Linear biologic model (limitations)
Masters and Johnson’s linear, 4-stage biologic model of sexual response for both men and women assumes that men and women have similar sexual responses. Many women, however, do not move progressively and sequentially through the phases as described. Women may not even experience all of the phases—for example, they may move from sexual arousal to orgasm and satisfaction without experiencing sexual desire, or they can experience desire, arousal, and satisfaction but not orgasm.
• The biologic model may be limited because it does not take into account nonbiologic experiences such as pleasure and satisfaction. It also does not place sexuality into the context of the relationship.
• Much of female sexual desire is actually a reaction to a partner’s sexual interest rather than a spontaneous stirring of the woman’s own libido. Women have many reasons for engaging in sexual activity other than sexual hunger or drive, as the traditional model suggests.
Circular relationship model (advantages)
The circular, variable-stage relationship model of female sexual response acknowledges how emotional intimacy, sexual stimuli, and relationship satisfaction affect the female sexual response.
• Female sexual functioning proceeds in a more complex and circuitous manner than does male sexual functioning. Also, female functioning is dramatically and significantly affected by numerous psychosocial issues.
• Many women start from a point of sexual neutrality—where a woman is receptive to being sexual but does not initiate sexual activity—and the desire for intimacy prompts her to seek ways to become sexually aroused via conversation, music, reading or view-ing erotic materials, or direct stimulation. Once she is aroused, sexual desire emerges and motivates.
• The goal of sexual activity for women is not necessarily orgasm but rather personal satisfaction, which may be orgasm and/or feelings of intimacy and connection.
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Biologic drive
| Nonsexual rewards for | |
| participating in sex | Sexual satisfaction |
| Arousal and | Subjective | |
| responsive desire | ||
| arousal | ||
Figure II-10-1. Female Sexual Response Cycle
SEXUAL HISTORY-TAKING
The following questions should be asked of all new patients in developing a medical data base and problem list.
• Sexual activity. Start out with the following initial question: Is the patient currentlysexually active? If not now, has she been in past?
• Current history. If she is currently sexually active, ask the following: Is the relation-ship with men or women or both? Is the relationship satisfying? Does she have any difficulty lubricating? Does she have pain with intercourse?
• Previous history. What was her age at first intercourse? What is the number of life-time and current sexual partners? Does she have a history of sexual abuse or rape?
SEXUAL DYSFUNCTION
Each phase of the sexual response cycle can be dysfunctional.
• Desire disorders. Decreased sexual desire is the most common female sexual com-plaint. It may be organic (e.g., low androgens), medication related (e.g., selective serotonin reuptake inhibitors [SSRIs]), or psychological (e.g., poor partner relation-ship). Treatment can be difficult if it is relational in etiology.
• Excitement disorders. This usually results in difficulty in vaginal lubrication.The most common cause is estrogen deficiency. Treatment is highly successful.
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• Anorgasmia. This can be primary or secondary. Inadequate clitoral stimulation is themost common cause. Treatment is highly successful using initially self-stimulation then partner education.
• Dyspareunia. Since pain with intercourse may arise from both psychological or physi-cal causes, a thorough history and physical examination is essential. Treatment is directed at the specific cause found.
• Vaginismus. This occurs with painful reflex spasm of the paravaginal thigh adductormuscles. It is the only sexual dysfunction that can be diagnosed on physical examina-tion. Treatment is highly successful using vaginal dilators.
SEXUAL ASSAULT
A 21-year-old university student presents to the emergency department stating she was walking home after an evening class when she was assaulted by a male stranger and was raped. She is not crying or upset, but rather looks almost without emotions. She is accompanied by her female roommate.
Definition. Rape is defined as sexual activity without the individual’s consent occurring undercoercion.
Management
• Stabilization. The first step is to determine the patient’s vital signs and take whateveris needed to stabilize them. An informed consent needs to be obtained.
• History-taking. Record the events that happened in the patient’s own words. Alsoobtain a reproductive, obstetric, sexual, and contraceptive history.
• Examination. A thorough general and pelvic examination should be performed withphotographic or drawing documentation of any injuries or trauma.
• Specimens. A rape kit should be used to obtain biologic specimens (e.g., vaginal, oral,or anal specimens) for DNA or other evidence for use in potential legal proceedings. These must be appropriately labeled and documented, including signatures of receiv-ing authorities. Also obtain baseline laboratory tests: VDRL, HIV screen, pregnancy test, urine drug screen, and blood alcohol level.
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• Prophylaxis. Antibiotic therapy should be administered prophylactically for gonor-rhea (ceftriaxone 125 mg IM × 1), chlamydia (azithromycin 1 g PO × 1), and tricho-moniasis (metronidazole 2 g PO × 1). Antiviral HIV prophylaxis should be admin-istered within 24 hours after exposure, but no medication should be given after 36 hours. Active and passive immunization for hepatitis B is appropriate.
• Pregnancy prevention. Administer 2 tablets of high progestin OCPs immediately,repeating two tablets in 12 h. A newly released formulation of levonogesterol tablets (Plan B) are now available specifically for postcoital pregnancy prevention.
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Menstrual Abnormalities 11
MENSTRUAL PHYSIOLOGY
The menstrual cycle is the cyclic pattern of activity of hypothalamus, pituitary, ovary, and uterus that produces a rhythm of bleeding every month for 30 years or more during the active reproductive phase of a woman’s life.
Menarche is the first flow that signifies potential reproductivity. Menopause is the termination of the menstrual flow, which signifies diminished ovarian function.
Menstrual cycle occurs with the maturation of the hypothalamic–pituitary–ovarian axis. The hormones produced include gonadotropin-releasing hormone (GnRH) from the hypothalamus, which stimulates follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, which stimulate estrogen and progesterone from the ovarian follicle.
Layers of the Endometrium
Functionalis Zone. This is the superficial layer that undergoes cyclic changes during themenstrual cycle and is sloughed off during menstruation. It contains the spiral arterioles that undergo spasm with progesterone withdrawal.
Basalis Zone. This is the deeper layer that remains relatively unchanged during the menstrual cycleand contains stem cells that function to renew the functionalis. It contains the basal arteries.
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Phases of the Endometrium
Menstrual Phase. This is defined as the first 4 days of the menstrual cycle with the first dayof menses taken as day 1. It is characterized by disintegration of the endometrial glands and stroma, leukocyte infiltration, and red blood cell (RBC) extravasation. Sloughing of the func-tionalis and compression of the basalis occurs.
Proliferative Phase. This follows the menstrual phase and is characterized by endometrial growthsecondary to estrogen stimulation, including division of stem cells that migrate through the stroma to form new epithelial lining of the endometrium and new endometrial glands. The length of the spiral arteries also increases. An estrogen-dominant endometrium is unstable and, in the pres-ence of prolonged anovulation, will undergo hyperplasia with irregular shedding over time.
Secretory Phase. This follows the proliferative phase and is characterized by glandular secre-tion of glycogen and mucus stimulated by progesterone from the corpus luteum. Endometrial stroma becomes edematous, and spiral arteries become convoluted. A progesterone-dominant endometrium is stable and will not undergo irregular shedding. Regression of the corpusluteum occurs by day 23 if there is no pregnancy, causing decreased levels of progesterone and estradiol and endometrial involution. Constriction of the spiral arteries occurs 1 day before
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menstruation, causing endometrial ischemia and release of prostaglandins, followed by leukocyte infiltration and RBC extravasation. The resulting necrosis leads to painful cramps and men-struation. When a pregnancy occurs, the serum b-human chorionic gonadotropin (b-hCG) becomes positive at day 22–23 of the cycle. The b-hCG becomes positive when the zygote implants into the endometrium, usually 7–8 days after ovulation. Therefore, the serum b-hCG becomes positive before the missed period.
Menstrual Cycle Hormones
FSH stimulates the growth of granulosa cells and induces the aromatase enzyme that convertsandrogens to estrogens. It raises the concentration of its own receptors on the granulosa cells. It stimulates the secretion of inhibin from the granulosa cells and is suppressed by inhibin.
LH stimulates the production of androgens by the theca cells, which then get converted to estro-gens in the granulosa cells by the aromatase enzyme (2-cell theory). It raises the concentration of its own receptors in FSH-primed granulosa cells. The LH surge, which is dependent on a rapid rise in estrogen levels, stimulates synthesis of prostaglandins to enhance follicle rupture and ovulation. The LH surge also promotes luteinization of the granulosa cells in the dominant follicle, resulting in progesterone production as early as the 10th day of the cycle.
Estrogen is produced in the granulosa cells in response to even low FSH concentrations, andstimulates proliferative changes in the endometrium. It has a negative feedback to FSH at the hypothalamic–pituitary level, but has a positive feedback to increase GnRH receptor concen-trations. At low estrogen levels there is negative inhibitory feedback for LH release, but as the level of estradiol increase is sustained for 50 hours, there is a transition to a positive stimulatory feedback, leading to the LH surge.
Androgens include androstenedione and testosterone. They are precursors of estrogen and areproduced in the theca cells. In lower concentrations they stimulate aromatase enzyme activity, whereas at high levels they inhibit it. Androgens inhibit FSH induction of LH receptors.
Progesterone is produced by the corpus luteum and stimulates secretory changes in the endo-metrium in preparation for blastocyst implantation.
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Ovulation
LH
FSH
Estradiol
Progesterone
| Uterine endometrium Ovarian function |
Days
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| Oocyte | Graafian follicle | Corpus luteum Corpus albicans | ||
| Spiral | ||||
| Gland | Vein | artery | ||
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| 4 | 14 | 28 | ||||
| Menstrual | Proliferative | Secretory | ||||
| phase | phase | phase | ||||
Figure II-11-1. Menstrual Cycle: Pituitary, Ovarian, and Endometrial Correlations
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