O&G

Question 1

Two categories of vulval SCC?

Answer 1

Basaloid and warty (HPV related)
Keratinizing (not HPV related, more related to chronic inflammation)

Question 2

Name the precursor lesion for keratinizing SCC of the vulva and two risk factors for developing this?

Answer 2

Differentiated vulval intraepithelial neoplasm

Occurs most often in individuals with:
1. Vulval squamous cell hyperplasia
2. Lichen sclerosis

70% of vulval cancers develop from differentiated VIN (i.e. are not HPV related).

Question 3

Cause of condyloma acuminatum?
Is this a precursor for SCC?

Answer 3

Low-risk HPV strains (6 and 11)
Not a precursor for SCC

Question 4

Precursor lesion for basaloid and warty vulval SCC?

Answer 4

Classic vulval intra-epithelial neoplasia (VIN)

30% of vulval cancers develop from classic VIN and are caused by HPV infection, typically HPV 16

Question 5

Location of a Bartholin’s cyst

Answer 5

Posterolateral vaginal introitus
Below the level of the pubic symphysis

Question 6

What is a Gartner duct cyst and where is it located?

Answer 6

Wolffian duct/mesonephric duct remnant

Anterolateral vaginal wall
Above the level of the pubic symphysis

Question 7

Exophytic growth in the endocervical canal with a feeding vascular stalk - what is it and what is its malignant potential? What is the treatment?

Answer 7

Endocervical polyp
<1% risk of malignancy
Treated with surgical excision

Question 8

Endocervical polyp risk factors?

Answer 8

Tamoxifen use
Multiparity
Foreign body
Chronic cervicitis
Oestrogen secretion

Question 9

What is squamous metaplasia and what is its significance?

Answer has been edited using Pathology outlines as a guide

Answer 9

Squamous metaplasia is the normal process of progressive replacement of glandular epithelium by squamous epithelium - Direct extension of stratified squamous epithelium into endocervix.

Occurs at squamocolumnar junction.
Transformation zone = area of newly formed squamous epithelium.

Induced by estrogenic stimulation and vaginal acidic environment.

• Non-neoplastic condition but vulnerable to persistent HPV infection –> Immature basal epithelial cells are more accessible at this region.
• Risk for high grade squamous intraepithelial lesion defined by maturation status of squamous metaplasia

Question 10

List 7 risk factors for cervical SCC excluding high risk HPV?

Answer 10

1. Increased number of sexual partners
2. Young age at first sexual activity
3. Long term oral contraceptive use
4. History of STI
5. Low socioeconomic status
6. Immunosuppresion
7. Smoking

Question 11

Which HPV subtype causes the most cases of cervical cancer?

Answer 11

16 (60% of cervical SCC)

subtype 18 causes 10%

Question 12

Name a condition caused by low risk HPV subtypes, and what are those subtypes?

Answer 12

Subtypes 6 and 11

Condyloma Acuminatum

Question 13

In which cells does viral replication of HPV occur?

Answer 13

Mature squamous cells

i.e. not the immature basal epithelial cells - these are vulnerable to entry of HPV

Question 14

What is the pathogenesis of high-risk HPV acting as a carcinogen?

Answer 14

The oncoproteins E6 and E7 bind to tumour suppressor proteins as follows:
E6 –> binds to P53 and causes its degradation
E7 –> binds to RB and inactivates it
and interfere with their activity.

Question 15

Why do low risk HPV strains not act as carcinogens?

Answer 15

E6 in lower risk strains can’t bind P53
E7 in lower risk strains binds RB with less affinity

Question 16

What does koilocytic atypia suggest?

Answer 16

HPV infection

Koilocytic atypia relates to cellular changes seen in HPV infected cells i.e. nuclear atypia with perinuclear halos

Question 17

What are the histological features that form the basis for squamous intraepithelial lesion diagnosis?

Answer 17

Nuclear atypia

• Nuclear enlargement
• Nuclear pleomorphism (variation in size and shape)
• Hyperchromasia (dark nucleus)
• Irregular nuclei

Question 18

What histologic feature differentiates LSIL and HSIL?

Answer 18

LSIL - immature squamous cells confined to lower 1/3 of epithelium (80% related to HPV, 10x more common than HSIL)

HSIL - immature squamous cells within the upper 2/3 of the epithelium (100% related to HPV)

Question 19

Give approximate percentages for the regression, persistence, and progression of LSIL vs. HSIL?

Answer 19

LSIL - 60% regress, 30% persist, 10% progress to HSIL
HSIL - 30% regress, 60% persist, 10% progress to invasive carcinoma

Question 20

Associated abnormalities with Gartner duct cyst

Answer 20

Metanephric - ipsilateral renal dysplasia/agenesis, ectopic ureter, cross-fused ectopia

Mullerian - bicornuate uterus, didelphys, diverticulosis fallopian tubes

Question 21

Is HPV related cervical SCC keratinizing or non-keratinizing?

Answer 21

Trick question! Can be both

Question 22

List three sites of cervical cancer invasion by direct extension, and two sites of distal metastasis

Answer 22

1. Paracervical soft tissues
2. Bladder, ureters
3. Rectum

Distant mets:
Lung, liver

Question 23

Important histopathological staining in HPV

Answer 23

Ki-67 and p16 - simultaneous expression in the same cells.
Usually not seen in same cells, but with HPV infection it upregulates expression of both, suggestive of oncogenic transformation of infected cells (differentiated HSIL from LSIL)

Question 24

List three causes of haematometrocolpos, and indicate which is most common

Answer 24

1. Imperforate hymen (most common)
2. Stenosis due to cervical cancer (older age group), post-radiation, surgery
3. Mullerian duct anomalies such as vaginal septum, cervical agenesis

Question 25

Typical age group affected by cervical carcinoma

Answer 25

45-50

Question 26

Subtypes of cervical carcinoma, in order of most common to least common

Answer 26

SCC (keratinizing or non-keratinizing) Adenocarcinoma Adenosquamous and neuroendocrine

Question 27

Causes of haematometrocolpos

Answer 27

Imperforate hymen (2/3) Mullerian duct anomaly: vaginal septum, vaginal/cervical agenesis, uterus didelphys with one side obstructed Cloacal malformation: confluence of rectum, vagina, urethra into common channel, up to 50% present with hydrocolpos at birth Cervical or vaginal stenosis: post-radiation, surgery, cancer

Question 28

Trauma to which uterine layer is thought to cause endometrial synechiae / Asherman syndrome

Answer 28

Basalis layer of the endometrium, from prior pregancy or D&C

Question 29

Which hormone are endometrial polyps sensitive to?

Answer 29

Oestrogen Little/no response to progesterone. Tamoxifen is pro-oestrogenic in endometrium, but anti-oestrogenic in breast

Question 30

Most common cause of post-partum fever, and the causative organism?

Answer 30

Acute endometritis Group A Strep (strep pyogenes)

Question 31

Risk factors for chronic endometritis?

Answer 31

1. Chronic pelvic inflammatory disease (chlamydia) 2. IUD 3. RPOC 4. Disseminated TB 15% no cause is identified

Question 32

Diagnostic histological feature of chronic endometritis?

Answer 32

Plasma cell infiltration into the endometrial stroma

Question 33

Define adenomyosis and name two risk factors and one complication?

Answer 33

Adenomyosis: presence of endometrial tissue (stroma with or without glands, from the stratum basalis) in the myometrium, in continuity with the endometrium. Surrounding smooth muscle hypertrophy. Risk factors: tamoxifen in post menopausal women and multiparity Complication: ?? increase risk of endometrial carcinoma

Question 34

Three imaging findings in adenomyosis

Answer 34

Venetian blinds appearance Thickening of the junctional zone 50% have myometrial cysts

Question 35

Thick-walled cystic mass in the myometrium with internal haemorrhage, "miniature uterus" appearance, what is it?

Answer 35

Cystic adenomyosis

Question 36

List two differences between adenomyosis and adenomyoma?

Answer 36

Adenomyoma is a circumscribed mass and is frequently discontinuous with the endometrium. It abutts the junctional zone and usually seen in patients with adenomyosis.

Question 37

What is the most common tumour in women, what are its risk factors and what are the genetic mutations?

Answer 37

Leiomyoma Obesity, family history, oestrogen therapy Mutations: Most have a normal karyotype. - 40% have a chromosomal abnormality including chromosome rearrangements involving HMGIC, HMGIY. - MED12 mutations (in 70%)

Question 38

Two unusual variants of leiomyoma

Answer 38

Intravenous leiomyomatosis: extend into vessels and spreads hematogenously to other sites - most commonly vena cava and right atrium Disseminated peritoneal leiomyomatosis: benign small peritoneal nodules Others: Lipoleiomyoma, Parasitic, Benign metastasizing leiomyoma

Question 39

Causes/associations of endometrial hyperplasia

Answer 39

Associated with prolonged estrogenic stimulation of the endometrium: - Obesity (peripheral conversion of androgens to oestrogen) - Menopause - Prolonged HRT - Polycystic ovarian syndrome - Functioning granulosa cell tumour of ovary (producing oestrogen) - Tamoxifen (pro-estrogen effect in uterus) Other: - Diabetes - Cowden syndrome (germline PTEN mutation (also breast cancer increase)

Question 40

Common mutation in endometrial hyperplasia

Answer 40

PTEN (inactivation mutation)

Question 41

Most common location of leiomyosarcoma

Answer 41

Uterus

Question 42

Typical age and common mutation in leiomyosarcoma

Answer 42

40-60 years old MED12 - same mutation as leiomyoma (fibroid) and fibroadenoma/phyllodes in breast Can't be reliably distinguished from a degenerating fibroid on radiology

Question 43

Most common invasive cancer of the female genital tract

Answer 43

Endometrial cancer

Question 44

Describe Type 1 endometrial adenocarcinoma

Answer 44

- Most common, mainly endometrioid, age 55-65 - Precursor: endometrial hyperplasia - Risk factor: unopposed oestrogen exposure, obesity, hypertension, diabetes - Mutations: PTEN, ARID1A, PIK3CA (40%), POLE (<10%), KRAS (25%), FGF2, CTNNB1, TP53 - Associations: DNA mismatch repair gene defects 20% (HNPCC), microsatellite instability - 20% have squamous differentiation

Question 45

Describe Type 2 endometrial adenocarcinoma

Answer 45

- Age 65-75 - Risk factors: Endometrial atrophy, thin physique - Histology: serous (10%), clear cell, mixed mullerian tumour; poorly differentiated - Precursor: serous endometrial intraepithelial carcinoma - By definition are grade 3 poorly differentiated (marked cytologic atypia) - TP53 missense mutation (>90%). Aneuploidy, PIK3CA mutations - Aggressive, poorer prognosis: propensity to exfoliate, travel through fallopian tubes, implant on peritoneum and lymphatics. Often spread at time of diagnosis. - Similar to ovarian serous carcinoma

Question 46

4 major molecular subtypes of endometrial cancer

Answer 46

1. Ultramutated/POLE: Mutations of DNA polymerase E (POLE) so high somatic mutations (passenger) <10%, often T cells involved 2. Hypermutated/MSI: Microsatellite instability with mutations in or epigenetic silencing of mismatch repair genes leading to genomic instability and high burden of somatic mutations. Often T cells involved. Association with Lynch syndrome. 3. Copy number low/MSS: Microsatellite stable, often endometrioid morphology, PI3K/AKT 4. Copy number high/serous-like: aggressive with all serous or high-grade endometrioid morphology associated with TP53 mutations and genomic copy number variants (50% of poorly differentiated endometrial carcinomas)

Question 47

A young female has an IUD in situ and develops PID. What is a common pathogen?

Answer 47

Actinomycoses can be the cause with IUD. - especially with prolonged use >2 years. Spreads irrespective of anatomic barriers due to proteolytic enzymes --> infiltrative borders, forms sinus tracts and fistulae Other general common pathogens are gonorrhoea / chlamydia.

Question 48

What are the causes of haematosalpinx?

Answer 48

Tubal ectopic pregnancy (most common) Endometriosis, cervical obstruction, tubal carcinoma, fallopian tube torsion

Question 49

Typical locations for Salpingitis isthmica nodosa?

Answer 49

Intramural and isthmus portions of the fallopian tubes

Question 50

Typical age group for ovarian torsion

Answer 50

Bimodal with young women and post-menopausal women

Question 51

Risk factors for fallopian tube torsion

Answer 51

PID, hydrosalpinx, tubal neoplasm

Question 52

Associations of theca lutein cysts

Answer 52

Gestational trophoblastic disease (very high association), multifetal pregnancy, PCOS, diabetes, ovulation induction. Thought to originate from excess circulating gonadotropins i.e. beta-HCG.

Question 53

Most common ovarian germ cell tumour

Answer 53

Mature cystic teratoma

Question 54

List the areas affected by endometriosis in order of frequency from most common to least common

Answer 54

1. Ovary 2. Uterosacral ligaments 3. Rectovaginal septum 4. Cul de sac (rectouterine pouch) 5. Pelvic peritoneum 6. Serosa of large/small bowel/appendix 7. Mucosa of cervix/vagina/fallopian tubes 8. Laparotomy scars

Question 55

Three types of endometriosis

Answer 55

Superficial peritoneal, ovarian and deep infiltrating endometriosus

Question 56

Histological types of ovarian malignancy associated with endometriosis

Answer 56

Endometrioid, clear cell

Question 57

Typical age group for Brenner tumours (transitional cell). What is its histologic composition?

Answer 57

50-70 Benign unilateral tumours of normal ovarian fibrous stroma with nests of epithelial cells that resemble urinary tract transitional cells.

Question 58

What makes up Meigs syndrome?

Answer 58

Benign solid ovarian tumour (usually fibroma) Ascites Hydrothorax (usually right side)

Question 59

Genetic syndrome associated with ovarian fibroma and fibrothecoma

Answer 59

Gorlin-Goltz syndrome (Multiple BCCs, OKC, medulloblastoma)

Question 60

Types of sex-cord stromal tumours

Answer 60

Fibroma Fibrothecoma Granulosa cell tumours (feminising) Sertoli-Leydig cell tumours (masculinising/defeminising)

Question 61

Most common ovarian malignant germ cell tumour

Answer 61

Dysgerminoma Yolk sac tumour is second most common

Question 62

Most common age range of dysgerminoma

Answer 62

20-30s

Question 63

What do yolk sac tumours secrete and what is a pathognomonic histological finding of them?

Answer 63

AFP alpha-1-antitrypsin Schiller-Duval bodies (glomerulus like structure with central vessel)

Question 64

Most common ovarian malignancy

Answer 64

Serous tumours (40% of all ovarian cancers)

Question 65

Risk factors for ovarian serous carcinoma

Answer 65

Increased risk: Nulliparity, BRCA1 or BRCA 2, family history. Decreased risk: tubal ligation or oral contraceptives. Note: BRCA are usually high grade serous tumours with TP53 mutations

Question 66

Typical age group for serous tumours

Answer 66

20-45 (benign and borderline, carcinoma is usually a bit later unless familial)

Question 67

Common mutations in serous ovarian carcinoma

Answer 67

Low grade: KRAS, BRAF, ERBB2, PIK3CA, RB High grade: TP53

Question 68

Precursor lesions for low grade and high grade serous ovarian carcinoma

Answer 68

1. Micropapillary carcinoma growth pattern 2. Serous tubal intra-epithelial carcinoma (STIC) or serous inclusion cysts in the ovary

Question 69

What is the difference between type 1 and type 2 ovarian carcinomas?

Answer 69

Type 1 are low grade (include low grade serous, mucinous and endometroid) Type 2 are high grade (generally serous)

Question 70

Important histological finding in serous ovarian cancers

Answer 70

Papillary epithelium (increasing papillary projections/growth as tumours get more malignant). Psammoma bodies

Question 71

Typical age group and mutation for mucinous ovarian cancers

Answer 71

Middle age KRAS

Question 72

Describe the tissues contained in immature teratomas

Answer 72

Embryonal elements resembling immature fetal tissues (e.g. primitive neuroepithelium, the proportion of which determines grade)

Question 73

Typical age group for immature teratomas

Answer 73

Young females, mean age of 18

Question 74

What is struma ovarii?

Answer 74

A specialised teratoma composed of mature thyroid tissue. 5-15% can be hyperthyroid. Generally benign. Usually unilateral, but can have mature teratoma on contralateral side.

Question 75

Pathophysiology of ovarian hyperstimulation syndrome

Answer 75

Exogenous LH + FSH -> hyperstimulation -> ovary secretes vasoactive angiogenic substances -> leaky vessels -> fluid shift into extracellular space (ascites, pleural effusion)

Question 76

Common locations of a tubal ectopic pregnancy

Answer 76

Ampullary (70%), isthmal (12%), fimbrial (11%)

Question 77

Risk factors for ectopic pregnancy

Answer 77

Most important predisposing factor is PID (35-50%) - resulting in chronic salpingitis Previous ectopic pregnancy IUCD (2x risk) IVF Peritubal scarring and adhesions (i.e. from appendicitis, endometriosis, previous surgery)

Question 78

Associations with cystic hygroma

Answer 78

Turners, trisomy 21 and trisomy 18 Cardiac anomalies, foetal alcohol syndrome

Question 79

Risk factors for placenta previa

Answer 79

Previous placenta praevia Previous C section Increased maternal age Increased parity

Question 80

Association and risk factors of placental abruption

Answer 80

1. Placenta praevia (13-14x increased risk) 2. Pre-eclampsia and maternal hypertension Previous placental abruption Prolonged rupture of membranes Extremities of maternal age Trauma

Question 81

Hydatiform moles are histologically characterised by

Answer 81

cystic swelling of the chorionic villi and variable trophoblastic proliferation

Question 82

How to distinguish gestational trophoblastic disease from retained products of conception?

Answer 82

Both have elevated hCG - In GTD, this will be peristently elevated - In RPOC, this will fall to pre-pregnancy levels over 2-3 weeks.

Question 83

What is the definition of gestational trophoblastic disease?

Answer 83

Spectrum of tumours and tumour like conditions characterised by proliferation of placental tissue, either villous or trophoblastic.

Question 84

Pathogenesis of a complete mole?

Answer 84

Results from fertilisation of an empty ovum (lost its female chromosomes) meaning all genetic material is paternally derived. Ninety percent are 46, XX karyotype. No fetal parts are identified.

Question 85

Pathogenesis of a partial mole

Answer 85

Results from fertilisation of an egg with two sperm. Karyotype is triploid (e.g 69,XXY) or tetraploid (92, XXYY). Fetal tissues are typically present.

Question 86

Risk of progression to invasive mole and choriocarcinoma for: - Complete mole - Partial mole

Answer 86

Complete mole - 15% risk of invasive mole, 2.5% risk of choriocarcinoma Partial mole - small risk of invasive mole, no risk of choriocarcinoma.

Question 87

Histology of a hydatiform mole

Answer 87

Enlarged, oedematous chorionic villi covered by extensive trophoblastic proliferation (grossly look like cystic, grapelike structures). Involves all or most of the villous tissue in complete mole. In partial mole only a fraction of villi are enlarged.

Question 88

Presentation of hydatiform mole

Answer 88

Usually present with spontaneous pregnancy loss or abnormal villous enlargement on ultrasound. Patients have elevated hCG which must be monitored for 6-12 months to ensure resolution (persistence = invasive mole).

Question 89

Pathogenesis of an invasive mole

Answer 89

Invasion of myometrium by hydropic chorionic villi, accompanied by proliferation of both syncytiotrophoblasts and cytotrophoblasts. Villi can invade parametrium and blood vessels, may embolise to distant sites (brain and lung) - not true metastases as emboli do not grow and will eventually regress.

Question 90

Definition of gestational choriocarcinoma

Answer 90

Malignant neoplasm of trophoblastic cells derived from a previously normal or abnormal pregnancy.

Question 91

Important features of gestational choriocarcinoma

Answer 91

- Presents with irregular vaginal spotting (bloody, brown fluid). - hCG is markedly elevated - Preceded by complete hydatiform mole (50%), previous abortions (25%), normal pregnancy (22%) or ectopic pregnancy (remainder). - Rapidly invasive and metastasises widely - high propensity for haematogneous spread to lungs (50%), vagina (40%), brain, liver, bone, kidney. - Responds well to chemotherapy once identified

Question 92

Characteristic histology of choriocarcinoma

Answer 92

Proliferating syncytiotrophoblasts and cytotrophoblasts, chorionic villi are absent

Question 93

Important features of non-gestational choriocarcinoma

Answer 93

Malignant germ cell tumour with extraembyronic differentiation. Develops from germ cells in the ovaries and rarely mediastinum. Most exist in combination with other germ cell tumours (pure choricarcinoma is rare). Morphologically identical to gestational choriocarcinoma except paternally derived DNA is absent. Ovarian tumours are more aggressive and have typically metastasised widely to lung, liver and bone at time of diagnosis. Resistant to chemotherapy, often fatal

Question 94

Definition of placental site trophoblastic tumours

Answer 94

Neoplastic proliferation of extravillous trophoblasts (intermediate trophoblasts)

Question 95

Important features of placental site trophoblastic tumours

Answer 95

Rare, less than 2% of gestational trophoblastic neoplasms. Presents as a uterine mass +/- abnormal uterine bleeding or amenorrhea. Can occur 2 weeks - 14 years following gestation (normal pregnancy 50%, spontaneous abortion 20%, molar pregnancy 10%). hCG is moderately elevated. Malignant trophoblastic cells diffusely infiltrate the uterus. Frequently penetrates blood vessels or extends through the uterine serosa to surrounding structures. Excellent prognosis with localised disease. 10-15% die with diseeminated disease

Question 96

Definition of pre-eclampsia

Answer 96

Systemic syndrome of late pregnancy characterised by widespread maternal endothelial dysfunction. Presents during pregnancy with hypertension, oedema, proteinuria.

Question 97

Complications of pre-eclampsia

Answer 97

Hypercoagulability Acute renal failure Pulmonary oedema 10% of women develop HELLP syndrome

Question 98

What is HELLP syndrome?

Answer 98

Haemolytic anaemia, elevated liver enzymes and low platelets.

Question 99

What distinguishes gestational hypertension from pre-eclmapsia?

Answer 99

Presence of proteinuria in pre-eclampsia

Question 100

What is the cardinal histological feature of endometrial hyperplasia?

Answer 100

Increased gland:stroma ratio

Question 101

Histology of pre-eclampsia

Answer 101

Placenta changes: 1. Infarcts 2. Exaggerated ischaemic change in the chorionic villi and trophoblasts 3. Frequent retroplacental haemorrhage due to instability of placental vessels 4. Abnormal decidual vessels (atherosis (fibrinoid necrosis), lack of normal physiologic remodelling, may have thrombi) In other end organs (liver, kidney, brain and pituitary): - Gross and microscopic foci or haemorrhage - Fibrin thrombi within the small vessels - If severe, may have haemorrhagic necrosis in the liver and bilateral renal cortical necrosis.

Question 102

Most common pathogen implicated in PID?

Answer 102

Niesseria gonorrhoea

Question 103

Corpus luteal cysts are lined by?

Answer 103

Luteinised granulosa cells

Question 104

PID in the setting of postpartum or miscarriage: causative pathogen and one difference in how it spreads compared to other causes of PID?

Answer 104

Commonly polymicrobial Spreads via lymphatics or blood rather than along mucosal surfaces (so the inflammation is usually more subserosal than mucosal) (PID from gonorrhoea/chlamydia spreads along mucosal surfaces from the endocervical mucosa --> tubes and ovaries but for some reason spares the endometrium)

Question 105

List 5 chronic sequelae/complications of PID

Answer 105

1. Infertility 2. Ectopic pregnancy 3. Hydrosalpinx 4. Chronic PID 5. Adhesions

Question 106

List three causes of hydrosalpinx and one pathognomonic radiological sign for it

Answer 106

1. Prior PID 2. Endometriosis 3. Prior pelvic infections (diverticulitis, appendicitis) The waist sign - indentation of a cystic tubular structure on both sides

Question 107

Aetiology of endometrial synechiae?

Answer 107

Trauma to the basalis layer of the endometrium (i.e. prior pregnancy or D&C) leads to scarring and adhesions of the uterine walls, with partial or complete obliteration of uterine cavity. Presents with menstrual abnormalities, infertility, recurrent pregnancy loss.

Question 108

Definition of endometrial hyperplasia

Answer 108

Abnormal proliferation of endometrial glands relative to stroma (increasing gland-to-stroma ratio).

Question 109

Two histological categories of endometrial hyperplasia

Answer 109

1. Typical hyperplasia - cardinal feature is increased gland-to-stroma ratio. Caused by peristent estrogen stimulation. Rarely progress to carcinoma. 2. Atypical hyperplasia (endometrial intraepithelial neoplasia) - complex patterns of proliferating glands with nuclear atypia. Associated with increased risk of endometrial carcinoma. Managed by hysterectomy.

Question 110

Complications of chorioangioma and when do they usually occur?

Answer 110

Polyhydramnios (most common), fetal anaemia, hydrops, fetal growth restriction, high output cardiac failure Usually when large (>5cm) or multiple

Question 111

Blood test which may be a sign of chorioangioma

Answer 111

Maternal serum AFP

Question 112

Three criteria for twin to twin transfusion syndrome

Answer 112

Shared placenta, size differential (at least 25%), disproportionate fluid (small fetus oligo, large fetus polyhydramnios)

Question 113

Types of endometrial stromal tumours

Answer 113

Two categories: 1. Adenosarcomas (malignant stromal tumours with benign endometrial glands) 2. Endometrial stromal neoplasms (two subtypes: benign stromal nodules and malignant stromal sarcomas)

Question 114

Features of uterine adenosarcoma

Answer 114

Predominate in the fourth and fifth decades Diagnosed based on presence of malignant appearing stroma with benign but abnormally shaped endometrial glands. Generally low grade Can resemble a benign polyp on macroscopic assessment → Must be distinguished as management is different. Treated with oophorectomy (lesions are estrogen sensitive)

Question 115

Mutations associated with stromal sarcoma

Answer 115

Low grade: fusion of JAZF1 and SUZ 12 genes High grade: Different translocations.

Question 116

Clinical features of stromal sarcomas

Answer 116

Approximately one half recur. Distant metastases can occur decades after initial diagnosis. 50% five year survival rate (less for high grade).

Question 117

What is lobular endocervical glandular hyperplasia and what is the clinical significance?

Answer 117

Non-invasive proliferation of endocervical glandular cells, showing gastric type differentiation. Associated with underlying malignancy or small progression to malignancy (atypical lobular endocervical glandular hyperplasia)

Question 118

Types mesenchymal elements in malignant mixed mullerian tumours (carcinosarcoma)

Answer 118

Homologous contains uterine mesenchymal elements (i.e stromal sarcoma, leiomyosarcoma) Others contain heterologous malignant mesenchymal cells from outside of the uterus (i.e. rhabdomyosarcoma, chondrosarcoma).

Question 119

Features of malignant mixed mullerian tumours

Answer 119

Occur in postmenopausal women. Present with bleeding. Outcome is determined by depth of invasion, stage, and differentiation of the mesenchymal component - heterologous mesenchymal elements have a worse prognosis. Overall five year survival rates are 25-35% with high-stage disease.

Question 120

Pathogenesis of mixed mullerian tumours?

Answer 120

Uncertain but molecular studies support the theory that the epithelial cells undergo differentiation into the mesenchymal cells (share driver mutations, appear to be derived from a single cell line). Metastases only contain epithelial component.

Question 121

Features of leiomyosarcoma

Answer 121

Occur in perimenopausal, age 40-60 Rare tumor, mostly found in uterine corpus (can occur anywhere there is smooth muscle). Two distinctive growth patterns: bulky masses that invade into the uterine wall or polypoid masses that project into the uterine lumen. Diagnostic triad (distinguishes from leiomyoma): marked cytologic atypia, tumor cell necrosis and increased mitoses . Poor prognosis even at low stage (overall five year survial is 40%, 10-15% for anaplastic lesions).

Question 122

USS on a young girl shows a cystic adnexal mass containing echogenic nodule with posterior acoustic shadowing - what is the diagnosis?

Answer 122

Rokitansky nodule aka dermoid plug - eccentric solid echogenic nodule with posterior acoustic shadowing within a cystic mass - mature cystic teratoma. Other key signs include: dot-dash sign tip of iceberg sign 2+ germ cell layers involved, mature tissues contained, 1% malignant transformation (SCC, melanoma, thyroid), paraneoplastic syndromes such as limbic encephalitis, bilateral in 10%

Question 123

Dysgerminoma: benign or malignant? Bilateral or unilateral? Name a mutation associated?

Answer 123

Malignant Unilateral 1/3 have activating KIT mutation

Question 124

Typical age presentation for granulosa cell tumours? Which hormone do granulosa cell tumours produce?

Answer 124

- composed of combinations of granulosa cells and theca cells. - Can elaborate large amounts of oestrogen so can cause precocious sexual development and endometrial hyperplasia. - 2/3rds present in postmenopausal women. - Granulosa cells elaborate inhibin which can be a useful tumour marker.

Question 125

Sertoli-leydig cell tumours presentation?

Answer 125

Recapitulate cells of the testes and commonly produce masculinization or defeminization

Question 126

Karyotype of all benign teratomas?

Answer 126

46,XX

Question 127

List the two most common malignant germ cell tumours

Answer 127

1. Dysgerminoma 2. Yolk sac tumour

Question 128

List the most common ovarian malignancies in order of frequency (i.e. percentage of all malignant ovarian tumours)

Answer 128

1. Serous adenocarcinoma 2. Endometrioid carcinoma 3. Undifferentiated carcinoma 4. Clear cell carcinoma 5. Metastatic ovarian tumours 6. Mucinous adenocarcinoma

Question 129

Histo appearances to differentiate benign, borderline, and malignant serous ovarian tumours

Answer 129

benign: single layer ciliated columnar epithelium borderline: micropapillary architecture with no stromal invasion malignant: multilayered cells, micropapillary architecture, underlying stromal invasion

Question 130

Gross morphological appearance difference between benign and malignant serous ovarian neoplasm

Answer 130

Benign: looks like a functional ovarian follicular cyst Malignant: cystic mass with substantial solid component

Question 131

Endometrioid ovarian carcinoma: What percentage is bilateral? What percentage is associated with endometriosis? What percentage is associated with concurrent endometrioid endometrial carcinoma?

Answer 131

1. 40% 2. 15-20% 3. 15-30%