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97 Cards in this Set
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preeclampsia in 26th week, what's the tx?
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Labetolol
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What's more safe/effective: male or female sterilization
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female
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fibroids present as
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bleeding
and little less often: pain |
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emergency contraceptives
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oral hormones, prohibit LH surge and ovulation, change endometrium, change tubal motility, do not disrupt pregnancy, 72h
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pseudostratification of endometrial cells
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complex endometrial hyperplasia
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hCG is made by
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Syncytiotrophoblast
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corpus luteum makes
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progesterone
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26yo, hirsutism, G0, infertility, acne,
pelvic ultrasound shows: |
multiple bilateral cysts
PCOS |
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is endometrioid adenocarcinoma dependent on estrogen for growth and proliferation?
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yes
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is endmoetrial hyperplasia dependent on estrogen for growth and proliferation?
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yes
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are leiomata dependent on estrogen for growth and proliferation?
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yes
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is papillary serous endometrial carcinoma dependent on estrogen for growth and proliferation?
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no
this is an endometrial CA, but it's not as common and not necessarily dependent on estrogen; not the classical presentation - thin older lady |
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is endometriosis dependent on estrogen for growth and proliferation?
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yes
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contraindications to using corticosteroids prenatally include
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chorioamnionitis (helps fetal lung maturity, helps decrease incidence of necrotizing enterocolitis, prevent interventricular hemorrhages)
not contraindications: maternal asthma, 26wk gestation, pre-eclampsia, premature rupture of membranes |
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most effective, most convienient method of contraception
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IUD
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split of wins causing : conjoined twins
what was the date? |
post 13 days
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mono-amniotic twins
when did the split occur? |
8-13days
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3rd trimester bleeding can be due to
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abruptio placentae - massive bleeding
placentae previa - painless bleeding vasa previa (obstetric complication defined as "fetal vessels crossing or running in close proximity to the inner cervical os") placenta accreta - painful bleeding |
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majority of chomosomal abnormalities occur in early conception due to
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no disjunction in maternal meiosis I
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indications for early delivery in pre-eclampsia
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rising liver enzymes
falling platelet count anuria HELLP (hemolysis, elevated liver enzymes, low platelets) worsening peripheral edema - is not indicative for early delivery |
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gestational DM is a risk for
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developing DM later in life (30-50% chance)
fetal macrosomia neonatal hypoglycemia |
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non-coiled umbilical artery is associated
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single umbilical artery
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endometriosis
causes pain when? |
powder-burn implants
most likely causing pain in: luteal phase |
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benign cystic teratomas in ovaries
incidence? unilateral?/bilateral? malignant? |
are not rare - 29% of all ovarian neoplasms
are bilateral in 10-15% can contain fully developed teeth risk of malignancy is very low in women of reproductive age managed by surgical excision |
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most common origin of breast CA
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TDLU
terminal duct lobular unit the epithelial cells - that's where the milk is made; here most CA arise if circumscribed by myoepithelial cells is CIS |
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where in the breast do we see the sarcomas of the breast
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Stroma:
Dense fibroconnective tissue – sarcomas of the breast |
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cancer close to the nipple in the ducts
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DIS
papillary CA most of the lesions here are benign |
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TDLU in post-menopausal woman
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atrophy - no more lobules
looks like a male breast |
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categories of benign breast disease
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Nonproliferative disease -Inflammatory conditions
-Fibrocystic changes Proliferative (Premalignant) -May mimic cancer clinically |
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inflammatory conditions
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Acute mastitis – usually during lactation, bacterial infection, erythema and swelling can mimic inflammatory breast cancer
Duct ectasia – dilatation of ducts, inspissated secretions, inflammation of lobules |
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Fibrocystic changes
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Lumpy, sometimes tender breasts
Very common – 60% of women, usually premenopausal Composed of cysts (fluid filled sacs, tender), fibrosis, adenosis Mass effect, tiny microcalcifications on mammogram, need biopsy to distinguish from cancer |
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Proliferative Lesions Without Atypia
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Usual ductal hyperplasia – very common, several cell layers with mixed cell population, ER+; look ugly but are benign
Sclerosing adenosis – proliferation of glands within a fibrotic stroma, microcalcifications Intraductal papilloma – growth inside duct, can cause nipple discharge; tree in the duct, if there are many many - they might get malignant Fibroadenoma – most common benign growth in younger pt, not precancerous, can go away; but they can become bad - Phylloides tumor |
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Proliferative Lesions with Atypia
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Premalignant
Miniature version of carcinoma in situ Homogeneous cell population (clonal) Cytologic atypia Atypical ductal hyperplasia ADH (they have high risk of going to CA) Atypical lobular hyperplasia ALH (no E-cadherin - so looks like they hate each other; also they have high risk of going to CA) ALH -> 4x higher chance to go to invasive BC (if it's already lobular insitu, the risk to become malignant is 8-10x higher) also, if it's ALH, but they have a + family Hx - the risk is also 8.4x |
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what drives the changes from nl to proliferative?
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Estrogen, Progesterone, other growth factors
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10% of breast CA are hereditary:
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Mutant gene defective in DNA repair
Passed from parents to offspring Early onset breast cancer (25-50 years) Multiple family members affected BRAC-1 and BRAC-2 account for half early onset (vs the later onset of sporadic cancer <50yo) |
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Carcinoma in situ in breast
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Lobular carcinoma in situ (LCIS) - less common (NO E-CADHERIN)
Ductal carcinoma in situ (DCIS) – more common (will not kill the pt, but eventually they'll become malignant; they're on a continuum between non-comedo- comedo-high grade) 1970, 3% of all new cases 2005, 30% of cases due to screening |
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Invasive Breast CA types?
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Invasive: cells invade outside duct basement membrane into stroma and potentially into blood vessels (systemic spread)
Requires surgery and systemic therapy Extremely heterogeneous behavior from patient to patient (indolent/aggressive) based on gene signature Paradigm for targeted therapy ER+: Tamoxifen, other endocrine therapies Her-2+: Trastuzumab Typically subset by histologic differentiation (degree of microscopic atypia) TYPES: Infiltrating “ductal” carcinoma, no special type (NOS); most common; 2/3 in post-menopausal LN - (75%) ER + (78%) PR + (50% ) HER + (25%) Infiltrating carcinoma: tubular, mucinous, medullary, lobular classic (these have much better prognosis) 10-15% of all cancers Rarely metastasize, excellent prognosis Tubular, mucinous-low grade, ER+ Medullary-high grade, ER- but still good prognosis |
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who is the silent killer of women?
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ovarian CA,
we don't have markers, we don't have goo tx |
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ovarian tumors
rate |
Ovarian tumors are common in women.
- 2/3 occur during the reproductive age - 80% benign: 60% < 40years - 20% malignant and borderline: 90% >40 years |
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what's in the ovarian stroma?
epithelium? |
Ovarian stroma
- Spindled shaped stromal cells - Lipid-droplets - Luteinized stromal cells - Leydig cells B. Surface epithelium (like mesothelium of the peritoneum) - Similar to the adjacent peritoneum - Ciliated cuboidal to columnar |
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classification of ovarian tumors
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Surface epithelial-stromal tumors
Sex cord-stromal tumors Germ cell tumors Secondary tumors |
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presentation of ovarian tumors
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Mild early symptoms/asymptomatic - “silent killer”
Abdominal distention, ascites, pain Urinary/Gastrointestinal tract symptoms Abnormal vaginal bleeding associated with functioning tumors Estrogenic/androgenic symptoms < 5 cm malignant in 5% of the cases 5-10 cm malignant in 12% of the cases > 10 cm malignant in 60% of the cases Bilateral tumors are malignant twice as often as unilateral tumors |
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ovarian tumor risk:
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Incessant ovulation Inc risk 1.5 - 3.2 (Nulliparity)
Oral contraceptive Dec risk 0.4- 0.7 Family history - 10% BRAC-1, 2 mutations (altered DNA repair) |
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Surface Epithelial Stromal Tumors
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2/3 of all ovarian tumors, 90% of all ovarian cancers
Classification: Cell type: Serous, Mucinous, Endometroid, Clear, Transitional (looks like urothelium), Squamous Exophytic/intracystic Cell proliferation, nuclear atypia or invasion: Benign 70% Borderline No invasion 10% Carcinoma Invasion 20% |
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Serous Tumors
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30% of all ovarian tumors; look like mesothelium (peritoneal)
Most are benign or borderline, 25% are malignant Cystic neoplasms, mostly uniloculated, lined by ciliated cuboidal Cells - Marker WT-1 They can be bilateral Psammoma bodies common finding |
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Mucinous tumors
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25% of all ovarian neoplasms
Most are benign or borderline, 15% are malignant Cystic neoplasms, mostly multiloculated, lined by tall columnar Cells with apical mucin - mucinous Less frequently bilateral |
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Endometrioid Tumors
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2- 4 % of all ovarian neoplasms
Almost 1/2 are associated with ipsilateral ovarian or pelvic endometriosis - Most are carcinomas - 30% of the cases are associated with endometrial adenocarcinoma probably related to same risk factors - Tubular glands similar to endometrial tissue |
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Sex Cord-Stromal Tumors
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Most common functioning ovarian tumors with endocrine manifestations
Classification: Derived from the ovarian stroma, that originates from the sex cords of the embryonic gonad: - Sertoli and Leydig - Masculinizing effect - Granulosa and theca - Feminizing effect |
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Granulosa Cell Tumors
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1-2% of all ovarian tumors
Most common estrogenic ovarian tumor Symptoms: abnormal uterine bleeding Rarely androgenic Unilateral 90% benign Call-Exner bodies, inhibin + 10yr survival 85% |
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Sertoli-Leydig Cell Tumors (Androblastoma)
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0.5% of all ovarian tumors
Peak occurrence during reproductive years Unilateral Androgenic virilization in 30-50% Histology: reminiscent of fetal testis Mostly benign |
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Germ Cell Tumors
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20 % of all ovarian tumors
Capable of developing complex and highly differentiated tissues Classification: Benign (95%) teratomas Malignant 5% |
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Teratomas ovarian
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Tissues derived from two or three embryonic layers in any combination
Most common ovarian neoplasm Young females Can have malignant transformation in post-menopausal women Tissues found are mature: Sometimes in organoid arrangement Ectodermal: Skin and adnexa, glia, cerebrum, cerebellum, choroid plexus and retina Endodermal: Respiratory, gastrointestinal, thyroid Mesodermal: Muscle, adipose tissue, bone, teeth, cartilage |
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Malignant germ cell tumors
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Girls and young women
Dysgerminoma – (seminoma) marker PLAP [Monotonous cell population of round cells Excellent prognosis: Stage I 95%, Radiosensitive and chemosensitive tumor] Yolk sac tumor – marker AFP [Histological hallmark: Papillary projections surrounded by embryonic epithelial cells, Schiller-Duval bodies - Survival: Stage I 80%, advanced stage 40% ] Choriocarcinoma – marker β HCG [Highly malignant; Advanced stage at presentation Rare Young patients, before puberty Most are associated with other tumors Poor prognosis; chemotherapy resistant ] |
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secondary tumors of ovaries
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Metastatic tumors involve the ovaries more often than any other site
Occur in 30% of women dying of cancer, maybe the initial manifestation GI tract - the signet cell from stomach (krukenberg) cervical, breast.... |
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Abnormal Uterine Bleeding
causes by Age Groups |
Adolescence:
Anovulatory cycle Reproductive age: Complications pregnancy – abortion, ectopic pregnancy, Organic lesions – leios, polyps, hyperplasia, cancer Anovulatory cycle DUB Perimenopausal: Anovulatory cycle Organic – cancer, hyperplasia, polyps Postmenopausal: #1 Endometrial Atrophy #2Organic – cancer, hyperplasia, polyps |
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biochemical changes are according to the main goals of:
1) proliferative 2) secretive 3) menstrual breakdown |
1) growth
2) maturation 3) apoptosis |
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Functional Disorders of Endometrium (No organic lesion) DUB
1) low estrogen 2) high estrogen 3) low progesterone |
1) low estrogen
-no follicle development -amenorrhea, oligomenorrhea, infertility 2) high estrogen -anovulatory cycle (most common cause) -metrorrhagia 3) low progesterone -defective corpus luteum, intermenstrual bleeding, irregular cycles -infertility |
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3 versions of DUB
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heavy uterine bleeding
prolonged uterine bleeding intermenstrual bleeding |
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AUBNon-proliferative/ Non malignant
causes |
a) Inflammation PID – chronic endometritis
b) IUD c) Retained POC |
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AUBProliferative Causes – Benign
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1) Polyp:
- Single or multiple - May cause bleeding Adenocarcinoma - Clonal > in patients on Tamoxifen Contain glands and stroma 2) Leiomyoma: - ”Fibroids” - Common 40y → 40% - Hormonal influence - Pain, intermenstrual bleeding - Examination to exclude malignancy -decrease after menopause (they're responsive to E ) -the large one's on the outside, cause the pain, but the submucosal ones cause the abnormal bleeding -made of smooth muscle 3)Endometrial Hyperplasia Simple (more related to high E): Without atypia – cancer risk: 1% With atypia - rare Complex (already has genetic changes closer to malignancy) Without atypia – cancer risk: 3% With atypia – cancer risk: 25 -40% |
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Endometrial Adenocarcinoma
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Post menopausal women 80%
Risks – High estrogenic states: HRT Tamoxifen Ovarian Neoplasm Obesity Reproductive factors types: Endometriod - most common - early stage - good prognosis Papillary serous - less common - aggressive - older patients |
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leiomysarcoma of uterus
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leiomysarcoma - rare
- cellular - necrosis - ↑mitoses bad spindle, fish-flesh like |
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Carcinosarcoma of uterus
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Carcinosarcoma
worst of all - malignant glands - malignant stroma - 2-5% of uterine malignancies - postmenopausal - poor prognosis homologous heterologous (chondrosarcoma, osteosarcoma) seen in older pt |
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Molar Pregnancy Hydatidiform Mole
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Complete
Origin – Fertilization of empty ovum Diploid – No maternal DNA More Common in Asian Women (Indonesia 10/1000 deliveries Clinical Symptoms: Excessive Uterine Size for Gestational Age Pre-eclampsia Hyperemesis Lab: Increased β-HCG Appearance and Histology: Enlarged villi (Up to 2 cm), grape-like clusters Microscopically: Large villi with central cisterns and circumferential proliferation of trophoblasts Androgenic diploid, p57 immunostain neg. No fetal tissue After evacuation, levels of β-HCG decrease Chemotherapy may be needed 2% may progress to choriocarcinoma Partial mole/incomplete mole: Origin: Union of oocyte with either a diploid spermatozoid or with two spermatozoids Triploid – DNA Analysis – p57 immunostain+ Incidence is similar as complete mole Appearance and Histology: Large and small villi Less formation of central cisterns Less trophoblastic proliferation A fetus with multiple congenital malformations may be seen Rarely progress to choriocarcinoma Choriocarcinoma: Malignant tumor of admixed proliferating trophoblasts No villi 1 in 24,000 pregnancies in USA, 1 in 2,500 in Ibadan, Nigeria Uniquely sensitive to chemotherapy, cure rate of >95% Lab: Markedly elevated increased β-HCG Normal pregnancies after treatment |
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choriocarcinoma of ovary vs choriocarcinoma of uterus
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choriocarcinoma ovary: chemoresistant
choriocarcinoma uterus - from a molar pregnancy : uniquely sensitive to chemo |
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uterine cancer types
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Adenocarcinoma (90% of all uterine malignancies)
-Endometrioid (garden variety adenocarcinoma) -Adenosquamous -Mucinous -Papillary serous (bad actor) -Clear cell (bad actor) -Rare subtypes – primary squamous Sarcomas (3-5% of all uterine malignancies) -Leiomyosarcoma -Endometrial stromal sarcoma Mixed homologous müllerian sarcoma (if malignant mesodermal elements are normally present in the uterus) -Mixed heterologous müllerian sarcoma Extension from cervical or ovarian cancers |
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endmetrial adenocarcinoma
incidence |
highest incidence, best survival
endometrial > ovarian > cervical Ovarian (worst) > cervical > endometrial (best) |
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endometrial CA types
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Type I (90%)
Estrogen Related Younger and heavier patients e.g. PCO Low grade Perimenopausal Exogenous estrogen Type II (10%) Aggressive Unrelated to estrogen stimulation Occurs in older & thinner women Potential genetic basis Lynch syndrome Familial trend [breast CA, uterine CA, colon CA] |
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endometrial CA risks
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Peak incidence in late 50s-early 60s
Associated with prolonged and uninterrupted exposure to estrogenic stimulation (endogenous or iatrogenic) Other risk factors: obesity, previous irradiation, early menarche, late menopause, hypertension, diabetes On a stage for stage basis the survival is slightly worse in african-american women than Caucasian women. AA women tend to present with later stage disease; almost always this is a failure to detect disease earlier because of either lack of access to healthcare system or delays in getting through our system |
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endometrial hyperplasia
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“overgrowth” of endometrium secondary to prolonged unopposed estrogen
May be generalized or focal Seen in adolescents through menopause Progression to carcinoma is possible, esp. with atypical histology Presents with abnormal uterine bleeding, typically following amenorrheic intervals If detected and properly treated should never progress to cancer obesity |
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endometrial hyperplasia is associated with (other risks)
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Anovulatory cycles in teens
Granulosa cell tumors of the ovary Polycystic ovary syndrome Adrenal cortical hyperplasia Iatrogenic unopposed estrogen (women with a uterus should not, as a rule, ever receive estrogen therapy alone without progesterone) Paradoxically, use of some anti-estrogens such as Tamoxifen |
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management of endometrial hyperplasia
with or without atyppia |
we can treat and cure this medically
progestin |
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endometrial carcinoma presentation
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Abnormal bleeding (>90%)
Abnormal cells detected on Pap – not so common as you would think Screening asymptomatic low risk patients is not cost effective. |
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HNPCC
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Hereditary nonpolyposis colorectal cancer (HNPCC) [Lynch syndrome] is a colon cancer, characterised by a risk of other cancers of the endometrium, ovary, stomach, small intestine, hepatobiliary tract, upper urinary tract, brain, and skin. The increased risk for these cancers is due to inherited mutations that impair DNA mismatch repair.
Endometrial cancer is most common malignancy: 40-60% lifetime risk, then colon cancer, then ovarian cancer |
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Endometrial carcinomaDiagnosis
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Endometrial biopsy (office procedure)
Dilation & curettage (D&C) Hysteroscopy with directed biopsy The latter two are done in the OR Transvaginal sonography can be suggestive but rarely diagnostic Opportunity to diagnose early Rare cases in young women desiring fertility preservation can be managed with aggressive progesterone therapy provided a narrow set of strict criteria are met Most everyone else will be treated primarily with surgery Radiation therapy as primary treatment reserved for patients who are too high-risk to undergo surgery |
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Endometrial carcinomaSurgical staging
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Abdominal exploration
Total hysterectomy Bilateral salpingo-oophorectomy Peritoneal cytology Pelvic and para-aortic node sampling Directed biopsies as needed Omentum, diaphragm, bowel surface, liver NOTE: the trend in the past five years has been to perform this surgery laparoscopically, with or without the Robot Stage 1 - uterus only stage 2 - uterus + cervix stage 3 - uterine serosa, adnexa, vagina, pelvic/aortic mets stage 4 - bladder, bowel, inguinal node, distant mets We can get some valuable information in the operating room about the risk factors the individual patient has for spread, and can make a “tailored” staging decision. Ideally, all patients should be surgically staged, but staging is not without potential complications so we are flexible We also have some idea pre-op about who has to be staged – e.g. high grade on biopsy, visible cervical lesion biopsy proven, elevated CA-125 Properly staged patients may be able to avoid post-operative pelvic (or other) radiation therapy Most patients with rarer subtypes (papillary serous, clear cell) are treated like ovarian cancers even if stage I because they tend to behave that way |
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Endometrial Cancer: Pre-op Evaluation
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CA125
Chest X-ray Mammogram Colon Evaluation. Transvaginal Ultrasound Others as indicated. Like physical exam. And, maybe even talk to the patient and take a real history |
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Endometrial Cancer: Poor Prognostic Factors
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Increasing age (over 65)
Stage (> IB) Vascular invasion Grade Histologic Subtypes (Clear-cell, Serous, Adenosquamous) Aneuploidy Altered oncogene/tumor suppressor gene expression Very elevated serum CA-125 in absence of surgical evidence of spread. (This creates a problem for us because we have to counsel the patient as well as decide on possible therapy, and it’s not clear what the best therapy should be in the absence of a “site”. ) Some patients with early cancers require less surgical staging because they have a much lower risk of having metastases - endometroid... |
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Endometrial Cancer: Adjuvant Therapy
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Brachytherapy
External beam radiotherapy Hormonal therapy Cytotoxic chemotherapy Combination therapy – chemo and hormonal |
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Endometrial Cancer: Recurrence
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responds less to chemo than ovarian
80% of recurrences happen first 3 years Most will be symptomatic Rare to cure distant recurrences 50% vaginal recurrences cured |
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Endometrial Cancer: Who Needs an Endometrial Biopsy?
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Postmenopausal bleeding
Postmenopausal women with endometrial cells on Pap Perimenopausal intermenstrual bleeding Abnormal bleeding with history of anovulation Thickened endometrial stripe via sonography* Older than age 40 with anovulatory bleeding Younger than age 40 with Abnormal uterine bleeding PLUS risk factors (e.g., PCOS, obesity) Atypical endometrial cells or atypical glandular cells on Pap at any stage of menstrual cycle Any endometrial cells on Pap during secretory phase of menstrual cycle – never heard of this one |
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uterine sarcomas
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All of the information we discussed was about the 90% of uterine cancers. What about the other 10%?
Presentations the same Surgery the same Survival NOT the same Post-operative therapy, if required, generally less effective For uterine sarcomas it is critical that the disease be surgically confined to the uterus. Even when it is, up to 50% of patients will recur |
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risk of ovarian mass being cancer increases with...
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Large size
Bilaterality Solid vs. cystic Radiologic appearance: Complex, papillary,density, pulsatility of blood flow Age of pt. outside reproductive span (Age of patient Premenarchal: risk of malignancy 5x Postmenopausal: risk of malignancy 10×) Ascites Elevated serum tumor markers |
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Adnexal massesIndications for surgery
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Cyst > 5 cm (persistent)
Solid Papillary appearance on sonography Initial size > 10 cm Ascites Age of patient outside reproductive range Torsion or rupture suspected |
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ovarian endometriosis is the most common cause of ...
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pelvic pain and infertility in women in the US
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Benign ovarian massesFunctional (Follicular) cysts
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Most common cystic mass in reproductive-age women
Rarely >6 cm Spontaneously resolve May rupture or undergo torsion Prevention: hormonal contraception |
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Corpus luteum cysts
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Usually <5 cm
May hemorrhage or undergo torsion Self-resolving |
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Cystic teratoma(Dermoid cyst)
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Cysts associated with endometriosis
Can fill with blood and become “chocolate cyst" |
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Ovarian fibroma(Thecoma)
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Solid
More common in older women Spindle cells and fibrous bands |
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Ovarian Cancer
numbers/incidence |
90% are epithelial in origin
1 in 56 women will develop ovarian cancer 4th most common fatal cancer in U.S. 27,000 new cases annually; 16,000 deaths annually in US High mortality in advanced stage disease (when it is most commonly diagnosed) |
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Ovarian CancerRisk factors
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Family history
BRCA1 or BRCA2 mutation Nulligravid ??Use of fertility (ovulation inducing) drugs |
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Abdominal distension
Ascites (amount does not corrlate With size of CA) Bowel obstruction Vague abdomnial/GI |
Ovarian cancerClinical features
|
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Ovarian cancerPresenting symptoms
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Abdominal pain
Abdominal swelling/increased abdominal girth Vomiting Altered bowel habits urinary frequency or retention clinical: Abdominal distension Ascites (amount does not corrlate With size of CA) Bowel obstruction Vague abdomnial/GI |
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Growth pattern of ovarian cancer
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Main mode of spread is by implantation on peritoneal surfaces
Lymphatic spread also important Omentum usually involved |
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Ovarian CancerManagement
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Surgery: for staging and “debulking”
Second-look after initial treatment Chemotherapy Adjunctive or salvage Radiation Limited role |
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Screening for ovarian cancer
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Physical exam
Fact: Most ovarian cancer not detected before Stage III or IV Imaging Fact: No imaging technique can definitively diagnose or rule out ovarian malignancy Serologic testing Fact: No serum marker with sufficiently high sensitivity or specificity, especially in early stage cancer, even for serum markers such as CA-125; it’s good for monitoring – but the big limiting factor is that the lvl is normal for 25% In women under age 50, elevated CA-125 is associated with malignancy less than 25% of the time increased with: Acute PID Active hepatitis Pericarditis Adenomyosis Acute pancreatitis Pneumonia Benign ovarian neoplasm Chronic liver disease Polyarteritis nodosa Endometriosis Cirrhosis Surgery Functional ovarian cyst Colitis Renal disease Meig’s syndrome Congestive heart failure Systemic lupus Menstruation Diabetes erythematosus Ovarian hyperstimulation Diverticulitis Uterine fibroids Mesothelioma Nonmalignant ascites |
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Protective factorsagainst ovarian cancer
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Pregnancies
Current or former use of OCPs Tubal ligation Breast feeding Prophylactic oophorectomy: not 100% |