Ovarian Cancer

Types of Ovarian Cancer
--Epithelial
--Germ Cell
– Dysgerminoma
– Immature teratoma
– Endodermal sinus tumor
– Embryonal carcinoma
– Polyembryonal
– Choriocarcinoma
– Mixed
-- Sex Cord Stromal
– Granulosa cell
– Sertoli-Leydig
– Gynandroblastoma
– Unclassified
--Metastatic
– Breast
– Kruckenberg- Primary usually stomach, signet ring cells on pathology

Ovarian Cancer Risks
--Increase Risk
– Age most important independent risk factor
– Family history
– BRCA1 (60x increased risk), BRCA2 (30x), HNPCC (13x)
– Nulliparity, infertility, endometriosis
--Decrease Risk
– Prophylactic oophorectomy
– Oral contraceptive pills

Exam
--Physical
– Malignancy: irregular, solid consistency, is fixed, nodular, or bilateral, is associated with ascites

§ Ultrasound
– Low positive predictive value for cancer
– Cancer: excrescences, ascites, and mural nodules
– Benign: unilocular, thin-walled sonolucent cysts with smooth, regular borders, regardless of menopausal status or cyst size

Labs
§ Tumor markers
– Epithelial: CA 125, elevated in 80%
§ 35 U/mL is upper limit of normal
§ Also elevated in many benign conditions
– Malignant germ cell tumors: b-hCG, LDH, AFP
– Embryonal carcinoma: AFP, BhCG
– Endodermal Sinus tumor: AFP
– Granulosa cell tumors: inhibin

Work-up
§ Premenopausal
– Symptomatic : evaluate as appropriate for tuboovarian abcess, ectopic, torsion, ruptured ovarian cyst
– B-HCG, CBC, transvaginal USN, cervical cultures
Work-up
§ Postmenopausal
– Exclude common diagnoses: endometriosis, cyst, abcess
– Higher index for suspicion: transvaginal USN, CA 125
– Unless simple cysts, most likely will need surgery
– Need breast exam, digital rectal, mammography

Treatment of Epithelial Ovarian Cancer

§ Chemotherapy

   Radiotherapy
§ Cytoreductive surgery (debulking)
§ Debulking
§ Carboplatin and Paclitaxel
– First line
– Mechanism of action
§ Carbo: binds and crosslinks DNA
§ Taxol: promotes formation and inhibits disassembly of stable microtubules, inhibiting mitosis
– Side effects
§ Carbo: thrombocytopenia, leukopenia, anemia, vomiting, hair loss
§ Taxol: neutropenia, leukopenia, anemia,
hair loss, muscle pain, vomiting, diarrhea

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Endometrial Cancer

Symptoms

n Post menopausal bleeding
n Endometrial cells on Pap
n Perimenopausal with irregular heavy menses, increasingly heavy menses
n Premenopausal with abnormal uterine bleeding with history of anovulation
Differential Diagnosis for PMB
n Exogenous estrogen use- ie tamoxifen
n Atrophic endometritis/vaginitis
n Endometrial/cervical polyps
n Endometrial hyperplasia
n Endometrial Cancer
n Other gynecologic cancers
Risk factors for Endometrial Cancer
n Increased estrogen
– Hormone therapy
– Obesity
– Anovulation/PCOS
– Estrogen secreting tumors
– Older age
– Infertility
– Early menarche
– Late menopause
n Genetics
– HNPCC
– Caucasian
Preoperative Work-up
n Endometrial biopsy
n Ultrasound
n For suspected advanced stage may need:
– Cystoscopy
– Sigmoidoscopy
– Pelvic and Abdominal CT
n Labs
– CBC
– Chem 7
– Liver function tests
– EKG, CXR
Endometrial Hyperplasia (EIN)
n Precursor to endometrial cancer
– Risk of progression related to cytologic atypia
n Presents with abnormal bleeding
n Simple
– Benign irregular dilated glands
– No atypia: 1% progress
– Atypia: 8% progress
n Complex
– Proliferation of glands with irregular outlines, back to back crowding of glands, but no atypia
– No atypia: 3% progress
– Atypia: 29% progress
Staging of Endometrial Cancer
n I: Confined to uterine corpus
– IA: limited to endometrium
– IB: invades less than ½ of myometrium
– IC: invades more than ½ of myometrium

n II: invades cervix but not beyond uterus
– IIA: endocervical gland involvement only
– IIB: cervical stroma involvement

n III: local and/or regional spread
– IIIA: invades serosa/adnexa, or positive cytology
– IIIB: vaginal metastasis
– IIIC: metastasis to pelvic or para-aortic lymph nodes

n IVA: invades bladder/bowel mucosa
n IVB: distant metastasis
Five Year Survival
n Stage I: 81-91%
– 72% diagnosed at this stage
n Stage II: 71-78%
n Stage III: 52-60%
n Stage IV: 14-17%
– 3% diagnosed at this stage
Spread Patterns
n Direct extension
– most common
n Transtubal
n Lymphatic
– Pelvic usually first, then para-aortic
n Hematogenous
– Lung most common
– Liver, brain, bone
Treatment
n Stage IB or less: total hyst/BSO/PPALND, cytology
n Stage IC to IIB: total hyst/BSO/PPALND, cytology, adjuvant pelvic XRT
n Stage III: total hyst/BSO/PPALND, cytology, adjuvant chemotherapy
n Stage IV: palliative XRT and chemotherapy
Histologic Types
n Estrogen dependent
– Endometrioid- most common
n Non estrogen dependent- worse prognosis
– Papillary Serous
– Clear cell
– Adenosquamous
– Undifferentiated
Other Types of Uterine Cancer
n Leiomyosarcoma
– Rapidly growing fibroid should be evaluated
n Stromal sarcoma
n Carcinosarcoma (MMMT)

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Endometriosis

What is Endometriosis?
n Chronic condition.
n Characterized by the growth of endometrial tissue in other sites outside the endometrial   cavity.
¨ Pelvic cavity
¨ Ovaries
¨ Uterosacral ligaments
¨ Pouch of Douglas
What are the symptoms?
n Dysmenorrhea - recurrent painful periods
n Dyspareunia - painful intercourse
n Chronic lower abdominal and back pain
n Non-cyclic or cyclic pelvic pain
n Adnexal masses
n Subfertility
n Symptoms range from severe to minimal to no symptoms at all.
How common is endometriosis?
n Incidence is 40-60% in women with dysmenorrhea.
¨ And 20-30% in women with subfertility.
n Most common age of diagnosis is 40.
What are the causes of endometriosis?
n Retrograde menstruation
¨ Postulated in the early 1920s by Dr Sampson.
¨ Many women experience retrograde menstruation but do not go on to develop endometriosis.
¨ This theory also fails to explain why endometriosis can be found in remote areas such as the lungs, breasts, lymph nodes and even the eyes.

n The transplantation theory
¨ That endometriosis spreads via the circulatory and lymphatic system.
n Coelomic Metaplasia -
¨ This theory holds that certain cells, when stimulated, can transform themselves into a different kind of cells.
n The hereditary theory
¨ Women with family members who have endometriosis are more likely, or are susceptible to developing the disease.
n Environmental factors
¨ A great deal of research is clearly highlighting that women who are exposed to environmental toxins are at much greater risk of developing Endometriosis along with other serious health disorders.
How do you diagnose endometriosis?
n Accurate history
¨ Dysmenorrhea, pelvic pain etc.
n Physical exam
¨ Tenderness in the posterior fornix or adnexal masses
n Laparoscopy is the only diagnostic test that can reliably rule out endometriosis.
¨ Gold standard.
When do you perform laparoscopy?
n Severe pain over several months.
n Pain requiring systemic therapy.
n Pain resulting in days off from work or school.
n Pain requiring admission to the hospital.
What are the medical treatment options?
n Oral contraceptives
n Progestins
n Androgenic agents
n GnRH analogues
¨ All suppress ovarian activity and menses and cause atrophy of the endometriotic implants.
n Base decision of treatment on side effect profile.
n Endometriomas are not amenable to medical treatment.
¨ Randomized controlled trials that compare excision or drainage and ablation of endometriomas >3 cm reported recurrence rates reduced and improved spontaneous pregnancy rates.
What does surgical management entail?
n Laparoscopy or open procedures.
n Requires excision or ablation (by laser or cautery) of the implants.
n Surgical excision of endometriosis results in improved pain relief and improved quality of life after 6 months compared with diagnostic laparoscopy alone.
How often does endometriosis recur after surgery?
n Rate of recurrence is ~20% after 5 years.

What are the unanswered questions?
n Is medical or surgical management more effective?
n Does long term medical management reduce the recurrence of endometriosis?
n What is the benefit of surgery for rectovaginal disease?

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