UW. Precoucious puberty Flashcards
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> what evaluate?
BONE AGE
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> NORMAL BONE AGE –> what evaluate?
bone and pubic hair
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> NORMAL BONE AGE –> Isolated breast development –>?
PREMATURE THELARCHE
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> NORMAL BONE AGE –> Isolated pubic hair development –>?
PREMATURE ADRENARCHE
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> ADVANCED BONE AGE –> what evaluate?
LH levels
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> ADVANCED BONE AGE –> HIGH LH -> ????Dx
Central precocious puberty (eg idiopathic, CNS tumor)
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> ADVANCED BONE AGE –> LOW LH -> what test to do?
GnRH stimulation test
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> ADVANCED BONE AGE –> LOW LH -> GnRH stimulation test -> HIGH LH ->?DX
Central precocious puberty (eg idiopathic, CNS tumor)
UW. precoucious puberty algorithm.
Early secondary sexual development (girls <8y.o; boys <9y.o) -> ADVANCED BONE AGE –> LOW LH -> GnRH stimulation test -> LOW LH ->?DX
PERIPHERAL PRECOCIOUS PUBERTY (eg nonclassic congenital adrenal hyperplasia, gonadal/adrenal hyperplasia)
UW. precocious puberty age for girl?
<8
UW. precocious puberty age for boy?
<9
UW. High levels of androgens and estrogens also promote increased bone formation and cartilage growth, which leads to early pubertal growth spurts (increased height velocity) and advanced bone age.
However, estrogen stimulates growth plate closure, so patients will often have shorter than expected adult height.
UW. Why kids with precocious puberty will have shorter adult height?
However, estrogen stimulates growth plate closure, so patients will often have shorter than expected adult height.
UW. Central PP is distinguished from peripheral PP by an ….?
elevated LH level at baseline (due to hypothalamic secretion of GnRH) or following stimulation with a GnRH agonist.
UW. elevated sex hormones in patients with peripheral PP suppress LH levels via negative feedback.
.
UW. when suspect central - do what?
Patients with central PP require an MRI of the brain to evaluate for hypothalamic or pituitary tumor.
UW. Once a CNS tumor is excluded, the primary treatment for idiopathic central PP is …..???
GnRH agonist therapy, which prevents premature epiphyseal plate fusion and maximizes adult height potential.
UW. Secondary sexual characteristics include breast tissue (stimulated by estrogens), as well as acne, adult-type body odor, and pubic and axillary hair (stimulated by androgens)
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UW. cause of central PP?
results from early activation of the hypothalamic-pituitary-gonadal (HPG) axis. Pulsatile GnRH secretion stimulates elevated FSH and LH levels, as seen in this patient.
UW. cause of peripheral PP?
Caused by gonadal or adrenal release of excess sex hormones. Basal levels of FSH and LH are typically low due to negative feedback and remain low following GnRH agonist stimulation.
UW. If MRI negative –> ?
If MRI is negative, the cause is most likely idiopathic precocious puberty, and GnRH therapy can be initiated.
GnRH desensitizes the pituitary and suppresses FSH and LH secretion to slow pubertal progression and maximize height potential.
UW. how bone is evaluated?
assess skeletal maturity via x-ray examination of the wrist and differentiate true precocious puberty (advanced bone age) from isolated premature thelarche/adrenarche (normal bone age).
UW. advanced bone age SD?
advanced bone age (>2 standard deviations above chronologic age)
UW. ). Nonclassic CAH is typically due to??
A partial 21-hydroxylase deficiency, in which adrenal glucocorticoid and mineralocorticoid synthesis is low but adequate, preventing the adrenal crises and salt wasting seen in classic CAH.
Instead, symptoms are due only to excess 17-hydroxyprogesterone, which is converted to adrenal androgens, causing premature development of secondary sexual characteristics. Because the HPG axis is not activated prematurely, testicular volume is often at a prepubertal stage at presentation. Nonclassic CAH tends to present in childhood rather than in infancy (as with classic CAH
UW. Obese children are at high risk for precocious development as adiposity can trigger ….?
excess insulin production, which then stimulates the adrenal glands to produce sex hormones.
UW. Isolated premature adrenarche is caused by?
by early activation of adrenal androgens.
UW. Isolated premature adrenarche CP?
body odor, oily skin, acne, and pubic and axillary hair.
UW. Isolated premature adrenarche estrogen and testosterone levels?
levels remain normal
therefore, there are no other signs of premature puberty (eg, breast development, testicular enlargement) or virilization (eg, clitoromegaly).
UW. Isolated premature adrenarche is generally benign but a risk factor for developing polycystic ovary syndrome, type 2 diabetes mellitus, and metabolic syndrome, especially in obese patients.
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