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19 Cards in this Set

  • Front
  • Back
What characterizes PCOS?
Chronic anovulation w/ formation of multiple ovarian cysts.
Why is there hyperandrogenism in PCOS?
There is increased pituitary stimulation by GnRH which leads to increased production of LH but not FSH.
What are the most common clinical manifestations of PCOS?
Infertility, hirsutism, amenorrhea, and obesity.
Why are there also increased levels of estrone in addition to androgen in PCOS?
Peripheral conversion of androgen results in increased estrogen. There is an increase in "circulating" estrogen NOT "total" estrogen because the polycystic ovary does not secrete increased estrogen. Also, SHBG is decreased due to the inc androgen.
What's the role of the increased levels of free estradiol in PCOS?
The increased free estradiol contributes to the abnormal gonadotropin secretion by increasing the pituitary sensitivity to GnRH.
What are the results of the increase levels of LH and relatively decreased levels of FSH in PCOS?
The elevated LH level increases androgen level and results in anovulation. The decreased FSH decreases the aromatase activity, which causes androgen to accumulate in the follicle causing atresia. The consequence is absence of a dominant follicle and development of multiple small follicles which become atretic.
Why are there also increased levels of ADRENAL steroid production in PCOS?
There is increased ACTH.
What is Late Onset CAH due to?
It is the result of allelic variants of enzyme deficiencies.
What do patients w/ LOCAH exhibit?
Elevated levels of adrenal androens, hirsutism, and irregular ovulation.
What is the genetic explanation for pts w/ LOCAH caused by 21-hydroxylase deficiency.
The 21-hydroxylase enzyme is coded for by chormosome 6 and is closely linked to the HLA-B locus. Homozygotes for the mild allele, and heterozygotes for one severe and one mild allele present w/ LOCAH.
How can we screen for LOCAH caused by 21-hydroxylase deficiency?
A 17-hydroxyprogesterone (17-OHP4) level drawn during the follicular phase is useful for screening. Low levels (<3 ng/ml) rule out 21-hydroxylase deficiency. High levels (>8 ng/ml) are diagnostic.
What are the characteristics of the typical patient presenting w/ Cushing's Syndrome?
30-40 yrs old, obese, hypertensive, with purple striae on the skin.
What's the first step in diagnosing Cushing's Syndrome?
A 24 hr urine collection looking for free cortisol.
What's an alternative to the 24 hr urine test in diagnosing Cushing's Syndrome?
The dexamethasone suppression test. Dexamethasone is given at midnight, and plasma cortisol level is drawn at 8 am. Low values (<6 ug/dl) rule out Cushing's. High values (>10 ug/dl) are diagnostic.
What is the second step in diagnosing Cushing's Syndrome?
The low-dose dexamethasone suppression test. Pts are given 2 mg of dexamethasone every day for 2 days. In pts w/ Cushing's, regardless of etiology, cortisol secretion is NOT suppressed in response to the low dose.
What are the levels of ACTH in a pt w/ a cortisol secreting tumor?
The ACTH levels are low.
What are the levels of ACTH in a pt w/ an ACTH secreting tumor?
The ACTH levels are high.
What is the high-dose dexamethasone suppression test used for?
To determine the source of plasma ACTH.
What is the metyrapone test?
Metyrapone inhibits cortisol synth at several steps. ACTH-producing pituitary adenomas (and normal pts) respond to a decrease in cortisol by increasing ACTH production. Non-pituitary tumors producing ACTH cause profound suppression of the hypothalamic-pituitary axis, and there is no increase in ACTH in response to metyrapone.