The Female Genital Tract

Figure 13.1

Normal external genitalia, gross

In the left panel, adult external genitalia include the labia majora (∗), labia minora (♦), clitoris (▲), vaginal orifice (□), and perineum (□) extending to the anus (▼). In the right panel, the appearance of the genitalia at birth illustrates the relationship of the vaginal orifice (□), perineum (□), and anus (▼) The external genitalia are covered by keratinizing stratified squamous epithelium.

Figure 13.2

Normal internal genitalia, gross

The gross appearance of a normal uterus from a young woman includes the fundus (∗), lower uterine segment (♦), cervix (▼), vaginal cuff (▲), right fallopian tube (▶), left fallopian tube (◀), right ovary (□), and left ovary (□). In the developing embryo, primordial germ cells from the yolk sac wall migrate to the urogenital ridge to become ovarian germ cells within the epithelium and stroma derived from urogenital ridge mesoderm. The unfused portions of the müllerian (paramesonephric) ducts form the fallopian tubes, and the fused portions become the uterus and vagina, whereas the distal fused ducts contact the urogenital sinus to become the vestibule of the external genitalia.

Figure 13.3

Normal internal genitalia, radiograph

This is a hysterosalpingogram, in which a catheter is introduced through the cervix (▲) to fill the endometrial cavity (♦) with contrast material. Contrast material extends into the right fallopian tube and left fallopian tube, eventually spilling out through the fimbriated ends of the fallopian tubes (oviducts) in the right adnexal (▶) and left adnexal (◀) regions, indicating normal tubal patency. Some contrast material here has also backfilled into the vagina. This radiographic study may be undertaken as part of an infertility work-up.

Figures 13.4 and 13.5

Bartholin gland cyst, MRI and microscopic

A small, bright cyst (▶) of the Bartholin gland is seen in the left panel . These paired glands are 0.5 cm in size and produce mucinous secretions emptying through ducts onto the vaginal vestibule surface. A gland duct can become obstructed, leading to cystic glandular enlargement with inflammation and infection, producing a fluctuant labial mass with pain and discomfort. A Bartholin cyst can reach 3 to 5 cm in size. In the right panel, the cyst with flattened transitional or squamous lining (◀) is at the far right, with remaining adjacent normal glands at the left.

Figure 13.6

Lichen sclerosus, gross

The pale white patches (◀) of leukoplakia seen here on the vulva with accompanying atrophy and fibrosis can narrow the introitus and produce discomfort as well as pruritus, dyspareunia, dysuria, or bleeding. This process can develop slowly and involve progressively more labial skin surface in women, particularly after menopause. Lichen sclerosus increases the risk for secondary infection. Less than 5% of these lesions progress to differentiated vulvar intraepithelial neoplasia, not associated with human papillomavirus.

Figure 13.7

Lichen sclerosus, microscopic

There is atrophy of the vulvar squamous epithelium with thinning, loss of rete pegs, hydropic degeneration of basal keratinocytes (◀), dermal dense band collagenous fibrous thickening (▪), and sometimes a bandlike infiltrate of lymphocytes (not present here). These findings suggest an autoimmune process. Local irritation, ischemic stress, and reduced 5α-reductase activity may play a role in its etiology. Lichen simplex chronicus also appears as patches of leukoplakia, but has pronounced hyperkeratosis and dermal inflammation.

Figure 13.8

Lichen simplex chronicus, microscopic

Note the thickened (acanthotic) epidermis and overlying keratin (♦) layer (hyperkeratosis), giving a grossly white appearance (leukoplakia). There is no atypia of the keratinocytes. This lesion arises from mechanical irritation with rubbing or scratching pruritic skin to relieve pruritus. This squamous cell hyperplasia does not show atypia, but may appear next to differentiated vulvar intraepithelial neoplasia.

Figure 13.9

Papillary hidradenoma, microscopic

The vulva has modified apocrine sweat glands from which a papillary hidradenoma may arise. It forms a sharply circumscribed nodule, most commonly in the labia majora or interlabial folds. A vulvar carcinoma may be suspected because the hidradenoma tends to ulcerate. Microscopic appearance is similar to an intraductal papilloma of the breast. As shown here, there is a regular papillary growth pattern with tubular ducts lined by a single or double layer of nonciliated columnar cells, with a layer of flattened “myoepithelial cells.” This lesion underlies the epithelium at the upper right. Myoepithelial elements are characteristic of sweat glands and sweat gland tumors.

Figures 13.10 and 13.11

Condyloma acuminata, gross and microscopic

Note the pale pink lesions (◀) on the vulva shown in the left panel. These warty (verrucous) excrescences can involve the perineum, vulva, and perianal region, typical of sexually transmitted human papillomavirus (HPV) infection, often HPV subtypes 6 and 11. The lesions can be solitary or multiple. The squamous epithelium becomes thickened, and there is perinuclear vacuolization to produce the characteristic cytologic “koilocytotic atypia” (▲) seen in the right panel. Condylomata are benign and do not progress to malignancy. They may remain the same size, regress spontaneously, or enlarge slowly.

Figure 13.12

Vulvar dysplasia, microscopic

Dysplasia (♦) may involve the vulvar epithelium as a consequence of human papillomavirus (HPV) infection. Note the overlying hyperkeratosis (∗) (which produces a grossly visible area of leukoplakia), acanthosis, and club-shaped rete ridges. Normal (but atrophic) keratinizing squamous epithelium (▪) is at the left. Most cases of vulvar intraepithelial neoplasia do not progress to invasive cancer, but the risk is greater with HPV subtypes 16 and 18. Many lesions are multicentric, and some occur in association with cervical or vaginal squamous carcinoma. In older women, differentiated vulvar carcinomas may be preceded by lichen sclerosus, not HPV infection.

Figure 13.13

Clear cell carcinoma, microscopic

Neoplasms of the vagina are rare. Note the vacuolated cells forming irregular clusters with ill-defined glandular lumens. Red, granular foci that appear on the vaginal mucosa are called adenosis and may precede clear cell carcinoma, a lesion most likely to occur in a young woman whose mother was given diethylstilbestrol (DES) during pregnancy. These cancers are rare, even in women with this history. DES exposure increases the risk for clear cell carcinoma arising in the upper vagina and cervix of adolescents and young adults. Clear cell carcinoma often becomes invasive before detection and is difficult to cure.

Figure 13.14

Normal cervix, gross

Note the smooth, glistening mucosal surface. There is a small rim of vaginal cuff (♦) seen in this hysterectomy specimen. The cervical os is small and round, typical of a nulliparous woman. The os attains a fish-mouth shape after one or more pregnancies. The os leads into the endocervical canal. This little os can dilate to 10 cm during the birth process.

Figure 13.15

Normal cervix, microscopic

This is normal cervical nonkeratinizing squamous epithelium. The squamous cells show maturation from the basal layer (◀) toward the overlying surface at the left. A Pap smear is obtained by scraping or brushing the surface of the cervix (and sometimes the vagina) to obtain cells that are placed in a fixative solution, stained, and examined cytologically. The maturation pattern of these cells gives an indication of the woman’s hormonal status and changes during the normal menstrual cycle. Inflammatory cells and infections can be seen on a Pap smear. Dysplastic and malignant changes can also be detected.

Figure 13.16

Normal cervix and vagina, gross

The normal adult vaginal mucosa (□) in reproductive-age women has a wrinkled appearance. The cervix (∗) has been opened anteriorly at autopsy to reveal an endocervical canal leading to the lower uterine segment (♦) on the right that has an erythematous appearance extending to the cervical os (▪), consistent with chronic inflammation. The cervix has an underlying dense fibromuscular stroma that appears white on cut section.

Figure 13.17

Nabothian cyst, gross

A large translucent Nabothian cyst (□) is seen extending from the stroma around the outer endocervical canal in an exophytic manner into the canal. Inflammation with cervicitis may produce submucosal gland obstruction so that glandular cystic dilation occurs. These cysts are filled with a clear, mucoid fluid. These are common lesions, generally ranging from a few millimeters to 1 cm in size. They are benign.

Figure 13.18

Normal cervical transformation zone, microscopic

Normal ectocervix with stratified nonkeratinizing squamous epithelium (▼) merges at the transformation zone (squamocolumnar junction) into endocervix lined by tall mucinous columnar cells (◀), as seen here at low magnification. Underlying endocervical glands in the stroma are also lined by tall mucinous columnar cells. The thick mucus from these glands is protective, but becomes thinner following ovulation to enhance passage of spermatozoa.

Figure 13.19

Chronic cervicitis, gross

Inflammation typically begins at the squamocolumnar junction of the cervix and can extend to involve the ectocervical squamous epithelium. The uterus has been opened anteriorly here to reveal the endocervical canal (∗) and lower uterine segment (▪). Note the erythematous appearance (♦) of this inflamed cervical epithelium. During reproductive years, estrogen levels promote maturation with glycogen uptake of cervical and vaginal squamous epithelium, and this glycogen provides a substrate for the normal vaginal bacterial flora keeping the pH low to inhibit proliferation of pathogenic organisms.

Figure 13.20

Chronic cervicitis, microscopic

Chronic cervicitis seen here at the squamocolumnar junction of the cervix has small, round, dark-blue lymphocytes along with red blood cells in the submucosa. Chronic cervicitis is quite common. Bacterial organisms, including streptococci, staphylococci, enterococci, and coliforms, and the fungus Candida, and the protozoan Trichomonas vaginalis, may contribute to cervicitis and vaginitis, which typically have a clinical course marked by episodes of acute inflammation that blend into chronic inflammation. The repair reaction to the inflamed and eroded epithelium may produce mildly atypical–appearing cells (“inflammatory” atypia) on a Pap smear.

Figure 13.21

Chronic cervicitis, microscopic

A predominantly lymphocytic infiltrate extends around this submucosal endocervical gland in the stroma of the cervix beneath the surface epithelium. Overlying cervical epithelial erosion, ulceration, and repair may accompany this inflammation. Local trauma or chemical irritation from douches, creams, tampons, or other items may contribute to inflammation. There is some degree of cervicitis in many women, but the amount of inflammation is minimal, and usually no significant health problems are related to it.

Figure 13.22

Cervical squamous metaplasia, microscopic

In this endocervical gland, the normal columnar epithelium (▶) is transforming to non-keratinizing squamous-appearing epithelium (♦) as a consequence of an ongoing inflammatory process. Metaplasia is a potentially reversible process in which one type of epithelium is exchanged for the normal epithelium. Metaplasia may be the first step in epithelial cellular alteration leading to dysplasia.

Figure 13.23

Bacterial vaginosis, wet mount, microscopic

The surface squamous epithelial cells shown have refractile bacteria plastered over their surfaces, a morphologic appearance called “clue cells” (their appearance is a “clue” to the diagnosis) and indicative of bacterial vaginosis. Normal vaginal flora includes large Gram-positive rods of lactobacilli maintaining a normal acid pH. Bacterial vaginosis includes Gram-negative cocci of Gardnerella vaginalis and small curved rods of Mobiluncus spp., among others. Inflammatory cells and infectious agents such as Candida albicans, trichomonads, and “clue cells” can also be detected on a Pap smear.

Figure 13.24

Human papillomavirus (HPV) effect, microscopic

This cervical biopsy shows a thickened squamous epithelium at the left with a vacuolated appearance (▲), called koilocytotic change (compare with normal cervical epithelium at the right). Condyloma acuminatum of external genitalia has a similar appearance. These changes typically result from HPV infection. Most healthy women clear an HPV infection after several years. HPV can be subtyped into high-risk and low-risk varieties. High-risk varieties include HPV subtypes 16 and 18. The E6 and E7 oncoproteins in these HPV subtypes bind to p53 and promote its degradation, while E7 binds to RB and up-regulates DNA synthesis.

Figure 13.25

Cervical squamous dysplasia, Pap smear

Pap smear screening has reduced the incidence of and death rate from cervical carcinoma because dysplasias and early carcinomas can be detected and treated to prevent invasive carcinomas. The cytologic features of normal squamous epithelial cells can be seen at the center top and bottom, with orange to pale blue, platelike squamous cells with small pyknotic nuclei. Dysplastic cells in the center extending to the upper right have larger, darker, more irregular nuclei (▲). Lesions with mild dysplasia are cervical intraepithelial neoplasia (CIN) I, or low-grade squamous intraepithelial lesion. A high-grade squamous intraepithelial lesion correlates with moderate to severe dysplasias (CIN II or III).

Figure 13.26

Cervical squamous carcinoma, Pap smear

This Pap smear shows more pleomorphic, darker, and larger cells (▼) indicative of a carcinoma. The neutrophilic inflammation and red blood cells in the background are characteristic of a more aggressive, ulcerative, and invasive lesion. It is essential to follow up an abnormal Pap smear showing dysplasia or carcinoma with a biopsy and treatment. Risk factors for cervical neoplasia include early age at first intercourse, multiple sexual partners, increased parity, male sexual partners with multiple previous sexual partners, and exposure to high-risk human papillomavirus subtypes 16 and 18 (causing 70% of cancers), as well as 31, 45, 33, 35, 39, 51, 52, 56, 58, 66, 68, and 70.

Figure 13.27

Cervical intraepithelial neoplasia grade I, microscopic

In this biopsy, the dysplastic, disordered cells (♦) occupy less than one third of the squamous epithelial thickness above the basal lamina, so this is LSIL (CIN I). Note the clear koilocytotic change in some cells, consistent with human papillomavirus effect. The term atypical squamous cells of undetermined significance may be applied in some Pap smear reports when there are abnormal cells, but an exact classification is not possible, and further follow-up is warranted. The term low-grade squamous intraepithelial lesion (LSIL) denotes mild dysplasia that likely will regress within 2 years.

Figure 13.28

Cervical intraepithelial neoplasia grade II (HSIL), microscopic

In this cervical biopsy sample, the dysplastic, disordered cells occupy about one third ♢ to one half ♦ the thickness of the epithelium, and the basal lamina is still intact, so this is CIN II. Moderate to severe dysplasias (CIN II and III) correlate with a high-grade squamous intraepithelial lesion (HSIL) and infection with more aggressive forms of human papillomavirus. There is continued expression of E6/E7 oncogenes with destabilizing influences on the cell cycle. There is up-regulation of p16/INK4 with increased expression of p16, a cyclin-dependent kinase inhibitor. Nevertheless, dysplasias tend to progress over many years, giving plenty of opportunity to find the early lesions with periodic Pap smear screening and treatment by excising the dysplastic areas. Colposcopy may aid in detection of the abnormal areas for removal.

Figure 13.29

HSIL (CIN III), microscopic

In this biopsy, there is severe cervical squamous dysplasia extending from the center to the right, compared with normal nondysplastic epithelium at the left. Note how the dysplastic cell nuclei are larger and darker, and the dysplastic cells have a disorderly arrangement within the epithelium. This dysplastic process involves the full thickness of the epithelium, but the basal lamina (▲) is intact, so this is a high-grade squamous intraepithelial lesion (HSIL), also designated as severe dysplasia/carcinoma in situ under the CIN III heading. HSIL has significant risk for progression to invasive carcinoma.

Figure 13.30

Squamous cell carcinoma, gross

This hysterectomy specimen shows a cervical squamous cell carcinoma (▶) from 3 o’clock to 7 o’clock around the cervical os. It is a red to tan to yellow mass that is exophytic (growing outward and extending above the surrounding normal smooth tan epithelium). It is still limited to the cervix (stage I). The 5-year survival rate for cervical intraepithelial neoplasia is essentially 100%, and it is more than 95% for microinvasive carcinomas (stage Ia). Five-year survival rates of 80% to 90% occur when the neoplasm is more invasive but still confined to the cervix (stage Ib). Cervical carcinomas may begin appearing in the second decade, but the peak incidence is in the fifth decade.

Figure 13.31

Squamous cell carcinoma, gross

This total abdominal hysterectomy with bilateral salpingo-oophorectomy on sectioning in half through the anterior uterus shows an advanced cervical squamous cell carcinoma (▲) that has spread to the vagina. This stage II cervical carcinoma has extended beyond the cervix, but not to the pelvic side wall. The 5-year survival rate is 75%. In stage III, the carcinoma has spread to the pelvic side wall, and the 5-year survival is less than 50%.

Figure 13.32

Squamous cell carcinoma, gross

This is a pelvic exenteration done for stage IV cervical carcinoma, which involves bladder or rectum or extends beyond the true pelvis. Dark vulvar skin (□) leads to the vagina (▼) and to the cervix (▲) in the center, where an irregular tan tumor mass (♦) is seen infiltrating upward into the bladder (∗). A slit like endometrial cavity (×) is surrounded by myometrium at the mid-right. The rectum (□) and sigmoid colon are at the bottom extending to the right. The 5-year survival rate approaches 5%, but that is still 1 in 20, and the quality of life with a reconstructed ileal bladder and colostomy (or Koch pouch) after exenteration is adequate for an active lifestyle. Advanced cancers require a realistic, but not futile, approach.

Figure 13.33

Cervix, squamous cell carcinoma, CT scan

CT scan of the pelvis shows a large mass (♦) with heterogeneous attenuation from necrosis and air-filled spaces arising in the cervix and extending anteriorly to the bladder (▼) and posteriorly to the rectum (▲). This squamous cell carcinoma of the cervix has invaded rectum and bladder and is stage IV.

Figure 13.34

Cervix, squamous cell carcinoma, microscopic

Nests (▲) of squamous cell carcinoma are invading downward and undermining the mucosa. There is loss of the epithelial surface from ulceration at the left, compared with thickened but non-neoplastic epithelium at the upper right, below which are dark blue lymphocytes of a chronically inflamed stroma. Most cervical carcinomas are composed of large pink keratinizing or nonkeratinizing squamous cells. Less than 5% are composed of small undifferentiated cells or neuroendocrine cells. Adenocarcinomas arising in the cervix are uncommon.

Figure 13.35

Endometrial hormonal cycle, diagram

The normal endometrial hormonal cycle averages 28 days. The proliferative (follicular) portion of the cycle varies among women, but tends to remain the same for any one woman. The time from ovulation to menstruation in the secretory (luteal) portion of the cycle is a constant 14-day period, with early, mid, and late phases. The menstrual portion of the cycle averages 3 to 7 days. This cycle is controlled by follicle-stimulating hormone (FSH) and luteinizing hormone (LH) secretion from the adenohypophysis, which is under negative feedback control by ovarian steroids, mainly estradiol, and by inhibin (which selectively suppresses FSH). FSH secretion is inhibited as estrogen levels increase about 8 to 10 days before ovulation. In the latter half of the follicular phase, LH begins to increase, reaching a peak, along with estradiol secretion, that is driven by positive feedback from increasing progesterone levels, to trigger ovulation. The luteal phase is marked by decreasing FSH and LH with increasing progesterone and estrogen levels. If fertilization does not occur, estrogen and progesterone levels decrease to trigger menses with sloughing of the endometrial stratum functionalis layer.

Figure 13.36

Endometrium, proliferative, microscopic

The proliferative (follicular) phase is the variable part of the menstrual cycle, but averages about 14 days in many women. In this phase, tubular endometrial glands lined by tall columnar cells and surrounded by a dense stroma are proliferating to build up the amount of functional endometrium after completion of the previous cycle with shedding from menstruation. Mitoses within these proliferating glands can be seen.

Figure 13.37

Endometrium, early secretory, microscopic

This appearance with prominent clear subnuclear vacuoles (◀) in the tall columnar cells lining these larger endometrial glands is consistent with postovulatory day 2 of the luteal phase of the menstrual cycle. The histologic changes after ovulation are constant over the next 14 days to menstruation and can be used to date the endometrium with biopsy for diagnostic purposes.

Figure 13.38

Endometrium, mid-secretory, microscopic

The mid-secretory endometrium of the normal menstrual cycle shows prominent clear stromal edema (▪). The endometrial glands are becoming larger and more tortuous as well. Some of the stromal cells have pink cytoplasm, representing the decidualizing effect (♦) of the increasing estrogen and progesterone levels in the luteal phase of the cycle after the LH surge has induced ovulation.

Figure 13.39

Endometrium, late secretory, microscopic

The tortuosity of the endometrial glands is apparent in this late secretory endometrium of the luteal phase of the normal menstrual cycle, and there are pink intraluminal secretions (◀) within the large glands. There is more pronounced pink decidualization of the surrounding stroma. Such an endometrium is now able to support implantation with continued development of a blastocyst from a fertilized ovum.

Figure 13.40

Endometrium, menstrual, microscopic

The menstrual phase endometrium is marked by breakdown of the glands and stroma from cellular intrinsic apoptosis triggered by declining estrogen and progesterone levels. There is hemorrhage and leukocyte infiltration. The upper two thirds of the endometrium, the functionalis layer, is shed. From the lower third, the basalis layer, which does not respond in similar manner to the ovarian hormones, will arise a new endometrial lining in the next cycle.

Figure 13.41

Endometrium, anovulatory cycle, microscopic

Dysfunctional uterine bleeding is most often due to anovulatory cycles, which are most apt to occur during the reproductive years just after menarche and just before menopause. Endocrine abnormalities of the pituitary or ovary may also be implicated, as may obesity or any chronic disease state. The failure of ovulation leads to an inadequate luteal phase with prolonged estrogenic stimulation without the progestational phase. This produces a persistent proliferative endometrial pattern and eventual stromal breakdown with bleeding. The biopsy sample seen here, on what should be postovulatory day 8, shows minimal glandular development and stromal hemorrhage.

Figure 13.42

Endometrium, oral contraceptive effect, microscopic

The endometrial stroma here is markedly decidualized, with large cells having abundant pink cytoplasm, whereas the few endometrial glands (◀) are small and inactive. These changes prevent successful implantation of the blastocyst, but the primary effect of contraceptive agents is prevention of ovulation. The effect on the endometrium is not permanent, and the endometrium typically returns to normal cyclical changes when the oral contraceptives are discontinued.

Figure 13.43

Endometrium, postmenopausal, microscopic

Note the thin endometrial layer with dense stroma containing small tubular endometrial glands scattered amid other cystically dilated glands (♦) that are lined by flat, atrophic-appearing epithelial cells. After menopause, which typically occurs in the late 40s to early 50s, there is reduced ovarian function with subsequent loss of regular hormonal cycles and decreased ovarian output of the estrogen and progesterone necessary to drive endometrial growth and cycling. Levels of FSH and LH from the pituitary increase as a result of the loss of the feedback loop through the ovaries.

Figure 13.44

Acute endometritis, microscopic

There are scattered neutrophils (▶) within these endometrial glands and stroma, indicative of acute endometritis, a condition that is most often a complication of childbirth (“puerperal sepsis” or “postpartum fever”); causative organisms include group B Streptococcus and Staphylococcus aureus . Retained products of conception after delivery increase the risk for endometritis. With good obstetric care, this condition is uncommon, but throughout human history, it accounted for significant maternal morbidity and mortality, as Dr. Semmelweis observed and addressed. Chlamydial infections also may produce an acute or chronic endometritis.

Figure 13.45

Chronic endometritis, microscopic

Collections of lymphocytes (◀) within the endometrial stroma are shown. At higher magnification, plasma cells would be identified. Chronic endometritis is present to a milder degree when an intrauterine device is present (the low-grade inflammation induced by some of these devices, designed to create a spermicidal environment, secondarily prevents implantation). The more marked inflammation seen here can occur postpartum, typically with retained products of conception, post abortion, or with chronic pelvic inflammatory disease. In one sixth of patients, there is no definable cause. Affected women can have pelvic pain, fever, vaginal discharge, and infertility.

Figure 13.46

Granulomatous endometritis, microscopic

This endometrial stroma contains ill-defined granulomas (∗) with epithelioid macrophages having abundant pink cytoplasm, and a multinucleated Langhans giant cell. The granulomatous form of chronic endometritis can be due to drainage of tuberculous salpingitis into the endometrial cavity. This can occur in a patient with disseminated tuberculosis.

Figure 13.47

Adenomyosis, MRI

In this T2-weighted MR image of the pelvis in midline sagittal view, the uterus shows abnormally low T2 signal intensity with obliteration of the junctional zone, consistent with adenomyosis (♦). The uterus is enlarged by this process. The bladder anteriorly (▪) is filled with bright fluid, whereas the sigmoid (□) and rectum posteriorly appear dark. Note the normal appearance of the sacrum (+). This obese patient has abundant subcutaneous adipose tissue (∗). Pathogenesis may involve overexpression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor 1-α, increasing the number of small vessels in the endomyometrial junctional zone, identified on MRI as ≤5 normally, increasing with age, and at least 1.1 mm with adenomyosis.

Figure 13.48

Adenomyosis, gross

The thickened and spongy-appearing myometrial wall of this sectioned uterus is typical of adenomyosis, a condition in which endometrial glands with (or without) stroma are located within the myometrium. Twenty percent of uteri examined after hysterectomy have some degree of adenomyosis, usually not as florid as this case. The uterus may become enlarged, usually symmetrically, and there may be menometrorrhagia, dysmenorrhea, dyspareunia, or pelvic pain. Fertility can be reduced. (An incidental small round white leiomyoma [▶] also is shown.)

Figure 13.49

Adenomyosis, microscopic

Downward growth of the endometrium more than 2 mm from the stratum basalis into the myometrium may account for adenomyosis. In this section through the myometrium, a cluster of endometrial tissue can be seen with glands (♦) and surrounding stroma, typical of adenomyosis. Because these foci are derived from the endometrial stratum basalis, there is usually no significant menstrual cycle bleeding within the foci themselves. This condition can lead to spontaneous pre-term delivery and pre-term premature rupture of the membranes.

Figure 13.50

Endometriosis, gross

About 10% of women have endometrial glands and stroma found outside the uterus, a very disabling and painful condition, even when just a few of these small foci are present. Clinical features include dyspareunia, pelvic pain, dysmenorrhea, and infertility. There is bleeding into these foci of endometriosis, and the blood is dark (from deoxygenation and from breakdown to hemosiderin), giving them the gross appearance of “powder burns.” The small nodular foci (▶) are seen here just beneath the serosa of the posterior uterus in the pouch of Douglas. Such endometriotic lesions can be identified and obliterated by cauterization during laparoscopy.

Figure 13.51

Endometriosis, gross

Typical locations for endometriosis include ovaries, uterine ligaments, rectovaginal septum, pelvic peritoneum, and laparotomy scars. Endometriosis may be found at more distant locations, such as appendix and vagina. This is a section through an enlarged 12-cm ovary to show a cystic cavity filled with old blood typical of endometriosis with formation of an endometriotic, or “chocolate,” cyst. The chocolate cyst is so named because the old blood in the cystic space formed by the hemorrhage is broken down to produce hemosiderin, which has a brown to black color.

Figure 13.52

Endometriosis, microscopic

A focus of endometriosis (◀) with a small cluster of endometrial glands and stroma with hemorrhage is seen within smooth muscle, adjacent to mucosa of appendix at the left. Theories for the origin of endometriosis include metaplastic change in coelomic epithelium, regurgitation of menstrual tissue out the fallopian tube with implantation onto the peritoneum, Müllerian embryonic rests, or vascular dissemination of endometrial tissues through veins or lymphatics. Endometriotic stromal cells express high levels of aromatase that increase estrogen production, and pro-inflammatory cytokines such as prostaglandin are released. There is an increased risk for development of endometrioid and clear cell carcinomas in foci of endometriosis.

Dec 29, 2020 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on The Female Genital Tract

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