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27 Cards in this Set
- Front
- Back
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1. What is an abnormal increase in Terminal hair from Vellus hair due to?
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a. Androgen excess or ↑ 5α-reductase activity (converts testosterone to DHT).
b. DHT is believed to be the main stimulant in terminal hair development. |
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2. Regulation of two inner layers of adrenal cortex (Fasiculata (cortisol) and reticulosa (androgens)?
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a. ACTH
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3. Regulation of outer layer of adrenal cortex (glomerulosa-aldosterone)?
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a. Renin-angiotensin system.
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4. What stimulates theca cells in ovaries and what do they produced?
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a. Stimulated by LH.
b. Produce androstenedione and testosterone. |
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5. What happens to androstenedione and testosterone after production by Theca cells in ovaries?
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a. They are then aromatized to estrone and estradiol by granulosa cells in response to FSH.
b. Elevated levels of FSH and LH may therefore lead to elevated levels of androgens. |
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6. Note: Bc synthesis of steroid hormones in the adrenal cortex is stimulated by ACTH as a non-differentiated step, elevated ACTH increases all the steroid hormones, including androgens.
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6. Note: Bc synthesis of steroid hormones in the adrenal cortex is stimulated by ACTH as a non-differentiated step, elevated ACTH increases all the steroid hormones, including androgens.
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7. From where is DHEAS derived almost entirely and what is the implication?!?!?
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a. From the adrenal glands.
b. So its elevation is used as marker for adrenal androgen production as opposed to ovarian. |
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8. What appears to lead to excess androgen production in the ovary?
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a. An increase in LH or in the LH:FSH ratio.
b. Elevated androgens leads to hirsutism and possibly virilism. |
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9. Presentation of CAH from 21α-OH deficiency?
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a. Do not synthesize cortisol or mineralocorticoids and thus present w/salt wasting and adrenal insufficiency at birth.
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10. CAH from 21α-OH deficiency presentation in FM infants?
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a. Ambiguous genitalia due to androgen excess.
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11. 2 other types of CAH that can be assoc. w/virilization?
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a. 11β-OH and 3β-hydroxysteroid dehydrogenase (3β-HSD).
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12. What should be tested for when CAH is suspected?
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a. 17α-hydroxyprogesterone (17-OHP) levels
b. If elevated (>200 ng/dL), the diagnosis can be confirmed w/ACTCH stimulation test. c. 17-OHP is checked 1 hour later. d. A marked increase in 17-OHP is consistent w/CAH. e. Lower elevated values are seen in late-onset CAH and heterozygote carriers for the 21α-OH deficiency. |
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13. Cause of androgen excess in PCOS?
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a. Excess LH stimulation leading to cystic changes in the ovaries and increased ovarian androgen secretion.
b. Typically, the LH:FSH ratio is >3:1. |
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14. Theca Lutein cysts SE?
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a. Produce an excess amount of androgens that are secreted into the circulation.
b. These cysts may be present in either normal or molar pregnancy. c. The ovaries are enlarged, and pts present w/hirsutism and, occasionally, virilization. |
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15. Diagnosis of Theca lutein cysts?
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a. Ovarian biopsy.
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16. When does Stromal hyperplasia occur and SE?
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a. Between age 50-70.
b. Can cause hirsutism. c. The ovaria are uniformly enlarged. |
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17. Functional ovarian tumours that can lead to hirsutism and virilization?
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a. Sertoli-Leydig- usually younger women.
b. Granulosa-theca cell tumours c. Hilar (leydig) cell tumours- even rarer than Sertoli-leydig and occur in postmenopausal women.- secrete androgens. d. Germ cell tumours |
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18. Luteoma?
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a. In pregnancy, there may be a luteoma.
b. A benign tumours that grows in response to hcg. c. Can result in high levels of testosterone and androstenedione and virilization in up to 25% of pts. d. There will also be virilization of 65% of female fetuses. e. These findings resolve in postpartum period. |
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19. Lab studies for hirsutism?
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a. Free testosterone- confirms androgen excess.
b. 17-OHP- If elevated suggests CAH. c. DHEAS (suggests adrenal source) |
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20. What ratio of LH:FSH suggests PCOS?
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a. >3:1.
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21. Evaluation of hirsute woman w/normal free testosterone?
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a. Assay 5α-reductase activity to see determine if increased peripheral enzymatic activity is responsible.
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22. Tx of adrenal nonneoplastic androgens?
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a. Suppression can be achieved with:
1. Glucocorticoids. b. Finasteride inhibits 5α-reductase, diminishing peripheral conversion of testosterone to DHT. c. Antiandrogens such as spironolactone have been helpful but are temporizing at best. |
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23. Tx of ovarian nonneoplastic androgens?
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a. Can be suppressed w/oral contraceptives that will suppress LH and FSH as well as increase SHBG.
b. Progesterone alone may help pts w/contraindications to oestrogen use. i. Progesterone decreases levels of LH and thus androgen production. c. GnRH agonists can also be used to suppress LH and FSH. However, this leads to a hypoestrogenic state and requires further concomitant oestrogen replacement. |
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24. Most widely used method of reversible contraception in the world?
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a. IUD baby!
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25. Primary MOA of IUD?
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a. Sterile inflammatory response resulting in sperm being engulfed, immobilized, and destroyed by inflammatory cells.
b. Also thought to inhibit tubal motility. c. Progesterone in Mirena thickens the cervical mucus and atrophies the endometrium to prevent implantation. d. Copper in the Paraguard is thought to hamper sperm motility and capitation so sperm rarely reach the tubes and are unable to fertilize ovum. |
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26. Infection prophylaxis for IUD placement?
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a. Screen for chlamydia and gonorrhea prior to placement.
b. No abx. |
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27. Other benefits of Mirena IUD?
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a. Has been found to decrease Menorrhagia (90% less blood loss) and dysmenorrhea.
b. It is also as effective as oral progestins in treating endometriosis, endometrial hyperplasia, and cancer. c. Also protects the user from PID. |
