Ovaries Flashcards
Clinical features of ovarian disease
Clinically silent for a long time beaause there is a lot of space, mostly mass effects that are late due to pressure or swelling which causes discomfort, heaviness, frquent micturition,
- rarely hormonal- endometrium(menstrual irregularities, Breast enlargment, hirsutism, Infertility, failure to ovulate
- per-vaginal examination- early detection.
Investigations in ovarian tumors
ultrasound, CT scan, Large mass, abdominal palpation, estimation of hormones, FNAC pouch of douglas, tymor mass per abdome
- ascitiv fluit tap, microscopy
- excision biopsy.
genearl ovarian tumor facts
- less common than uterus or breast but more deadly because of late detection
- 4th most common cancer after lung breast colon
- pregnancy and oral contraceptives reduce the risk of ovarian cancer.
Cysts of ovary
related to follicles,
Etiology
- follicular cysts- lined by layers of cuboidal grnulosa
- corpus luteal cysts, ruptured and sealed off hemorrhagic cysts with lutinised cells. eventually these will involute
- chocolate cysts- endometeriosis
Pathogenesis- chocolate cysts- repeated cyclical hemorrhage- chocolate color, induce fibrosis, adhesions, pain,
Morphology- usually less than 1-5 cms, sometimes large 4-5 cm
- lining may atrophy due to pessure
- chocolate cysts- consist of normal looking endometrial glands +stroma+RBC+hemosiderin. May extend along pelvic ligaments,
Chocolate cysts associations- infertility
Clinical- silent, pain, endometrial hyperplasia
Diagnosis- ultrasound.
polycystic ovarian disease(PCOD) (Stein Leventhal syndrome
Epidemiology: young women, post menarche,
Etiology: excess androgens secreted by ovary and adrenals (may be under influence of abnormal pituatary)
Morphology- large thich capsule, multiple unruptured follicles as cysts, lined by granulosa cells and hypertrophied theca interna cells
- thick, hypertrophited stroma
- persistent anovulation, no CL
Pathogenesis- androgens converted to estrogen by adipose tissue, excess estrogens inhibit release of FSH by pituitary and stimulate the release of GnRH by hypothalamus
- GnRH acts on pituitary to release LH
- LH elevated, FSH levels fall, LH:FSH ration elevated greater than 3
- persistently elevated LH stimulates theca cells in ovary to produce excess androgens,
- cycle continues unabated.
Clinical:
- Persistent anovulation, Oligomenorrhea, secondary amenorrhea, infertility, facial hair, obesity, voice changes.
- high LH, Low FSH, HIgh Androgens. ultrasound shows bilaterally enlarged ovaries with multiple subcapsular cysts.
- Hyper insulinemia due to peripheral resistence to insulin
Complications: excess estrogen-endometrial hyperplasia, stimulates adipose cells in body- obesity
-excess androgens- hirsutism, virilization, androgens processed through adipose tissue and liver–> excess estrogens.
Diagnosis/treatment- hormonal assay, transvaginal ultrasound.
-hormonal break the cycle, chlomiphene, induce ovulation, early years- wedge resectino of ovary
Tumors of Ovary
Epidemiology6% of all cancer in women, 80% benign (20-45 years) 20% malignant940-65 years, often bilateral, more in nulliparous, family history, oral contraceptives REDUCE RISK
-problem is late detection and rarely functional.
Classification- cell of origin:
- surface epithelium(60-70%)- serous, mucinous, endometriod, brenner
- Germ cell(15-20%)- teratoma, dysgerminoma, endodermal sinus(Yolk sac)
- Stroma cell(5-10%)- granulosa, theca, fibroma, sertoli leydig cell
- metastasis(5%)- stomach, colon endometrium, breast
Morphology-Cysitc- generally benign, Solid homogenous- benign, solid variegated- malignant
Pathogenesis:
-spread: peritoneum, ascities omental pancakes, LN-iliac, paraaortic, Blood- lungs.
Clinical: abdmonial distension, pelvic diiscomfort, cystic mass palpated in right iliac fossa.. ultrasound, cystic mass in adnexa
Surface epithelial tumors
towards fallopian tube- -cells with cilia- serious
- towards endocervix- tall mucin secreting cell- mucinous
- Towards endometrium- nonciliated columnar cell- endometrioid
- toards transitional epitheleum, transitional cells- brenner’s tumor
Bordelrine tumor
Benign- cystadenomas
Borderline- intermediate, carcinoma of low malignat potential
Malignant- cystadenocarcinoma.
Gross- small to very large filling abdomen
Bengin- cystic, unilocular, no papillae, smooth
malignant: solid, multiloculor, nodular, papillae
Serous tumors-
lined by single layer of tall columnar ciliated cells, 30 % of all ovarian tumors 60% benign, 15% bordelrine, 25% malignant
Morphology: cysts filled with serous fluid
-20% benign bilateral, 2/3 of malignant are bilateral.
-10-15 cm diameter, lining smooth and glistening
-papillae polyps in benign, but more numerous in malignant
-psammoma bodies in both benign and malignant
-solid nodules indicate serosal peneration/malignancy
- serous tumors can reach very large sizes and fill abodmen
Malignancy- solid, mor papillae, more polyps.
VARIANT- cystadenofibroma- abundant fibrous tissue under epithelium, usually benign.
Borderline- multi layering, moderate mitosis, nulcear atypia, but no stromal invastion- 10year SR=75%
Malignant- multilayering, nuclear atypia and stromal invasion 10year SR=10-30%
Mucinous tumors
25% of ovarian tumors
Morphology
Multiolculate cyst, sticky, gelatinous material rich in glycoproteins
-no papillae, polyps or psammoma, few locules,
-micro- Tall columnar cells with apical mucus vacuole, no cilia
Benign- 80%- 5% benign are bilateral,
Borderline-10-15% Complication-Pseudomyxoma peritonei, 10 year SR- 70%
Malignant5-10%- 15% bilateral- multiloculation and solid nodules- 10 year SR- 35% (Better than serous)
- Complication- pseudomyxoma peritonie
Assocation: mixed dermoid cysts, Brenner’s tumor
Pseudomyxoma peritonei
2-5 % of mucinous tumors show this complication
-peritoneal cavity filled with mucoid material, mated tumor implants all over the abdomen on serosal surfaces.
complication of mucocele of the appendix and carcinoma of the appendix. fecolith blocking the lumen of appendix. - only mucocele due to carcinoma can lead to this.
Endometroid tumors
mostly behave as carcinomas, 10% o all ovarian carcinomas, 15-30% associated with concomitant endometrial carcinoma ( not metastasis
Morphology
- Gross: solid and cystic, small, papillae, velvety surface
- Micro- Resemble endometrial carcinoma not normal endometrium as seen in endometriosis
- 40% bilateral, 5 year SR 4-50%
Complication variant- clear cell carcinoma
Brenner’s tumor
Morphology
transitional epithelial cells like urinary bladder( may come from urogenital ermants
plus dense fibrous tissue, small multiple nodules (not cysts) clinically silent and usually benign, occasionally malignant
Clincal features- abdominal pain, swelling, tumor mass or compression, GI symptoms, dysuria, increased frequncy urine, pelvic pressure, resection of tumor leads to cure. .
-malignant- progressive weakness weight loss cachexia
Spread: seeding into peritoneum- massive ascites,
- tumor implants grow on the surface of other structures- dont invade)
- regional lympho nodes can be involved
- to liver, lung, GIT, 50% to opposite ovary
- diagonsis are generally late
CA 125
Diagnositc value as a screening test for ovarian malignancy-
- increased CA 125 seen in blood of 75-95 of women with epithelial ovarian cancers.
- tumor limited to ovary- 50% are negative
- increased in a varity of benign lesions of ovary and nonovarian cancers
- may be useful in screening asymptomatic postmenopausal women for ovarian malignancy
- greater value in monitoring response to therapy
Germ cell tumor
acute pain in the iliac fossa, can resemble appendicitis, twisted ovarian lesion,
-lesion is cystic and solid full of sebacoius material, hair and some teeth.
epidemiology- 15-20% o all ovarian tumors, 95% benign cystic teratomas,
5% in children and young adults- malignant
-teratoma dysgerminaoma, endodermal sinus tumor, choriocarcinoma- nongestational.
