Reproductive System

佚名

T he reproductive system must function properly to ensure survival of the species. The male reproductive system produces sperm and delivers them to the female reproductive tract. The female reproductive system produces the ovum. If a sperm fertilizes an ovum, this system also nurtures and protects the embryo and developing fetus and delivers it at birth. The functioning of the reproductive system is determined not only by anatomic structure, but also by complex hormonal, neurologic, vascular, and psychogenic factors.

Anatomically, the main distinction between the male and female is the presence of conspicuous external genitalia in the male. In contrast, the major reproductive organs of the female lie within the pelvic cavity.

MALE REPRODUCTIVE SYSTEM

The male reproductive system consists of the organs that produce sperm, transfer mature sperm from the testes, and introduce them into the female reproductive tract, where fertilization occurs.

Besides supplying male sex cells (in a process called spermatogenesis), the male reproductive system plays a part in the secretion of male sex hormones. The penis also functions in urine elimination.

Reproductive organs

The male reproductive organs include the penis, scrotum, testes, duct system, and accessory reproductive glands.

Penis

The penis consists of three cylinders of erectile tissue: two corpora cavernosa, and the corpus spongiosum, which contains the urethra. The glans or tip of the penis contains the urethral meatus, through which urine and semen pass to the exterior, and many nerve endings for sexual sensation.

Scrotum

The scrotum, which contains the testes, epididymis, and lower spermatic cords, maintains the proper testicular temperature for spermatogenesis through relaxation and contraction. This is important because excessive heat reduces the sperm count.

Testes

The testes (also called gonads, which is a term for any reproductive organ, or testicles) produce sperm in the seminiferous tubules.

The testes form in the abdominal cavity of the fetus and descend into the scrotum during the seventh month of gestation.

Duct system

The vas deferens connects the epididymis, in which sperm mature and ripen for up to 6 weeks, and the ejaculatory ducts. The seminal vesicles ― two convoluted membranous pouches ― secrete a viscous liquid of fructose-rich semen and prostaglandins that probably facilitates fertilization.

Accessory reproductive glands

The prostate gland secretes the thin alkaline substance that comprises most of the seminal fluid; this fluid also protects sperm from acidity in the male urethra and in the vagina, thus increasing sperm motility.

The bulbourethral (Cowper's) glands secrete an alkaline ejaculatory fluid, probably similar in function to that produced by the prostate gland. The spermatic cords are cylindrical fibrous coverings in the inguinal canal containing the vas deferens, blood vessels, and nerves.

Testosterone

The testes produce and secrete hormones, especially testosterone, in their interstitial cells (Leydig's cells). Testosterone affects the development and maintenance of secondary sex characteristics and sex drive. It also regulates metabolism, stimulates protein anabolism (encouraging skeletal growth and muscular development), inhibits pituitary secretion of the gonadotropins (follicle-stimulating hormone and interstitial cell-stimulating hormone), promotes potassium excretion, and mildly influences renal sodium reabsorption.

In males, the reproductive and urinary systems are structurally integrated; most disorders, therefore, affect both systems. Congenital abnormalities or prostate enlargement may impair both sexual and urinary function. Abnormal findings in the pelvic area may result from pathologic changes in other organ systems, such as the upper urinary and GI tracts, endocrine glands, and neuromusculoskeletal system.

FEMALE REPRODUCTIVE SYSTEM

Female reproductive structures include the mammary glands, external genitalia, and internal genitalia. Hormonal influences determine the development and function of these structures and affect fertility, childbearing, and the ability to experience sexual pleasure.

In no other part of the body do so many interrelated physiologic functions occur in such proximity as in the area of the female reproductive tract. Besides the internal genitalia, the female pelvis contains the organs of the urinary and GI systems (bladder, ureters, urethra, sigmoid colon, and rectum). The reproductive tract and its surrounding area are thus the site of urination, defecation, menstruation, ovulation, copulation, impregnation, and parturition.

Mammary glands

Located in the breasts, the mammary glands are specialized accessory glands that secrete milk. Although present in both sexes, they normally function only in females.

External structures

Female genitalia include the following external structures, collectively known as the vulva: mons pubis (or mons veneris), labia majora, labia minora, clitoris, and the vestibule. The perineum is the external region between the vulva and the anus. The size, shape, and color of these structures ― as well as pubic hair distribution and skin texture and pigmentation ― vary greatly among individuals. Furthermore, these external structures undergo distinct changes during the life cycle.

Mons pubis

The mons pubis is the pad of fat over the symphysis pubis (pubic bone), which is usually covered by the base of the inverted triangular patch of pubic hair that grows over the vulva after puberty.

Labia majora

The labia majora are the two thick, longitudinal folds of fatty tissue that extend from the mons pubis to the posterior aspect of the perineum. The labia majora protect the perineum and contain large sebaceous glands that help maintain lubrication. Virtually absent in the young child, their development is a characteristic sign of onset of puberty. The skin of the more prominent parts of the labia majora is pigmented and darkens after puberty.

Labia minora

The labia minora are the two thin, longitudinal folds of skin that border the vestibule. Firmer than the labia majora, they extend from the clitoris to the posterior fourchette.

Clitoris

The clitoris is the small, protuberant organ located just beneath the arch of the mons pubis. The clitoris contains erectile tissue, venous cavernous spaces, and specialized sensory corpuscles that are stimulated during coitus. It's homologous to the male penis.

Vestibule

The vestibule is the oval space bordered by the clitoris, labia minora, and fourchette. The urethral meatus is located in the anterior portion of the vestibule, and the vaginal meatus is in the posterior portion. The hymen is the elastic membrane that partially obstructs the vaginal meatus in virgins. Its absence doesn't necessarily imply a history of coitus, nor does its presence obstruct menstrual blood flow.

Several glands lubricate the vestibule. Skene's glands (also known as the paraurethral glands) open on both sides of the urethral meatus; Bartholin's glands, on both sides of the vaginal meatus.

The fourchette is the posterior junction of the labia majora and labia minora. The perineum, which includes the underlying muscles and fascia, is the external surface of the floor of the pelvis, extending from the fourchette to the anus.

Internal structures

The internal structures of the female genitalia include the vagina, cervix, uterus, Fallopian tubes (or oviducts), and ovaries.

Vagina

The vagina occupies the space between the bladder and the rectum. A muscular, membranous tube approximately 2 to 3 inches (5 to 7.5 cm) long, the vagina connects the uterus with the vestibule of the external genitalia. It serves as a passageway for sperm to the Fallopian tubes, a conduit for the discharge of menstrual fluid, and the birth canal during parturition.

Cervix

The cervix is the most inferior part of the vagina, protruding into the vaginal canal. The cervix provides a passageway between the vagina and the uterine cavity.

Uterus

The uterus is the hollow, pear-shaped organ in which the conceptus grows during pregnancy. The thick uterine wall consists of mucosal, muscular, and serous layers. The inner mucosal lining (the endometrium) undergoes cyclic changes to facilitate and maintain pregnancy.

The smooth muscular middle layer (the myometrium) interlaces the uterine and ovarian arteries and veins that circulate blood through the uterus. During pregnancy, this vascular system expands dramatically. After abortion or childbirth, the myometrium contracts to constrict the vasculature and control loss of blood.

The outer serous layer (the parietal peritoneum) covers all of the fundus, part of the corpus, but none of the cervix. This incompleteness allows surgical entry into the uterus without incision of the peritoneum, thus reducing the risk for peritonitis in the days before effective antibiotic therapy.

Fallopian tubes

The Fallopian tubes extend from the sides of the fundus and terminate near the ovaries. Each tube has a fimbriated (fringelike) end adjacent to the ovary that serves to capture an oocyte after ovulation. Through ciliary and muscular action, these small tubes carry ova from the ovaries to the uterus and facilitate the movement of sperm from the uterus toward the ovaries. The same ciliary and muscular action helps move a zygote (fertilized ovum) down to the uterus, where it may implant in the blood-rich inner uterine lining, the endometrium.

Ovaries

The ovaries are two almond-shaped organs, one on either side of the pelvis, situated behind and below the Fallopian tubes. The ovaries produce ova and two primary hormones ― estrogen and progesterone ― in addition to small amounts of androgen. These hormones in turn produce and maintain secondary sex characteristics, prepare the uterus for pregnancy, and stimulate mammary gland development. The ovaries are connected to the uterus by the utero-ovarian ligament.

In the 30th week of gestation, the fetus has about 7 million follicles, which degenerate, leaving about 2 million present at birth. By puberty, only 400,000 remain, and these ova precursors become Graafian follicles in response to the effects of pituitary gonadotropic hormones (follicle-stimulating hormone [FSH] and luteinizing hormone [LH]). Fewer than 500 of each woman's ova mature and become potentially fertile.

The menstrual cycle

Maturation of the hypothalamus and the resultant increase in hormone levels initiate puberty. In the young girl, the appearance of pubic and axillary hair (pubarche) and the characteristic adolescent growth spurt follow breast development (thelarche) ― the first sign of puberty. The reproductive system begins to undergo a series of hormone-induced changes that result in menarche, or the onset of menstruation (or menses).

The menstrual cycle consists of three different phases: menstrual, proliferative (estrogen dominated), and secretory (progesterone dominated). (See Understanding the menstrual cycle .)

At the end of the secretory phase, the uterine lining is ready to receive and nourish a zygote. If fertilization doesn't occur, increasing estrogen and progesterone levels decrease LH and FSH production. Because LH is needed to maintain the corpus luteum, a decrease in LH production causes the corpus luteum to atrophy and halt the secretion of estrogen and progesterone. The thickened uterine lining then begins to slough off, and menstruation begins again.

In the nonpregnant female, LH controls the secretions of the corpus luteum, thereby increasing progesterone levels in the bloodstream. In the pregnant woman, human chorionic gonadotropin (HCG), produced by the nascent placenta, controls these secretions.

If fertilization and pregnancy occur, the endometrium grows even thicker and vascular ingrowth occurs. After implantation of the zygote (about 5 or 6 days after fertilization), the endometrium becomes the decidua. Trophoblastic cells produce HCG soon after implantation, stimulating the corpus luteum to continue secreting estrogen and progesterone, which prevents further ovulation and menstruation.

HCG continues to stimulate the corpus luteum until the placenta (the vascular organ that develops to transport materials to and from the fetus) forms and starts producing its own estrogen and progesterone. After the placenta takes over hormonal production, secretions of the corpus luteum are no longer needed to maintain the pregnancy, and the corpus luteum gradually decreases its function and begins to degenerate. This is termed the luteoplacental shift and commonly occurs by the end of the first trimester.

PATHOPHYSIOLOGIC MANIFESTATIONS

Alterations may occur in the structure, process, or function of both the male and female reproductive systems.

Sexual maturation alteration

Sexual maturation, or puberty, can be affected by various congenital and endocrine disorders. The timing of puberty may be too early (precocious puberty) or too late (delayed puberty). Precocious puberty is the onset of sexual maturation before age 9 years in boys and before age 8 years in girls. It occurs more often in girls than boys. In girls, the cause is most commonly idiopathic, whereas in boys it is more likely to be organic.

In delayed puberty, there's no evidence of the development of secondary sex characteristics in a boy age 14 years or a girl age 13 years. There's usually no evidence of hormonal abnormalities. The hypothalamic-pituitary-ovarian axis, a system that stimulates and regulates the production of hormones necessary for normal sexual development and function, is intact, but maturation is slow. The cause is unknown.

Hormonal alterations

Complex hormonal interactions determine the normal function of the female reproductive tract and require an intact hypothalamic-pituitary-ovarian axis. A defect or malfunction of this system can cause infertility due to insufficient gonadotropin secretions (both LH and FSH). The ovary controls, and is controlled by, the hypothalamus through a system of negative and positive feedback mediated by estrogen production. Insufficient gonadotropin levels may result from infections, tumors, or neurologic disease of the hypothalamus or pituitary gland. A mild hormonal imbalance in gonadotropin production and regulation, possibly caused by polycystic disease of the ovary or abnormalities in the adrenal or thyroid gland that adversely affect hypothalamic-pituitary functioning, may sporadically inhibit ovulation. Because gonadotropins are released in a pulsatile fashion, a significant disturbance in this pulsatility will adversely affect ovulatory function.

Male hypogonadism, or an abnormal decrease in gonad size and function, results from decreased androgen production in males, which may impair spermatogenesis (causing infertility) and inhibit the development of normal secondary sex characteristics. The clinical effects of androgen deficiency depend on age at onset. Primary hypogonadism results directly from interstitial (Leydig's cell) cellular or seminiferous tubular damage due to faulty development or mechanical damage. Androgen deficiency causes increased secretion of gonadotropins by the pituitary in an attempt to increase the testicular functional state and is therefore termed hypergonadotropic hypogonadism. This form of hypogonadism includes Klinefelter's syndrome (47 XXY), Reifenstein's syndrome, male Turner's syndrome, Sertoli-cell-only syndrome, anorchism, orchitis, and sequelae of irradiation.

Secondary hypogonadism is due to faulty interaction within the hypothalamic-pituitary axis, resulting in failure to secrete normal levels of gonadotropins, and is therefore termed hypogonadotropic hypogonadism. This form of hypogonadism includes hypopituitarism, isolated FSH deficiency, isolated LH deficiency, Kallmann's syndrome, and Prader-Willi syndrome. Depending on the patient's age at onset, hypogonadism may cause eunuchism (complete gonadal failure) or eunuchoidism (partial failure).

Symptoms vary depending on the specific cause of hypogonadism. Some characteristic findings may include delayed bone maturation, delayed puberty; infantile penis and small, soft testes; less than average muscle development and strength; fine, sparse facial hair; scant or absent axillary, pubic, and body hair; and a high-pitched, effeminate voice. In an adult, hypogonadism diminishes sex drive and potency and causes regression of secondary sex characteristics.

Menstrual alterations

Alterations in menstruation include the absence of menses, abnormal bleeding patterns, or painful menstruation. Menopause is the cessation of menstruation. It results from a complex continuum of physiologic changes ― the climacteric ― caused by declining ovarian function. The climacteric produces various changes in the body, the most dramatic being the cessation of menses.

Premature menopause, the gradual or abrupt cessation of menstruation before age 35 years, occurs without apparent cause in about 5% of women in the United States. Certain diseases, especially autoimmune diseases such as premature ovarian failure, may cause pathologic menopause. Other factors that may precipitate premature menopause include malnutrition, debilitation, extreme emotional stress, pelvic irradiation, and surgical procedures that impair ovarian blood supply. Artificial menopause may follow radiation therapy or surgical procedures such as removal of both ovaries (bilateral oophorectomy). Hysterectomy decreases the interval before menopause even when the ovaries are not removed. It's speculated that hysterectomy may decrease ovarian blood flow in some fashion.

Ovarian failure, in which no ova are produced, may result from a functional ovarian disorder from premature menopause. Amenorrhea is a natural consequence of ovarian failure.

Pain is often associated with the menstrual cycle; in many common diseases of the female reproductive tract, such pain may follow a cyclic pattern. A patient with endometriosis, for example, may report increasing premenstrual pain that decreases at the end of menstruation. For a description of the types of abnormal menstrual bleeding, see Abnormal premenopausal bleeding .

Sexual dysfunction

Sexual dysfunction includes arousal problems, orgasmic problems, and sexual pain (dyspareunia, vaginismus). Dysfunction may be caused by a general medical condition, psychological condition, substance use or abuse, or a combination of these factors.

Arousal disorder is an inability to experience sexual pleasure. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV), the essential feature is a persistent or recurrent inability to attain or to maintain an adequate lubrication-swelling response of sexual excitement until completion of the sexual act. Orgasmic disorder, according to DSM-IV, is a persistent or recurrent delay in or absence of orgasm after a normal sexual excitement phase.

Both arousal and orgasmic disorders are considered primary if they exist in a female who has never experienced sexual arousal or orgasm; they are secondary when a physical, mental, or situational condition has inhibited or obliterated a previously normal sexual function. The prognosis is good for temporary or mild disorders resulting from misinformation or situational stress but is guarded for disorders that result from intense anxiety, chronically discordant relationships, psychological disturbances, or drug or alcohol abuse in either partner.

The following factors, alone or in combination, may cause arousal or orgasmic disorder:

• certain drugs, including central nervous system depressants, alcohol, street drugs, and, rarely, oral contraceptives
• general systemic illnesses, diseases of the endocrine or nervous system, or diseases that impair muscle tone or contractility
• gynecologic factors, such as chronic vaginal or pelvic infection or pain, congenital anomalies, and genital cancers
• stress and fatigue
• inadequate or ineffective stimulation
• psychological factors, such as performance anxiety, guilt, depression, or unconscious conflicts about sexuality
• relationship problems, such as poor communication, hostility, or ambivalence toward the partner, fear of abandonment or independence, or boredom with sex.

All these factors may contribute to involuntary inhibition of the orgasmic reflex. Another crucial factor is the fear of losing control of feelings or behavior. Whether these factors produce sexual dysfunction and the type of dysfunction depend on how well the woman copes with the resulting pressures. Physical factors may also cause arousal or orgasmic disorder.

Female sexual function and responses decline, along with estrogen levels, in the perimenopausal period. The decrease in estradiol levels during menopause affects nerve transmission and response in the peripheral vascular system. As a result, the timing and degree of vasoconstriction during the sexual response is affected, vasocongestion decreases, muscle tension decreases, and contractions are fewer and less intense during orgasm.

A female with arousal disorder has limited or absent sexual desire and experiences little or no pleasure from sexual stimulation. Physical signs of this disorder include lack of vaginal lubrication or absence of signs of genital vasocongestion.

Dyspareunia is genital pain associated with intercourse. Insufficient lubrication is the most common cause. Other physical causes of dyspareunia include:

• endometriosis
• genital, rectal, or pelvic scar tissue
• acute or chronic infections of the genitourinary tract
• disorders of the surrounding viscera (including residual effects of pelvic inflammatory disease or disease of the adnexal and broad ligaments).

Among the many other possible physical causes are:

• deformities or lesions of the introitus or vagina
• benign and malignant growths and tumors
• intact hymen
• radiation to the pelvis
• allergic reactions to diaphragms, condoms, or other contraceptives.

Psychological causes include:

• fear of pain or injury during in