Endocrinology- Puberty, Metabolism and other hormones Flashcards
Define Precocious puberty. What is the initial evaluation
Onset of secondary sexual characteristics (breast tissue, acne, pubic/axillary hair) in girls <8 and boys <9.
Bone age evaluation to asses skeletal maturation is initial assessment
what are precocious puberty signs of excess androgens
acne
body odor
axillary and pubic hair
what are precocious puberty signs of excess estrogen
breast development
Vaginal bleedings
Premature epiphyseal fusion
advanced bone age
When would abdomina/ pelvic U/S be indicated for precocious puberty?
Concern for peripheral production of endogenous hormones (ovarian/ adrenal tumor).
Findings: advance bone age with suppressed LH& FSH levels
Hypothyroidism and precocious puberty
TSH activates FSH receptor–> increased estrogen.
Presents with signs of hypothyroidism, great tissue, vaginal bleeding.
Diagnosis: Precocious puberty, normal bone age, pubic hair, obesity
Premature adrenarche
Early activation of adrenal androgens: Adipose tissue –> XS insulin –> adrenal glands produce ↑ sex hormones
Diagnosis: precocious puberty, advanced bone age, elevated FAH and LH
Central precocious puberty
causes of central precocious puberty
hypothalmic glioma,
pituitary hamartoma,
pituitary microadenoma
Idiopathic precocious puberty
Test for central precocious puberty
LH elevated at basal or becomes elevated after GnRH stimulation.
Diagnosis: precocious puberty, advance bone age, low LH even with stimulation
Peripheral precocious puberty
Causes of peripheral precocious puberty
non classic congenital adrenal hyperplasia
congenital adrenal hyperplasia
Mechanism of [nonclassic] congenital adrenal hyperplasia in precocious puberty
21-hydroxylase deficiency impart conversions of 17-hydrxyprogesterone to 11-deoxycortisol.
17-hydroxyprogesterone is shunted toward adrenal androgen over production
Key findings of non classic congenital adrenal hyperplasia
in non classic CAH sufficient glucocorticoid and mineralocorticoid levels are maintained therefore patients have normal electrolytes
PCOS malignancy risk
Decreased progesterone due to chronic anovulatory cycles causes unbalanced endometrium proliferation by estrogens.
Increased risk for endometrial hyperplasia and cancer
S&S refeeding syndrome
Arrhythmia CHF Pulmonary edema Peripheral edema Seizures Wernikie encephalopathy