pediagenosis
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Saturday, November 13, 2021

ADNEXAL TORSION

ADNEXAL TORSION

ADNEXAL TORSION

ADNEXAL TORSION


Adnexal torsion is the twisting of part or all of the adnexa on its mesentery, resulting in tissue ischemia and frank infarction. This usually involves the ovary but may include the fallopian tube as well. Although this accounts for only 2% to 3% of all gynecologic operative emergencies, it is nonetheless a significant event that often results in the loss of the ovary. Torsion of the adnexa is usually associated with the presence of an ovarian, tubal, or a paratubal mass (50% to 60% have an ovarian tumor or cyst). The risk of torsion is higher during pregnancy (20% of cases) or after ovulation induction. The average age of patients suffering adnexal torsion is in the mid-20s.

SEROUS CYSTOMA AND CYSTADENOMA

SEROUS CYSTOMA AND CYSTADENOMA

SEROUS CYSTOMA AND CYSTADENOMA

SEROUS CYSTOMA AND CYSTADENOMA


Cystadenomas are the most common ovarian neoplasms. Benign ovarian tumors are most frequently diagnosed at the time of routine examination and are asymptomatic. They are divisible, according to their lining epithelium, into serous and mucinous varieties. Approximately 90% of ovarian tumors encountered in younger women are benign and metabolically inactive. More than 75% of the benign adnexal masses are functional. Functional cysts are not true neoplasms but rather are anatomic variants resulting from the normal function of the ovary.

TERATOMA

TERATOMA

TERATOMA

TERATOMA


The most common ovarian tumor in young, reproductive-age women is the cystic teratoma, or dermoid, which originates from a germ cell and contains elements from all three germ cell layers. These tumors may be benign or malignant (1% to 2% malignant, usually in women older than 40 years). They account for 20% to 25% of all ovarian tumors and one-third of all benign tumors. A dermoid cyst may be microscopic in size or may reach proportions up to 40 cm. Bilateral involvement occurs in 25% of cases. The tumors are usually round or oval, doughy and rather heavy, with a smooth, opaque, gray-white, or yellow surface. Their lardaceous contents tend to harden when chilled. The open specimen reveals fatty, sebaceous material, strands of long hair and an intracystic plug, covered by scalp-like skin. The tufts of hair originate mostly in this skin-lined area. The color of the hair bears no relation to that of the host. The remainder of the cyst lining appears smooth and glistening or rough and granular. Cartilage, bone, and teeth are found in two-thirds of the cases.

MUCINOUS CYSTADENOMA

MUCINOUS CYSTADENOMA

MUCINOUS CYSTADENOMA

MUCINOUS CYSTADENOMA


Mucinous (pseudomucinous) cystadenomas are cystic neoplasms of the ovary in which the lining epithelium is mucus-producing. They are usually unilateral, multilocular, lobulated, smooth-surfaced, tensely cystic, pedunculated, and benign. They represent the most common type of ovarian cyst, occurring with slightly greater frequency than the serous cystadenomas. Usually, they are encountered during the reproductive years (20 to 50 years), rarely before puberty or after the menopause. In contrast to serous epithelial growths, they are less likely to be bilateral (10%) or papillary (10%) and are rarely malignant (5% to 15%). Mucinous cystadenomas may be minute in size or may fill the abdomen: mammoth ovarian cysts are apt to be of the mucinous type. Generally, they are recognized and are removed before reaching a diameter of 15 to 30 cm. Torsion of the pedicle is common (20%). Ascites is rare but may occur. Hydrothorax and hydroperitoneum, as encountered in Meigs syndrome, have been described. Intracystic hemorrhage, secondary suppuration, and spontaneous rupture are rare. Penetration of the capsule, with implantation and growth of mucinous epithelium in the peritoneal cavity, may cause pseudomyxoma peritonei. The rate of growth is generally slow. Rupture of a cyst by trocar, aspiration, or handling should be avoided. Unilateral removal of ovary and tube is the therapy of choice, at which time the specimen must be carefully examined for evidences of localized, firm infiltrations in the cyst wall.

 PAPILLOMA, SEROUS ADENOFIBROMA, AND CYSTADENOFIBROMA

PAPILLOMA, SEROUS ADENOFIBROMA, AND CYSTADENOFIBROMA

 PAPILLOMA, SEROUS ADENOFIBROMA, AND CYSTADENOFIBROMA

PAPILLOMA, SEROUS ADENOFIBROMA, AND CYSTADENOFIBROMA


The serous epithelial tumors of the ovary include three subgroups in which the fibromatous elements over-shadow the proliferation of “serous” epithelium. Although histogenetically similar, they present gross and microscopic differences. These variants may be classified as surface papillomas, adenofibromas, and cystadenofibromas. Adenofibromas are most commonly found as ovarian masses but may also occur in the cervix or uterine body. Adenofibromas are also closely related to cystadenofibromas that contain cystic areas but still contain more than 25% fibrous connective tissue.

PAPILLARY SEROUS CYSTADENOMA

PAPILLARY SEROUS CYSTADENOMA

PAPILLARY SEROUS CYSTADENOMA

PAPILLARY SEROUS CYSTADENOMA


Papillary serous cystadenomas are serous cysts that manifest intra or extracystic papillary growths in addition to adenomatous proliferations. Papillary serous cystadenomas are commonly multilocular, spherical, and lobulated. When papillations are confined to the inner wall, the cyst is apt to be unilateral and may attain a large size. When external and internal papillary masses are present, they are usually smaller and more frequently bilateral. Aside from their papillary structures, these neoplasms grossly resemble the serous cystadenomas. They are irregular in contour, with variations in the size of the component cysts, the color of the serous contents, and the thickness and completeness of the intervening septa. The papillary excrescences are the most striking feature of these tumors. They may involve isolated segments of one or more locules or the entire inner surface. They may be flat, warty, nodular, or villous. Fine, pedunculated, branching papillae may coalesce and form large cauliflower masses. Increased congestion may impart a red or raspberry color. Edema and myxomatous changes may induce a dead-white, swollen, translucent appearance. Necrosis and fatty changes may result in a grayish-yellow hue. Calcium deposits in the form of psammoma bodies render the papillations sandy to the touch.

INFECTIONS

INFECTIONS

INFECTIONS

INFECTIONS


Infections of the ovaries are usually secondary, with most the result of cervical gonococcal or chlamydial infections that have ascended into the upper genital tract (pelvic inflammatory disease [PID]). Tubercular infections and infections in the gastrointestinal tract (particularly in association with appendicitis) also occur. Transmission may be through direct contact with infections of contiguous organs; lymphatic spread, particularly of streptococcal infections of the uterus to the ovarian hilum; and hematogenous extension from distant foci, as may occur in mumps, scarlatina, measles, diphtheria, tonsillitis, typhoid fever, and cholera.

ENDOMETRIOSIS II—PELVIS

ENDOMETRIOSIS II—PELVIS

ENDOMETRIOSIS II—PELVIS

ENDOMETRIOSIS II—PELVIS


Endometriosis refers to the growth of endometrium outside of its normal intrauterine location (ectopic) that retains the histologic characteristics and biologic response of the endometrium. It is nonneoplastic, that is, incapable of autonomous growth, but it is dependent on estrogenic and progesterone stimulation. Endometriosis may arise by one of several proposed mechanisms—lymphatic spread, metaplasia of coelomic epithelium or müllerian rests, seeding by retrograde menstruation, or direct hematogenous spread. Instances of presumed iatrogenic spread (surgical) have been reported. A role for an immunologic defect is debated but remains to be conclusively established. The greatest incidence occurs between 30 and 40 years of age and may be found in 5% to 15% of women, 20% of gynecologic laparotomies, 30% of chronic pain patients, and 30% to 50% of infertility patients.

PHYSIOLOGIC VARIATIONS, NONNEOPLASTIC CYSTS

PHYSIOLOGIC VARIATIONS, NONNEOPLASTIC CYSTS

PHYSIOLOGIC VARIATIONS, NONNEOPLASTIC CYSTS

PHYSIOLOGIC VARIATIONS, NONNEOPLASTIC CYSTS


The preponderance of small cystic structures within the ovary represents physiologic variations of the normal ovulatory cycle. These follicle and corpus luteum derivatives are nonneoplastic, that is, they are incapable of autonomous growth. Their clinical recognition and differentiation from true ovarian cysts are most important. A small neoplastic ovarian cyst may be simulated by a single, large follicle cyst, by multiple cystic follicles, or by a corpus luteum cyst. A large or cystic corpus luteum of pregnancy may be mistaken for an ectopic pregnancy or an ovarian cyst. A corpus luteum hematoma may present with signs comparable to those associated with torsion of a small cyst. A ruptured graafian follicle or ruptured hemorrhagic corpus luteum may be misdiagnosed as acute appendicitis or ruptured tubal pregnancy. It is not uncommon to find adnexal cysts during pelvic ultrasonography performed for other reasons, and these are generally not of any clinical significance. Follicle cysts are distended atretic follicles more than 6 to 8 mm in diameter. They are usually not more than 1 to 2 cm in diameter, thin-walled, translucent, and filled with watery fluid. The cysts may project slightly above the surface of the ovary or may lie more deeply within the cortex. If pricked, the follicle fluid may spurt out under pressure. The inner lining appears smooth and glistening. Microscopically, the granulosa cell lining varies in thickness and may be well preserved or may show evidence of degeneration. On pelvic examination, a unilateral, smooth, cystic, slightly tender, movable, plum-sized ovary may be felt. Therapy is based on the principle that during the reproductive years a cystic ovary up to 6 cm in diameter is presumed, unless proved otherwise, to be a physiologic variation that will undergo subsequent resorption. The patient is reexamined at intervals. If the ovarian enlargement per- sists or increases in size, surgical intervention may be indicated.

GONADAL DYSGENESIS

GONADAL DYSGENESIS

GONADAL DYSGENESIS

GONADAL DYSGENESIS


Gonadal dysgenesis is a developmental abnormality of patients who do not carry the stigmata of Turner syndrome but still suffer absent menarche because of chromosomal abnormalities and abnormal (streak) gonads. These patients are generally tall (150 cm), are more normal in appearance, and are a chromosomally heterogeneous group: 46, XX, 46, XY, or mosaic X/XY karyotypes. Classic Turner syndrome is caused by the absence of one X chromosome. Turner syndrome is a collection of stigmata that include edema of the hands and feet, webbing of the neck, short stature, left-sided heart or aortic anomalies, and gonadal dysgenesis resulting in primary amenorrhea and infertility.

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