pediagenosis: Reproductive
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Showing posts with label Reproductive. Show all posts

Tuesday, November 16, 2021

CONDITIONS SIMULATING OVARIAN NEOPLASMS II

CONDITIONS SIMULATING OVARIAN NEOPLASMS II

CONDITIONS SIMULATING OVARIAN NEOPLASMS II

Mesenteric cyst. Rarely, a cyst of the mesentery of the transverse colon or small bowel or of the omentum may reach large proportions and simulate a pedunculated, freely movable, extrapelvic ovarian cyst.

CONDITIONS SIMULATING OVARIAN NEOPLASMS II


Polycystic kidney. The multilocular cystic replacement of the renal cortex and medulla may reach a huge size. On abdominal palpation the possibility of a large, adherent ovarian cyst may be suggested. Intravenous pyelography may demonstrate the bilateral renal involvement and characteristic elongation and spreading apart of the calyces. Abdominal ultrasonography will demonstrate the classic cystic nature of the kidneys and cysts, if present in the liver.

CONDITIONS SIMULATING OVARIAN NEOPLASMS I

CONDITIONS SIMULATING OVARIAN NEOPLASMS I

CONDITIONS SIMULATING OVARIAN NEOPLASMS I

Low-lying distended cecum. Normally, the cecum lies in the right iliac fossa upon the iliopsoas muscle, with its apex or lowest point a little to the mesial side of the middle of the inguinal ligament. In some cases, however, the cecum hangs over the pelvic brim or is lodged entirely within the pelvic cavity. It may be mistaken for an ovarian cyst.

CONDITIONS SIMULATING OVARIAN NEOPLASMS I


Redundant sigmoid colon. The sigmoid lies in close relationship to the uterine fundus within the true pelvis. When the redundant loop is filled with fecal material or gas, it may suggest the possibility of ovarian neoplasm.

DIAGNOSIS OF OVARIAN NEOPLASMS

DIAGNOSIS OF OVARIAN NEOPLASMS

DIAGNOSIS OF OVARIAN NEOPLASMS

Ovarian neoplasms may be found at any age. The majority occur during the reproductive years, though about 4% are present in children less than 10 years old. Of these, about half are malignant (dysgerminoma, solid teratoma, carcinoma, granulosa cell tumor) and the remainder benign (dermoid and epithelial cysts). Malignancy may be expected in about 15% of all ovarian tumors. The highest incidence of ovarian malignancy occurs between 40 and 60 years of age.

DIAGNOSIS OF OVARIAN NEOPLASMS


The most important objective of the management of an ovarian mass is the timely diagnosis of its type and origin. Subsequent therapy and assessment of risk are based on the correct diagnosis. For acutely symptomatic cysts, rapid evaluation and intervention may be necessary.

SECONDARY OVARIAN CARCINOMA

SECONDARY OVARIAN CARCINOMA

SECONDARY OVARIAN CARCINOMA

SECONDARY OVARIAN CARCINOMA


Metastatic cancer of the ovary accounts for only about 5% of ovarian cancer. The ovary is particularly prone to metastatic invasion by carcinoma. The primary sites include the breast, stomach, small and large intestine, appendix, liver, gallbladder, bile ducts, pancreas, uterus, tubes, opposite ovary, bladder and ureters, lungs, and meninges. Frequently, metastases are from primary tumors that originate elsewhere in the female reproductive tract, particularly from the endometrium and fallopian tube. Secondary ovarian carcinoma is most frequently seen from the fourth to the sixth decades of life. The ovaries are bilaterally involved in 66% to 75% of cases. Ascites is often evident (50%). The ovarian neoplasms may be asymptomatic or may manifest symptoms and signs similar to those produced by primary ovarian carcinoma. In the presence of a known primary lesion and palpable enlargement of the ovaries, the diagnosis of secondary carcinoma may reasonably be suspected. Similarly, the discovery of bilateral, solid ovarian growths on pelvic examination is an indication for a thorough search for a primary source elsewhere. Esophagoscopy, gastroscopy, sigmoidoscopy, or colonoscopy should be considered as a part of the evaluation when a gastrointestinal source is being sought.

PRIMARY SOLID CARCINOMA

PRIMARY SOLID CARCINOMA

PRIMARY SOLID CARCINOMA

PRIMARY SOLID CARCINOMA

Primary solid ovarian carcinomas, also designated as the undifferentiated or unclassified group, may be arbitrarily divided on the basis of the architectural pattern of the epithelial and connective tissue elements into solid adenocarcinoma, medullary carcinoma, scirrhous carcinoma, alveolar carcinoma, plexiform carcinoma, clear cell, endometrioid, and adenocarcinoma with squamous cell metaplasia (adenoacanthoma). Primary solid carcinomas of the ovary are less common than the cystic variety. They may be unilateral or bilateral, small or large, ovoid or round, smooth or nodular, grayish- pink in color and solid. The consistency and color are dependent upon the proportionate amounts of epithelial and connective tissue elements. If very cellular, they are apt to be relatively soft, meaty, and pink, often with areas of degeneration. If less cellular, they may be firm and whitish gray. Focal necrosis, hemorrhage, cavitation, deposition of calcium, and psammoma bodies are not infrequent. In advanced cases, penetration of the capsule, infiltration, extension, and metastases occur.

PRIMARY CYSTIC CARCINOMA

PRIMARY CYSTIC CARCINOMA

PRIMARY CYSTIC CARCINOMA

PRIMARY CYSTIC CARCINOMA


Ovarian cancer represents the second most common malignancy of the genital tract (after endometrial cancer), but is the most common fatal gynecologic cancer. The lifetime risk of developing ovarian cancer is approximately 1 in 70. Papillary serous cystadenocarcinomas make up a high proportion of most reported series of ovarian carcinomas. Roughly half of all ovarian cystic cancers occur after menopause, with an average age of 59 years, and the highest rate between 60 and 64 years. Despite this, only one-quarter to one-third of ovarian tumors in postmenopausal women are malig- nant. A family pattern is recognized in a small percentage of cases. There is an association with abnormalities of the breast cancer (BRCA1 and BRCA2) gene. Hereditary ovarian cancers are rare but usually fatal; 95% of ovarian cancers are sporadic. More than 95% of patients with ovarian cancer have no risk factor. Oral contraception, high parity, tubal ligation, hysterectomy, and breast-feeding reduce risk.

STROMATOGENOUS NEOPLASMS

STROMATOGENOUS NEOPLASMS

STROMATOGENOUS NEOPLASMS

STROMATOGENOUS NEOPLASMS


Ovarian fibromas are benign stromatogenous tumors. The most common benign ovarian tumor, this tumor is composed of stromal cells (fibroblasts). Although benign, these tumors are sometimes associated with ascites and hydrothorax (Meigs syndrome, 1% of patients). They may be minute or may reach a diameter of more than 27 cm. Unilateral involvement is usual (90%). Multiple fibromas of a single ovary occur occasionally (10%). Though encountered at any age, the majority are found postmenopausally. Because of its weight, torsion of the pedicle is apt to occur.

DYSGERMINOMA, BRENNER TUMOR

DYSGERMINOMA, BRENNER TUMOR

DYSGERMINOMA, BRENNER TUMOR

DYSGERMINOMA, BRENNER TUMOR


The dysgerminoma is an ovarian tumor made up of germ cells and stroma that appear analogous in structure to the seminomas found in the male testes. Although rare, these tumors are the most common malignant germ cell tumors (1% to 2% of ovarian malignancies). At times, they may be associated with evidence of sexual underdevelopment or pseudoher-maphroditism. Although found at all ages, at least 75% of cases occur in young individuals between 10 and 30 years of age. Unilateral involvement is usual (90%).

Saturday, November 13, 2021

ENDOCRINOPATHIES II—POLYCYSTIC OVARY SYNDROME

ENDOCRINOPATHIES II—POLYCYSTIC OVARY SYNDROME

ENDOCRINOPATHIES II—POLYCYSTIC OVARY SYNDROME

ENDOCRINOPATHIES II—POLYCYSTIC OVARY SYNDROME


In 1935, Stein and Leventhal described a group of patients in whom the symptoms of amenorrhea, sterility, slight hirsutism, and occasional obesity were associated with the presence of bilaterally enlarged, polycystic ovaries. The syndrome is now known as polycystic ovary syndrome (PCOS). The exact pathophysiology of PCOS is not well established, but increased amplitude of gonadotropin-releasing hormone (GnRH) pulsation and abnormal secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) during puberty are thought to result in androgen excess. Elevated levels of LH persist and may be used to help establish the diagnosis. Insulin resistance is a prominent aspect of this syndrome (40% of patients). It is clear that there is a genetic predisposition to PCOS; however, it is likely that several genes are involved.

ENDOCRINOPATHIES I—LUTEINIZATION

ENDOCRINOPATHIES I—LUTEINIZATION

ENDOCRINOPATHIES I—LUTEINIZATION

ENDOCRINOPATHIES I—LUTEINIZATION


In the presence of a hydatidiform mole or chorioepithelioma, the ovarian response to the elevated gonadotropin level may be markedly exaggerated and give rise to multiple theca lutein cysts. A palpable enlargement of the ovary due to theca lutein cysts occurs in about 60% of hydatidiform moles and 10% of choriocarcinomas. The lesions may be small or may reach proportions up to 20 to 30 cm in diameter. Smaller theca lutein cysts may be found in multiple gestations. Bilateral involvement is usual, though often asymmetric. The ovaries are polycystic and irregularly oval in shape, with a lobulated, smooth surface. The individual cysts are of variable size, thin-walled, gray or translucent, and often tinged with yellow. On section, a multilocular or honeycombed appearance is noted. The contained fluid may be clear, amber, or blood-tinged. The more solid portions of ovarian tissue may be edematous, with minute cystic cavities. Microscopically, the theca interna cells are strikingly hyperplastic and luteinized. The wall of a theca lutein cyst includes an inner lining of cicatricial tissue and an outer, thickened layer of luteinized theca cells. On occasion, areas of granulosa cells may be seen internal to the theca layer, with evidences of proliferation and luteinization. Isolated islands of luteinized theca cells may be scattered through the ovarian parenchyma. The multicystic ovaries may be asymptomatic or may manifest symptoms related to their increased size and weight. Following termination of the pathologic pregnancy, they gradually regress and disappear within a few to several weeks.

MASCULINIZING NEOPLASMS

MASCULINIZING NEOPLASMS

MASCULINIZING NEOPLASMS

MASCULINIZING NEOPLASMS


Masculinizing tumors are rare sex cord tumors of the ovary (<0.5% of ovarian tumors) that carry male elements and may be associated with virilization. Tumors vary in size but generally are 5 to 15 cm in diameter. For the sake of simplicity, they may be divided into two categories: the Sertoli-Leydig cell tumor (formerly arrhenoblastoma) and the adrenal rest tumor. The picture of virilization associated with these neoplasms is the result of defeminization and masculinization. Defeminization is manifested by amenorrhea, infertility, loss of feminine contour, decrease in size of the breasts, genital hypoplasia, and coarse skin texture. Masculinization is evident in hirsutism, male escutcheon, enlargement of the clitoris, increased muscular development, acne, and hoarseness of the voice. Metabolic disturbances, including hypertension and disorders of carbohydrate metabolism, are relatively uncommon with the adrenal rest tumors but may occur with Sertoli-Leydig cell tumors. Plasma levels of testosterone, androstenedione, and other androgens may be elevated; urinary 17-ketosteroid values are usually normal. (Androgen secretion by the tumor may result in erythrocytosis.) Laboratory studies cannot reliably differentiate between virilization caused by adrenal tumors and virilization caused by ovarian sources. Symptoms referable to the presence of a pelvic mass, torsion of a pedicle, necrosis, hemorrhage, and ascites may occur.

FEMINIZING NEOPLASMS

FEMINIZING NEOPLASMS

FEMINIZING NEOPLASMS

FEMINIZING NEOPLASMS


The granulosa cell tumor is a feminizing neoplasm composed of cells that resemble, in appearance and arrangement, the granulosa cells of the graafian follicle. It is the most common of the hormonal tumors of the ovary, comprising 6% of all ovarian tumors. Unlike theca cell tumors, it may be found in the prepubertal years (5%). The degree of hormonal activity is variable. The clinical characteristics depend upon age: in child-hood, hyperestrogenism is responsible for the syndrome of precocious pseudopuberty manifested by the premature development of secondary sex characteristics (feminine contour, breast growth, pubic and axillary hair, enlargement of the genitalia, anovulatory menses, acyclic uterine bleeding, hyperplastic endometrium, and estrogenic vaginal smears); during sexual maturity, the granulosa cell tumor may induce irregular vaginal bleeding; postmenopausally, irregular uterine bleeding, a marked estrogenic vaginal smear, and endometrial proliferation or hyperplasia. Breast enlargement, uterine fibroids, endometrial hyperplasia with polyps, and a concomitant endometrial carcinoma may develop. The tumor, by virtue of its size and weight, may give rise to abdominal pain, pressure symptoms, and torsion of the pedicle with infarction, hemorrhage, rupture, ascites (10%), and Meigs syndrome. Prognosis does not correlate with the histologic pattern of the tumor: 90% of tumors found are stage I and the prog- nosis is good (90% 10-year survival); a poorer prognosis is found with tumors 15 cm that have ruptured or have a high mitotic rate or aneuploidy.

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.

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