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TN Gyneco > 19. Gynecological Oncology > Flashcards

19. Gynecological Oncology Flashcards

1
Q

Name: Differential diagnosis of pelvic mass (Figure)

A
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2
Q

Describe etiology: Endometrial carcinoma (6)

A
  • most common gynecological malignancy in North America (40%); 4th most common cancer in women
  • 2-3% of women develop endometrial carcinoma during lifetime
  • mean age is 60 yr
  • majority are diagnosed in early stage due to detection of symptoms
  • 85-90% 5 yr survival for stage I disease
  • 70-80% 5 yr survival for all stages
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3
Q

Describe: Incidence of Malignant Gynecological Lesions in North America (6)

A

endometrium > ovary > cervix > vulva > vagina > fallopian tube

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4
Q

Name: Risk Factors for Endometrial Cancer (7)

A

COLD NUT

  • Cancer (ovarian, breast, colon)
  • Obesity
  • Late menopause
  • Diabetes mellitus
  • Nulliparity
  • Unopposed estrogen: PCOS, anovulation, HRT
  • Tamoxifen: chronic use
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5
Q

True or false

Postmenopausal bleeding = endometrial cancer until proven otherwise

A

True

(95% present with vaginal bleeding)

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6
Q

An endometrial thickness of __ mm or more is considered abnormal in a postmenopausal woman with vaginal bleeding

A

5 mm

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7
Q

Describe: Type 1 Endometrial Cancer (2)

A

Characterized as estrogen-related (i.e. excess/unopposed estrogen):

  • Endometrioid
  • Includes well-differentiated endometrioid adenocarcinoma

(Both types related to estrogen, but Type II to a lesser degree)

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8
Q

Name risk factors: Type 1 Endometrial Cancer (8)

A
  • PCOS
  • Diabetes mellitus
  • Unbalanced HRT (balanced HRT is protective)
  • Nulliparity
  • Late menopause (>55 yr), early menarche Estrogen-producing ovarian tumours (e.g. granulosa cell tumours)
  • HNPCC (hereditary non-polyposis colorectal cancer)/Lynch II syndrome
  • Tamoxifen
  • Increasing age and family history are risk factors for both types
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9
Q

Describe clinical features: Type 1 Endometrial Cancer (3)

A
  • ~80% of cases
  • Postmenopausal bleeding in majority
  • Abnormal uterine bleeding in majority of affected pre-menopausal women (menorrhagia, intermenstrual bleeding)
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10
Q

Describe: Type 2 Endometrial Cancer (2)

A

Characterized as non-estrogen related: Non-endometrioid

  • Includes serous, clear cell, grade 4 endometrioid and undifferentiated carcinomas, as well as carcinosarcoma
  • More aggressive histologic subtypes; prognosis typically worse than type I, with a poorer 5 yr survival

(Both types related to estrogen, but Type II to a lesser degree)

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11
Q

Name risk factors: Type 2 Endometrial Cancer (4)

A
  • (Increasing age and family history are risk factors for both types)
  • Parous women
  • Increasing age of menarche and number of children not significantly associated with reduced risk in clear-cell endometrial carcinoma
  • Has been associated with p53 mutations
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12
Q

Describe clinical features: Type 2 Endometrial Cancer (3)

A
  • ~15% of cases
  • Post-menstrual bleeding
  • Abnormal uterine bleeding
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13
Q

Describe screening: Endometrial Cancer (3)

A
  • no known benefit for mass screening
  • annual endometrial sampling starting at age 30-35 only for women at high risk (HNPCC [Hereditary Non-Polyposis Colorectal Cancer]/ Lynch II syndrome)
  • routine pelvic ultrasound should not be used as screening test (high false positives)
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14
Q

Describe investigations: Endometrial Cancer (3)

A
  • endometrial sampling
    • office endometrial biopsy
    • D&C ± hysteroscopy
  • ± pelvic ultrasound (in women where adequate endometrial sampling not feasible without invasive methods)
    • not acceptable as alternative to pelvic exam or endometrial sampling to rule out cancer
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15
Q

Name prognostic factors: Endometrial Cancer (6)

A

Most important is FIGO stage

Other Prognostic Factors:

  • Age
  • Grade
  • Histologic subtype
  • Depth of myometrial invasion
  • Presence of lymphovascular space involvement (LVSI)
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16
Q

Describe: FIGO Staging of Endometrial Cancer (2009)

A
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17
Q

Describe treatment: Endometrial carcinoma (4)

A
  • surgical: hysterectomy/bilateral salpingo-oophorectomy (BSO) and pelvic washings ± pelvic and para- aortic node dissection ± omentectomy
    • goals: diagnosis, staging, treatment, defining optimal adjuvant treatment
    • laparoscopic approach associated with improved quality of life (optimal for most patients)
  • adjuvant radiotherapy (for improved local control in patients at risk for local recurrence) and adjuvant chemotherapy (in patients at risk for distant recurrence or with metastatic disease): based on presence of poor prognostic factors in definitive pathology
  • chemotherapy: often used for recurrent disease (if high grade or aggressive histology)
  • hormonal therapy: progestins can be used for recurrent disease (especially if low-grade)
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18
Q

Describe complications of therapy: Endometrial carcinoma (5)

A

Surgical Complications

  • Surgical site infection
  • Lymphedema

Radiation Complications

  • Radiation fibrosis
  • Cystitis
  • Proctois
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19
Q
A
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20
Q

Name symptoms: Uterine Sarcoma (4)

A

BAD-P

  • Bleeding
  • Abdominal distention
  • Foul-smelling vaginal Discharge
  • Pelvic pressure
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21
Q

A rapidly enlarging uterus, especially in a postmenopausal woman, should prompt consideration of what? (2)

A
  • leiomyosarcoma.
  • Nevertheless, all postmenopausal patients with an enlarging uterus should have an endometrial biopsy
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22
Q

Describe: UTERINE SARCOMA (4)

A
  • rare; 3-9% of all uterine malignancies
  • arise from stromal components (endometrial stroma, mesenchymal or myometrial tissues)
  • behave more aggressively and are associated with worse prognosis than endometrial carcinoma; 5 yr survival is 35%
  • vaginal bleeding is most common presenting symptom
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23
Q

Name types of: Uterine Sarcoma (4)

A
  • Pure type
    • Leiomyosarcoma
    • Endometrial Stromal Sarcoma (ESS)
    • Undifferentiated Sarcoma
  • Mixed type
    • Adenosarcoma
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24
Q

Describe epidemiology: Leiomyosarcoma (3)

A
  • Most common type of uterine sarcoma
  • Average age of presentation is 55 yr but may present in pre-menopausal women
  • Often coexist with benign leiomyomata (fibroids)
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25
Q

Describe features: Leiomyosarcoma (3)

A
  • Histologic distinction from leiomyoma
    • Increased mitotic count (> 10 mitoses/10 high-power fields)
    • Tumour necrosis
    • Cellular atypia
  • Rapidly enlarging fibroids in a pre-menopausal woman
  • Enlarging fibroids in a postmenopausal woman
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26
Q

Describe diagnosis: Leiomyosarcoma (2)

A
  • Often post-operatively after uterusremoved for presumed fibroids
  • Stage using FIGO 2009 staging for leiomyosarcomas and ECC
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27
Q

Describe tx: Leiomyosarcoma (5)

A
  • Hysterectomy/BSO usually
  • No routine pelvic lymphadenectomy
  • Chemotherapy is used in cases of metastatic disease
  • Radiation therapy does not improve local control or survival
  • Poor outcomes overall, even for early-stage disease
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28
Q

Describe epidemiology: Endometrial Stromal Sarcoma (ESS) (1)

A

Usually presents in perimenopausal or postmenopausal women with abnormal uterine bleeding

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29
Q

Describe features: Endometrial Stromal Sarcoma (ESS) (2)

A
  • Abnormal uterine bleeding
  • Good prognosis
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30
Q

Describe diagnosis: Endometrial Stromal Sarcoma (ESS) (2)

A
  • Diagnosed by histology of endometrial biopsy or D&C
  • Stage using FIGO 2009 staging for leiomyosarcomas and ECC
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31
Q

Describe tx: Endometrial Stromal Sarcoma (ESS) (4)

A
  • Hysterectomy & BSO (remove ovaries as ovarian hormones may stimulate growth)
  • No routine pelvic lymphadenectomy
  • Adjuvant therapy based on stage and histologic features (hormones and/or radiation)
  • Hormonal therapy (progestins) may be used for metastatic disease
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32
Q

Describe epidemiology: Undifferentiated Sarcoma (1)

A

Rare; less common than leiomyosarcoma, endometrial stromal sarcoma

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33
Q

Describe features: Undifferentiated Sarcoma (2)

A
  • Severe nuclear pleomorphism, high mitotic activity, tumour cell necrosis, and lack smooth muscle or endometrial stromal differentiation
  • Poor prognosis
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34
Q

Describe diagnosis: Undifferentiated Sarcoma (1)

A

Often found incidentally post-operatively for abnormal bleeding

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35
Q

Describe tx: Undifferentiated Sarcoma (2)

A
  • Treatment primarily surgical
  • Radiation and/or chemotherapy for advanced diseased or unresectable disease
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36
Q

Describe epidemiology: Adenosarcoma (2)

A
  • The rarest of the uterine sarcoma
  • Mixed tumour of low malignancy potential
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37
Q

Describe features: Adenosarcoma (2)

A
  • Present with abnormal vaginal bleeding
  • Polypoid mass in uterine cavity
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38
Q

Describe dx: Adenosarcoma (3)

A
  • Mixture of benign epithelium with malignant low-grade sarcoma
  • Often found incidentally at time of hysterectomy for PMB
  • Stage using FIGO 2009 staging for adenosarcoma
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39
Q

Describe tx: Adenosarcoma (1)

A

Treatment is surgical with hysterectomy and bilateral salpingo-oophorectomy

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40
Q

Describe: FIGO Staging of Uterine Sarcoma (2009) (Figure)

A
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41
Q

Most (70%) epithelial ovarian cancers present at stage __

A

III disease

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42
Q

Name: Ovarian Tumour Markers (10)

A

Ovarian Tumour Markers

  • Epithelial cell: CA-125
  • Stromal
  • Granulosa cell: inhibin
  • Sertoli-Leydig: androgens
  • Germ cell
  • Dysgerminoma: LDH
  • Yolk sac: AFP
  • Choriocarcinoma: β-hCG
  • Immature teratoma: none
  • Embryonal cell: AFP + β-hCG
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43
Q

Describe: Benign ovarian tumours (5)

A
  • many are asymptomatic
  • usually enlarge slowly, if at all
  • may rupture or undergo torsion, causing pain
  • pain associated with torsion of an adnexal mass usually originates in the iliac fossa and radiates to the flank
  • peritoneal irritation may result from an infarcted tumour (rare)
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44
Q

Describe epidemiology: malignant ovarian tumours (6)

A
  • lifetime risk 1.4%
  • in women >50 yr, more than 50% of ovarian tumours are malignant
  • causes more deaths in North America than all other gynecologic malignancies combined
  • 4th leading cause of cancer death in women
  • 85% epithelial; 15% non-epithelial
  • 10-15% of epithelial ovarian cancers are related to hereditary predisposition
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45
Q

Name: Risk Factors (for epithelial ovarian cancers) (5)

A
  • early menarche and/or late menopause
  • personal history of breast, colon, endometrial cancer
  • family history of breast, colon, endometrial, ovarian cancer
  • Lynch syndrome and BRCA mutations
  • use of fertility drugs
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46
Q

Name: Protective Factors (for epithelial ovarian cancers) (2)

A
  • OCP: likely due to ovulation suppression (significant reduction in risk even after 1 yr of use)
  • pregnancy/breastfeeding
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47
Q

Name Prophylactic Measures for malignant ovarian tumours (2)

A
  • salpingectomy (prophylactic)
  • BSO (prophylactic hysterectomy or tubal ligation performed for this reason in high-risk women [i.e. BRCA mutation carriers])
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48
Q

Describe screening: Malignant ovarian tumours (3)

A
  • no effective method of mass screening
  • routine CA-125 level measurements or U/S not recommended
    • high false positive rates
  • controversial in high-risk groups: transvaginal U/S and CA-125, starting age 30 (no consensus on interval)
    • familial ovarian cancer (>1 first degree relative affected, BRCA-1 mutation)
    • other cancers (e.g. endometrial, breast, colon)
    • BRCA-1 or BRCA-2 mutation: recommendation is prophylactic bilateral oophorectomy after age 35 or when childbearing is completed
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49
Q

Describe clinical features: Malignant ovarian tumours (2)

A
  • most women with epithelial ovarian cancer present with advanced stage disease as patients often asymptomatic until disseminated (symptoms with early-stage disease are vague and non-specific)
  • when present, symptoms may include:
    • abdominal symptoms (nausea, bloating, pain, dyspepsia, anorexia, early satiety)
    • symptoms of mass effect
      • increased abdominal girth (from ascites or tumour itself)
      • urinary urgency and frequency
      • constipation
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50
Q

Diagnosis of ovarian tumours requires what? (1)

A

surgical pathology

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51
Q

Any adnexal mass in postmenopausal women should be considered what? (1)

A

malignant until proven otherwise

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52
Q

Describe: Omental Cake (2)

A
  • a term for ascites plus a fixed upper abdominal and pelvic mass;
  • almost always signifies ovarian cancer
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53
Q

Describe: Malignant Ovarian Tumour Prognosis 5 Year Survival (4)

A
  • Stage I 75-95%
  • Stage II 60-75%
  • Stage III 23-41%
  • Stage IV 11%
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54
Q

Describe: Low Malignant Potential (also called “Borderline”) Tumours (6)

A
  • a subcategory of epithelial ovarian cancer (~15% of all epithelial ovarian tumours)
  • pregnancy, OCP, and breastfeeding are protective factors
  • tumour cells with histologically malignant characteristics arise from the ovarian surface, but do not invade ovarian stroma
  • able to metastasize, but not commonly
  • treated primarily with surgery (BSO/omental biopsy ± hysterectomy)
    • chemotherapy has limited benefit: can be treated with hormonal manipulation (letrozole)
  • generally slow growing, excellent prognosis
    • 5 yr survival >99%
    • recurrences tend to occur late, may be associated with low-grade serous carcinoma
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55
Q

Name ovarian tumours (16)

A
  • FUNCTIONAL TUMOURS (all benign)
    • Follicular Cyst
    • Corpus Luteum Cyst
    • Theca-Lutein Cyst
    • Endometrioma
    • Polycystic Ovaries
  • BENIGN GERM-CELL TUMOURS
    • Benign Cystic Teratoma (dermoid)
  • MALIGNANT GERM-CELL TUMOURS
    • Dysgerminoma
    • Immature Teratoma
    • Yolk Sac Tumour
    • Ovarian Choriocarcinoma
  • EPITHELIAL OVARIAN TUMOURS (malignant or borderline)
    • Serous
    • Mucinous
  • SEX CORD STROMAL OVARIAN TUMOURS
    • Fibroma/Thecoma (benign)
    • Granulosa-Theca Cell Tumours (benign or malignant)
    • Sertoli-Leydig Cell Tumour (benign or malignant)
  • METASTATIC OVARIAN TUMOURS
    • From GI Tract, Breast, Endometrium, Lymphoma
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56
Q

Describe ovarian tumour: Follicular Cyst

  • Description
  • Presentaiton
  • Ultrasound/Cytology
  • Treatment
A
  • Description: Follicle fails to rupture during ovulation
  • Presentation:
    • Usually asymptomatic
    • May rupture, bleed, tort, infarct causing pain ± signs of peritoneal irritation
  • Ultrasound/Cytology: 4-8 cm mass, unilocular, lined with granulosa cells
  • Treatment:
    • Symptomatic or suspicious masses warrant surgical exploration Otherwise if <6 cm, wait 6 wk then re-examine as cyst usually regresses with next cycle
      OCP (ovarian suppression): will prevent development of new cysts
    • Treatment usually laparoscopic (cystectomy vs. oophorectomy, based on fertility choice)
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57
Q

Describe ovarian tumour: Corpus Luteum Cyst

  • Description
  • Presentaiton
  • Ultrasound/Cytology
  • Treatment
A
  • Description: Corpus luteum fails to regress after 14 d, becoming cystic or hemorrhagic
  • Presentation:
    • More likely to cause pain than follicular cyst
    • May delay onset of next period
  • Ultrasound/Cytology:
    • Larger (10-15 cm) and firmer than follicular cysts
  • Treatment: Same as for follicular cysts
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58
Q

Describe ovarian tumour: Theca-Lutein Cyst

  • Description
  • Presentaiton
  • Ultrasound/Cytology
  • Treatment
A
  • Description: Due to atretic follicles stimulated by abnormal β-hCG levels
  • Presentation: Associated with molar pregnancy, ovulation induction with clomiphene
  • Ultrasound/Cytology: -
  • Treatment:
    • Conservative
    • Cyst will regress as β-hCG levels fall
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59
Q

Describe ovarian tumour: Benign Cystic Teratoma (dermoid)

  • Description
  • Presentaiton
  • Ultrasound/Cytology
  • Treatment
A
  • Description:
    • Single most common ovarian germ cell neoplasm
    • Elements of all 3 cell lines; contains dermal appendages (sweat and sebaceous glands, hair follicles, teeth)
  • Presentation:
    • May rupture, twist, infarct
    • 20% bilateral
    • 20% occur outside of reproductive yr
  • Ultrasound/Cytology:
    • Smooth-walled, mobile, unilocular
    • Ultrasound may show calcification which is pathognomonic
  • Treatment: Treatment usually laparoscopic cystectomy; may recur
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60
Q

Describe general information: Malignant germ-cell tumours

  • Description
  • Presentation
  • Treatment
A
  • Description: Rapidly growing, 2-3% of all ovarian cancers
  • Presentation: Usually children and young women (<30 yr)
  • Treatment: Surgical resection (often conservative unilateral salpingo- oophorectomy ± nodes) ± chemotherapy
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61
Q

Describe ovarian tumour: Dysgerminoma

  • Description
  • Presentaiton
  • Treatment
A
  • Description: Produces LDH
  • Presentation: 10% bilateral
  • Treatment: When diagnosed at stage IA, no adjuvant treatment is indicated If diagnosed at advanced stage, very responsive to chemotherapy, therefore complete resection is not necessary for cure
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62
Q

Describe ovarian tumour: Immature Teratoma

  • Description
  • Presentaiton
  • Treatment
A
  • Description: No tumour marker identified
  • Presentation: Almost always unilateral
  • Treatment:
    • When diagnosed at stage IA Grade 1, no adjuvant treatment is indicated
    • When diagnosed at Grade 2-3, either adjuvant chemotherapy or surgical staging
    • If diagnosed at advanced stage, very responsive to chemotherapy, therefore complete resection is not necessary for cure
63
Q

Describe ovarian tumour: Yolk Sac Tumour

  • Description
  • Presentaiton
  • Treatment
A
  • Description: Produces AFP
  • Presentation: Abdominal pain and pelvic mass
  • Treatment:
    • When diagnosed at stage IA Grade 1, no adjuvant treatment is indicated
    • If diagnosed at advanced stage, very responsive to chemotherapy, therefore complete resection is not necessary for cure
64
Q

Describe ovarian tumour: Ovarian Choriocarcinoma

  • Description
  • Presentaiton
  • Treatment
A
  • Description: Produces hCG
  • Presentation: Precocious puberty and irregular vaginal bleeding
  • Treatment:
    • When diagnosed at stage IA Grade 1, no adjuvant treatment is indicated
    • If diagnosed at advanced stage, very responsive to chemotherapy, therefore complete resection is not necessary for cure
65
Q

Describe ovarian tumour: Epithelial ovarian tumours (General info)

  • Description
  • Ultrasound/Cytology
  • Treatment
A
  • Description:
    • Derived from mesothelial cells lining peritoneal cavity
    • Classified based on histologic type 80-85% of all ovarian neoplasms (includes malignant)
  • Ultrasound/Cytology: Varies depending on subtype
  • Treatment:
    • Borderline: Cystectomy vs. unilateral salpingo-oophorectomy
    • Malignant
      • Early stage (stage I): Hysterectomy/BSO/staging (omentectomy, peritoneal biopsies, washings, pelvic and para-aortic lymphadenectomy)
      • Advanced stage: Upfront cytoreductive (debulking) followed by adjuvant chemotherapy consisting of IV carboplatic/paclitaxel vs. intraperitoneal chemotherapy (stage III) neoadjuvant chemotherapy with IV carboplatin/ paclitaxel, followed by delayed debulking with further adjuvant IV chemotherapy
66
Q

Describe ovarian tumour: Serous epithelial ovarian tumour

  • Description
  • Presentaiton
  • Ultrasound/Cytology
A
  • Description:
    • Most common ovarian tumour
    • 50% of all ovarian cancers
    • 75% of epithelial tumours
    • 70% benign
  • Presentation: 20-30% bilateral
  • Ultrasound/Cytology:
    • Lining similar to fallopian tube epithelium
    • Often multilocular Histologically contain
    • Psamomma bodies (calcified concentric concretions)
67
Q

Describe ovarian tumour: Mucinous epithelial ovarian tumour

  • Description
  • Presentaiton
  • Ultrasound/Cytology
  • Treatment
A
  • Description: 20% of epithelial tumours
  • Presentation:
    • Rarely complicated by Pseudomyxoma peritoneii: implants seed abdominal cavity and produce large quantities of mucin
  • Ultrasound/Cytology:
    • Resembles endocervical epithelium
    • Often multilocular
    • May reach enormous size
  • Treatment:
    • Poor response to chemotherapy
    • If mucinous, remove appendix as well to rule out possible source of primary disease
68
Q

Describe ovarian tumour: Sex cord stromal ovarian tumours

  • Treatment
A
  • Surgical resection of tumour
  • Chemotherapy may be used for unresectable metastatic disease
69
Q

Describe ovarian tumour: Fibroma/Thecoma (benign)

  • Description
  • Presentaiton
  • Ultrasound/Cytology
A
  • Description: From mature fibroblasts in ovarian stroma
  • Presentation:
    • Non-functioning
    • Occasionally associated with Meig’s syndrome (benign ovarian tumour and ascites and pleural effusion)
  • Ultrasound/Cytology:
    • Firm, smooth rounded tumour with interlacing fibrocytes
70
Q

Describe ovarian tumour: Granulosa-Theca Cell Tumours (benign or malignant)

  • Description
  • Presentaiton
  • Ultrasound/Cytology
    *
A
  • Description: Can be associated with endometrial cancer Inhibin is tumour marker
  • Presentation: Estrogen-producing: feminizing effects (precocious puberty, menorrhagia, postmenopausal bleeding)
  • Ultrasound/Cytology: Histologic hallmark of cancer is small groups of cells known as Call-Exner bodies
71
Q

Describe ovarian tumour: Sertoli-Leydig Cell Tumour (benign or malignant)

  • Description
  • Presentaiton
A
  • Description: Can measure elevated androgens as tumour markers
  • Presentation: Androgen-producing: virilizing effects (hirsutism, deep voice, recession of front hairline)
72
Q

Describe ovarian tumour: Metastatic ovarian tumours From GI Tract, Breast, Endometrium, Lymphoma

A

4-8% of ovarian malignancies
Krukenberg tumour – metastatic ovarian tumour (usually GI tract, commonly stomach or colon, breast) with “signet-ring” cells

73
Q

Describe: Investigation of Suspicious Ovarian Mass (5)

A
  • women with suspected ovarian cancer based on history, physical, or investigations should be referred to a gynecologic oncologist
    • bimanual examination
      • solid, irregular, or fixed pelvic mass is suggestive of ovarian cancer
    • RMI (Risk of Malignancy Index) is best tool available to assess likelihood of ovarian malignancy and need for pre-operative gynecologic oncology referral (see sidebar)
  • physical exam findings largely dependent on stage of disease
  • blood work: CA-125 for baseline, CBC, liver function tests, electrolytes, creatinine
  • radiology
    • transvaginal ultrasound best to visualize ovaries
    • CT abdomen and pelvis to look for metastatic disease
    • bone scan or PET scan not indicated
  • try to rule out other primary source if suspected, based on:
    • occult blood per rectum: endoscopy ± barium enema
    • gastric symptoms: gastroscopy ± upper GI series
    • abnormal vaginal bleeding: endometrial biopsy to rule out concurrent endometrial cancer; abnormal cervix: need to biopsy cervix (not Pap smear); breast lesion identified or risk factors present: mammogram
74
Q

Describe: A Risk of Malignancy Incorporating CA-125, Ultrasound, and Menopausal Status for the Accurate Pre-Operative Diagnosis of Ovarian Cancer ()

A

RMI = U x M x CA-125

Ultrasound Findings (1 pt for each)

  • Multilocular cyst
  • Evidence of solid areas
  • Evidence of metastases
  • Presence of ascites
  • Bilateral lesions

U = 1 (for U/S scores of 0 or 1)

U = 4 (for U/S scores of 2-5)

Menopausal Status

  • Postmenopausal: M = 4
  • Premenopausal: M = 1

Absolute Value of CA-125 Serum Level

  • For RMI>200: gynecologic oncology referral is recommended
75
Q

Describe: FIGO Staging for Primary Carcinoma of the Ovary (Surgical Staging) (2014) (Figure)

A
76
Q

Describe: Fallopian Tube tumour (4)

A
  • least common site for carcinoma of female reproductive system (0.3%)
  • usually serous epithelial carcinoma
  • new evidence shows that some serous ovarian cancers originate in the fallopian tube
  • more common in fifth and sixth decade
77
Q

Describe clinical features: Fallopian Tube tumour (4)

A
  • classic triad present in minority of cases, but very specific
    • watery discharge (most specific): “hydrops tubae profluens”
    • vaginal bleeding or discharge in 50% of patients
    • crampy lower abdominal/pelvic pain
    • most patients present with a pelvic mass (see Ovarian Tumours, GY41 for guidelines regarding diagnosis/investigation)
78
Q

Describe tx: Fallopian Tube tumour (4)

A
  • as for malignant epithelial ovarian tumours
79
Q

Describe: BENIGN CERVICAL LESIONS (2)

A
  • Nabothian cyst/inclusion cyst: no treatment required
  • endocervical polyps: treatment is polypectomy (office procedure)
80
Q

Describe epidemiology: MALIGNANT CERVICAL LESIONS (4)

A
  • majority are SCC (95%); adenocarcinomas increasing (5%); rare subtypes include small cell, adenosquamous
  • 8000 deaths annually in North America
  • annual Pap test reduces a woman’s chance of dying from cervical cancer from 0.4% to 0.05%
  • average age at presentation: 52 yr old
81
Q

Describe etiology: MALIGNANT CERVICAL LESIONS (9)

A
  • at birth, vagina is lined with squamous epithelium; columnar epithelium lines only the endocervix and the central area of the ectocervix (original squamocolumnar junction)
  • during puberty, estrogen stimulates eversion of a single columnar layer (ectopy), thus exposing it to the acidic pH of the vagina, leading to metaplasia (change of exposed epithelium from columnar to squamous)
    • a new squamocolumnar junction forms as a result
  • the transformation zone (TZ) is the area located between the original and the current squamocolumnar junction
  • the majority of dysplasias and cancers arise in the TZ of the cervix
  • must have active metaplasia in presence of inducing agent (HPV) to get dysplasia
  • dysplasia progresses to carcinoma in situ (CIS), which further progresses to invasion
  • slow process (~10 yr on average)
  • growth is by local extension
  • metastasis occurs late
82
Q

Name risk factors: MALIGNANT CERVICAL LESIONS (5)

A
  • HPV infection
    • high risk of neoplasia associated with types 16, 18
    • low risk of neoplasia associated with types 6, 11
    • >99% of cervical cancers contain one of the high risk HPV types
  • high-risk behaviours (risk factors for HPV infection)
    • multiple partners
    • other STs (HSVm trichomonas)
    • early age at first intercourse
    • high-risk male partner
  • smoking
  • poor screening uptake is the most important risk factor for cervical cancer in Canada
  • at-risk groups include:
    • immigrant Canadians
    • First Nations Canadians
    • geographically-isolated Canadians
    • sex-trade workers
    • low socioeconomic status Canadians
83
Q

Name: Causes of elevated CA-125 (6)

A
  • Age influences reliability of test as a tumour marker
  • 50% sensitivity in early-stage ovarian cancer (poor), therefore not good for screening

Malignant

  • Gyne: ovary, uterus
  • Non-Gyne: pancreas, stomach, colon, rectum

Non-Malignant

  • Gyne: benign ovarian neoplasm, endometriosis, pregnancy, fibroids, PID
  • Non-Gyne: cirrhosis, pancreatitis, renal failure
84
Q

Cervical cancer is most prevalent in which countries? (1)

A

developing countries and, therefore, is the only gynecologic cancer that uses clinical staging; this facilitates consistent international staging with countries that do not have technologies, such as CT and MRI

85
Q

Describe anatomy: Cervix (8) (Image)

A
86
Q

Name clinical features: Malignant cervical lesions (4)

A
  • SCC: exophytic, fungating tumour
  • adenocarcinoma: endophytic, with barrel-shaped cervix
  • early
    • asymptomatic
    • discharge: initially watery, becoming brown or red
    • postcoital bleeding
  • late
    • 80-90% present with bleeding: either postcoital, postmenopausal or irregular bleeding
    • pelvic or back pain (extension of tumour to pelvic walls)
    • bladder/bowel symptoms
  • signs
    • friable, raised, reddened, or ulcerated area visible on cervix
87
Q

Describe: Decision making chart for Pap test (Figure)

A
88
Q

Describe diagnosis: Malignant cervical lesions (8)

A
  • colposcopy is a clinical procedure that facilitates identification and biopsy of suspicious cells
  • in colposcopy:
  • apply acetic acid and identify acetowhite lesions, punctation, mosaicism, and abnormal blood vessels to guide cervical biopsy
  • endocervical curettage (ECC) if entire lesion is not visible or no lesion visible
  • diagnostic excision (LEEP) if:
    • unsatisfactory colposcopy (poor visualization/access to transformation zone)
    • discrepancy between cytology, colposcopy, and histological findings
    • positive findings/glandular abnormalities in endocervical curettage
    • suspicious for adenocarcinoma in situ (consider cold-knife conization)
    • recurrence of lesion post-ablation or excision
    • inability to rule out invasive disease, i.e. large lesions (lesions extending into endocervical canal, extending widely on cervix, or onto vaginal epithelium)
  • consider cold-knife conization (in OR) if glandular abnormality suspected based on cytology or colposcopic findings due to concern for margin interpretation
  • tests permitted for FIGO clinical staging include: physical exam (including examination under anesthesia), cervical biopsy (including cone biopsy), proctoscopy/cystoscopy, intravenous pyelogram, ultrasound liver/kidneys, CXR, LFTs
  • MRI and/or CT and/or PET scan often done to facilitate planning of radiation therapy, results do not influence clinical stage
89
Q

Describe: The Bethesda Classification System (2)

A
  • is based on cytological results of a Pap test that permits the examination of cells but not tissue structure.
  • Cervical intraepithelial neoplasia (CIN) or cervical carcinoma is a histological diagnosis, requiring a tissue sample via biopsy of suspicious lesions seen during colposcopy
90
Q

With development of hypertension early in pregnancy (i.e. <20 wk), think what? (1)

A

gestational trophoblastic disease

91
Q

What is indicated for monitoring response to treatment of malignant cervical lesions? (1)

A

CA-125

92
Q

Describe: FIGO Staging Classification of Cervical Cancer (Clinical Staging) (2018) (Figure)

A
93
Q

Name: Causes of Elevated CA-125 (6)

A

Causes of Elevated CA-125

  • Age influences reliability of test as a tumour marker
  • 50% sensitivity in early stage ovarian cancer (poor) – therefore not good for screening

Malignant

  • Gyne: ovary, uterus
  • Non-Gyne: pancreas, stomach, colon, rectum

Non-Malignant

  • Gyne: benign ovarian neoplasm, endometriosis, pregnancy, fibroids, PID
  • Non-Gyne: cirrhosis, pancreatitis, renal failure
94
Q

Describe: Cervical Cancer Prognosis 5 yr Survival (6)

A
  • Stage 0 99%
  • Stage I 75%
  • Stage II 55%
  • Stage III 30%
  • Stage IV 7%
  • Overall 50-60%
95
Q

How to prevent cervical cancer? (2)

A

2 vaccines currently approved (Gardasil®, Cervarix®)

96
Q

Describe: Cervarix

  • Viral Strains Covered
  • Route of Administration
  • Schedule of Dosing
  • Side Effets
  • Approved Age
A
  • Viral Strains Covered: 16, 18
  • Route of Administration: IM
  • Schedule of Dosing: 0, 1, 6 mo
  • Side Effects:
    • Local: redness, pain, swelling
    • General: headache, low grade fever, GI upset
  • Approved Age: Females age 10-25
97
Q

Describe: Gardasil

  • Viral Strains Covered
  • Route of Administration
  • Schedule of Dosing
  • Side Effets
  • Approved Age
  • Contraindications
A
  • Viral Strains Covered: 6, 11, 16, 18
  • Route of Administration: IM
  • Schedule of Dosing: 0, 2, 6 mo
  • Side Effects:
    • Local: redness, pain, swelling
    • General: headache, low grade fever, GI upset
  • Approved Age: Females age 9-45, males age 9-26
  • Contraindications: Pregnant women and women who are nursing (limited data)
98
Q

Describe HPV Vaccine (5)

A
  • should be administered before onset of sexual activity (i.e. before exposure to virus) for optimal benefit of vaccination
  • may be given at the same time as hepatitis B or other vaccines using a different injection site
  • not for treatment of active infections
  • most women will not be infected with all four types of the virus at the same time, therefore vaccine is still indicated for sexually active females or those with a history of previous HPV infection or HPV- related disease
  • conception should be avoided until 30 d after last dose of vaccination
99
Q

Describe management Cervical Cancer: CIN I (4)

A
  • Preferred option for biopsy-proven CIN I is observation
  • Repeat assessment and cytology in 12 mo
  • Management according to cytology results
  • If after HSIL or AGC:
    • Cytology and histology should be reviewed
    • If discrepancy remains, excisional biopsy may be considered
100
Q

Describe management Cervical Cancer: CIN II and CIN III (3)

A
  • Women ≥25 yr
    • CIN II or III should be treated
    • Excisional procedures preferred for CIN III
    • Those with positive margins should have follow-up with colposcopy and directed biopsies and/or endocervical curettage
  • Women <25 yr
    • Same treatment for CN II and CN III: observe with colposcopy at 6-mo intervals for up to 24 mo before treatment considered
  • During pregnancy
    • CIN II or III suspected or diagnosed during pregnancy: repeat colposcopy and treatment delayed until 8-12 wk after delivery
101
Q

Describe management Cervical Cancer: Stage IA1 (no LVSI) (2)

A
  • LEEP if future fertility desired (and lesion ≤2 cm)
  • Simple hysterectomy if future fertility is not desired
102
Q

Describe management Cervical Cancer: Stage IA2, IB1 (6)

A
  • Typically treated with radical hysterectomy and pelvic lymphadenectomy (sentinel nodes under study)
  • If high chance of adjuvant radiation then consider primary chemoradiation as more morbidity occurs from double-modality treatment (surgery and radiation)
  • Equal cure rates may be obtained with primary radiation therapy; advantage of surgery: may accurately stage and grade and more targeted adjuvant therapy
  • Advantage is that ovaries can be spared if pre-menopausal
  • For fertility preservation (if tumour <2 cm), may have radical trachelectomy (removal of cervix and parametria) and nodes instead of radical hysterectomy for early-stage disease
  • Chemoradiation therapy if adverse high-risk prognostic factors on radical surgical specimen, such as: positive pelvic lymph nodes, positive parametria, and/or positive margins or adverse cervical factors (2 or more): deep stromal invasion, size >4 cm, LVSI
103
Q

Describe management Cervical Cancer: Stages IB2 (>4 cm), II, III, IV (4)

A
  • Primary chemoradiation therapy
  • CT assess extent of disease: evaluate pelvic and para-aortic nodes
  • For positive nodes on PET: primary chemoradiation with extended field RT
  • Hysterectomy generally not suggested following primary treatment with curative intent
104
Q

Describe incidence: Abnormal Pap Tests in Pregnancy (1)

A
  • incidence: 1/2200
105
Q

What to do with abnormal pap tests in pregnancy? (4)

A
  • if abnormal Pap or suspicious lesion, refer to colposcopy
  • if diagnostic conization required, should be deferred until second trimester (T2) to minimize risk of pregnancy loss
  • if invasive cancer ruled out, management of dysplasia deferred until completion of pregnancy (may deliver vaginally)
  • if invasive cancer present, management depends on prognostic factors, degree of fetal maturity, and patient wishes
    • general recommendations in T1: consider pregnancy termination, management with either radical surgery (hysterectomy vs. trachelectomy if desires future fertility), or concurrent chemoradiation therapy
    • recommendations in T2/T3: delay of therapy until viable fetus and C-sectionfor delivery with concurrent radical surgery or subsequent concurrent chemoradiation therapy
106
Q

Name: Non-Neoplastic Disorders of Vulvar Epithelium (3)

A
  • biopsy is necessary to make diagnosis and/or rule out malignancy:
    • Hyperplastic dystrophy (squamous cell hyperplasia)
    • Lichen sclerosis
    • Mixed dystrophy (lichen sclerosis with epithelial hyperplasia)
107
Q

Describe: Hyperplastic dystrophy (squamous cell hyperplasia) (4)

A
  • surface thickened and hyperkeratotic
  • pruritus most common symptom
  • typically postmenopausal women
  • treatment: 1% fluorinated corticosteroid ointment bid for 6 wk
108
Q

Describe: Lichen sclerosis (5)

A
  • subepithelial fat becomes diminished; labia become thin, atrophic, with membrane-like epithelium and labial fusion
  • pruritus, dyspareunia, burning
  • ‘figure of 8’ distribution
  • most common in postmenopausal women but can occur at any age
  • treatment: ultrapotent topical steroid 0.05% clobetasol x 2-4 wk then taper down, can consider long-term suppression twice a week
109
Q

Describe: Mixed dystrophy (lichen sclerosis with epithelial hyperplasia) (2)

A
  • hyperkeratotic areas with areas of thin, shiny epithelium
  • treatment: fluorinated corticosteroid ointment
110
Q

Name benign vulvar tumours (4)

A
  • papillary hidradenoma
  • nevus,
  • fibroma
  • hemangioma
111
Q

Describe epidemiology: MALIGNANT VULVAR LESIONS (2)

A
  • 5% of genital tract malignancies
  • 90% SCC; remainder melanomas, basal cell carcinoma, Paget’s disease, Bartholin’s gland carcinoma
    • Type I disease: HPV-related (50-70%)
      • more likely in younger women
      • 90% of vulvar intraepithelial neoplasia (VIN) contain HPV DNA (usually types 16, 18)
    • Type II disease: not HPV-related, associated with current or previous vulvar dystrophy
      • usually postmenopausal women
112
Q

Name risk factors: MALIGNANT VULVAR LESIONS (5)

A
  • HPV infection
  • VIN: precancerous change which presents as multicentric white or pigmented plaques on vulva (may only be visible at colposcopy)
    • progression to cancer rarely occurs with appropriate management
    • treatment: local excision (i.e. superficial vulvectomy ± split thickness skin grafting to cover defects if required) vs. ablative therapy (i.e. laser, cauterization) vs. local immunotherapy (imiquimod)
  • history of cervical cancer
  • cigarette smoking
  • immunodeficiency
113
Q

Describe clinical features: MALIGNANT VULVAR LESIONS (5)

A
  • many patients asymptomatic at diagnosis (many also deny or minimize symptoms)
  • most lesions occur on the labia majora, followed by the labia minora (less commonly on the clitoris or perineum)
  • localized pruritus or lesion most common
  • less common: raised red, white or pigmented plaque, ulcer, bleeding, discharge, pain, dysuria
  • patterns of spread
    • local
    • groin lymph nodes (usually inguinal, then spreading to pelvic nodes)
    • hematogenous
114
Q

Describe investigations: MALIGNANT VULVAR LESIONS (2)

A
  • ± vulvar biopsy
  • always biopsy any suspicious lesion
    • do not remove entire lesion (allows for site identification through sentinel LN injection if malignant)
115
Q

Describe prognosis: MALIGNANT VULVAR LESIONS (3)

A
  • depends on stage: particularly nodal involvement (single most important predictor followed by tumour size)
  • lesions >4 cm associated with poorer prognosis
  • overall 5 yr survival rate: 79%
116
Q

Describe tx: MALIGNANT VULVAR LESIONS (4)

A
  • T1 lesions (tumour confined to vulva; no extension to adjacent perineal structures): radical local excision
  • T2 lesions (tumour of any size with extension to adjacent perineal structures): modified radical vulvectomy
  • T3 lesions (extension to any of: proximal 2/3 of urethra, proximal 2/3 of the vagina, bladder mucosa, rectal mucosa, or fixed to pelvic bone): chemoradiation followed by selective resection of residual primary
  • node positive disease: adjuvant chemoradiation or radiation therapy
117
Q

Any suspicious lesion of the vulva should be __

A

Any suspicious lesion of the vulva should be biopsied

118
Q

Name benign vaginal lesions (4)

A
  • inclusion cysts
  • endometriosis
  • Gartner’s duct cysts
  • urethral diverticulum
119
Q

Describe: inclusion cysts (2)

A
  • cysts form at site of abnormal healing of laceration (e.g. episiotomy)
  • no treatment required
120
Q

Describe: endometriosis (2)

A
  • dark lesions that tend to bleed at time of menses
  • treatment: excision
121
Q

Describe: Gartner’s duct cysts (2)

A
  • remnants of Wolffian duct, seen along side of cervix
  • treatment: conservative unless symptomatic
122
Q

Describe: urethral diverticulum (2)

A
  • can lead to recurrent urethral infection, dyspareunia
  • treatment: surgical correction if symptomatic
123
Q

Describe epidemiology: Malignant vaginal lesions (3)

A
  • primary carcinomas of the vagina represent 2-3% of malignant neoplasms of the female genital tract
  • 80-90% are SCC
  • more than 50% diagnosed between 70-90 yr old
124
Q

Name risk factors: Malignant vaginal lesions (2)

A
  • associated with HPV infection (analogous to cervical cancer)
  • increased incidence in patients with prior history of cervical and vulvar cancer
125
Q

Describe investigations: Malignant vaginal lesions (6)

A
  • cytology
  • significant false negative rate for existing malignancy (i.e. if gross lesion present, biopsy)
  • colposcopy
  • Schiller test (normal squamous epithelium takes up Lugol’s iodine)
  • biopsy, partial vaginectomy (wide local excision for diagnosis)
  • rule out disease on cervix, vulva, or anus (most vaginal cancers are metastatic from one of these sites)
  • staging
126
Q

Describe clinical features: Vaginal Intra-Epithelial Neoplasia (VAIN) (1)

A

Grades: analogous to cervical dysplasia

127
Q

Describe clinical features: Squamous Cell Carcinoma (SCC) (6)

A
  • Most common site is upper 1/3 of posterior wall of vagina
  • Asymptomatic
  • Painless discharge and bleeding
  • Vaginal discharge (often foul-smelling)
  • Vaginal bleeding especially during/post-coitus
  • Urinary and/or rectal symptom 2° to compression
128
Q

Describe clinical features: Adenocarcinoma (2)

A
  • Most are metastatic, usually from cervix, endometrium, ovary, or colon Most primaries are clear-cell adenocarcinomas
  • 2 types: non-DES and DES syndrome
129
Q

Describe treatment of Malignant vaginal lesions: Stage 1 (2)

A
  • radiation therapy: for tumours >2 cm diameter or tumour involvement of the mid- to low-grade vagina
  • surgical excision: radical hysterectomy, upper vaginectomy, and bilateral pelvic lymphadenectomy
130
Q

Describe treatment of Malignant vaginal lesions: Stage 2-4 (2)

A

chemoradiation

131
Q

Describe: Gestational Trophoblastic Disease/Neoplasia (1)

A
  • refers to a spectrum of proliferative abnormalities of the trophoblast
132
Q

Describe epidemiology: Gestational Trophoblastic Disease/Neoplasia (4)

A
  • 1/1000 pregnancies
  • marked geographic variation (as high as 1/125 in Taiwan)
  • 80% benign, 15% locally invasive, 5% metastatic
  • cure rate >95%
133
Q

Describe: Complete HYDATIDIFORM MOLE (5)

A
  • most common type of hydatidiform mole
  • diffuse trophoblastic hyperplasia, hydropic swelling of chorionic villi, no fetal tissues or membranes present
  • 46XX or 46XY, chromosomes completely of paternal origin (90%)
  • 2 sperm fertilize empty egg or 1 sperm with reduplication
  • 15-20% risk of progression to malignant sequelae
134
Q

Describe risk factors: Complete HYDATIDIFORM MOLE (2)

A
  • geographic (South East Asia most common)
  • others (maternal age >40 yr, β-carotene deficiency, vitamin A deficiency not proven)
135
Q

Describe clinical features: Complete HYDATIDIFORM MOLE (8)

A
  • clinical features often present during apparent pregnancy with abnormal symptoms/findings
    • vaginal bleeding (97%)
    • hyperemesis gravidarum (26%)
    • excessive uterine size for LMP (51%)
    • hyperthyroidism (7%)
    • theca-lutein cysts >6 cm (50%)
    • β-hCG >100,000 IU/L
    • preeclampsia (27%)
    • no fetal heartbeat detected
136
Q

With development of hypertension early in pregnancy (i.e. <20 wk), think what? (1)

A

gestational trophoblastic disease

137
Q

Describe: Partial (or Incomplete) hydatidiform Mole (4)

A
  • focal trophoblastic hyperplasia and hydropic villi are associated with fetus or fetal parts
  • often triploid (XXY, XYY, XXX) with chromosome complement from both parents
    • usually related to single ovum fertilized by two sperm
  • low risk of progression to malignant sequelae (<4%)
  • associated with fetus, which may be growth-restricted, and/or have multiple congenital malformations
138
Q

Describe clinical features: Partial (or Incomplete) hydatidiform Mole (2)

A
  • typically present similar to threatened/spontaneous/missed abortion
  • pathological diagnosis often made after D&C
139
Q

Describe investigations: Hydatidiform mole (4)

A
  • quantitative β-hCG levels (tumour marker) abnormally high for gestational age
  • U/S findings
    • if complete: no fetus (classic “snow storm” due to swelling of villi)
    • if partial: molar degeneration of placenta ± fetal anomalies, multiple echogenic regions corresponding to hydropic villi, and focal intrauterine hemorrhage
  • CXR (may show metastatic lesions)
  • features of molar pregnancies at high risk of developing persistent GTN post-evacuation
    • local uterine invasion as high as 31%
    • β-hCG >100,000 IU/L
    • excessive uterine size
    • prominent theca-lutein cysts
140
Q

Describe treatment: Hydatidiform mole (4)

A
  • suction D&C with sharp curettage and oxytocin
  • Rhogam® if Rh negative
  • prophylactic chemotherapy of no proven benefit
  • chemotherapy for GTN if develops after evacuation
141
Q

Describe folllow-up: Hydatidiform mole (3)

A
  • contraception required to avoid pregnancy during entire follow-up period
  • serial β-hCGs (as tumour marker) every week until negative x 3 (usually takes several wk), then monthly for 6-12 mo prior to trying to conceive again
  • increase or plateau of β-hCG indicates GTN: patient needs chemotherapy
142
Q

Describe: Invasive Mole or Persistent gestational trophoblastic neoplasia (GTN) (3)

A
  • diagnosis made by rising or plateau in β-hCG, development of metastases following treatment of documented molar pregnancy
  • histology: molar tissue from D&C
  • metastases are rare (4%)
143
Q

Describe: Choriocarcinoma (4)

A
  • often present with symptoms from metastases
  • highly anaplastic, highly vascular
  • no chorionic villi, elements of syncytiotrophoblast and cytotrophoblast
  • may follow molar pregnancy, abortion, ectopic, or normal pregnancy
144
Q

Describe: Placental-Site Trophoblastic Tumour (3)

A
  • rare aggressive form of GTN
  • abnormal growth of intermediate trophoblastic cells
  • low β-hCG, production of human placental lactogen (hPL), relatively insensitive to chemotherapy
145
Q

Describe classification of: Gestational trophoblastic neoplasia (2)

A
  • non-metastatic
  • metastatic
146
Q

Describe: Non-metastatic Gestational trophoblastic neoplasia (4)

A
  • ~15% of patients after molar evacuation
  • may present with abnormal bleeding
  • all have rising or plateau of β-hCG
  • negative metastases on staging investigations
147
Q

Describe: Metastatic Gestational trophoblastic neoplasia (5)

A
  • 4% of patients after treatment of complete molar pregnancy
  • metastasis more common with choriocarcinoma, which tends toward early vascular invasion and widespread dissemination
  • if signs or symptoms suggest hematogenous spread, do not biopsy (they bleed)
    • lungs (80%): cough, hemoptysis, CXR lesion(s)
    • vagina (30%): vaginal bleeding, “blue lesions” on speculum exam
    • pelvis (20%): rectal bleeding (if invades bowel), U/S lesion(s)
    • liver (10%): elevated LFTs, U/S or CT findings
    • brain (10%): headaches, dizziness, seizure (symptoms of space-occupying lesion), CT/MRI findings
  • highly vascular tumour, which is more likely to bleed and result in anemia
  • all have rising or plateau of β-hCG
148
Q

Describe: Classification of metastatic Gestational trophoblastic neoplasia (GTN) (3)

A
  • divided into good prognosis and bad prognosis
  • features of bad prognosis
    • long duration (>4 mo from antecedent pregnancy)
    • high pre-treatment β-hCG titre: >100,000 IU/24 h urine or >40,000 IU/L of blood
    • brain or liver metastases
    • prior chemotherapy
    • metastatic disease following term pregnancy
  • good prognosis characterized by the absence of each of these features
149
Q

Name the primary site for metastatic Gestational trophoblastic neoplasia (GTN) (1)

A

Lungs are the primary site for malignant GTN metastases; when pelvic exam and chest x-ray are negative, metastases are uncommon

150
Q

Describe investigations for staging: Gestational trophoblastic neoplasia (GTN) (5)

A
  • blood work: CBC, electrolytes, creatinine, β-hCG, TSH, LFTs
  • imaging: CXR, U/S pelvis only
  • if CXR shows lung metastasis then CT abdo/pelvis, MRI brain
  • if suspect brain metastasis but CT brain negative, consider lumbar puncture for CSF β-hCG
  • ratio of plasma β-hCG:CSF β-hCG <60 indicates metastases
151
Q

Describe: FIGO Staging and Management of Malignant Gestational trophoblastic neoplasia GTN (Figure)

A
152
Q

Describe: WHO Prognostic Score for Gestational trophoblastic neoplasia GTD (2011) (Figure)

A
153
Q

Describe follow-up: Gestational trophoblastic neoplasia GTD (3)

A
  • contraception for all stages to avoid pregnancy during entire follow-up period
  • stage I, II, III
    • weekly β-hCG until 3 consecutive normal results
    • then monthly x 12 mo
  • stage IV
    • weekly β-hCG until 3 consecutive normal results
    • then monthly x 24 mo
154
Q

Describe diagnosis: Gestational trophoblastic neoplasia GTD (4)

A
  • β-hCG plateau: <10% drop in β-hCG over four values in 3 wk (e.g. days 1, 7, 14, and 21) OR
  • β-hCG rise >20% in any two values over two wk or longer (e.g. measure at days 1, 7, 14) OR
  • β-hCG persistently elevated >6 mo OR
  • metastases on work-up

TN Gyneco (20 decks)

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