Endocrinology- Puberty, Metabolism and other hormones Flashcards

1
Q

Define Precocious puberty. What is the initial evaluation

A

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

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2
Q

what are precocious puberty signs of excess androgens

A

acne
body odor
axillary and pubic hair

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3
Q

what are precocious puberty signs of excess estrogen

A

breast development
Vaginal bleedings
Premature epiphyseal fusion
advanced bone age

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4
Q

When would abdomina/ pelvic U/S be indicated for precocious puberty?

A

Concern for peripheral production of endogenous hormones (ovarian/ adrenal tumor).

Findings: advance bone age with suppressed LH& FSH levels

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5
Q

Hypothyroidism and precocious puberty

A

TSH activates FSH receptor–> increased estrogen.

Presents with signs of hypothyroidism, great tissue, vaginal bleeding.

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6
Q

Diagnosis: Precocious puberty, normal bone age, pubic hair, obesity

A

Premature adrenarche

Early activation of adrenal androgens: Adipose tissue –> XS insulin –> adrenal glands produce ↑ sex hormones

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7
Q

Diagnosis: precocious puberty, advanced bone age, elevated FAH and LH

A

Central precocious puberty

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8
Q

causes of central precocious puberty

A

hypothalmic glioma,
pituitary hamartoma,
pituitary microadenoma
Idiopathic precocious puberty

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9
Q

Test for central precocious puberty

A

LH elevated at basal or becomes elevated after GnRH stimulation.

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10
Q

Diagnosis: precocious puberty, advance bone age, low LH even with stimulation

A

Peripheral precocious puberty

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11
Q

Causes of peripheral precocious puberty

A

non classic congenital adrenal hyperplasia

congenital adrenal hyperplasia

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12
Q

Mechanism of [nonclassic] congenital adrenal hyperplasia in precocious puberty

A

21-hydroxylase deficiency impart conversions of 17-hydrxyprogesterone to 11-deoxycortisol.

17-hydroxyprogesterone is shunted toward adrenal androgen over production

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13
Q

Key findings of non classic congenital adrenal hyperplasia

A

in non classic CAH sufficient glucocorticoid and mineralocorticoid levels are maintained therefore patients have normal electrolytes

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14
Q

PCOS malignancy risk

A

Decreased progesterone due to chronic anovulatory cycles causes unbalanced endometrium proliferation by estrogens.

Increased risk for endometrial hyperplasia and cancer

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15
Q

S&S refeeding syndrome

A
Arrhythmia 
CHF
Pulmonary edema 
Peripheral edema
Seizures 
Wernikie encephalopathy
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16
Q

mechanism of refeeding syndrome

A

Increased insulin activity causes electrolyte derangement as the body shifts from prolonged catabolism to anabolism.

Increased cellular uptake of phosphorous (main deficient), K and Mg.