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41 Cards in this Set
- Front
- Back
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When a woman is exposed to excess androgens, terminal hair first appears on
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the lower abdomen and around the nipples, next around the chin and upper lip, and finally between the breasts and on the lower back.
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When a woman is exposed to excess androgens, terminal hair first appears on
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the lower abdomen and around the nipples, next around the chin and upper lip, and finally between the breasts and on the lower back.
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Treatment of androgen excess should be directed at
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suppressing the source of androgen excess or blocking androgen action at the receptor site.
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Treatment of androgen excess should be directed at
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suppressing the source of androgen excess or blocking androgen action at the receptor site.
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he following three androgens may be measured when evaluating a woman with hirsutism and virilization.
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Dehydroepiandrosterone (DHEA): a weak androgen secreted principally by the adrenal glands. (This is generally measured as dehydroepiandrosterone sulfate [DHEA-S] because of its longer half-life, making it a more reliable measure.)Androstenedione: a weak androgen secreted in equal amounts by the adrenal glands and ovaries.Testosterone: a potent androgen secreted by the adrenal glands and ovaries and produced in adipose tissue from the conversion of androstenedione.
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he following three androgens may be measured when evaluating a woman with hirsutism and virilization.
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Dehydroepiandrosterone (DHEA): a weak androgen secreted principally by the adrenal glands. (This is generally measured as dehydroepiandrosterone sulfate [DHEA-S] because of its longer half-life, making it a more reliable measure.)Androstenedione: a weak androgen secreted in equal amounts by the adrenal glands and ovaries.Testosterone: a potent androgen secreted by the adrenal glands and ovaries and produced in adipose tissue from the conversion of androstenedione.
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he following three androgens may be measured when evaluating a woman with hirsutism and virilization.
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Dehydroepiandrosterone (DHEA): a weak androgen secreted principally by the adrenal glands. (This is generally measured as dehydroepiandrosterone sulfate [DHEA-S] because of its longer half-life, making it a more reliable measure.)Androstenedione: a weak androgen secreted in equal amounts by the adrenal glands and ovaries.Testosterone: a potent androgen secreted by the adrenal glands and ovaries and produced in adipose tissue from the conversion of androstenedione.
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In addition, testosterone is also converted within hair follicles and within genital skin to dihydrotestosterone (DHT), which is an androgen even more potent than testosterone.
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This metabolic conversion is the result of the local action of 5α-reductase on testosterone at these sites.
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In addition, testosterone is also converted within hair follicles and within genital skin to dihydrotestosterone (DHT), which is an androgen even more potent than testosterone.
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This metabolic conversion is the result of the local action of 5α-reductase on testosterone at these sites.
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Adrenal androgen production is controlled by reciprocal feedback regulation through pituitary secretion of
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adrenocorticotropic hormone (ACTH). ACTH stimulates the adrenal cortical production of cortisol. In the metabolic
P.322 sequence of cortisol production, DHEA is one precursor hormone. In enzymatic deficiencies of adrenal steroidogenesis (21-hydroxylase deficiency and 11β-hydroxylase deficiency), DHEA accumulates and is further metabolized to androstenedione and testosterone. |
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Adrenal androgen production is controlled by reciprocal feedback regulation through pituitary secretion of
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adrenocorticotropic hormone (ACTH). ACTH stimulates the adrenal cortical production of cortisol. In the metabolic
P.322 sequence of cortisol production, DHEA is one precursor hormone. In enzymatic deficiencies of adrenal steroidogenesis (21-hydroxylase deficiency and 11β-hydroxylase deficiency), DHEA accumulates and is further metabolized to androstenedione and testosterone. |
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DHEA accumulates and is further metabolized to androstenedione and testosterone in...
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n enzymatic deficiencies of adrenal steroidogenesis (21-hydroxylase deficiency and 11β-hydroxylase deficiency), DHEA accumulates and is further metabolized to androstenedione and testosterone. The flow of adrenal hormone production is shown in Figure 36.2.
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DHEA accumulates and is further metabolized to androstenedione and testosterone in...
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n enzymatic deficiencies of adrenal steroidogenesis (21-hydroxylase deficiency and 11β-hydroxylase deficiency), DHEA accumulates and is further metabolized to androstenedione and testosterone. The flow of adrenal hormone production is shown in Figure 36.2.
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Ovarian androgen production is regulated by
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luteinizing hormone (LH) secretion from the pituitary gland. LH stimulates theca-lutein cells surrounding the ovarian follicles to secrete androstenedione and, to a lesser extent, testosterone. These androgens are precursors for estrogen production by granulosa cells of the ovarian follicles. In conditions of sustained or increased LH secretion, androstenedione and testosterone increase.
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Ovarian androgen production is regulated by
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luteinizing hormone (LH) secretion from the pituitary gland. LH stimulates theca-lutein cells surrounding the ovarian follicles to secrete androstenedione and, to a lesser extent, testosterone. These androgens are precursors for estrogen production by granulosa cells of the ovarian follicles. In conditions of sustained or increased LH secretion, androstenedione and testosterone increase.
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Ovarian androgen production is regulated by
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luteinizing hormone (LH) secretion from the pituitary gland. LH stimulates theca-lutein cells surrounding the ovarian follicles to secrete androstenedione and, to a lesser extent, testosterone. These androgens are precursors for estrogen production by granulosa cells of the ovarian follicles. In conditions of sustained or increased LH secretion, androstenedione and testosterone increase.
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) estrone in greater concentration than estradiol,
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pcos
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) estrone in greater concentration than estradiol,
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pcos
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string of pearls
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PCOS
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string of pearls
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PCOS
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string of pearls
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PCOS
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string of pearls
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PCOS
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string of pearls
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PCOS
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string of pearls
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PCOS
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re ovarian neoplasms that secrete testosterone.
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Sertoli-Leydig cell tumor
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re ovarian neoplasms that secrete testosterone.
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Sertoli-Leydig cell tumor
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lab studies of sertoli-leydig cell tumors
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suppression of FSH and LH, low plasma androstenedione, and marked elevation of testosterone. An ovarian mass may be palpable on pelvic examination. Once the diagnosis is suspected, there should be no delay in surgical removal of the involved ovary. The contralateral ovary should be inspected, and if it is found to be enlarged, it should be bisected for gross inspection.
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lab studies of sertoli-leydig cell tumors
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suppression of FSH and LH, low plasma androstenedione, and marked elevation of testosterone. An ovarian mass may be palpable on pelvic examination. Once the diagnosis is suspected, there should be no delay in surgical removal of the involved ovary. The contralateral ovary should be inspected, and if it is found to be enlarged, it should be bisected for gross inspection.
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lab studies of sertoli-leydig cell tumors
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suppression of FSH and LH, low plasma androstenedione, and marked elevation of testosterone. An ovarian mass may be palpable on pelvic examination. Once the diagnosis is suspected, there should be no delay in surgical removal of the involved ovary. The contralateral ovary should be inspected, and if it is found to be enlarged, it should be bisected for gross inspection.
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The most common cause of increased adrenal androgen production is adrenal hyperplasia as a result of 21-hydroxylase deficiency; 21-hydroxylase catalyzes the conversion of
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progesterone and 17α-hydroxyprogesterone to desoxycorticosterone and compound S.
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The most common cause of increased adrenal androgen production is adrenal hyperplasia as a result of 21-hydroxylase deficiency; 21-hydroxylase catalyzes the conversion of
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progesterone and 17α-hydroxyprogesterone to desoxycorticosterone and compound S.
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The diagnosis of 21-hydroxylase deficiency is made by measuring increased 17-OH progesterone in plasma during the follicular phase (preferably measured while fasting). Patients with classic 21-hydroxylase deficiency will have significantly elevated
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plasma 17-OH progesterone levels, usually over 2000 ng/dL.
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The diagnosis of 21-hydroxylase deficiency is made by measuring increased 17-OH progesterone in plasma during the follicular phase (preferably measured while fasting). Patients with classic 21-hydroxylase deficiency will have significantly elevated
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plasma 17-OH progesterone levels, usually over 2000 ng/dL.
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A less-common cause of adrenal hyperplasia is
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11β-hydroxylase deficiency. The enzyme 11β-hydroxylase catalyzes the conversion of desoxycorticosterone to cortisol. A deficiency in this enzyme also results in increased androgen production. The clinical features of 11β-hydroxylase deficiency are mild hypertension and mild hirsutism. The diagnosis of 11β-hydroxylase deficiency is made by demonstrating increased plasma desoxycorticosterone.
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A less-common cause of adrenal hyperplasia is
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11β-hydroxylase deficiency. The enzyme 11β-hydroxylase catalyzes the conversion of desoxycorticosterone to cortisol. A deficiency in this enzyme also results in increased androgen production. The clinical features of 11β-hydroxylase deficiency are mild hypertension and mild hirsutism. The diagnosis of 11β-hydroxylase deficiency is made by demonstrating increased plasma desoxycorticosterone.
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Treatment of CAH is aimed at
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restoring normal cortisol levels. In CAH, cortisol production is reduced secondary to enzymatic block. This decreased cortisol production results in a compensatory increase in ACTH secretion to attempt to stimulate cortisol production. This increased ACTH production results in the oversecretion of precursor molecules proximal to the enzymatic block, which results in oversecretion of androgens.
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Treatment of CAH is aimed at
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restoring normal cortisol levels. In CAH, cortisol production is reduced secondary to enzymatic block. This decreased cortisol production results in a compensatory increase in ACTH secretion to attempt to stimulate cortisol production. This increased ACTH production results in the oversecretion of precursor molecules proximal to the enzymatic block, which results in oversecretion of androgens.
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Usually, prednisone, 2.5 mg daily
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Treatment of CAH
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Usually, prednisone, 2.5 mg daily
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Treatment of CAH
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treatment of constitutional hirsutism is primarily androgen blockade and mechanical removal of the excess hair.
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Spironolactone 100 mg/day is the most commonly used androgen blocke
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treatment of constitutional hirsutism is primarily androgen blockade and mechanical removal of the excess hair.
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Spironolactone 100 mg/day is the most commonly used androgen blocke
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