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18 Cards in this Set
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Polycystic Ovarian Syndrome (PCOS)
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*hyperandrogenism:
increased pulse amplitude of GnRH & incr sensitivity of ant pit to GnRH ==>inappropriate release of LH ==>hyperandrogenism |
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presentaton of Polycystic Ovarian Syndrome
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1. MC=infertility
2. 2nd MC=hirsuitism -amenorrhea>dysmenorrhea -obesity -virilization |
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do all pts PCOS pts have hirsutism?
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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)
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PCOS pts without hisutism most likely have what serum level compared to pts w/hirsutism?
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compared to pts w/hirsutism, they have lower levels of 3a-androstenediol-G (indicating decr conversion of test==>DHT)
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what is LH:FSH ratio in pts w/hirsutism?
why? |
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) |
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serum levels in PCOS
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*incr free estradiol and test
*no incr in total estradiol *high LH (but nl FSH) -incr androgen==>decr SHBG==>incr FREE estradiol and test |
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what happens to follicle in PCOS
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undegoes atresia
-tonically elevated LH and androgen==>anovulation -androgen accumulates in follicle==>atresia ==>no dominant follicle and multiple small follcles that ultimatelly become atretic` - |
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Tx PCOS if pt does not want to immediately get pregnant
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OCP's
(OCP's inhibit LH release, and SHBG) |
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Tx PCOS if woman does not want to beecome pregnancy but who cannot/chooses not to take birth control pills
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cyclic progestin therapy (to prevent endometrial hyperplasia)
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Tx PCOS for women who wish to become pregnant
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ovulation induction w/clomiphene citrate (estrogen antagonist) or gonadotropins (FSH)
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Presentation for late-onset CAH
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hirsuitism
elevated adrenal androgens irregular ovulation Lab: elevated levels of androgens |
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Et of late-onset CAH
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MCC is 21-hydroxylase def
-classic CAH assoc w/HLA-B47 -late-onset CAH assoc w/chrom 6 and HLA-B14 |
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how many "severe" alleles result in classic 21-hydroxylase def
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2 out of 3 (3 alleles code for 21-hydroxylast enzyme, producing nol, mild, and severe deficiency)
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21-hydroxylase enzyme def:
how inherited? what pop? |
auto rec;
confined to Jews in US |
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MCC Cushing's
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ACTH-secreting pit adenoma
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presentation of Cushing's
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30-40 y/o
obese hypertensive menstrual irreg, sign of hyperandrogenism xs glucose & incr insulin |
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Evaluation for Cushing's
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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 |
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metyraprone test
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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 |