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18 Cards in this Set

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Polycystic Ovarian Syndrome (PCOS)
increased pulse amplitude of GnRH & incr sensitivity of ant pit to GnRH
==>inappropriate release of LH
presentaton of Polycystic Ovarian Syndrome
1. MC=infertility
2. 2nd MC=hirsuitism

do all pts PCOS pts have hirsutism?
no, not all have hirsutism even though they do have increased circulating androgens. they don't have hirsutism b/c they have decr conversion of test==>DHT as reflected by decr levels of 3a-androstenediol-G (DHT metabolite)
PCOS pts without hisutism most likely have what serum level compared to pts w/hirsutism?
compared to pts w/hirsutism, they have lower levels of 3a-androstenediol-G (indicating decr conversion of test==>DHT)
what is LH:FSH ratio in pts w/hirsutism?

high (LH:FSH > 3:1)
*increased adrogen synthesis by ovaries and adrenal glands (but no incr in TOTAL estradiol since polycystic ovary does not secrete estrogen)
*incr androgen==>decreased SHBG==>incr levels of FREE estradiol and test
==>incr pit sensitivity to GnRH from hypothalamus
==>tonically elevated LH (but no parallel incr in FSH)
serum levels in PCOS
*incr free estradiol and test
*no incr in total estradiol
*high LH (but nl FSH)

-incr androgen==>decr SHBG==>incr FREE estradiol and test
what happens to follicle in PCOS
undegoes atresia
-tonically elevated LH and androgen==>anovulation
-androgen accumulates in follicle==>atresia
==>no dominant follicle and multiple small follcles that ultimatelly become atretic`
Tx PCOS if pt does not want to immediately get pregnant

(OCP's inhibit LH release, and SHBG)
Tx PCOS if woman does not want to beecome pregnancy but who cannot/chooses not to take birth control pills
cyclic progestin therapy (to prevent endometrial hyperplasia)
Tx PCOS for women who wish to become pregnant
ovulation induction w/clomiphene citrate (estrogen antagonist) or gonadotropins (FSH)
Presentation for late-onset CAH
elevated adrenal androgens
irregular ovulation

Lab: elevated levels of androgens
Et of late-onset CAH
MCC is 21-hydroxylase def
-classic CAH assoc w/HLA-B47
-late-onset CAH assoc w/chrom 6 and HLA-B14
how many "severe" alleles result in classic 21-hydroxylase def
2 out of 3 (3 alleles code for 21-hydroxylast enzyme, producing nol, mild, and severe deficiency)
21-hydroxylase enzyme def:

how inherited? what pop?
auto rec;
confined to Jews in US
MCC Cushing's
ACTH-secreting pit adenoma
presentation of Cushing's
30-40 y/o
menstrual irreg, sign of hyperandrogenism
xs glucose & incr insulin
Evaluation for Cushing's
1st Step: 24-hour urine collection for free cortisol

OR Overnight Suppression Test (use Low-dose Dexamethasone):

-give low-dose (1 mg) dexamethasone (looks like cortisol):
-collect urine at 8am:

-Low cortisol (<6 mg/dl)
==>not Cushing's
-High cortisol (>10 mg/dl) are ==>Dx Cushing's

2. If Dx Cushing's, now must determine cause via high-dose dexamethasone supp test:
-administer very high does of dexamethasone:

-suppress ACTH==>pit adenoma
-does not suppress==>ectopic tumors secreting ACTH
metyraprone test
metyrapone inhibits cortisol syntehsis at several steps
*ACTH-producing pit adenoma (and nl pts) should respond to marked decr in cortisol by incr ACTH

1. 11-deoxycortisol (cortisol precursor) measured
-increased ACTH (>5 mg/dl)==>pit dz
-no incr ACTH
==>non-pit tumors producing ACTH
(there is no incr b/c non-pit tumors producign ACTH profoundly suppress hypo-pit axis==>no incr ACTH in response to metyrapone)

-3x increase in urinary 12-hydroxysteroids (cortisol precursor)==>pituitary adenoma