Flashcards in Pediatric Growth and Puberty Deck (27):
What hormone mediates the following growth phases: intrauterine, early infancy, childhood, pubertal growth?
intrauterine: IGF-1, IGF-2
early infancy: nutrition (via insulin and IGFs)
childhood: GH (thyroid hormone required)
pubertal growth: androgens stimulate growth and estrogens stimulate GH secretion and growth plate closure
Describe the hormonal control of GH.
GHRH tonically stimulates, somatostatin comes and goes, controls most of the pulsatile secretion, occuring primarily at night
How does GH act on bone metabolism?
increases osteoclast differentiation and activity
increased osteoblast activity
increase in bone mass by endocrine bone formation
promotes epiphyseal growth, stimulates differentiation of prechondrocytes and the local expression of IGF-1 which increases clonal expansion of osteoblasts
How does GH act on adipose tissue?
has insulin-like effects:
inhibits lipoprotein lipase (LPL)
stimulate hormone sensitive (HSL)
decreases glucose transport
How does GH act on muscle?
increases amino acid transport
increases nitrogen retention
increases metabolically active tissue and increases energy expenditure
may effect muscle fiber distribution
What factors impact intrinsic/genetic height potential?
family tendency: mid-parental height
genetic/epigenetic factors: birth size, syndromes and mutations, body proportions
What is genetic channeling?
phenomenon that birth length is not predictive of adult height and children will fall into their MPH growth curve as they finish out their first year
What are the features of constitutional delay in growth and puberty?
attenuated post-natal puberty
delayed bone age
normal growth rate
exaggerated per-pubertal growth deceleration
delayed puberty onset
normal adult height
frequent family history of "late bloomers"
What are the features of familial short stature?
normal/near normal growth rate
bone age approximates chronological age
growth trajectory fits parental heights
body proportions show mild short limb-ness
Give examples of non-familial intrinsic short stature.
cranial spinal radiation
(bone and chronological age same, velocity is near normal, and ***height trajectory is below mid-parental height)
What are the features of attenuated growth?
growth rate is slow for age (downward crossing percentiles)
bone age is delayed in proportion to growth deceleration
How might you differentiate between endocrine and disease state causes of attenuated growth?
if stature is affected more than weight, consider and endocrine problem
if stature is affected less than/equal to weight, consider underlying disease
What labs are important for evaluation of attenuated growth?
TTG, ESR (celiac and IBD chronic disease)
dynamic evaluation of GH/IGF+/- pubertal axis
What are treatments available for GH deficiency?
daily subcutaneous injections of recombinant hGH
(better outcome with early initiation, higher dose and delay in puberty)
treatments are expensive and vary often by access
What are features of accelerated growth?
seen as upward crossing of percentiles
over-nutrition is the most common cause (weight will be effected earlier and more severely than height)
can include conditions: precocious puberty, hyperhthyroidism, familial or Klinefelter's syndrome, GH excess
Contrast adrenarche and gonadarche.
andrenarche: manifestations of adrenal androgens
gonadarche: response of ovaries/testicles to nocturnal LH secretion
What substance is through to initiate the production of GnRH in puberty?
What initiates breast development and pubic hair development?
breasts- estrogen exposure
pubic hair- androgen exposure
Describe the tanner stages of breast development.
II- breast budding
III- continued enlargement
IV: areola and papilla form secondary mound
V: mature female breasts
What age of breast development, menses or start of puberty in men would you consider delayed?
> 13.5 years for breasts
> 15.5 years for menses
> 15 yrs in boys
Describe the characteristics of premature thelarche with premature adrenarche. (hormones, bone age and onset of true puberty)
no gondatropin activation
minimal/no growth or bone age acceleration
normal onset of true puberty
What is the difference between central and peripheral precocious puberty?
central precocious puberty is gonadotropin-dependent (organic causes in males- tumors, alt. source of sex steroids and females are often idiopathic)
peripheral precocious puberty is gondaotropin independent
What are the two subtypes of delayed puberty?
hypogonadotropic hypogonadism (central inactivity causes gonadotropins to be low)
hypergonadotropic hypogonadism (peripheral under activity causes lack of feedback and gonadotropins are high)
What are possible causes of peripheral precocious puberty?
sex steroid independent of the CNS can be:
gonadal origin- sex hormone secreting gonadal tumors
activating mutations of GT receptor syndromes
adrenal origin- congenital adrenal hyperplasia, virilizing adrenal tumors
What are important distinctions/ diagnostic tests for evaluating a male with precocious puberty?
must determine source of the testosterone causing puberty and distinguishing between testes and adrenals can be important, there are also liver tumors that can produce hCG
also consider familial male precocious puberty; constitutional delayed growth/puberty can be hard to distinguish from hypogonadotropic hypogonadism
Contrast primary and secondary causes of hypogonadotropic hypogonadism.
primary: hypopituitarism, Kallman syndrome
secondary: anorexia, athletic triad, male obesity, chronic disease, malnutrition, endocrine disease (hypothyroidism, hyperprolactinemia)