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NGD > Puberty > Flashcards

Puberty Flashcards

1
Q

Normal pubertal onset

A

reactivation of HPG axis: increased nocturnal pulsatile secretion of LH and early morning secretion of gonadal steroid hormones
Appearance of an LH-predominant response during GnRH stimulation testing
usually preceded 2-3 years by a rise in adrenal androgen levels (Adrenarche) which occurs independently of GnRH

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2
Q

FSH/LH testing in childhood

A

Can’t measure since axis is shut down
over time, develop decreased sensitivity to negative feedback –> can ramp up FSH/LH to drive through puberty during adolescence

Can test during mini puberty (less than 6 mo)

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3
Q

Signs of onset of normal puberty in girls

A

85% Thelarche (breast development) first sign
15% pubarche, first outward sign
want to see thelarche first, since pubarche before thelarche is likely pathological

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4
Q

Signs of onset of normal puberty in boys

A

nearly all: gonadarche, testicular enlargement to volume >=4 cc (length >=2.5 cm), first outward sign of puberty
must palpate testicles, pubarche in isolation doesn’t count

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5
Q

Pubertal onset timing for girls

A

White NA girls:

  • thelarche mean 10
  • pubarche 10.5
  • menarche 12.9

Black NA girls

  • thelarche 8.9
  • pubarche 8.8
  • menarche 12.2

Asian girls also thought to mature earlier

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6
Q

Normal pubertal progression in girls

A

peak growth velocity at Tanner 3 (earlier than boys)
mean growth after menarche ~3 cm
breasts, pubes, flow, grow
- may get growth spurt before breasts, since estrogen is potent at the bones

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7
Q

Pubic hair Tanner staging

A 
I: none
II: sparse, pigmented, long, striahgt
III:darker, coarser, curlier
IV: adult, but decreased distribution
V: adult in quantity and type with spread to medial thighs
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8
Q

Breast development Tanner staging

A 
I: preadolescent
II: breast budding
III: continued enlargement
IV: areola and papilla form secondary mound
V: mature female breast
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9
Q

Normal pubertal onset timing for boys

A

96% between 9-14 NA boys
no significant difference between black and white males
first sign: testicular enlargement

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10
Q

Testicular volume

A

prepubertal 2.0 cm, 1-3 cc
early puberty should be around 4 cc
adult 4-6 cm, 15-25 cc

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11
Q

Normal pubertal progression for boys

A

voice breaks around age 13
axillary, facial hair appear at about age 14
gynecomastia frequent at Tanner 4 due to peak in testosterone and peripheral aromatization
peak growth velocity at Tanner 4
continued virilization into late teens

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12
Q

Growth spurt

A

Gonadal steroid hormone induced increase in GH secretion
Peak growth v at 11.5 in girls, 13.5 in boys
~15% adult height achieved in puberty
99% reached at bone age 15 in girls, 17 in boys

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13
Q

Precocious puberty Dx in girls

A

breast budding/pubic hair before 8

menarche befoer 10

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14
Q

Precocious puberty Dx in boys

A

testicular enlargement or pubic hair before 9

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15
Q

Physical examination of precocious puberty

A

follow growth curve
Tanner staging
Isosexual pubertal development (evidence of sex hormone production consistent with sex)
Contrasexual pubertal development - worrisome (clitoromegaly, hirsutism, gynecomastia - for real breast tissue, not fat)
Otehr disease processes?
- CNS disease or abnormalities
- Cafe au lait spots or other neurocutaneous lesions
- endocrine disease

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16
Q

DDx of precocious puberty

A

GnRH-dependent (always isosexual, true, central)

GnRH-independent ( can be iso or contrasexual, peripheral)

17
Q

GnRH dependent precocious puberty

A

central

idiopathic (75% girls, less than 10% boys)

18
Q

CNS lesions associated with central precocious puberty

A

Hypothalamic hamartoma (17-30% girls, 50% boys)
optic glioma (neurofibromatosis)
Craniopharyngioma, dysgerminoma, other tumors
arachnoid/suprasellar cyst
hydrocephalus
congenital defects: myelodysplasia, septo-optic dysplasia
infectious: encephalitis, abscess, meningitis, granuloma
abuse, hemorrhage, trauma, irradiation
tuberous sclerosis

19
Q

Growth in central precocious puberty

A

decreased final height due to premature fusion of epiphyses
deficit not as great as previously thought in many children
adult height lowest in those with earliest onset of puberty
- early diagnosis is important, if therapy to be effective in preserving height

20
Q

Other side effects of central precocious puberty

A

co-existing pathology

Psychological issues

21
Q

GnRH-independent precocious puberty in girls etiology

A

exogenous gonadal hormones (BCPs, estrogen creams)
- massive soy consumption?
Severe primary hypothyroidism (TSH spillover on FSH receptor)
Ovarian tumours/cysts
Adrenal tumours
McCune-Albright syndrome

22
Q

McCune-Albright syndrome

A

precocious puberty, menarche
bony lesions - polyostotic fibrous dysplasia
irregular cafe-au-lait spots
may have other autonomous endocrine tumours - toxic thyroid nodules, pituitary adenomas
may have non-endocrine invovement - hepatobiliary, cardiac

23
Q

GnRH-independent precocious puberty in boys - etiology

A

Untreated CAH
exogenous gonadal hormones (anabolid steroids)
hCG-secreting dysgerminoma/hepatoma (LH receptor)
testicular tumors
adrenal tumors
testotoxicosis (autonomous LH receptor)

24
Q

Premature thelarche

A

may appear at any age, usually younger than 5
common condition of isolated breast development that usually resolves within 6 mo - 1 year
often asymmetrical, may regress
etiology unknown - ?transient ovarian follicle
maybe the first sign of true precocious puberty
may be associated with “smoldering early puberty”
generally benign, if bone age is not advancing

25
Q

Premature adrenarche

A

usually warrants some investigation
increasingly common especially in obese girls
may also have BO, axillary hair, acne, hirsutism, acanthosis nigricans (insulin resistance)
R/O non-classical or late-onset CAH
generally benign if bone age not advancing
associated with later development of PCOS in many girls

26
Q

Gynecomastia

A

65% of normal boys at Tanner 4
resolves in 75% within a year
more noticeable in obese boys
consider possibility of Klinefelter: palpate small testicles
Also consider medications, marijuana
- usually affect liver function so estrogen levels increase

27
Q

Precocious puberty: investigations before referral

A

measure height and growth velocity carefully
bone age
TSH
LH, FSH, DHEAS, estradiol or testosterone - not always helpful
All hormone levels should be obtained as early in day as possible (pulsatile secretion)

28
Q

Precocious puberty: investigations at endocrinologist

A

GnRH stim test, look for rise of LH to >=6-8U/L (normal unactivated axis should not respond)
If central precocious puberty: MRI head
Other tests as indicated:
- Hormones: testosterone, DHEAS, estradiol
- tumors, CAH: 17-OHP, DHEAS, androstenedione, renin, aldosterone
- Boys: betahCG
- US: abdominal, testicular, pelvic
_ Cushing: 24h urine free cortisol
- Contrasexual development: karyotype

29
Q

Treatment of CPP consideration

A 
Patient's age and Tanner stage
rate of pubertal development
bone age advancement and predicted adult height
coexisting pathology
compelling psychosocial considerations
30
Q

DevoProvera

A

CPP

Injections can be given to control menstrual periods and some sexual behaviours without affecting adult height

31
Q

GnRH agonists

A

GnRH stimulates gonadotropin secretion if given in PULSES
CONTINUOUS: inhibition of gonadotropin secretion
analogues are true agonists of natural GnRH with substitutions at 6th aa
inhibit gonadotropin secretion because of prolonged half-life
can halt pubertal development and menses
absolute indication still not clear
may cause some regression of secondary sex characteristics
Appears to increase final height most in those who start puberty earliest and those wiht most advanced bone age
not currently recommended for use in girls who begin puberty at age 6-8 with slowly progressive puberty and/or acceptable predicted adult height

32
Q

Leuprolide acetate

A

The only GnRH agonist licensed for treatment of CPP in Canada
IM q3-4 weeks
requries frequnet physical monitoring of growth/bone age, pubertal progression/regression, predicted adult height

33
Q

Delayed puberty dx in girls

A

no breast development by age 13 or no menarche by age 16

absence of menarche within 5 years of pubertal onset

34
Q

Dx delayed puberty in boys

A

no increase in testicular length (>2.5 cm, volume 4 cc) by age 14

35
Q

DDx of delayed puberty

A

Hypergonadotropic:

  • ovarian/testicular dysgenesis: Turner, Klinefelters
  • Gonadal toxins: chemo/radiotherapy
  • Enzyme: 17alpha hydroxylase, 177 ketosteroid reductase
  • androgen insensitivity

Hypogonadotropic:

  • multiple trophic hormone deficiencies/isolated GH deficiency
  • Kallman: isolated GnRH deficiency
  • systemic conditions, nutrition and psychogenic, increased energy expenditure
  • other endocrine causes: hypothyroidism, GC excess, hyperPRL
  • Constitutional (CDGA)
36
Q

Investigations of delayed puberty before referral

A

measure height and growth velocity
bone age
TSH/possibly fT4, prolactin
LH, FSH helpful if elevated (hypergonadotropic hypogonadism)
Karyotype as indicated for Turner, Klinefelter

37
Q

Treatment of CDGA considerations

A

Considerations: age, Tanner stage
coexisting pathology
psychosocial

38
Q

Tx of CDGA boys

A

best - watchful waiting coupled with explanation of wide variation of pubertal development
6 mo course of low dose depot testosterone will increase growth rate by ~75%, and advance pubic hair by one stage, without deleterious effect on height potential
usually not initiated before age 13 (minimum bone age 11) otherwise puberty will not be sustained

39
Q

Tx of CDGA girls

A

minimum bone age 10 to initiate therapy
most start at ethinyl estradiol at 2.5 microg/d with max dose of 5
usually not initiated befoer age 13 (minimum bone age 11) - otherwise puberty will not be sustained

NGD (16 decks)

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