Gestational Trophoblastic Disease by MWEBAZA VICTOR .pptx

M W E B A Z A
VICTOR. J
M B c h B 5 T H Y E A R ( O B G Y N )
Ugandan
mwebazavictor1997@gmail.com
Kampala international university western
campus
Jinja site light under the care of
Jinja Regional Referral Hospital OBGYN
dept
GESTATIONAL TROPHOBLASTIC DISEASES
Presentation TWO
1st/AUG/2022 @ 8:00AM
Modulated and Mentored by Doctor petrus
(gynaecology and obstetrics CONSULTANT)
@ KIUWC

Topic : Gestational trophoblastic
disease (GTD)
Gestational trophoblastic disease (GTD) is a
heterogeneous spectrum of diseases with abnormal
trophoblastic proliferation ranging from benign to
malignant state. It has varying degree of spread
from local invasion to distant metastasis.
S i m p l e r e c a p o n e m b r y o g e n e s i s
f o r 5 t o 1 0 m i n u t e s u s i n g l a n g h m a n
e m b r y o l o g y t e x t b o o k 8 t h e d i t i o n
10/18/2022 MWEBAZA VICTOR GTD presentation

The cells that form gestational trophoblastic
tumours are called trophoblasts and come
from tissue that grows to form the placenta
during pregnancy.
There are several different types of GTD.
Hydatidiform moles are benign in most cases,
but sometimes may develop into invasive
moles, or, in rare cases, into choriocarcinoma,
which is likely to spread quickly, but which is
very sensitive to chemotherapy, and has a very
good prognosis.

Types of G.T.D
one benign tumour, and four malignant tumours
The benign tumour Hydatidiform mole
The four malignant tumours
1. Invasive mole
2. Choriocarcinoma
3. Placental site trophoblastic tumour
4. Epithelioid trophoblastic tumour

Risk factors for Development of
GTN
1. Advanced maternal age (>40 years)
2. b-hCG >100,000 IU/L
3. Increased uterine size
4. Bilateral ovarian enlargement (>8 cm)
5. USG—uterine invasion
6. Increased uterine vascularity (USG Doppler)

Classification
of GTD (WHO).
A. Benign trophoblastic
lesions
1. Placental site nodule
2. Exaggerated placental
reaction
B. H ydatidiform moles
(HM)
1. Complete hydatidiform
mole
2. „
Partial hydatidiform
moles
C. Gestational
trophoblastic neoplasia
1. „
Invasive mole
2. Choriocarcinoma
3. „
Placental site
trophoblastic tumor
4. „
Epithelioid trophoblastic
tumors
10/18/2022
MWEBAZA VICTOR GTD presentation

Risk factors of GTD.
Race: Asians compared to
North Americans or
Europeans
Age: Extremes of age (<16
and >45)
Parity: Increasing parity
Diet: Risks of CHM is
increased when dietary
intake of animal fat, beta-
carotene or vitamin A is
less
Genetics: Autosomal
recessive disorder (familial
recurrent HM) chromosome
19q
Risk of recurrence is increased
up to 25% when there is
previous 2 or more molar
pregnancy
(CHM: complete hydatidiform
mole)

Incidence of GTD
The incidence of GTN is about 1 in 5,000 pregnancies
in oriental countries and 1 in 50,000 in Europe and
North America. More than 50% occur after molar
pregnancy, about 25% after abortion and/or ectopic
pregnancy and a few after normal pregnancy. Non
metastatic (locally invasive) lesions develop in 15%
and metastatic lesions develop in about 4% of
patients after molar evacuation.
While GTD overwhelmingly affects women
of child-bearing age, it may rarely
occur in postmenopausal women.

1. HYDATIDIFORM MOLE—
MOLAR PREGNANCIA
Molar pregnancy is an abnormal form of
pregnancy in which a non-viable fertilized egg
implants in the uterus and will fail to come to
term. A molar pregnancy is a gestational
trophoblastic disease which grows into a mass
in the uterus that has swollen chorionic villi.
These villi grow in clusters that resemble
g r a p e s .

An hydatidiform mole is a pregnancy or conception
in which the placenta contains grape like
vesicles (small sac) that are usually visible
with the naked eyes
These vesicles are due to distention of the
chorionic villi by fluids
On microscopy there is hypertrophy of the
trophoblastic cells
NOTICE Hydatidiform mole will almost always end
as a spontaneous abortion

Molar pregnancies are categorized as partial
moles or complete moles, with the word mole
being used to denote simply a clump of
growing tissue, or a growth.

1.1. Complete mole
o An "empty" ovum (i.e. absent or inactivated
maternal chromosome) is fertilized by either a
haploid sperm that then duplicates or two
separate spermatozoa.
o Have a 46XX /46YY karyotype 4 and 8% have 46,xy
karyotype. These arise from dispermy i.e.
fertilization of the ‘empty’ ovum by two separate
haploid sperms
o There is absence of embryonic material
o Its diffuse in nature, Hyperplasia usually present to
variable degrees
o Uterine size large for dates10/18/2022
MWEBAZA VICTOR GTD
presentation

o Complete hydatidiform moles have a 2–4% risk of
developing into choriocarcinoma in Western
countries and 10–15% in Eastern countries and a
15% risk of becoming an invasive mole.
o About the theca lutein cysts, >25% develop
depending on the diagnostic modality
o About immuno staining its negative for P57
o No fetal parts
o Increased or elevated hCG
o All villi hydropin with no normal adjacent villi
o Risk of choriocarcinoma is 15%
o Post molar invasion and malignancy is 15% and
4% respectively

Classic signs and symptoms a complete
mole.
1. Vaginal bleeding
2. Hyperemesis ( severe vomit)
3. Size inconsistent with gestational age( with no fetal
heart beating and fetal movement)
4. Preeclampsia
5. Theca lutein ovarian cysts
6. Hyperthyroidism signs and symptoms
Sometimes symptoms of hyperthyroidism are seen, due to the
extremely high levels of hCG, which can mimic the effects
of thyroid-stimulating hormone.

Differentials of complete molar
1. Hyperemesis gravidarum
2. Hypertension in pregnancy
3. Hyperthyroidism
4. Abortion
5. Multiple pregnancy
6. Polyhydramnios

1.2. Partial mole
o 90% of the time, they exhibit triploidy. The
additional haploid component is paternal
(diandry). An oocyte retains its female nucleus
o but is fertilized by two haploid sperms
 69 XXX, 69 XXY, rarely 69 XYY

o Embryonic material present
o Focal in nature, Hyperplasia mild and focal
o Small for the dates or norm
o About immuno staining there is a positive P57
o Development of theca lutein cysts is rare
o Post molar invasion and malignancy is <5%
o Mild to norm increase in hCG
o Fetal parts present
o Risk of choriocarcinoma 0.5%
o Normal adjacent villi may be present

Signs and Symptoms of Partial
Mole
1. Vaginal bleeding
2. Absence of fetal heart tones
3. Uterine enlargement and preeclampsia is
reported in only 3% of patients.
4. Theca lutein cysts rare.
5. Hyperemesis is rare.

Diagnosis of hydatidiform mole
o Quantitative beta-HCG; Serum beta-hCG (raised
more than 100,000 i.u. per ml)
o CBC
o CXRAY
o Ultrasound is the criterion standard for
identifying both complete and partial molar
pregnancies. The classic image On ultrasound,
the mole resembles a bunch of grapes ("cluster
of grapes" or "honeycombed uterus" or
"snow-storm")
o definitive diagnosis requires histopathological
examination.
10/18/2022

o The most common symptom of a mole is
vaginal bleeding during the first trimester
o however very often no signs of a problem
appear and the mole can only be diagnosed
by use of ultrasound scanning. (routine check)
o Occasionally, a uterus that is too large for the
stage of the pregnancy can be an indication.
NOTE: Vaginal bleeding does not always
indicate a problem!

Management of a complete mole
oSuction dilation and curettage :
To remove benign hydatidiform moles
When the diagnosis of hydatidiform mole is established,
the molar pregnancy should be evacuated.
An oxytocic agent should be infused intravenously after
the start of evacuation and when moderate amount of
trophoblastic tissue has been removed to avoid risk of
dissemination of trophoblastic tissue into circulation
and continued for several hours to enhance uterine
contractility

Suction curettage should be followed by gentle
sharp curettage to obtain tissue for histology
The procedure should be done in operation
theatre under GA or SA with blood available,
If the uterus is larger than 14 weeks one hand
should be placed on top of the fundus, uterus
should be massaged to stimulate uterine
contraction and reduce the risk perforation.

oRemoval of the uterus (hysterectomy) :
used rarely to treat hydatidiform moles if
future pregnancy is no longer desired. If the
patient desires surgical sterilization, hysterectomy
may be performed with the mole in situ.
- Ovaries may be preserved at the time of surgery,
even though prominent theca lutein cysts are
present.
- Large ovarian cysts may be decompressed by
aspiration.
- Hysterectomy does not prevent metastasis, therefore
patient will still require follow-up with assessment of
hCG levels.

oChemotherapy with a single-agent drug
Prophylactic (for prevention) chemotherapy at
the time of or immediately following molar
evacuation may be considered for the high-
risk patients( to prevent spread of disease )

High-risk postmolar trophoblastic
tumor
1. Pre-evacuation uterine size larger than expected
for gestational duration
2. Bilateral ovarian enlargement (> 9 cm theca
lutein cysts)
3. Age greater than 40 years
4. Very high hCG levels(>100,000 m IU/ml)
5. Medical complications of molar pregnancy such
as toxemia, hyperthyrodism and trophoblastic
embolization (villi come out of placenta )
6. repeat hydatidiform mole

Follow-up
Patients with molar pregnancy are curative over 80% by
treatment of evacuation.
The follow-up after evacuation is key necessary
o uterine involution,
o Regression cystic ovarian enlargement (theca lutein
cysts)
o cessation of bleeding
o Quantitative serum hCG levels
should be obtained every 1-2 weeks until negative for
three consecutive determinations, Then monthly for 6
months, Followed by every 3 months for 1 years.
@Weekly to non-detectable levels (i.e.
<5MIu/ml) on 3 m .Then monthly for 6
months. Then bimonthly for 6 months

Follow-up
o Physical examination to r/o metastatic disease
is equally important. Ask for headache, visual
disturbance, cough, difficult in breathing,
involution of the uterus
o Investigations; FBC, base line chest X-ray and
abdominal and pelvic US scan
o Contraception should be practiced during this
follow-up period for atleast 1 yr.

NOTE: Avoid IUCD --- Risk of perforation
Avoid Depo---Irregular bleeding
At completion of follow-up pregnancy may be
undertaken

1. Hemorrhage
2. Sepsis
3. Perforation during Evacuation
4. Thyroid storm
5. Persistent GTD
Complications of molar pregnancy

Persistent gestational trophoblastic
neoplasia (GTN)
Persistent GTN is evidenced by persistence of
trophoblastic activity following evacuation of
molar pregnancy. This is clinically diagnosed
when the patient presents with
(a) Irregular vaginal bleeding;
(b)Subinvolution of the uterus;
(c) Persistence of theca lutein cysts;
(d)Level of hCG either plateaus or re-elevates
after an initial fall.

After molar evacuation serum β-hCG becomes
normal in about 7–9 weeks. Post molar GTN of
serious nature may be either invasive mole or
choriocarcinoma but GTN after nonmolar
pregnancy is always a choriocarcinoma.

All patients with persistent GTT should undergo
a careful pre-treatment evaluation, include:-
1. Complete history and physical exam.
2. Serum h CG level.
3. LFT, RFT, Thyroid fn test.
4. Peripheral WBC & platelet counts.
- Metastatic work –up should include
CXR, CT-Scan
USS or CT-Scan of abdomen and pelvis
CT or MRS Scan of the head.

HINT ON Theca lutein cyst
Theca lutein cyst is a type of bilateral functional
ovarian cyst filled with clear, straw-coloured
fluid.
To be classified a functional cyst, the mass must reach
a diameter of at least three centimetres.
These cysts result from exaggerated physiological
stimulation (hyperreactio luteinalis) and are usually
associated with markedly elevated levels of beta-
human chorionic gonadotropin (beta-hCG). They
are thus associated with gestational trophoblastic
disease (molar pregnancy), diabetes mellitus,
alloimmunisation to Rh-D, and multiple gestations.

Women who smoke have a twofold increase for functional cysts.

2. PLACENTAL SITE
TROPHOBLASTIC TUMOR
PSTT tumour arises from the trophoblasts of the
placental bed. Incidence is less than 1% of all
patients with GTN. 40–50% of these patients
develop metastases. Tumor cells infiltrate the
myometrium and grow between smooth-muscle
cells
Syncytiotrophoblast cells are generally
absent, instead intermediate
trophoblast cells are predominant.
β-hCG secretion is low but human placental
lactogen (hPL) is secreted and this is monitored
during the follow up. 10/18/2022

The entity is not responsive to
chemotherapy. Hysterectomy is the
preferred treatment. Serial serum
hPL may be a reliable marker
and hPL is useful for immunohistochemical
staining toconfirm the diagnosis.
Tend to remain confined to the uterus,
metastasizing late in their course.
In contrast to other trophoblastic tumors,
placental site tumors are relatively
INSENSITIVE to chemotherapy.

Management of Non-metastatic
PGTD
Single agent is used. Methotrexate or
Actinomycin D.
For those beyond 40 yrs and /or have
completed their families or have
more than 4 children chemotherapy
followed by surgery on the 3rd day is
recommended.

3. EPITHELIOID
TROPHOBLASTIC TUMOR
(ETT):
It is a variant of PSTT (WHO, 2003). Both are
relatively chemoresistant and recurrence rate
for the both are high (20–30%) despite
surgery or chemotherapy.

4. INVASIVE GTN
(Chorioadenoma destruens)
Invasive mole comprises about 15% of all GTN.
The prominent features of this type of mole are
invasive and destructive potentialities. Invasive mole
shows abnormal penetration through the muscle
layers of the uterus.
The uterine wall may be perforated at multiple areas
showing purple, fungating growth with
massive intraperitoneal hemorrhage.
The neoplasm may invade the pelvic blood vessels and
metastasizes to vagina or distant sites as like those
in choriocarcinoma.

Diagnosis of invasive mole
On laparotomy:
1. Perforation of the uterus through which purple
fungating growth is visible
2. Hemoperitoneum.
Histology:
There is penetration of the uterine wall by the
hyperplasic trophoblastic cells which still retain
villus structures. There is no evidence of muscle
necrosis . The materials for uterine curettage are
often deceptive as the lesion may be deep inside
the myometrium.
Persistent high level of urinary or serum hCG

5. CHORIOCARCINOMA
A malignant form of GTD which can develop
from a hydatidiform mole or from
placental trophoblast cells
associated with a healthy fetus ,an
abortion or an ectopic pregnancy.
Characterized by abnormal trophoblastic
hyperplasia and anaplasia , absence of
chorionic villi

Choriocarcinoma is a h i g h l y m a l i g n a n t
t u m o r arising from the chorionic epithelium
Is purely an epithelial tumor composed of anaplastic
syncytiotrophoblastic and cytotrophoblastic cells
Histologically – No villi.
Sheets of anaplastic trophoblastic cells on a
background of Hemorrhage and necrosis.
Occurs in about 5% of patients after molar pregnancy
evacuation

About 3–5% of all patients with molar
pregnancies develop choriocarcinoma.
Amongst all patients with choriocarcinoma,
around 50% develop following a hydatidiform
mole
Trophoblastic disease following a normal
pregnancy is either choriocarcinoma or PSTT
and not a benign or invasive mole.

Pathology
The primary site is usually anywhere in the
uterus. Rarely, it starts in the tube or ovary.
Ovarian choriocarcinoma (nongestational)
may also be associated with malignant
teratoma or dysgerminoma.
The lesion is usually localized nodular type. It
looks red, hemorrhagic, and necrotic. At
times, the lesion is diffuse involving the entire
endometrium.

Ovarian Enlargement due to’
Bilateral lutein cysts are present in about 30%.
These are due to excessive production of
chorionic gonadotropin.

Cause of choriocarcinoma
Choriocarcinoma of the placenta during
pregnancy is preceded by:
1. hydatidiform mole (50% of cases)
2. spontaneous abortion (20% of cases)
3. ectopic pregnancy (2% of cases)
4. normal term pregnancy (20–30% of cases)
5. hyperemesis gravidarum

Signs and symptoms
1. increased quantitative chorionic gonadotropin
(the "pregnancy hormone") levels
2. vaginal bleeding
3. shortness of breath
4. haemoptysis (coughing up blood)
5. chest pain
6. chest X-ray shows multiple infiltrates of various
shapes in both lungs
7. can present with decreased thyroid-stimulating
hormone (TSH) due to hyperthyroidism.

Treatment of gestational
choriocarcinoma
Since gestational choriocarcinoma (which arises
from a hydatidiform mole) contains paternal
DNA (and thus paternal antigens), it is
exquisitely sensitive to chemotherapy. The
cure rates, even for metastatic gestational
choriocarcinoma, more than 90% when using
chemotherapy for invasive mole and
choriocarcinoma.

Medical management.
As of 2019, treatment with either single-agent
Methotrexate or Actinomycin-D is
recommended for low-risk disease,
while intense combination regimens including
EMACO (etoposide, Methotrexate,
Actinomycin D, cyclophosphamide and
vincristine (Oncovin) are recommended for
intermediate or high-risk disease

EMA-CO Chemotherapy for poor
Prognostic Disease
Etoposide(VP-16) 100mg/M2 IV daily×2 days
(over 30-45 minutes)
Methotrexate 100mg/M2
IV losding dose,
then 200mg/M2
over 12 hours day 1
Actinomycin D 0.5mg IV daily×2 days
Folinic acid
15mg IM or p.o. q 12 hours×4 starting 24
hours after starting methotrexate
Cyclophosphamide 600mg/M2 IV on day8
Oncovin (vincristine) 1mg/M2 IV on day8
(Repeat every 15 days as toxicity permits)

Surgical management
Hysterectomy (surgical removal of the uterus)
can also be offered to patients > 40 years of
age or those for whom sterilisation is not an
obstacle. It may be required for those with
severe infection and uncontrolled bleeding.

ANATOMICAL STAGING OF GTT (FIGO)
1. Stage I. [confirmed to uterus]
2. Stage II [extends outside uterus but limited
to the pelvic structures (adnexae, vagina,
broad ligaments)]
3. Stage III [Extend to the lung with/without
genital tract involvement.]
4. Stage IV [Metastasis to the liver, Brain,
Kidney, GIT etc]

WHO Prognostic Scoring System
Score
Prognostic factor 0 1 2 4
Age(years) ≤40 >/=40 — —
Pregnancy history
Hydatidiform
mole
Abortion,
ectopic
Term
pregnancy
—
Interval (months)
of treatment
<4 4-6 7-12 >12
Initial hCG(mIU/ml) <103 103-104 104-105 >105
Largest tumor(cm) <3 3-5 >5 —
Sites of metastasis Lung
Spleen,
kidney
GI tract Liver, Brain
No. of metastasis — 1-4 4-8 >8
Previous failed
chemotherapy
(treatment)
— — Single drug
2 or more
drugs

In this scoring system, women with a score of 7 or
greater are considered at high risk.

FIGO Staging System for
Gestational Trophoblastic Tumors
Substages assigned for each stage as follows:
A: No risk factors present
B: One risk factor
C: Both risk factors
Risk factors used to assign substages:
1. Pretherapy serum hCG > 100,000 mlU/ml
2. Duration of disease >6 months

Becoming pregnant again after GTD
Most women with GTD can become pregnant again
and can have children again.
In the past, it was seen as important not to get
pregnant straight away after a GTD. Specialists
recommended a waiting period of 6 months after
the hCG levels become normal. Recently, this
standpoint has been questioned. New medical data
suggest that a significantly shorter waiting period
after the hCG levels become normal is reasonable
for approximately 97% of the patients with
hydatidiform mole. 10/18/2022 MWEBAZA VICTOR GTD presentation

GTD coexisting with a normal fetus,
also called "twin pregnancy"
In some very rare cases, a GTD can coexist with a
normal fetus. This is called a "twin pregnancy".
These cases should be managed only by
experienced clinics, after extensive consultation
with the patient. Because successful term if the
mother wishes, following appropriate counselling.
The probability of achieving a healthy baby is
approximately 40%, but there is a risk of
complications, e.g. pulmonary embolism and
preeclampsia

Treatment summary on GTD
1. Nonmetastatic GTD
2. Low-Risk Metastatic GTD
3. High-Risk Metastatic GTD

Treatment of Nonmetastatic GTD
1. Hysterectomy is advisable as initial treatment
in patients with Nonmetastatic GTD who no
longer wish to preserve fertility
2. This choice can reduce the number of course
and shorter duration of chemotherapy.
3. Adjusted single-agent chemotherapy at the
time of operation is indicated to eradicate
any occult metastases and reduce tumor
dissemination.

4. Single-agent chemotherapy is the treatment
of choice for patients wishing to preserve
their fertility.
5. Methotrexate(MTX) and Actinomycin-D are
generally chemotherapy agents
6. Treatment is continued until three
consecutive normal hCG levels have been
obtained and two courses have been given
after the first normal hCG level.

Treatment of Low-Risk Metastatic
GTD
1. Single-agent chemotherapy with MTX or
Actinomycin-D is the treatment for patients
in this category
2. If resistance to sequential single-agent
chemotherapy develops, combination
chemotherapy would be taken
3. Approximately 10-15% of patients treated
with single-agent chemotherapy will require
combination chemotherapy with or without
surgery to achieve remission

Treatment of High-Risk Metastatic
GTD
1. Multiagent chemotherapy with or without
adjuvant radiotherapy or surgery should be
the initial treatment for patients with high-
risk metastatic GTD
2. EMA-CO regimen formula is good choice for
high-risk metastatic GTD
3. Adjusted surgeries such as removing foci of
chemotherapy-resistant disease, controlling
hemorrhage may be the one of treatment
regimen

Follow-up After Successful
Treatment
Quantitative serum hCG levels should be
obtained monthly for 6 months, every two
months for remainder of the first year, every 3
months during the second year
Contraception should be maintained for at least
1 year after the completion of chemotherapy.
Condom is the choice.

Final Prognosis
Cure rates should approach 100% in
nonmetastatic and low-risk metastatic GTD
Intensive multimodality therapy has resulted in
cure rates of 80-90% in patients with high-risk
metastatic GTD

A GIRL CHILD
NEED TO BE
LOVED AND
CARED FOR.
FEMALE
LIVES
MATTER –
MWEBAZA
VICTOR

References of Mwebaza victor’s
work
1. DC Dutta’s Textbook of Gynecology
2. ^ "choriocarcinoma" at Dorland's Medical Dictionary
3. ^ Rosenberg S, DePinho RA, Weinberg RE, DeVita VT,
Lawrence TS (2008). DeVita, Hellman, and Rosenberg's
Cancer: Principles & Practice of Oncology. Hagerstwon,
MD: Lippincott Williams & Wilkins. ISBN 978-0-7817-7207-
5. OCLC 192027662.
4. ^ Kufe D (2000). Benedict RC, Holland JF (eds.). Cancer
medicine (5th ed.). Hamilton, Ont: B.C. Decker. ISBN 1-
55009-113-1. OCLC 156944448.
5. ^ Gerson RF, Lee EY, Gorman E (November 2007).
"Primary extrauterine ovarian choriocarcinoma mistaken
for ectopic pregnancy: sonographic imaging findings". AJR.
American Journal of Roentgenology. 189 (5): W280–
W283. doi:10.2214/AJR.05.0814. PMID 17954626.

6. Gestational trophoblastic disease: Epidemiology, clinical
manifestations and diagnosis. Chiang JW, Berek JS. In:
UpToDate [Textbook of Medicine]. Basow, DS (Ed).
Massachusetts Medical Society, Waltham, Massachusetts, USA,
and Wolters Kluwer Publishers, Amsterdam, The Netherlands.
2010.
7. ^ Chittenden B, Ahamed E, Maheshwari A (August 2009).
"Choriocarcinoma in a postmenopausal woman". Obstetrics and
Gynecology. 114 (2 Pt 2): 462–5.
doi:10.1097/AOG.0b013e3181aa97e7. PMID 19622962.
S2CID 35996436.
8. ^ Gestational trophoblastic disease: Pathology. Kindelberger
DW, Baergen RN. In: UpToDate [Textbook of Medicine]. Basow,
DS (Ed). Massachusetts Medical Society, Waltham,
Massachusetts, USA, and Wolters Kluwer Publishers,
Amsterdam, The Netherlands. 2010
9. ^ "Gestational Trophoblastic Disease Treatment (PDQ®)–
Patient Version - National Cancer Institute". www.cancer.gov.
2020-05-11. Retrieved 2021-02-16.

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