2d:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/0fma7nlq6immz.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/1chr5wkk3j58k.js","/_next/static/immutable/chunks/37kmmh_zm4dov.js","/_next/static/immutable/chunks/311zvdjfxff-f.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js"],"default"] 2e:T52d8,

Summary Table

Feature	Detail
Risk Factors	Extremes of reproductive age (< 20 or > 35, with sharp increase > 40), prior molar pregnancy, folate deficiency, Southeast Asian descent
Etiology	Abnormal fertilization leading to trophoblastic proliferation without viable fetal development; complete mole (46,XX or 46,XY, entirely paternal origin) vs. partial mole (triploid 69,XXX/XXY, one ovum + two sperm)
Patient Presentation	Vaginal bleeding in the first trimester, uterine size larger than expected for gestational age (complete mole), hyperemesis, passage of grape-like vesicles
Classic Physical Exam	Boggy, enlarged uterus disproportionate to dates; absence of fetal heart tones (complete); passage of vesicular tissue per vaginum
Key Diagnostic Results	Markedly elevated beta-hCG (often > 100,000 mIU/mL in complete mole), "snowstorm" pattern on pelvic ultrasound, no fetal parts in complete mole
Management	Suction curettage (evacuation), serial beta-hCG monitoring post-evacuation, reliable contraception for 6 to 12 months
Keywords	"Grape-like vesicles," "snowstorm on ultrasound," "uterus large for dates," "markedly elevated hCG," "theca lutein cysts"

1. Pathophysiology

Hydatidiform mole is a form of gestational trophoblastic disease (GTD) arising from abnormal fertilization. The core defect is an imbalance in parental genetic contribution, which causes unchecked trophoblastic proliferation and hydropic degeneration of chorionic villi.

In a complete mole, an empty ovum (one that has lost its maternal nuclear DNA) is fertilized by one sperm that duplicates its chromosomes (46,XX) or, less commonly, by two sperm (46,XY). The entire genome is paternal. Because trophoblast differentiation is driven by the paternal genome while embryonic tissue differentiation relies on the maternal genome, you get massive trophoblastic growth with no fetal tissue. The villi become universally swollen and edematous, forming the characteristic grape-like vesicles. The all-paternal genome drives aggressive trophoblastic proliferation, which explains the markedly elevated beta-hCG and the higher risk of progression to gestational trophoblastic neoplasia (GTN), approximately 15 to 20%.

In a partial mole, a normal ovum retains its maternal DNA but is fertilized by two sperm, producing a triploid karyotype (69,XXX or 69,XXY). Because maternal genetic material is present, some fetal tissue or fetal parts may develop, though the fetus is never viable. The trophoblastic proliferation is focal rather than diffuse, hCG levels are less dramatically elevated, and the risk of malignant transformation is lower (around 1 to 5%).

The markedly elevated hCG in complete moles has direct clinical consequences. Theca lutein cysts form bilaterally in the ovaries because excessive hCG overstimulates the granulosa and theca cells. The hCG can also cross-react with the TSH receptor due to structural similarity of their alpha subunits, causing secondary hyperthyroidism with tachycardia, tremor, and heat intolerance. Severe nausea (hyperemesis) is driven by the very high hCG levels as well.

The reason a patient presents with first-trimester bleeding is that the hydropic villi outgrow their blood supply and disrupt the decidual-trophoblast interface, leading to hemorrhage into the uterine cavity.

2. Classification and Clinical Manifestation

Feature	Complete Mole	Partial Mole
Karyotype	46,XX (most common) or 46,XY; entirely paternal	69,XXX or 69,XXY; triploid (2 paternal + 1 maternal set)
Fertilization event	Empty ovum + 1 sperm (duplication) or 2 sperm	Normal ovum + 2 sperm
Fetal tissue	Absent	Present (but abnormal and nonviable)
Villous edema	Diffuse, all villi affected	Focal, only some villi hydropic
Trophoblastic proliferation	Diffuse and pronounced	Focal and mild
Uterine size	Larger than dates (classic)	Small or appropriate for dates
beta-hCG level	Markedly elevated, often > 100,000 mIU/mL	Mildly to moderately elevated
Ultrasound appearance	"Snowstorm" pattern, no fetal parts	Mixed echogenic mass, may show fetal parts or gestational sac
Theca lutein cysts	Common (bilateral, due to high hCG)	Rare
Hyperthyroidism	May occur	Rare
Risk of GTN	15 to 20%	1 to 5%
Typical presentation	Vaginal bleeding, uterus large for dates, hyperemesis	Often diagnosed incidentally after missed abortion or incomplete miscarriage

A key exam point: complete moles present dramatically (large uterus, very high hCG, snowstorm on ultrasound), while partial moles present subtly and are frequently diagnosed only after pathologic examination of products of conception from a presumed miscarriage.

3. Diagnostic Workup

Test	Role	Key Finding
Quantitative serum beta-hCG	Best initial test / screening	Disproportionately elevated for gestational age; often > 100,000 mIU/mL in complete mole
Pelvic ultrasound	Best initial imaging and often sufficient for diagnosis	"Snowstorm" or "cluster of grapes" pattern (complete); mixed echogenicity with possible fetal parts (partial)
Histopathology of evacuated tissue	Most accurate / confirmatory test (gold standard)	Hydropic villi, trophoblastic proliferation; immunostaining for p57 (absent in complete mole, present in partial mole)
Chest X-ray	Baseline for staging	Rule out pulmonary metastases (trophoblastic emboli)
TSH, free T4	If symptomatic	Secondary hyperthyroidism from hCG cross-reactivity with TSH receptor
CBC, type and screen	Pre-procedural	Anemia from vaginal bleeding; blood type for Rh status

Quantitative beta-hCG is the first test you order when a molar pregnancy is suspected. A level that is far higher than expected for the stated gestational age, particularly in a patient with first-trimester bleeding and an enlarged uterus, should immediately raise suspicion. In a complete mole, values above 100,000 mIU/mL are typical.

Pelvic ultrasound is the best initial imaging study. In a complete mole, you see a heterogeneous echogenic mass filling the uterine cavity with multiple small cystic spaces ("snowstorm" appearance) and no identifiable fetal pole or cardiac activity. In a partial mole, the ultrasound may show a gestational sac with abnormal placental tissue and, in some cases, identifiable but abnormal fetal structures. Bilateral theca lutein cysts may be visible on the ovaries if hCG is very high.

The gold standard for diagnosis is histopathologic examination of the evacuated tissue. The pathologist looks for hydropic swelling of chorionic villi and the degree of trophoblastic proliferation. A critical immunohistochemical marker is p57, a maternally imprinted, paternally silenced gene product. In a complete mole, because no maternal genome is present, p57 staining is negative in villous cytotrophoblast and stromal cells. In a partial mole, p57 is positive because maternal DNA is present. This distinction is high-yield when a vignette asks how to differentiate complete from partial mole on pathology.

A baseline chest X-ray is obtained before or shortly after evacuation to screen for pulmonary metastases, which is relevant for staging if GTN develops.

4. Management and Treatment

Phase	Intervention	Details
Pre-evacuation	Labs, imaging, stabilization	CBC, beta-hCG, TSH, type and screen, chest X-ray; treat hypertension or hyperthyroidism if present
Evacuation	Suction curettage	Preferred method regardless of uterine size; IV oxytocin started as the cervix is dilated to reduce hemorrhage
Rh prophylaxis	RhoGAM (anti-D immunoglobulin)	Given to all Rh-negative patients
Post-evacuation monitoring	Serial beta-hCG	Weekly until undetectable for 3 consecutive values, then monthly for 6 months (complete) or 6 months total (partial)
Contraception	Reliable method for monitoring period	Oral contraceptive pills preferred; avoid pregnancy until hCG surveillance is complete (6 to 12 months)
If hCG plateaus or rises	Evaluate for GTN	Staging workup and initiation of chemotherapy (methotrexate for low-risk, multi-agent for high-risk)

Suction curettage is the treatment of choice for uterine evacuation, regardless of uterine size. Hysterotomy and induction with prostaglandins or oxytocin are avoided as primary methods because they increase the risk of trophoblastic dissemination and hemorrhage. IV oxytocin is infused once cervical dilation begins to promote uterine contraction and minimize blood loss. Sharp curettage may follow suction to ensure the cavity is completely evacuated.

For patients who have completed childbearing, hysterectomy is an alternative. The uterus is removed with the mole in situ. However, even after hysterectomy, hCG monitoring is still required because trophoblastic tissue may have already spread hematogenously.

Serial beta-hCG monitoring is the cornerstone of post-evacuation management. After evacuation, hCG should fall progressively. The levels are checked weekly. Once hCG reaches undetectable levels for three consecutive weekly measurements, monitoring switches to monthly. For a complete mole, monthly surveillance continues for 6 additional months after the first undetectable value. For a partial mole, the monitoring period is typically 6 months total from evacuation. During this entire surveillance window, the patient must use reliable contraception (oral contraceptive pills are acceptable and do not increase GTN risk) because a new pregnancy would produce hCG and confound the monitoring.

If beta-hCG plateaus (remains unchanged across four measurements over three weeks) or rises (increases across three consecutive weekly measurements), the diagnosis shifts to gestational trophoblastic neoplasia. The patient then undergoes staging workup (pelvic ultrasound, CT chest/abdomen/pelvis, brain MRI if indicated) and receives chemotherapy. Single-agent methotrexate is first-line for low-risk GTN. Multi-agent regimens (EMA-CO: etoposide, methotrexate, actinomycin D, cyclophosphamide, vincristine) are used for high-risk disease.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Threatened abortion	First-trimester vaginal bleeding, cramping	Uterine size appropriate for dates, normal hCG trend, viable fetal pole with cardiac activity on ultrasound
Ectopic pregnancy	Elevated hCG, vaginal bleeding, no intrauterine pregnancy on ultrasound	hCG is elevated but usually much lower than molar range; adnexal mass or free fluid present; no "snowstorm" pattern
Hyperemesis gravidarum	Severe nausea and vomiting in first trimester	In simple hyperemesis, hCG is elevated but not to molar levels; ultrasound shows normal intrauterine pregnancy
Twin gestation	Uterus larger than dates, elevated hCG	Ultrasound shows two gestational sacs with fetal poles/cardiac activity; hCG elevated but not disproportionately
Choriocarcinoma	Very high hCG, trophoblastic tissue, vaginal bleeding	Choriocarcinoma is a malignant GTN that can arise after any pregnancy (not just molar); pathology shows absence of chorionic villi (sheets of malignant cytotrophoblast and syncytiotrophoblast without villous structures)
Incomplete/missed abortion	Vaginal bleeding, passage of tissue, abnormal ultrasound	hCG levels declining (not rising or disproportionately high); ultrasound shows retained products but no "snowstorm" or vesicular pattern; partial mole can initially look identical, so always send tissue for pathology

The most tested distractor pair is complete mole vs. partial mole within the same question. Vignettes will present features that overlap and ask you to distinguish them. The discriminators: complete mole has no fetal tissue, diffusely hydropic villi, very high hCG, and uterus larger than dates. Partial mole may show fetal parts, triploid karyotype, and less dramatic hCG elevation.

Another common distractor is choriocarcinoma vs. complete mole. Both produce very high hCG and vaginal bleeding. The key: choriocarcinoma is a malignancy that invades myometrium and metastasizes hematogenously (lung most common), and histology shows no chorionic villi (pure malignant trophoblastic tissue). A mole retains villous architecture on pathology.

6. Traps and High-Yield Pearls

The most common way students get questions on hydatidiform mole wrong is by failing to distinguish complete from partial mole based on the clinical and pathologic clues in the vignette. Test-writers love to present a partial mole that was initially misdiagnosed as a spontaneous abortion. The trap: the student sees "vaginal bleeding" and "passage of tissue" and jumps to missed abortion without recognizing the clue of a mildly elevated hCG or triploid karyotype on genetic analysis. The teaching point is that all products of conception from first-trimester losses should undergo pathologic examination to rule out molar pregnancy.

Another frequent trap involves the post-evacuation surveillance period. Students forget that hCG must be monitored to undetectable and then continued monthly, and that pregnancy must be avoided during this window. A vignette may describe a patient whose hCG was falling and who then becomes pregnant, making it impossible to interpret whether a subsequent hCG rise represents recurrence or a new pregnancy. The tested concept: reliable contraception is not optional but a mandatory part of management.

Students also miss the association between complete mole and secondary hyperthyroidism. When a vignette pairs first-trimester bleeding with tachycardia, tremor, and weight loss, the test is checking whether you recognize hCG cross-reactivity with the TSH receptor rather than attributing these symptoms to anxiety or a separate thyroid disorder.

Finally, remember that suction curettage is always the answer for evacuation, not medical induction. And if hCG plateaus or rises after evacuation, the next step is staging and chemotherapy, not repeat curettage.

1e:["$","$L2d",null,{"article":{"id":"fb275b25-aad5-4dca-9e0e-cec1fcde709f","title":"Mola Hidatidosa","content":"$2e","category":"Reproduksi","created_at":"2026-05-16T06:57:03.406443+00:00","status":"published","subcategory":null},"questionCount":5,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]