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PA29.2-10 | Female Genital Tract — Graded Quiz

Graded 12 questions · Untimed · 2 attempts

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Q1 PA29.9 1 pt

A 38-year-old woman with polycystic ovary syndrome (PCOS) and a BMI of 34 presents with irregular, heavy menstrual bleeding for 18 months. She is nulliparous and has never taken oral contraceptives. Transvaginal ultrasound shows endometrial thickness of 18 mm. Endometrial biopsy shows markedly crowded glands with a gland:stroma ratio >3:1, back-to-back architecture, intraluminal epithelial tufting, nuclear stratification, and rounded nuclei with prominent nucleoli. No stromal invasion is identified. What is the MOST appropriate classification and the most critical management decision at this point?

A Non-atypical endometrial hyperplasia — progestogen therapy for 6 months and reassess; < 5% risk of progression to carcinoma
B Atypical endometrial hyperplasia/Endometrial Intraepithelial Neoplasia (EIN) — discuss hysterectomy as definitive treatment given the nuclear atypia, as approximately 25–30% of such specimens contain concurrent or subsequent invasive carcinoma
C FIGO Grade 1 endometrioid adenocarcinoma — the glandular crowding with nuclear atypia represents stromal invasion and mandates surgical staging
D Disordered proliferative endometrium — this is expected in PCOS patients and does not warrant treatment beyond cycle regulation with progestogens

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Q2 PA29.2 1 pt

A 68-year-old thin, non-diabetic woman with no history of exogenous estrogen use presents with one episode of postmenopausal bleeding. Endometrial biopsy shows a serous papillary carcinoma. CA-125 is 185 U/mL. Peritoneal washings are positive for malignant cells. Hysterectomy + bilateral salpingo-oophorectomy shows a 0.4 cm tumour confined to an endometrial polyp with no myometrial invasion. What is the MOST accurate characterisation of stage and prognosis?

A FIGO Stage IA with excellent prognosis — despite serous histology, minimal or absent myometrial invasion at Stage IA has the same prognosis as Grade 1 endometrioid carcinoma
B FIGO Stage IIIA (positive peritoneal cytology) — serous carcinoma disseminates transcoelomic even from minimal primary disease, and positive washings upgrade stage with significantly worse prognosis than endometrioid Stage IA
C FIGO Stage IVB — the positive peritoneal cytology indicates distant metastasis equivalent to peritoneal carcinomatosis
D The stage is FIGO IA but the diagnosis should be revised to an endometrioid carcinoma — serous carcinoma cannot arise in an endometrial polyp without myometrial invasion

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Q3 PA29.7 1 pt

A 34-year-old nulliparous woman presents with 6 months of secondary dysmenorrhoea and deep dyspareunia. Laparoscopy reveals a right ovarian 'chocolate cyst' (4 cm), powder-burn lesions in the pouch of Douglas, and dense filmy adhesions fixing the uterus in retroversion. A biopsy from the posterior broad ligament shows endometrial glands and stroma with haemosiderin-laden macrophages. CA-125 is 78 U/mL. She wishes to conceive. Which statement BEST characterises the RISK of malignancy in this setting?

A CA-125 of 78 U/mL mandates immediate oophorectomy as this level indicates malignant transformation of the endometrioma to clear cell carcinoma
B Endometriosis-associated ovarian carcinoma (EAOC) is a genuine risk — most commonly clear cell or endometrioid carcinoma arising within an endometrioma — but the overall absolute risk is low (~1–2%), and CA-125 elevation alone is insufficient to diagnose malignancy in active endometriosis
C Endometriosis is categorically benign and confers no ovarian cancer risk; the CA-125 elevation is entirely explained by peritoneal inflammation
D The 4 cm size of the chocolate cyst is the primary concern — any endometrioma >3 cm requires immediate surgical removal due to exponential malignancy risk above this threshold

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Q4 PA29.8 1 pt

A 42-year-old multiparous woman with a 10-year history of heavy menstrual bleeding undergoes hysterectomy. The uterus weighs 360 g (normal ~70 g). Cut surface of the myometrium shows irregular, haemorrhagic, soft foci scattered throughout the posterior wall, without a discrete capsule. The endometrium is intact. Microscopically, endometrial glands and stroma are identified within the myometrium at multiple foci more than 2.5 mm below the endomyometrial junction, surrounded by hypertrophied smooth muscle. No mitoses or cytological atypia. CA-125 is normal. What is the MOST specific clinical predictor that distinguishes this from uterine leiomyomas preoperatively?

A Uterine size — leiomyomas cause irregular enlargement while adenomyosis causes uniform enlargement, distinguishable by bimanual examination
B The association with secondary dysmenorrhoea that begins at the onset of menstrual flow and worsens progressively over years, combined with a uniformly enlarged tender uterus — a pattern not typical of uncomplicated fibroids which cause menorrhagia without cyclical pain beginning at flow onset
C Serum CA-125 level — adenomyosis specifically elevates CA-125 to >200 U/mL while leiomyomas do not affect CA-125
D Age of onset — adenomyosis begins in the first decade of menstruation while leiomyomas exclusively affect perimenopausal women

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Q5 PA29.4 1 pt

A 55-year-old woman presents with a 6 cm bilateral complex ovarian mass found on routine pelvic ultrasound. She is otherwise asymptomatic. CA-125 = 850 U/mL. CT shows omental caking, ascites, and bilateral pleural effusions. Histology from an omental biopsy shows high-grade carcinoma with psammoma bodies and complex papillary architecture. TP53 is mutated; BRCA1 is mutated. Which statement about the ORIGIN and CLINICAL implications of this tumour is MOST accurate?

A This tumour originated from the ovarian surface epithelium and is best treated with primary debulking surgery followed by paclitaxel/carboplatin, with BRCA1 status informing hereditary risk counselling only
B Contemporary evidence supports a fallopian tube fimbrial origin for most high-grade serous carcinomas (HGSC); BRCA1 mutation identifies the patient as a candidate for PARP inhibitor maintenance therapy after platinum-based chemotherapy, and all first-degree relatives require BRCA cascade testing
C Bilateral ovarian involvement with omental caking proves haematogenous spread from a primary gastric or colonic mucinous primary (Krukenberg tumour), not an ovarian primary
D Psammoma bodies identify this as low-grade serous carcinoma, which is driven by KRAS/BRAF mutations and is not associated with BRCA1 mutations or PARP inhibitor sensitivity

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Q6 PA29.4 1 pt

A 19-year-old woman presents with a solid left ovarian mass. Serum AFP = 3,400 ng/mL; β-hCG = normal; LDH = elevated. Histology shows a solid tumour with interlocking cords of primitive germ cells around a central hyalinised fibrovascular core, forming papillary structures. PAS stain shows a bright red rim around the central core. IHC: AFP+, Gleason-staining positive for AFP on the papillary structures. What is the MOST complete diagnosis including the name of the pathognomonic structure?

A Dysgerminoma with AFP-positive variant — AFP elevation does not indicate yolk sac tumour elements as dysgerminoma can produce AFP at this age
B Yolk sac tumour (endodermal sinus tumour) — the pathognomonic structure is the Schiller-Duval body (papillary structure with hyalinised fibrovascular core lined by cuboidal cells, surrounded by a mantle of tumour cells), which recapitulates the endodermal sinus of Duval
C Immature teratoma Grade 3 — the high AFP reflects immature hepatic elements within the teratoma and the structures represent immature hepatic cords
D Choriocarcinoma — the combination of AFP elevation and primitive germ cells is diagnostic of gestational trophoblastic disease arising in a germ-cell tumour

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Q7 PA29.4 1 pt

A 50-year-old woman is admitted for evaluation of abdominal distension. She had a left salpingo-oophorectomy 2 years ago for a 'benign cystic ovarian mass' with 'abundant mucinous material.' Now, re-exploration reveals massive gelatinous material filling the peritoneal cavity with mucoid implants on the omentum and bowel serosa. Repeat appendix biopsy is non-contributory. Review of the original left ovary shows a multilocular mucinous cystadenoma without atypia. What MOST accurately explains this clinical scenario?

A Mucinous cystadenoma has undergone malignant transformation in situ within the peritoneal metastases — this is Stage IV mucinous carcinoma arising from the ovarian primary
B Pseudomyxoma peritonei most commonly originates from a low-grade appendiceal mucinous neoplasm (LAMN), not the ovary — the ovarian mucinous lesion was likely a secondary deposit; appendiceal primary must be definitively excluded by thorough pathological review
C This is a normal postoperative complication of spilling mucinous cyst contents at oophorectomy — the peritoneal mucin will reabsorb over time without surgical intervention
D Pseudomyxoma peritonei confirms a primary ovarian mucinous carcinoma because only ovarian mucinous tumours produce large volumes of intraperitoneal mucin

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Q8 PA29.4 1 pt

A 25-year-old woman is found to have a 3 cm solid right ovarian mass at routine scan. Serum LDH and PLAP are mildly elevated; AFP and β-hCG are normal. Histology shows solid nests of large cells with clear cytoplasm and central nuclei separated by fibrous septa containing a brisk lymphocytic infiltrate. PAS shows intracytoplasmic glycogen. No Schiller-Duval bodies are seen. IHC: OCT4+, CD117+, D2-40+, SALL4+, AFP negative. Five percent of cells have microfoci with syncytiotrophoblastic giant cells. What is the ONE most important treatment implication of this diagnosis?

A The syncytiotrophoblastic giant cells indicate choriocarcinoma elements requiring immediate BEP chemotherapy regardless of stage
B Dysgerminoma is exquisitely radiosensitive and chemosensitive (BEP protocol); even with para-aortic nodal disease (Stage II–III), >90% cure rate is achievable, making fertility-sparing surgery a viable option for Stage I and selected higher-stage patients
C The prognosis is equivalent to HGSC — aggressive debulking and platinum-based chemotherapy are required; fertility preservation is not possible
D OCT4 and CD117 positivity indicates that this is a primary small cell carcinoma of the ovary requiring immediate combination radiation + chemotherapy with no role for surgery

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Q9 PA29.5 1 pt

A 28-year-old woman has a uterine evacuation for a suspected molar pregnancy. Products of conception are sent for histology. The pathologist identifies: (i) Enlarged villi with central cisterns (cavities); (ii) Some villi with irregular, scalloped outlines; (iii) A few recognisable fetal blood vessels in some villi; (iv) Trophoblastic hyperplasia focally, predominantly syncytiotrophoblast only; (v) p57 immunostaining POSITIVE in villous stromal cells and cytotrophoblast. Karyotype is 69,XXY. What is the MOST accurate diagnosis and its malignant potential compared to the alternative molar diagnosis?

A Complete hydatidiform mole (46,XX) — the p57 positive staining confirms maternally expressed alleles and the triploid karyotype is a laboratory error
B Partial hydatidiform mole (69,XXY) — p57 is POSITIVE (maternally expressed gene present) in contrast to complete mole (p57 negative); malignant potential (persistent GTD) is ~2–4%, significantly lower than the 15–20% risk of complete mole
C Complete hydatidiform mole — the 69,XXY karyotype reflects a chromosomal error in an otherwise complete mole; p57 positivity is diagnostic of complete mole
D Hydropic abortion — the presence of fetal vessels and p57 positivity rules out any molar pregnancy; the enlarged villi are due to hydropic degeneration of a missed abortion

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Q10 PA29.5 1 pt

A 24-year-old woman presents with vaginal bleeding 8 weeks after an uneventful term delivery. β-hCG is 28,000 mIU/mL. MRI shows a 2.2 cm vascular uterine mass invading through the myometrium. Histology from a curettage specimen shows mononuclear intermediate trophoblastic cells infiltrating individually through the myometrium between smooth muscle fibres with minimal necrosis. The β-hCG is only mildly elevated relative to the tumour size. Inhibin A is strongly positive; hPL (human placental lactogen) is strongly positive. Multinucleated syncytiotrophoblast and chorionic villi are ABSENT. What is the MOST likely diagnosis and the critical therapeutic implication that distinguishes it from choriocarcinoma?

A Choriocarcinoma — the mononuclear cells are cytotrophoblast and the strong hPL is characteristic of choriocarcinoma; EMA/CO chemotherapy is the treatment of choice
B Placental site trophoblastic tumour (PSTT) — composed of intermediate trophoblast (hPL+, inhibin A+, β-hCG mildly elevated), relatively chemoresistant compared to choriocarcinoma; hysterectomy is the preferred treatment for Stage I disease because PSTT does not respond well to standard EMA/CO chemotherapy
C Epithelioid trophoblastic tumour (ETT) — the mononuclear cells forming nests with geographic necrosis and a hyalinised matrix are diagnostic; managed identically to choriocarcinoma with EMA/CO
D Invasive mole — the presence of molar villi is the defining feature; surgical evacuation cures most cases and chemotherapy is rarely required

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Q11 PA29.10 1 pt

A 52-year-old woman presents with a 7 cm solid right ovarian mass. Serum estradiol is markedly elevated; FSH is suppressed. She has endometrial hyperplasia on biopsy. Histology of the ovarian mass shows polygonal cells with abundant pale cytoplasm arranged in nests and microfollicular structures, with characteristic 'coffee-bean' nuclei (grooved, oval nuclei). Call-Exner bodies are identified. What additional finding would MOST likely be present on further investigation, and which marker best confirms this diagnosis?

A Serum CA-125 markedly elevated — high CA-125 confirms the sex cord–stromal origin of this granulosa cell tumour
B Serum inhibin B elevated and serum AMH elevated — inhibin B is the most sensitive and specific marker for adult granulosa cell tumour; endometrial hyperplasia confirms the estrogenic activity of the tumour
C Serum testosterone markedly elevated — granulosa cell tumours produce androgens, and virilisation with clitoromegaly would be the expected clinical finding
D Serum AFP markedly elevated — the 'coffee-bean' nuclei and Call-Exner bodies confirm a yolk sac tumour origin producing AFP

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Q12 PA29.6 1 pt

A 44-year-old woman presents with cervical discharge, pelvic pain, and cervical motion tenderness. A cervical smear shows short, cylindrical, intracellular Gram-negative diplococci within neutrophils. She is treated with dual antibiotics. Three months later she is asymptomatic but presents for infertility evaluation. Hysterosalpingography shows bilateral tubal occlusion. What is the MOST accurate pathological explanation for her infertility?

A Gonococcal endocervicitis directly causes fallopian tube lumen scarring through toxin production without ascending infection — the bilateral occlusion is a direct toxic effect on tubal smooth muscle
B Ascending infection from endocervicitis to endometritis and salpingitis (PID) causes peritubal adhesions and tubal lumen scarring; bilateral tubal occlusion from pelvic inflammatory disease is the most common cause of tubal-factor infertility worldwide, occurring even after a single episode of acute PID
C The antibiotic treatment caused iatrogenic tubal fibrosis as a side effect — rifampicin is tubulofibrogenic and is contraindicated in women of reproductive age
D N. gonorrhoeae selectively tropisms the ovarian cortex — bilateral tubal occlusion indicates ovarian fibrosis, not tubal pathology, and the primary fertility issue is ovarian reserve depletion

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