreting tumours
    - Elevated levels of LH& FSH
36
Q

What causes peripheral precocity in girls?

A
  1. ) Ovarian cysts
    - most common
    - breast development, vaginal bleeding-Ovarian torsion
  2. ) Ovarian tumours
    - Rare cause
    - Granulosa cell tumors—> isosexual precocity
    - Sertoli/leydig cell tumours, pure leydig cell tumours, gonadoblastoma—> contrasexual precocity( virilisation)
37
Q

What causes peripheral precocity in boys?

A
  1. ) Leydig cell tumors
    - asymmetric testicular enlargment
    - Testosterone secreting tumor, benign
    - Rx usually radical orchiectomy
  2. )Germ cell tumours
    - they secrete hCG
    - hCG secretion activates LH receptors on Leydig cells—> testosterone production
    - located in gonads,brain,liver,retroperitoneum, anterior mediastinum
  3. ) Familial male-limited precocious puberty (testotoxicosis):
    - Activating mutation in the LH receptor gene—> premature Leydig cell maturation& testosterone secretion
38
Q

What consequences can primary hypothyroidism have on puberty?

A
  • Early breast development, galactorrhoea, recurrent vaginal bleeding-premature testicular enlargement
  • Cross-reactivity & stimulation of the FSH receptor by high serum TSH levels -common alpha subunit
39
Q

Outline McCune Albright syndrome

A
  • Triad of peripheral precocious puberty, irregular cafe au lait spots, fibrous dysplasia of bone
  • Sequence of pubertal progression may be abnormal often presenting with vaginal bleeding
  • Tends to be within the midline, not crossing over
40
Q

What is premature thelarche?

A
  • A benign pubertal variant
  • Idiopathic
  • Arounds 2yrs of age
  • waxes and wanes, doesn’t progress
  • Isolated breast development/ Not beyond tanner stage 3
  • Absence of other secondary sexual characteristics
  • Normal height velocity for age
  • Normal or near normal bone age
  • LH& FSH between normal range
41
Q

What is premature adrenarche?

A
  • Pubic &/or axillary hair—> pubarche
  • Acne, BO, greasy skin
  • Mild increase in growth velocity& advanced bone age
  • Mild elevation in serum DHEAS for age
  • More common in girls, Afro caribbean & hispanic females
  • In patients with obesity & insulin resistance
  • Risk factor for later development of PCOS in girls
  • Can cause priming resulting in TCPP
42
Q

How can we treat premature preocity

A
  • Depends on cause
  • Reasurrance if it’s normal benign variation
  • Gonadotrophin independent: Anti-androgens/aromatase inhibitors
  • Gonadotrophin dependent : block with GnRH analogues
43
Q

Outline delayed puberty in girls

A
  • 13 yrs old and no breast development
  • No pubic hair by 14 yrs
  • More than 5 years between thelarche& menarche
  • No menarche by 16 years old without secondary sexual characteristics
44
Q

Outline delayed puberty in boys

A
  • Testicular volume less than 4ml by age 14
  • No pubic hair by 15 yrs old
  • More than 5 yrs to finish penile and testicular growth
45
Q

What are the different forms of gonadal failure

A
  1. ) Primary failure
    - hypergonadotrophic hypogonadism
    - increased levels of FSH&LH stimilating the gonads
    - Gonads not working; increased LH& FSH levels due to hypothalamus and pituitary still working
  2. ) Secondary failure:
    - hypogonadotrophic hypogonadism
    - hypothalamus/pituitary stops working so no testosterone release—> no stimulation of gonads
    - May stop due to trauma to the brain or craniofacial anomalies
46
Q

Explain the different types of secondary hypogonadism

A
  • Normal/low gonadotrophins
  • hypogonadotropic hypogonadism
    1. ) Congenital:
  • craniofacial anomalies/midline defects
  • GnRH deficit (eg Kallman, Prader Willi, Alteration of GnRH receptor)
    2. ) Acquired:
  • function loss: Eating disorders/athletes; chronic illness; Cushing;diabetes;hyperprolactinaemia;hypothyroidism
  • Physical: CNS tumors; Infiltrative disease; head trauma; head radiation
47
Q

What are the hypogonadotrophic hormones?

A

GnRH
FSH
LH

48
Q

Explain the different types of primary hypogonadism

A
  • High gonadotrophins
  • hypergonadotrophic hypergonadism
    1. ) Congenital:
  • Chromosome anomalies: Turner syndrome; Klinefelter syndrome
  • Testicular regression syndrome
  • Synthesis & action of sexual steroids
    2. ) Acquired:
  • surgery/trauma
  • chemo/radiotherapy
  • Autoimmune
  • Post infection
  • Metabolic galactosemia
49
Q

How can we diagnose delayed/early puberty?

A
  • Clinical history
  • growth charts
  • family history
  • Exercise,chronic illness, food habits
  • LH, FSH, testosterone, oestrogens, prolactin, TSH, karyotype
  • Bone age, brain MRI, pelvic Ultrasounds

Human development block (35 decks)

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