GTD Flashcards

1
Q

What WHO scores are counted as low risk GTN?

A

< 7

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2
Q

WHat WHO scores are counted as high risk GTN?

A

7 - 13

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3
Q

What WHO scores are considered extremely high risk?

A

> 13

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4
Q

What are the founr types of malignant GTN?

A

malignant invasive mole, Choriocarcinoma, placental site trophoblastic tumour (PSTT) and Epitherlioid trophoblastic tumour (ETT)

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5
Q

What is the significance of an atypical placental site nodule?

A

10 - 15% may coexist with or develop into PSTT / ETT

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6
Q

What % of cases of CHM will develop into GTN?

A

15-20%

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7
Q

What % of PHM will develop into GTN?

A

0.5 - 5%

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8
Q

What is the incidence of hydatidiform mole

A

1: 1000 and 1-3: 1000 in developed countries

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9
Q

What is the incidence of partial mole?

A

3: 1,000 pregnancies

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10
Q

RF for GTD?

A

Extremes of reproductive age <15 & >45
Hx of molar pregnancy - 10x risk after 1
Even more after 2.
Dietary deficiency of beta-carotene and animal fat is considerd to be a etiological factor for complete mole but not partial mole.

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11
Q

What is quiescent GTN?

A

Consistently low level of hCG; <200 mIU/mL)
persists for > 3 months after evacuation without detectable disease.
Very rare
? due to small focus of highly differentiated, noninvasive syncytiotrophoblast cells that produce small amounts of hCG and usually do not progress to invasive disease as long as cytotrophoblast or intermediate cells are absent.

Do not require Rx. 6 - 10 % will eventually develop active GTN, Monitor and avoid pregnancy.

quiescent GTN is far less common than active GTN after a molar pregnancy, patients who develop a persistent plateau or elevation of hCG at low levels during HM follow-up may reasonably be diagnosed with active GTN and treated.
Evidence of chemotherapy resistance (hCG level unresponsive to therapy presumably because the growth cycle of these cells is long and comparable to normal cells) combined with absence of any clinical or radiologic evidence of GTN supports the diagnosis of quiescent GTN and should prompt discontinuation of chemotherapy unless active GTN is documented by increasing hCG levels. Measurement of hyperglycosylated hCG (hCG-h) has been proposed for surveillance in patients with quiescent GTN, but the test is not commercially available.

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12
Q

What is a trophoblast?

A

Trophoblasts (from Greek to feed: threphein) are cells forming the outer layer of a blastocyst, which provides nutrients to the embryo, and develops into a large part of the placenta. They are formed during the first stage of pregnancy and are the first cells to differentiate from the fertilized egg.

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13
Q

What is a villous trophoblast?

A

Villous trophoblast cells consist of progenitors referred to as cytotrophoblast, which fuse to form syncytiotrophoblast

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14
Q

What are syncytiothrophoblasts?

A

syncytiotrophoblasts are a continuous, specialized layer of epithelial cells. They cover the entire surface of villous trees and are in direct contact with maternal blood. The surface area of syncytiotrophoblasts is about 5 square meters at 28 weeks’ gestation and reaches up to 11–12 square meters at term

Syncytiotrophoblast represent both the primary barrier regulating transport between maternal and fetal vascular compartments and, also the principal source of steroid and peptide hormones produced by the human placenta.

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15
Q

What are cytotrophoblasts?

A

Beneath the syncytiotrophoblasts are the cytotrophoblasts. Considered to be stem cells for syncytiotrophoblasts.
Continually differentiate into syncytiotrophoblasts during villous formation and development. Cytotrophoblast invasion into the uterine spiral arteries is accompanied by loss of the endothelial lining and musculoelastic tissue in these vessels. This process of invasion is necessary for placental vascular remodelling in the early stages of the implantation process.

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16
Q

What are the RF for post molar persistent tumour?

A
  • hCG > 100,000
  • Excessive uterine enlargement
  • Theca lutein cysts > 6cm
17
Q

What is the likelihood of developing GTD post complete mole?

A

~ 15 % will develop local invasion
~ 5% will develop metastatic disease.

18
Q

What is the likelihood of developing GTD post partial mole?

A

GTN, usually nonmetastatic, occurs in 1 to 4 % of patients after partial hydatidiform mole

19
Q

How often does GTN occur after a non-molar term pregnancy?

A
  • usually choriocarcinoma but rarely PSTT or ETT,
  • 2 to 7 : 100,000 pregnancies in Europe and North America,
    Southeast Asia and Japan - the incidence 5 to 200 : 100,000 pregnancies, respectively
20
Q

What % of women with metastatic GTN will have lung mets?

A

~80%

21
Q

What % of women with metastatic GTN will have Vaginal mets?

A

~30%

22
Q

WHO score - how many ares?

A

8

23
Q

WHO Score mnemonic?

A

HAM CLANS
H - HCG
A - Age
M - Months from preg

C - Chemo tried previously
L - Largest tumour
A - Antecedent pregnancy - types
N - Number of mets
S - Site of Mets

24
Q

Re second curette - what should you do?

A

Consider a second curette in the presence of disease in the uterus - not embedded in the wall. The risk of requiring chemotherapy increases with the level of hCG. Seckl et al, suggest 5000 as a cut off above which 70% of women will need chemotherapy anyway and you avoid any of the morbidity of curettage. There may also be an increased risk of perforation with a second curette.

25
Q

In a meta-analysis of 14 studies with 244 cases of complete HM with a coexisting foetus. GTN was diagnosed with what % of cases?

A

34%

26
Q

In a meta-analysis of 14 studies with 244 cases of complete HM with a coexisting foetus. Of the 182 women who did not terminate their pregnancy the overall birth rate was?

A

50%

27
Q

In a meta-analysis of 14 studies with 244 cases of complete HM with a coexisting foetus. of the 182 women who did not terminate their pregnanct the rate of IUFD was?

A

40%

28
Q

In a meta-analysis of 14 studies with 244 cases of complete HM with a coexisting foetus. Of the 182 women who continued their pregnancy what % of women had maternal complications?

A

80% - including Pre-eclampsia, hyperthyroidism, PTB and still birth
No maternal deaths were reported.

29
Q

In a meta-analysis of 14 studies with 244 cases of complete HM with a coexisting foetus. Of the 182 women who continued their pregnancy what % of women had died?

A

0 %

30
Q

What value of hCG in the CSF suggests occult CNS disease in GTD?

A

1:60 of serum level.

31
Q

What are the UK indications for the treatment of GTD?

A
  • Plateaued or rising hCG after evacuation
    • Heavy PV bleeding or evidence of GI or intraperitoneal haemorrhage
    • Histo evidence of choriocarcinoma
    • Evidence of metastases in the brain, liver or GI or >2cm on chest x-ray (<2cm can resolve spont)
    • Serum hCG >20,000 >4 weeks after evacuation
      unlikely to resolve spontaneously and increased risk of uterine rupture/perforation.
    • Raised hCG 6 months after evacuation - now omitted. In UK but still in FIGO - although that might be from 2002(~ 80 women) 98% to 0 and 1 had renal failure but was well
32
Q

According to the ESGO guideline - In women with a WHO score of 5 -6 what % would be expected to be cured by low risk treatment?

A

~ 30% - yes 30.

33
Q

What % of women with progress or on after primary chemotherapy for GTD? What % of those can still be salvaged by additional therapy?

A

About 20% of high-risk GTN patients will progress on or after primary chemotherapy, but these individuals still have an excellent outcome with ∼75%–80% still being salvaged.

34
Q

After treatment for GTN what % of women are able to achieve pregnancy?

A

83%

35
Q

What are three causes of persistently elevated low levels of hCG?

A
  • Heterophilic antibodies - cross-reacts with the assay. The antibodies do not pass into the urine. Both positive - likely real results.

Quiescent GTD - ? due to low levels of hCG that develop into GTN over time. ? a real entity

Pituitary hCG - rarely - normally 2-11mU/L. more common in post menopausal women and can be suppressed by HRT.

36
Q

What are the causes of an unexplained / persistently low level hCG

A
  1. GTD
  2. Non GTD tumour e.g. mixed germ cell tumour
  3. Pituitary hCG - COCP for 3/12. FSH, LH Estrogen
  4. Pregnancy
  5. Familial elevated hCG - vanishingly rare
  6. False +Ve - eg human anti-mouse antibody

Talk to clinical chemist, geneticist, GTD centre

37
Q

What is GTD and GTN?

A

GTD is an umbrella terms that includes molar pregnancy and GTN.
GTN - includes the four subtypes - invasive mole, choriocarcinoma, ETT nd PSTT

38
Q

On diagnosis of GTN what is the suggested work up - from the RANZCOG guideline and compared to Charing cross?

A

The RANZCOG guideline indicates that:
If the suction curette indicates Chorio, PSTT or ETT or in the presence of persistent disease.
That is a rise in hcg >10% over two weeks - e.g. thre values. Or there is a less than 10% fall in three weeks - over 4 consecutive footballer.

That they have…
- MDT review
- FBC, EUC, LFT, FP and hold, beta hcg and TFT
- Metastatic screen with
○ CT Heath chest abdo or pelvis. Add MRI head if choriocarcinoma ,pulmonary mets or neurological symptoms.

In the same situation Charing cross indicate to undertake Hx, exam, hcg, US pelvis and CXR.
- If the CXR is normal no further imaging and FIGO scoring / staging undertaken.
- If the CXR indicated mets - CT chest - if normal continue.
- IF mets >1cm then do MRI brain + CT A/P or MRI abdo then FIGO staging.

39
Q
A