GTD Flashcards

1
Q

How commonly does GTN develop after a complete and partial mole?

A

Complete 15-20%

Partial 0.5-5%

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2
Q

What type of pregnancy does GTN follow?

what are the rates?

A

50% occur after molar pregnancies, the rest after spont abortion, Ectopic, or term pregnancy

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3
Q

How common is molar pregnancies?

How common is choriocarcinoma?

A

1/714 live births. Higher occurrence is Asian women

FIGO says 1:1000

Choriocarcinoma 1-10 : 40 000

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4
Q

What are the risk factors for developing GTD

A

Extremes of age (as abnormal gametogenesis and fertilization)

Risk increases after 35, 5-10X higher after 45

Previous GTD
Increases the risk of recurrence by 10X

Diets deficient in folate, protein and carotene

Women with blood group A with blood group O partners are at 10 times higher risk

Women with blood group AB have a worse prognosis

Women with theca lutein cysts are at higher risk of developing malignant sequalae

Dietary deficiency in beta carotene and animal fat is associated with complete moles

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5
Q

How does cytogenetics help differentiate between partial and complete molar pregnancies?

A

A cyclin dependent kinase inhibitor P57 is encoded by paternal imprinted and maternally expressed genes and therefore is absent in CHM. PHM and hydropic gestations have strong p57 staining. P57 stain can be use to exclude a complete mole

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6
Q

what is the gross description and histology of complete molar pregnancies?

A

Gross:
Hydropic villi to semi transparent vesicles of variable sizes with absence of normal placenta (if early may have no abnormal villi)

Histology: Florid cistern formation, trophoblastic proliferation in the absence of fetal parts, significant cytological atypia and mitotic figures are common.

In T1 Polypoid appearance, abnormal villous stromal changes and mild to moderate trophoblastic hyperplasia.

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7
Q

What is the pathology of a complete molar pregnancy?

A

Complete moles usually (75–80%) arise as a consequence of duplication of a single sperm following fertilisation of an ‘empty’ ovum.

Some complete moles (20–25%) can arise after dispermic fertilisation of an ‘empty’ ovum.

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8
Q

what is the pathology of partial moles?

A

(90%) triploid in origin, with two sets of paternal haploid genes and one set of maternal haploid genes.

Partial moles occur, in almost all cases, following dispermic fertilisation of an ovum.

Ten percent of partial moles represent tetraploid or mosaic conceptions

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9
Q

What is the histology of a partial mole?

A

Histo: changes less marked compared to partial mode and fetal parts or cells are present

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10
Q

Histology of a choriocarcinoma

gross description?
genetics?

A

The tumor is bulky with hemorrhagic and necrotic areas. It can be found in the tubes, ovaries, lung, liver, spleen, kidneys, bowel or brain.

Most XX with highly complex karyotypes

Histology: absence of chorionic villi and presence of abnormal intermediate trophoblast and cytotrophoblasts with necrosis and haemorrhage.

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11
Q

Placental site trophoblastic tumor

Gross description and histology

A

Grossly: white, tan to yellow nodular masses varying from 1-10 cm in the endomyometrium, half of the cases invade the myometrium.

Histo: mononuclear intermediate trophoblast on the maternal side of the vascular bed. Tumor cells have irregular nuclear membranes, hyperchromatic nuclei and dense eosinophilic cytoplasm. Most tumors have a low mitotic count. Chorionic villi are absent.

Tumor cells procedure human placental lactogen (hPL) MUC-4, HSD3B1, HLA-G and Mel-CAM (CD146) Focal expression hcg and inhibin. Proliferation index is modestly increased with Ki-67 expressed in 10-30% of cells, higher then benign exaggerated placental site reaction. These have rare genetic imbalances.

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12
Q

Epithelial trophoblastic tissue

Gross and histological description

A

Epithelial Trophoblastic tumor

Grossly: white tan to brown, discrete nodules or cystic haemorrhagic masses invading deep into the surrounding tissues. Half in the cx or lower segment, some in the fundus and the broad ligament.

Histo: arises from chorionic type intermediate trophoblast. Relatively uniform intermediate trophoblastic cells with moderate eosinophilic to clear cytoplasm and round nuclei are surrounded by extensve necrosis and associated hyaline like matrix. Extensive necrosis – can co exist with other trophoblastic neoplasms.

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13
Q

How does GTN present

A
irregular vaginal bleeding,  
hyperemesis,  
excessive uterine enlargement  
Early failed pregnancy 
Hyperthryoidism 
Early onset pre eclampsia 
Abdo distention to theca tutein cysts 
Respiratory failure and seizures  
After a pregnancy with symptoms of metastasis pulmonary sx, neurological signs, spine, brain, - GTD should be considered with unusual sx and + hcg
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14
Q

What does a molar pregancy look like on USS

A

Multiple hypoechoic cystic structures - snowstorm appearance

Honeycomb - Rarely seen T1

T1 often cystic spaces and absence of fetal parts, maybe a deformed sac

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15
Q

How to manage an a molar pregnancy

A

Suction curettage under USS guidance
Fertility preserving
12-14 mm suction cannular
IV oxytocin infusion is started at the onset and continued for hours afterwards to enhance uterine contractility.
If uterus over 16 weeks then blood should be avaliable
Rh immunoglobulin (RhD is expressed in trophoblasts)

If over 40 and not wanting uterus then for hysterectomy
- decreases the chance of subsequent chemo

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16
Q

Complications of ERPOC for molar pregnancy

A

Complications - Excessive bleeding secondary to atony or perforation, pulmonary oedema (high output cardiac failure) trophoblast embolus entry of trophoblastic tissue into maternal circulation can result in ARDS and DIC

17
Q

How to manage persisting sx / vaginal bleeding ?

A

FU hcg and USS
Any woman who develops persistent vaginal bleeding after a pregnancy event is at risk of having GTN. A urine pregnancy test should be performed in all cases of persistent or irregular vaginal bleeding after a pregnancy event.

Symptoms from metastatic disease, such as dyspnoea or abnormal neurology, can occur very rarely. Several case series have shown that vaginal bleeding is the most common presenting symptom of GTN diagnosed after miscarriage, therapeutic termination of pregnancy or postpartum.

18
Q

How to manage twin pregnancy with co existing molar?

A

Prenatal invasive testing for fetal karyotype should be considered in cases where it is unclear if the pregnancy is a complete mole with a coexisting normal twin or a partial mole.

Prenatal invasive testing for fetal karyotype should also be considered in cases of abnormal placenta, such as suspected mesenchymal hyperplasia of the placenta.

The outcome for a normal pregnancy with a coexisting complete mole is poor, with approximately a 25% chance of achieving a live birth.
There is an increased risk of early fetal loss (40%) and premature delivery (36%). The incidence of pre-eclampsia is variable, with rates as high as 20% reported.

FIGO – increased rates GTN compared to singleton molar 15-20% to 30-45%

19
Q

How to dx GTN

A

Post molar GTN (FIGO 2000)

Plateau of hcg lasts more 4 measurements over 3 weeks or longer on day 1,7,14,21

Rise in hcg over 3 consecutive weekly measurements over 2 weeks or more on day 1,7,14

Histological dx of choriocarcinoma

20
Q

How long to follow up molar pregnancy hcgs?

A

Hcg 1-2 weeks is essential for early diagnosis of and management of post molar GTN

GTN very rare after hcg negative

Repeat hcgs PHM – 1 month post normalisation

CHM - Monthly hcg for 6/12 after normalisation

TOP not indicated if accidental pregnancy

FIGO says OCP now ok

Recurrence low 0.6-2% (increased if consecutive molar pregnancies)

If recurrent perhaps mutation NLRP7 and KHDC3L

21
Q

How to manage future pregnancies?

A

Early scan

Any miscarriage or failed future pregnancy should have its histology reviewed

Send placentas from any future pregnancy

Hcg follow up 6/52 post natal (can be a urine hcg)

22
Q

What is the long-term outcome of women treated for GTN?

A

Women who receive chemotherapy for GTN are likely to have an earlier menopause (1 - 3 years) increased risk of secondary cancers (developing acute myeloid leukaemia. There was also a 4.6 relative risk for developing colon cancer, 3.4 relative risk for melanoma and 5.79 relative risk for breast cancer

cure rates 95-100% if managed correctly