Download MBBS GTA Management Lecture PPT

Download MBBS (Bachelor of Medicine and Bachelor of Surgery) GTA Management PowerPoint PPT presentation

MANAGEMENT OF
GESTATIONAL
TROPHOBLASTIC
NEOPLASIA






PRE TREATMENT EVALUATION
History and clinical examination
Serum hCG
Lab evaluation ? RFT, LFT, WBC count, DLC, Platelet count, clotting profile
USG pelvis- excludes pregnancy
Chest X-Ray/CT scan
CT Abdomen and Pelvis
CT/MRI Head ? Brain metastases
Thyroid function test




LOW RISK GTN
METHOTREXATE
? Most common treatment ? single agent Mtx
? Recommended 8 day regimen ? Mtx alternating with Folinic acid
? Mtx 50mg/kg bodyweight I.M - on day 1,3,5,7 and oral folinic acid 7.5 ?15 mg
oral y on days 2,4,6,8
? Treatment repeated every 2 weeks.

Folinic Acid Rescue
Mtx ? Folinic acid antagonist ? inhibit
DNA synthesis
Side effects of Mtx-
o Mild stomatitis
o Pleurisy
o Infrequently pericarditis,peritonitis,pneumonitis
Hence folinic acid- Mtx ALTERNATE regimen :Protect normal mucosal and
serosal cel s.

Before each Mtx course ? CBC, RFT, LFT mandatory.
Courses repeated every 14 days.
Remission ? 3 normal consecutive weekly titers ----- hence weekly serum hCG, done till
normal 3 weeks
One more course ? after normalization of hCG
Pregnancy avoided for atleast one year after cessation of chemotherapy.

Drug Resistance
19 ? 33 % women develop Mtx resistance.
Detection ? increasing or plateauing levels of serum hCG
Second line drug ? Actinomycin D [ Dactinomycin]
Etoposide may also be effective
If still no response ? high risk protocol


DACTINOMYCIN
Superior efficacy as a single agent.
Pulse I.V Dactinomycin 1.25-2 mg /sq.m repeated every
14 days.
Side effects : alopecia, grade 4 toxicity.
Mtx resistant GTN often responds to dactinomycin.

HIGH RISK GTN
q More likely to develop drug resistance to single agent ? hence combination
chemotherapy.
q Highly effective regimen ? ETOPOSIDE + MTX+ DACTINOMYCIN alternating with
CYCLOPHOSPHAMIDE + VINCRISTINE [ONCOVIN] --- EMA-CO REGIMEN
q Cycle repeated every 2 weeks until serum hCG normal ? then 3 more cycles given
q Overal survival ? 86%


1 Quarter patients become refractory to or relapse.
Secondary treatment ?
Platinum based chemotherapy + possible surgical excision of resistance site
? EMA/EP regimen [ etoposide ? cisplatin ]
? paclitaxel + cisplatin alternating with paclitaxel + etoposide
? BEP regimen : bleomycin + etoposide +cisplatin



HYSTERECTOMY
INDICATIONS
? Invasive mole perforating the serosa causing an intraperitoneal bleed
? Uncontrol able vaginal bleeding
? Extensive uterine tumor to reduce burden and limit chemotherapy.


BRAIN METASTASES
Presenting features - seizures /
headaches /hemiparesis
Whole brain irradiation +
combination chemotherapy
Other choice ? intrathecal Mtx,
fortnightly
Moribund circumstances ?IC bleed
? emergency craniotomy + critical
care support

VAGINAL METASTASES
Profuse bleeding ? managed by packing/ wide local excision
Rarely, embolization of hypogastric arteries.

PULMONARY METASTASES
90% - remission with chemotherapy
Rarely ? thoracotomy and excision needed.

LIVER METASTASES
Difficult to treat with chemotherapy
Rarely need hepatic resection and arterial embolisation


POST TREATMENT SURVEILLANCE
Low risk GTN --- weekly hCG ? until titers undetectable for 3 consecutive weeks.
--- then monthly titers until level undetectable for 12 months
High risk GTN --- fol owed for 24 months, since chance of late relapse
Effective contraception during surveillance period.



PROGNOSIS
Overal cure rate for GTN ? 90%
Non and low risk mets ? excel ent prognosis ? 100% survival rate with single agent
therapy
High risk disease ? 86% with multiple agent therapy


POST TREATMENT SEQUELAE
PREMATURE OVARIAN FAILURE
PSYCHOSOCIAL PROBLEMS
RISK OF SECONDARY MALIGNANCY

SUBSEQUENT PREGNANCY
Advised not to become pregnant atleast for 1 year after chemotherapy
Send placenta for histological examination
Do serum hCG test 6 and 10 weeks after delivery
Lifelong fol owup


hCG - H
[Hyperglycosylated Hcg]
Variant of hCG ? produced by invasive
trophoblasts ? has double sized
oligosaccharides
Presence only in implantation phases of
normal pregnancy
Seen mainly in GTN
Action autocrine.
Main action ? promote trophoblast
growth and invasion


Phantom hCG
Due to presence of heterophile Abs in serum
Interfere with immunoassay ? cause false + result
This cause mild elevation of hCG
? clinicians erroneously treat with chemotherapy
Clarification :
? UTP : negative
? Serial dilations of serum sample : phantom hCG unchanged
? Different hCG assay by alternate method : absence of true hCG

DIAGNOSIS OF PSTT
? Presenting symptom ? 90% with bleeding
? Only mild elevation of serum Hcg
- due to predominance of intermediate trophoblast and lack of
syncytiotrophoblast
? Radiological evidence of uterine tumour
? Tumours stain intensively with antibodies to hPL
? However serum hPL not elevated hence hPL not for fol owup.

TREATMENT OF PSTT
Chemoresistant tumors.
Primary modality ? surgery
Simple hysterectomy + pelvic lymphadenectomy + ovary preservation
Lifelong fol ow up
Advanced disease or distant mets ? adjuvant chemotherapy

THANKYOU

This post was last modified on 12 August 2021