GTD Flashcards

1
Q

Types of GTD

A

Choriocarcioma
Molar pregnancy
Partial mole
Placental site strophoblastic tumour (PSTT)

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2
Q

Complete mole pathophysiology

A

Usually arise following duplication of a single sperm following fertilization of an empty ovum (75-80%)
20-25% dispermic fertilization of an empty ovum

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3
Q

Partial mole

A

90% triploid
Two sets of paternal haploid genes and one set of maternal haploid genes
Usually dispermic fertilization of an ovum
Usually evidence of a fetus or fetal blood cells

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4
Q

Incidence GTD

A

1/714
Complete mole 1:1000
Partial 3:1000

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5
Q

Presentation of mole

A

Irregular vaginal bleeding
HG
Excessive uterine enlargement
Early failed pregnancy

Rarer:
Hypothyroidism
Early onset PET
ARFailure - usually due to Mets

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6
Q

Treatment of mole

A

Suction curettage
Urinary preg test should be performed 3 weeks after medical management of failed pregnancy if products of conception are not sent for histology
Don’t use oxytocic infusions

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7
Q

Which women should be investigated for persistent GTN after a non-molar pregnancy

A

Any woman who develops persistent vaginal leading after a pregnancy event is at risk of having GTN
Need urine preg test

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8
Q

Follow up of GTD

A

Hcg normal within 56 days -> 6 months
Hcg not normal by 56 days, then 6 months after this has normalised
Need follow up after any future pregnancy (test hcg 6-8 weeks PP)

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9
Q

Treatment for GTN

A

Chemo for complete mole 15%, 0.5% partial mole
Low risk - methotrexate and folinic acid
High risk multi agent
Cure rate LR 100%, HR 95%

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10
Q

Long term outcomes

A

Earlier menopause

If have multi-agent chemo, may have increased risk of secondary cancers

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11
Q

Contraception following dx of GTD

A

Barrier only until hcg normal
Hcg normal - COC can be used
NO intrauterine devices until hcg normal - increased risk of perforation

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12
Q

Recurrent complete molar pregnancy genetic mutation

A

Autosomal recessively inherited NLRP7 on chromosome 19q

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13
Q

Origin of mole

A

Varying degrees of trophoblastic proliferation (cytotrophoblast and syncytiotrophoblast)
Vesicular swelling of placental villi (villous hydrops)

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14
Q

Risk factors molar pregnancy

A
Asian
Advanced or very young maternal age
Previous molar pregnancy
Increased risk malignant transformation if using OCP while hcg levels elevated
Familial -chromosome 19q-NLRP7
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15
Q

Histopathology

A

Complete: diffuse villous hydrops, diffuse trophoblast hyperplasia; macroscopic:cystic villi=clusters of grapes

Partial: focal villous hydrops with scattered abnormally sized/scalloped villi, focal trophoblastic hyperplasia, trophoblastic pseudoinclinations, identifiable fetal tissues

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16
Q

Risk of recurrence

A

1 mole 2%

2 20%

17
Q

USS appearance of CHM

A

Placental mass containing multiple echoes (snowstorm appearance) without an associated embryo and bilateral ovarian thecal luteal cysts

40-60%accuracy USS dx

18
Q

Work up required before chemotherapy

A
Clinical assessment
CNS assessment
Baseline hcg
TFTs
U/Es
LFTs
FBC
CXR
Pelvic US
Review of histopathology
19
Q

Choriocarcinoma

A

Hcg-secreting tumour

3% of molar pregnancies

20
Q

Choriocarcinoma pathology

A

Large haemorrhagic mass
Abnormal trophoblastic hyperplasia and anaplasia with the absence of chorionic villi, haemorrhage and necrosis, and with direct invasion into the myometrium and venous sinuses
Mets spread via vessels

21
Q

Placental site trophoblastic tumour

A

Mostly mononuclear intermediate trophoblast and syncytial elements without chorionic villi, infiltrating in sheets between myometrial fibers
Usually from non-molar pregnancies
Produce small amounts of hcg and human placental lactogen
Usually lymphatic spread
Treatment is usually hysterectomy and pelvic lymphadenectomy

22
Q

Invasive mole

A

10% of moles
15% met to lung and vagina
Usually diagnosed clinically