ePathoPlusPage

Female Reproductive System

Outline

A. Reproductive Structures

1. External genitalia (collectively referred to as vulva)

    a. mons pubis

    b. labia majora and labia minora

        vestibule

        Bartholin’s glands

    c. clitoris

    d. urethra

    e. vaginal opening = introitus

        hymen

    f. perineum

2. Internal genitalia

a. vagina

    b. uterus

        a. divided into three parts

            1. fundus

            2. cervix

            3. body

                wall of uterus composed of 3 layers

                    perimetrium

                    myometrium

                    endometrium (which has a basal layer and a

                    superficial layer)

    c. oviducts (Fallopian tubes)

    d. ovaries

B. Reproductive Function

1. Menstrual cycle

    a. menarchee = first menstrual bleeding

    b. menopause = last menstrual bleeding

2 Ovarian hormones

    a. Estrogen

        1. effect on growth and development

        2. effect on reproductive processes

        3. action on vagina, cervix and breasts

        4. general metabolic effects

    b. Progesterone (from corpus luteum)

        1.glandular development of breasts

        2. cyclic glandular development of endometrium

        3. smooth muscle relaxation

    c. Androgens

        1. can be converted into estrogens in peripheral fat tissue

3. Ovarian Follicle Development and Ovulation

Primary follicles, as a result of endocrine stimulation (increasing levels of FSH), develop into secondary follicles. Most mature secondary follicle continues to develop. This dominant follicle moves to periphery of ovary, it bursts, releasing oocyte into oviduct. Remains of dominant follicle become corpus luteum which secretes progesterone. Two possibilities

    a. fertilization occurs- implanted blastocyst produces human chorionic gonadotropin which prevents luteal regression so that the corpus luteum secretes progesterone for 3 months (maintainng pregnancy)

   b. fertilization does not occur- corpus luteum atrophies, becomes corpus albicans (white scar tissue in ovary), hormonal production of progesterone stops and menstruation occurs.

C. Menstrual Disorders

    1. Amenorrhea- absence of menstruationa.

        a. primary - failure to menstruate by age 16 or by age 14 if secondary sexual characteristics absent

        b. secondary - cessation of menses for at least 6 months in previously
        menstruating woman

    2. Oligomenorrhea- scant menstruation

    3. Menorrhagia- excessive menstruation

    4. Metorrhagia- bleeding between periods

    5. Menometrorrhagia- heavy bleeding both between and during menstrual cycle

    6. Dysmenorrhea- pain or discomfort with menstruation

    7. Premenstrual Syndrome

        a. symptoms begin 7- 10 days before menses

D. Alterations in Uterine Position and Pelvic Support

    1. Cystocele- herniation of blader into vagina

    2. Rectocele- herniation of rectum into vagina

    3. Enterocele - herniation of small bowel into vagina

    4. Uterine Prolapse (providentia uteri)- bulging of uterus into vagina

E. Inflammations and Infections

    1. Vaginitis

        a. caused by C. albicans

        b. caused by Trichomonas vaginalis

        c. bacterial vaginosis

    2. Atrophic vaginitis

    3. Cervicitis

4. Vulvitis

    5. Pelvic Inflammatory Disease (PID)

        a. endometritis (inflammation of uterus)

        b. salpingitis (inflammation of oviducts)

        c. oophoritis (inflammtion of ovaries)

F. Benign Growth and Aberrant Tissues

    1. Endometriosis - functional endometrial tissue found in ectopic sites

        a. mulberry spots

    2. Adenomyosis - endometrial glands and stroma found within myometrium, interspersed between smooth muscle fibers

    3. Leiomyomas (fibroids) - benign neoplasms of smooth muscle

G. Cancer of Genital Structures

    1. Cancer of Vulva

        a. about 5% of all cancers of female genital tract

        b. infection with certani strains of HPV increases risk

    2. Cancer of Vagina

            a. extremely rare- about 1-2% of female genital tract cnacrers

            b. higher incidence, though, in woman exposed to DES while in utero

    3. Cancer of Cervix

        a. if detected early readily cured (importance of PAP smear)

        b. considered a sexually transmitted disese

    4. Endometrial Cancer

        a. most common cancer of female pelvis (2X rate of cervical cancer)

        b. linked to exessive estrogen stimulation

    5. Ovarian Cancer

        a. second most common female genital tract cancer

        b. difficult to diagnose- CA 125 controversial value

H. Breast Cancer

    1. most common malignancy affecting American woman

    2. risk factors

    most significant risk factor is having a relative, mother or sibling, with  breast cancer

    3. medical treatment- use of tamoxifen in ER+

    4. surgical treatment.

  a. modified radical mastectomy- removal of entire breast, dissection of axillary lymph nodes, with or without removing pectoralis minor muscle

b. lumpectomy- removal of portion of breast tissue and axillary lymph nodesc.

c. radical mastectomy- removal of entire breast, axillary lymph nodes and pectoralis major muscle

Discussion  

To protect against infection the vagina has a pH of between 3.8 - 4.2. Such an acidic pH is bacteriostatic to most bacteria. This pH is achieved as a result of a symbiotic relationship with Doderleins bacilli. Estrogen increases the glycogen content of epithelial cells in the vagina. Doderleins bacilli ferment this glycogen to lactic acid, thus lowering the pH of the vagina. The use of antibiotics to treat an infection may also kill Doderlein bacilli and, thus, increase the risk of developing a vaginal infection. Also, after menopause (when estrogen levels dramatically drop), there is less glycogen, hence less fermentation. The loss of acidity due to this can lead to atrophic vagintis.

Both males and females produce FSH and LH. In females FSH leads to the production of estrogen by stimulating the theca interna of the developing follicle and LH leads to the production of progesterone by stimulating the corpus luteum. In males these hormones target the Sertoli cells and interstitial cells of Leydig respectively in order to bring about the maturation of sperm and the production of testosterone.

Ongoing research and clinical trial and error is providing more data regarding the use of estrogen replacement therapy. The benefits of estrogen replacement therapy in postmenopausal woman can occur in several areas: it can be of great benefit to woman with osteoporosis or with increased risk of osteoporosis (because of its effect on bone), it can also be potentially useful in reducing the risk of heart diseae (because of its effect on lipid metabolism). Some research even indicates it may play a role in preventing Alzheimer’s disease. The downside to estrogen replacement therapy is the increased risk of breast and endometrial cancer.

Tamoxifen works in the treatment of breast cancer since it interferes with the ability of cells to take up estrogen. Just as in prostate cancer, the principle here is that cancers of the reproductive system often feed on sex hormones. They need these hormones to grow. If you deprive them of the hormone they will "starve to death", so to speak. So with prostate cancers you give anti- androgens, with breast cancer you give anti- estrogens, or in this case, tamoxifen. Some woman with breast cancer, however, have cancer cells that are ER -, i.e they do not have receptors on their cell surface for estrogen. Obviously, in these cases (about one third of all breast cancers), tamoxifen is not useful. So successful has tamoxifen been in the treatment of breast cancer that studies are being done to determine its efficacy in preventing breast cancer in woman at high risk.