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Endometrial NeoplasiaEndometriosis ectopic endometrial glands / chocolate cysts / 1st - ovaries (associated w/ endometrioid carcinoma) / 2nd recto-vaginal septum / reproductive age / dysmenorrhea, menometrorrhagia, dyspareunia, infertility / pathogenesis: retrograde menstruation, implantation, coelomic metaplasia, lymphatic, hematogenous dissemination
simple: dilated glands, abundant stroma complex: crowded architecture, epithelium may be stratified, reduced stroma atypical simple or complex: 25% progress to carcinoma other endometrial CA usually has worse prognosis adenosquamous, clear cell carcinoma, squamous carcinoma, papillary serous carcinoma Endometrial Adenocarcinoma most common invasive neoplasm of female genital tract / 75% of endometrial CA 70% before age of 50 / peak 60 yrs Presentation: post-menopausal bleeding (90%), abnormal Pap (30%), bone pain Note: if endometrial biopsy (90% sensitivity) negative, proceed with hysteroscopy Risk factors: unopposed estrogen, obesity, nulliparity, low parity, anovulation, menopause > 50 yrs / diabetes, hypertension, breast/ovarian cancer, family history of endometrial cancer Type I pre and peri-menopausal, low grade, hyperplastic, secretory, responds to HRT, whites Type II post- menopausal, high grade, serous clear cell, progressive, does not respond to HRT, blacks endometrioid: most common / adenocarcinoma / may have squamous differentiation Method of Spread: direct extension, lymphatic (most), direct, peritoneal seeding, hematologic dissemination Treatment: TAH/BSO with surgical staging +/- postoperative radiation, hormonal therapy, single-agent chemotherapy / hormonal therapy for advanced/recurrent Prognosis: histological grade is the most important factor, then depth of myometrial invasion (> 1/3 worse), then histological type / pelvic node mets, tumor volume, involvement of cervix/adnexa, positive peritoneal washings Overall 5 yr survival is 65% / stage I (73%), stage II (56%), stage III (32%), stage IV(10%) / 75% of recurrence in first 2 yrs, 85% in first 3 yrs FIGO Grading I - III / increases with solid component / FIGO Staging I – IV is most common / abdominal abscesses is most common COD Follow-up: every 3 months for 2 yrs, then every 6 months for 3 yrs, then once yr Mesenchymal Tumors of Endometrium Leiomyoma most common uterine neoplasm / SMC / blacks > white / usually multiple / hyaline fibrosis / apoplectic leiomyoma: pregnancy, progestins / hemorrhage, edema, myxoid changes, mitoses apoplectic and marantic: hemorrhagic degeneration/necrosis due to hormonal effects Treatment: OCP’s, NSAIDS, surgery Malignant Mixed-Mullerian Tumor (MMMT) – poor prognosis 1st uterine sarcoma / associated with pelvic radiation / homologous or heterologous (muscle, cartilage, bone, fat) / rapid spread, poor prognosis for both types Leiomyosarcoma 2nd uterine sarcoma / mitotic and cellular atypical / not arising from leiomyoma Treatment: only proven treatment is surgical
homozygous 46 XX (started as one paternal X / RF: young/old, Asian, FH, infertility, smoking large edematous villi (grapes of wrath) / Symptoms: vaginal bleeding, preeclampsia, uterine enlargement, high hCG complications: DIC, infection, choriocarcinoma (2%) Partial hydatidiform mole (PHM) fetal tissue often present / triploidy (69XXY) results from dispermy / RF’s same as CHM w/out maternal age, ace / milder symptoms / does NOT lead to choriocarcinoma
mole, abortion, normal pregnancy / no chorionic villi / Treatment: chemotherapy Placental site trophoblastic tumor (PSTT) rare / intermediate trophoblast deeply invades myometrium Miscellaneous Endometrial stromal tumors stromal nodule: benign low-grade endometrial stromal sarcoma: responds to progestins high-grade endometrial stromal sarcoma: very poor prognosis Adenomyosis diffuse glands in inner myometrium / posterior wall Fallopian Tube Fallopian Tube Infection Acute salpingitis TORCH / abortion (Strep, Staph, coliform, anaerobes) / adhesions, hydrosalpinx, infertility Chronic salpingitis bilateral / hydrosalpinx, pyosalpinx / ectopic pregnancy Granulomatous salpingitis granulomas / epithelial hyperplasia / systemic / MTB or M. bovis Fallopian Tube Neoplasia Carcinoma of fallopian tube rare / similar to serous ovarian carcinoma Other Fallopian Paratubal cysts (hydatid of Morgagni) common / non-significant / Mullerian origin Ectopic pregnancy Cause of 9% of maternal deaths from exsanguinations / commonly rupture by 12th week Risk factors: prior ectopic, chlamydia (PID), tubal surgery, smoking, increasing age Diagnosis: absence of IUP (ultrasound) and positive B-hCG (< 6000) / transvaginal ultrasound 85% sensitive for IUP at 6-7 wks or B-hCG over 1500 / confusing factors: multiple gestations, failed IUP, obesity, fibroids, uterine axis Labs: normal hCG increase is 66% or more per/48 hrs (15% of normal IUP have lower bhCG) / 17% of ectopics have normal hCG doubling time / doubling rate at 6-7 wks is every 3.5 days Pathology: endometrium may be secretory (Arias-Stella) or normal appearing Treatment: laparoscopy, laparotomy or methotrexate if small/unruptured / single dose MTX (84% success rate) or multiple dosing regimen / with leucovorin rescue Absolute contraindications: breastfeeding, immunodeficiency, alcoholism, alcoholic liver disease, chronic liver disease, blood dyscrasias (bone marrow hypoplasia, leukopenia, thrombocytopenia, severe anemia), known sensitivity to MTX, active pulmonary disease, peptic ulcer disease, hepatic, renal, hematologic dysfunction Relative contraindications: gestational sac > 3.5 cm / embryonic cardiac motion Note: pt must avoid alcohol, folate, NSAIDS, sexual intercourse during treatment Precautions: get LFT, U/A, transvaginal ultrasound within 48 hrs of treatment, Treatment Success: increase in hCG during 1st 1-3 days of treatment, vaginal bleeding/spotting, 2/3 will have increasing abdominal pain Treatment Failure: severely worsening abdominal pain, hemodynamic instability, hCG does not decline by at least 15% between day 4 to 7 / increase or plateau of B-hCG after 1st week Ovary Cystic Ovarian Disease Follicular cysts asymptomatic or increased estrogen causing isosexual precocity, menstrual disturbances, endometrial hyperplasia / may rupture with hemoperitoneum / unilocular / serous, blood clot, or mixed contents / probably due to FSH, LH stimulation Treatment: observe, oral contraceptives, surgery after 6-8wks Corpus luteum cyst continued progesterone secretion / large luteinized granulosa cells / smaller theca lutein cells involution of CLC usually leads to corpus albicans cyst
present in 20s with oligomenorrhea, menometrorrhagia, infertility (amenorrhea), and hirsutism (androstenedione to testosterone), acanthosis nigricans / bilaterally enlarged ovaries / thick, fibrotic cortical tunica / cystic follicles / hyperplasia and luteinization of theca interna w/out CL formation Treatment: clomiphene (blocks pituitary ER), MPA, oral contraceptives, wedge resection / metformin (under investigation) Surface epithelial inclusion cysts invagination of surface epithelium / post-men. / psammoma bodies may give rise to epithelial neoplasms Ovarian Tumors General: 80% benign / 5th most common CA death in women (from intestinal obstructions); 65% of ovarian tumors and 90% of ovarian cancer is from coelomic epithelial, 10% Krukenberg (mets from GI, breast, endometrium) Risk factors: nulliparity, family history, BRCA1 gene (history of breast CA 2x risk), clomiphene, infertility (10% less risk per childbirth) / oral contraceptives may confer protection Presentation: abdominal pain/distention (pelvic fullness, vague discomfort), GI complaints (early satiety, constipation, bowel obstruction or “carcinomatous ileus”), urinary symptoms, weight loss, pancytopenia, abnormal uterine bleeding (less than cervical and endometrial CA), ascites (late), cachexia / majority present with stage 3 Diagnosis: difficult to diagnose early, high mortality when malignant / may have peritoneal carcinomatosis on paracentesis, but avoid cyst aspiration (may worsen spread) Ultrasound (malignant): > 8 cm / solid or cystic and solid / multilocular / bilateral / ascites Ddx: ovarian cysts, renal cysts, adrenal cysts, gall bladder, pancreas Method of Spread: direct exfoliation, lymphatics, hematogenous (lung, brain) Tumor markers: CA-125 not very specific, elevated (>35) with all female reproductive tumors plus pancreas, breast, lung, colon and pregnancy, endometriosis, PID and fibroids / AFP and hCG Staging: TAH/BSO, omentum, washings, appendix, paraaortic lymph nodes, peritoneal biopsy Treatment: see below Prognosis: 5 yr survival 30% (because 80% present at late stage); if caught early, survival is 90% Epithelial (70%) % of malignant ovarian bilateral prognosis Serous (fallopian) 40 30-60 good Endometrioid 20 40 very bad Mucinous (cervical) 10 10-20 - Clear (kidney) 6 40 poor Brenner (bladder) < 3 - excellent Undifferentiated 10 - poor
benign ovarian tumor, ascites, hydrothorax Epithelial Tumors 85% of ovarian tumors (usually > 40 yrs / peak in 70s / more in nulliparous or few pregnancies) 50% benign, large, bilateral, cystic 33% malignant 16% borderline (younger women, diagnosis from morphology, not stage) Stage I - IV (III allows for superficial liver mets)
borderline (15%): ciliated, stratification, solid buds, psammoma bodies, no invasion malignant (25%): invasion, fine papillae, irregular lumens, tight nests, solid sheets, psammoma bodies / can have primary peritoneal papillary serous carcinoma (and normal ovaries); treated with debulking and chemotherapy (carboplatin or cisplatin + paclitaxel); 10% remission at 2 yrs Endometrioid - very poor prognosis ⅓ accompanied by independent endometrial cancer / association with endometriosis usually carcinomatous
largest ovarian tumors / borderline version may be intestinal (85%) or mullerian origin / mucinous carcinoma exceeds 4 layers / borderline type may display pseudomyxoma peritonei (peritoneum fills with mucin, must be repeat / high association with Peutz-Jeghers syndrome / CA-125 not useful, but CEA is useful (highly associated with appendix tumor) benign (80%): simple cystadenoma borderline (10%): malignant (10%): Clear cell adenocarcinoma - poor prognosis unilocular / solid nodules / highly associated with endometriosis clear, hobnail, flattened pattern contain glycogen / aggressive tumor
98% benign / small, well demarcated nests of epithelial cells / fibrous stroma / may surround eosinophilic material / grooved, “coffee bean” nuclei Germ Cell Tumors -15-20% / 0-25+ yrs -resection and chemotherapy (BEP) is generally treatment of choice
young age / sudden onset abdominal pain / elevated a-FP / large tumor / reticular pattern / Schiller-Duval bodies (papillae, central vessel) / hyaline droplets (contain a-FP, PAS+, eosinophilic) / moderate prognosis with combination chemotherapy Embryonal – aFP and hCG [may differentiate into endodermal sinus tumor or choriocarcinoma] Polyembryonal – aFP and hCG Choriocarcinoma – hCG Dermoid cyst (Mature Teratoma) - good prognosis most common GCT / 96% benign / 15% bilateral / usually cystic / 2-3 embryonic layers / sebaceous, hair, teeth (ectodermal mostly) / Rokitansky’s protuberances / torsion may occur / occasionally develop squamous carcinoma (1-2%) Struma Ovarii (Monodermal Teratoma) thyroid tissue predominates / 1/3 associated with ascites / rarely associated with Meig’s syndrome / 5-10% malignant Immature Teratoma - poor prognosis young age / neuroectodermal elements / large / graded I - III with level of immaturity / 60% survival for all stages Sex-Cord Stromal Tumors -affects all ages -associated with Peutz-Jeghers
most common SCST / middle-age / associated with basal-cell nevus syndrome / 40% w/ ascites / 1% with Meig’s syndrome (ovarian tumor, ascites, hydrothorax) / storiform pattern Granulosa cell tumors usually estrogenic / usually post-menopausal (adult vs. juvenile form) / may present with precocious puberty / macro/microfollicular pattern (call-exner bodies) / insular, trabecular, diffuse, luteinized / thecomatous component / size <5cm most important factor Thecoma estrogenic / post-menopausal / benign Sertoli-Leydig cell tumors (Arrhenoblastomas) < 1% of solid ovarian tumors Presentation: testosterone/androgen levels higher than PCOS and virilization is much more pronounced Treatment: chemotherapy? / hormone therapy will not suppress androgens
signet-ring cells / primary stomach, GI tumor / usually bilateral / can cause mild, reactive hypersecretion of androgen Female Breast Estrogen - proliferation of duct cells Progesterone - proliferation of lobules, stroma and stromal edema Others: prolactin, human placental lactogen menstruation - sloughing of EC’s and reduced edema 90% benign (40% fibrocystic) / 10% Ca
90% of reproductive women / relative estrogen predominance Non-proliferative changes blue-dome cysts / fibrosis, cyst formation, apocrine metaplasia, sclerosing adenosis microcalcification, (acini with intralobular fibrosis) Proliferative changes (2x Ca risk) > 2 duct layers / papillomatosis (project into lumen) / EC hyperplasia (irregular spaces in dilated ducts bridged by EC’s), regular spaces may be Ca in situ / atypia or FH is 5x risk
unilateral / lactation / staphylococcus duct ectasia plasma cell mastitis / inspissation / mistaken for carcinoma fat necrosis resembles carcinoma, chalky nodule / foreign body rxn resolves w/ fibrosis granuloma (foreign substance) breast implant, self-induced, iatrogenic gynecomastia (male) Ddx: cirrhosis, testicular tumors (secreting estrogen), Klinefelter’s Benign tumors 90% of breast lumps are benign Fibroadenoma Most common tumor in < 30 yrs / reproductive age / fibrous, gland element (stroma compressed ducts) / upper outer quadrant / increased E sensitivity ~ / occasionally foci for carcinoma / juvenile form is fast-growing Cystosarcoma phyllodes - worse prognosis painless / older women / lobulated, enormous / larger stromal cells surround “leaf-like” glands / Phylloides – painless / treated with wide excision along with sarcomas Intraductal papilloma Most common cause of bloody nipple discharge / papillary architecture / near large ducts Treatment: excise duct system Adenoma of nipple elderly onset / crusted, ulcerated nodule beneath nipple / Treatment: excision Others lipoma, hemangioma, hamartoma Malignant Changes Non-invasive Intraductal carcinoma in situ (DCIS) most common / 28% become invasive / comedocarcinoma (necrosis) Treatment: almost as aggressive Lobular carcinoma in situ (LCIS) marker for invasive CA (30% develop invasive CA in same or contralateral breast) Invasive carcinoma (adenocarcinoma) Scirrhous carcinoma (ductal carcinoma) - poor prognosis majority / radiating, infiltrating / Black’s nuclear grading I - III (reverse of normal) Lobular carcinoma - worse 20% bilateral / multicentric / cells smaller than ductal carcinoma / “Indian filing” LCIS component / may co-exist with scirrhous (ductal carcinoma) Medullary carcinoma - good prognosis pushing borders / solid aggregates of tumor cells / reactive lymphocytes Colloid carcinoma (mucinous) - good prognosis clusters of malignant cells in lakes of mucin / infrequent node mets Paget’s Disease (different from bone disease) - poor prognosis not too common / form of ductal carcinoma / eczematoid nipple / Paget’s cells surrounded by clear halo / 40% have axillary node mets / poorer prognosis b/c skin involvement Breast CancerPathology: Infiltrating ductal carcinoma 70% Medullary carcinoma 6% Lobular carcinoma 5% Colloid, Tubular 19% Download 3.95 Mb. Share with your friends:
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