Female Sexual Dysfunction

1. Female Sexual Dysfunction Kecia Smette, D.O.

2. Female Sexual Dysfunction (FSD)-Defined • Involves any problem during any phase of the sexual response cycle that prevents an individual or couple from experiencing satisfaction from sexual activity1 • Includes disorders involving desire, arousal and orgasm8 • Also includes sexual pain disorders (dyspareunia, vaginismus)2 • All recognized by the DSM-IV

3. Prevalence • 43% of women (ranges 19-50%) most common in early adult and geriatric years2 • 31% of men1 • From National Health and Social Life Survey of 1992 (included 1749 women and 1410 men ages 18-59) • Masters and Johnson estimate sexual dysfunction plagues 50% of all marriages15

4. Four Types of FSD • 1. Hypoactive Sexual Disorder • 2. Sexual Arousal Disorder • 3. Orgasmic Disorder • 4. Sexual Pain Disorders Dysparunia Vaginismus

5. FSD-Hypoactive Sexual Disorder • Persistent or recurrent deficiency (or absence) of sexual fantasies or thoughts and/or the lack of receptivity to sexual activity • Disorder of desire • Most common sexual dysfunction15 • Individual libidinal drives differ • Low testosterone (?)

6. FSD-Sexual Arousal Disorder • Female Sexual Arousal Disorder (FSAD)-patients have the desire to have sex, but their genital area fails to respond in the normal way, making sex painful or impossible • Is the female equivalent of impotence • Usually psychological • Estrogen deficiency (?) 2,15

7. FSD-Orgasmic Disorder • Female Orgasmic Disorder-unable to achieve orgasm despite sufficient desire and arousal • Unlike men, in women, orgasm is a learned, not an automatic response

8. FSD-Orgasmic Disorder • 5-15% of women never have an orgasm (anorgasmia) • Usually the result of sexual inexperience, performance anxiety or past experiences that have led to inhibition of the sexual response8,15 • Hormones not implicated

9. Sexual pain disorders Dyspareunia • Dyspareunia • Superficial-occurs with attempted penetration usually due to anatomic or irritative condition. Actively find and treat condition • Vaginal –related to pain from friction tx: lubrication • Deep- pain from thrusting Tx: r/o pelvic disease. Encourage relaxation

10. Sexual pain disorders Vaginismus • Vaginismus- involuntary contraction of the muscles of the outer one third of the vagina • Often related to sexual phobias or past abuse • Can be complete or situational • Tx: counseling and progressive relaxation • Vaginal dilators (worn 15 min bid) achieve success rates of 90%

11. Causes of FSD • Risk Factors • Physical • Psychological / Psychosocial • Surgical (combination of effects)

12. FSD-Risk Factors7 • Hypertension • Smoking/substance abuse • Hyperlipidemia • Previous pelvic surgery

13. Physical Causes • Diabetes, heart disease, neurological disorders, hormonal imbalances • Chronic disease (liver or renal) • Arthritis • Urinary incontinence • Substance abuse • Pregnancy and postpartum states (prolonged with lactation) • Medications 1

14. Medications • Never underestimate them!!! • Influence • desire, • arousal, • ability to attain orgasm

15. Medications affecting desire2,15 • Psychoactive antipsychotics, barbiturates, benzodiazepines, SSRIs, Lithium, TCAs • Cardiovascular and antihypertensives antilipid meds, Beta blockers, Clonidine, Digoxin, Spironolactone • Hormonal Preparations Danazol, GnRh agonists, OCPs

16. Medications affecting desire2 • Others H2 receptor blockers Promotility agents Indomethacin Ketoconazole Phenytoin Sodium (Dilantin)

17. Medications affecting arousal2 • Anticholinergics • Antihistamines • Antihypertensives • Psychoactive meds (same plus, MAOIs)

18. Medications affecting orgasm2 • Methyldopa • Amphetamines • Antipsychotics, benzodiazepines, SSRIs, TCAs* • Trazadone • Narcotics *also associated with painful orgasm

19. Psychological / Psychosocial Causes • Stress, anxiety • Religious taboos2 • Sexual performance concerns • Marital/ relationship problems • Depression • Guilt • Past sexual trauma1

20. Surgical Effects • Combination of surgical and psychological effects • Gynecological malignancy 74% reported decreased desire 40% reported dyspareunia2

21. Surgical Effects • Breast Cancer survivors 21-39% incidence of sexual dysfunction (believed to be secondary to chemo or hypoestrogenism from ovarian failure)2 • Hysterectomy for Benign disease 30% reported decreased responses

22. Diagnosis • Complete History and physical examination is critical and should include: • Pap and pelvic exams • Attitude toward sex • Past trauma/sexual abuse • Relationship problems • Sexual orientation • Substance abuse1 • Medication History

23. Focused Physical Exam for the OB/GYN • Examination to include: 1. External genitalia 2. Monomanual exam 3. Bimanual exam 4. Speculum exam

24. External genitalia • Assess muscle tone (vaginismus) • Color and texture (vulvar dystrophy and dermatitis) • Skin turgor and thickness (atrophy) • Amount and distribution of pubic hair (atrophy)

25. External genitaliacontinued… • Visualize clitoris (adhesions) • Ulcers (HSV) • Cotton swab test (vulvar vestibulitis) • Palpate Bartholin glands (bartholinitis) • Assess posterior forchette and hymenal ring (episiotomy scars and strictures)

26. Monomanual exam2 • Palpation of rectovaginal surface (rectal disease) • Palpate levator ani (levator myalgia, vaginismus) • Palpate bladder and urethra (urethritis, cystitis, UTI) • CMT (infection, peritonitis) • Vaginal depth (post op changes, post radiation changes, stricture)

27. Bimanual exam2 • Palpate uterus (retrogression, fibroids, endometriosis) • Adnexa (masses, cysts, endometriosis) • Rectovaginal exam (endometriosis) • Guaiac test (bowel disease)

28. Speculum exam2 • Evaluate discharge, pH (vaginitis, atrophy) • Vaginal mucosa (atrophy) • Papanicolaou smear (HPV, cancer) • Assess for prolapse (cystocele, rectocele, uterine prolapse)

29. Diagnosis • If surgically or easily medically correctable (not hormonal)…correct the problem • If psychological/ psychosocial…refer to appropriate therapist • If hormonal in nature, use your history and physical exam to guide your treatment and remember your physiology…

30. Physiology of FSD • The power players are… • Estrogens • Androgens Testosterone (T) Dihydrotestosterone (DHT) Dehydroepiandrosterone Sulfate (DHEAS) Dehydroepiandrosterone (DHEA) Androstenedione (A) • Progestogens

31. Evils threatening the power players • Menopause • Bilateral oophorectomy • Premature/Pharmacologically induced ovarian failure

32. Menopause • Permanent cessation of menstruation caused by failure of ovarian follicular development and estradiol production in the presence of elevated gonadotropin levels • Average age of onset for perimenopause is 47.5 yrs with menopause occuring at 51-52 yrs15

33. “Evils” of Menopause • Total estrogen production decreases by 80% as estrone and estradiol levels fall • Androgen production declines by 50% • Androstenedione (the primary ovarian androgen) declines 75% • DHEAS (the principal adrenal androgen) decreases by 50%16 • Decreased estrogen to androgen ratio. More problematic in slim women.

34. Effects of Hypoestrogenism • Postmenopausal women produce about 3000 ug of androstenedione (A) qd. • 95% of this is adrenal in origin, the remaining 5% is ovarian • A is converted to estrone in peripheral body fat • A slim woman converts 1.5% of A, resulting in 40 ug of estrone/day • A heavier women converts 7% of A, resulting in 200 ug of estrone/day

35. Hot flashes Increased anxiety, depression, irritability, fatigue Associated with declining cognitive function Usually resolve in 5 yrs Estrogen increases levels of beta endorphin and beta lipotrophin Improves cognitive function, may delay onset of Alzheimer’s disease Studies by Paganini-Hill and Kawas Effects of Hypoestrogenism

36. Osteopenia and osteoporosis Skin thins, collagen levels fall Teeth fall out more easily Bone formation is unchanged, but low levels of estrogen result in increased bone absorption rates. E replacement believed to block actions of PTH responsible Manheux study shows increased skin thickness and collagen with E compared to placebo Effects of Hypoestrogenism15

37. Effects of Hypoestrogenism15 • Atrophy of urogenital tract • Topical estrogen helpful initally, but absorption is irregular. As epithelium thickens, systemic replacement is necessary to support the collagen content of the ligaments supporting the uterus (prevents descensus) and the facial tissue (prevents cystoceles, rectoceles, enteroceles)

38. Effects of Hypoestrogenism15 • E defiency at urinary tract leads to urge incontinence, frequency, dysuria and nocturia

39. Power Player #2…The Androgens9, 13, 14 • DHEA, DHEAS and A are considered proandrogens: they must be converted to testosterone (T) to express their effects • T is the most potent androgen • Plasma T levels range from 0.2 to 0.7 ng/mL • T is metabolized to DHT or E2 • Some studies show an increase libido at supraphysiolocial levels, but no consistent results on libido at physiologic levels16

40. The Androgens9, 13, 14 • DHEA benefits (at 50 mcg) • Increased bone density • Estrogenic stimulation of vaginal cytology

41. The Androgens9, 13, 14,16 • Enhancement of immune system • Does not reliably increase libido. Those most likely to benefit are young women with bilateral oophorectomies.

42. Premenopausal Testosterone: 1.7+/- 0.49 nmol/l SHBG: 4.3+/- 1.46 mg/l Postmenopausal Testosterone 1.3 +/-0.40 nmol/l SHBG 3.4+/-1.41 ml/l Serum levels of T and SHBG15

43. Effects of Hypoandrogenism15 • Decreases libido? • T is produced in ovarian stroma, and elevated levels of LH post menopausally continue to support T production. • More problematic for those with bilateral oophorectomies vs. menopausal women

44. Effects of Hypoandrogenism15 • Sherwin and Williams show IM T increased libido and coital activity • Myers, et al. oral T did not significantly alter libido or coital activity • Trial testing T patch vs. placebo found increases in libido and coitus • Gels and lozenges under investigation • Verdict: parenteral, but not oral, T seems to be effective for FSD with low desire/libido

45. Power Player #3The Progestogens9 • Progestogens are synthetic molecules with progestinic activity • Protectors of endometrium • May mildly inhibit sexual desire

46. The Progestogens9 • Vary in activity from strongly antiandrogenic, to neutral, to androgenic depending upon their structure, the molecule the are derived from (progesterone vs. 19-nortestosterone) and their interaction with different hormonal receptors • Can interact with progestinic, estrogenic, androgenic glucocorticoid and mineralocorticoid receptors. THUS, the consequent metabolic and sexual profile is very different12

47. General Treatment Guidelines 1, 2 • Education, Education, Education!! (anatomy, function, effects of aging) • Enhancing stimulation (erotic materials, masturbation)

48. General Treatment Guidelines 1, 2 • Distraction techniques (fantasy, Kegel exercises with intercourse, backgound music or television) • Encouraging non-coital behaviors (massage) • Minimize pain (positional, lubricants, warm baths, biofeedback, NSAIDS prior to intercourse)1,2

49. Treatment of Hypoactive Sexual Disorders2 • Difficult • Often secondary to boredom, lifestyle factors, medications, or other sexual dysfunction • No (reliable, recognized) medical therapy available2 • Estrogen therapy may help some, although this is not universal • Testosterone usage controversial

50. Estrogen for Treatment of Hypoactive Sexual disorders2 • Improves urogenital atrophy • Improves vasomotor symptoms • Improves menopausal mood disorders (depression) • Addition of progesterone believed to exhibit a negative impact by dampening mood and decreasing available androgens2