Gestational and Placental Disorders

Slide 1 · Gestational and

Placental Disorders

Placental structure • pregnancy loss • vascular pathology • inflammation • trophoblastic disease

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Map the maternal and fetal circulations and the trophoblast compartments.

Link early gestational disorders to their characteristic mechanisms and morphology.

Differentiate maternal and fetal vascular malperfusion and inflammatory lesions.

Explain the placental basis of preeclampsia and identify the major trophoblastic lesions.

Slide 3 · Why placental pathology matters

Can explain fetal intrauterine or perinatal death and fetal growth restriction.

Provides information about congenital abnormalities and maternal morbidity.

Identifies morphologic processes relevant to immediate neonatal and maternal care.

May inform counseling about recurrence risk in a later pregnancy.

Placental findings should be interpreted with gestational age and clinical context.

Slide 4 · The placenta is a dual-circulation exchange organ

Maternal spiral arteries

Intervillous space

Maternal veins

Two umbilical arteries

Fetal capillaries in villi

One umbilical vein

Molecule exchange across villous barrier; Blood remains in separate circulations

Maternal blood

Fetal blood

Slide 5 · Chorionic villi are exchange units

Syncytiotrophoblast boundary

Underlying cytotrophoblast

Villous stroma and fetal capillaries

Schematic villus cross-section—not histology

Slide 6 · Three functional trophoblast compartments

Syncytiotrophoblast

Maternal interface • exchange • endocrine function

Cytotrophoblast

Villous trophoblast epithelial compartment

Extravillous trophoblast

Anchorage • uterine invasion • vessel remodeling

The major trophoblast groups serve different, complementary placental functions.

Slide 7 · Villous trophoblast: Interface with maternal blood

The syncytiotrophoblast is the outer villous epithelial surface.

Cytotrophoblasts form an underlying trophoblast compartment.

Together they participate in hormone secretion, transport, and barrier function.

Fetal capillary endothelium completes the thin exchange boundary.

Slide 8 · Extravillous trophoblast establishes uterine perfusion

Uterine implantation

Trophoblast invasion

Spiral artery remodeling

Low-resistance inflow

Normal implantation converts maternal resistance vessels into high-capacitance placental inflow.

Slide 9 · Normal spiral artery transformation

Before remodeling

Narrow-caliber resistance vessel

Muscular vascular wall

Limited flow capacity

Physiologic remodeled artery

Extravillous trophoblast remodels wall

Smooth muscle diminished or removed

High-capacitance, low-resistance inflow

A failure of remodeling predisposes to placental ischemia.

Slide 10 · Maternal blood enters the intervillous space

Spiral arteries

Maternal intervillous blood

Exchange at villous surface

Endometrial veins

Perfusion of the intervillous space begins during early gestation; Exchange occurs without routine blood mixing.

Slide 11 · Fetal blood traverses the villous capillary tree

Two umbilical arteries

Chorionic plate branches

Villous capillaries

Single umbilical vein

Deoxygenated fetal blood is delivered to villi; Oxygenated blood returns to the fetus.

Slide 12 · Exchange barrier becomes thin in mature villi

Maternal intervillous blood

Syncytiotrophoblast

Fetal capillary endothelium

Fetal capillary network lies close to the trophoblast surface.

A thin epithelial–endothelial interface favors gas and nutrient exchange.

Maternal and fetal blood ordinarily remain in distinct compartments.

Slide 13 · Villous maturation changes histologic architecture

First trimester

Prominent inner cytotrophoblast layer

Outer syncytiotrophoblast well defined

Delicate central stroma

Third trimester

Dense fetal capillary network

Thinned vasculosyncytial membrane

Cytotrophoblast less conspicuous

Conceptual developmental comparison; Not a diagnostic micrograph.

Slide 14 · Normal exchange does not require blood mixing

Maternal blood bathes villi in the intervillous space.

Fetal blood remains within capillaries inside chorionic villi.

Small amounts of cell-free fetal DNA enter maternal blood, likely through syncytiotrophoblast shedding.

The latter principle supports prenatal genetic testing, without implying wholesale blood mixing.

Slide 15 · Approach placental disease by mechanism

Pregnancy establishment

Abortion • ectopic implantation

Perfusion abnormalities

Maternal and fetal malperfusion

Inflammation

Ascending or hematogenous infection

Trophoblast disorders

Hydatidiform mole • neoplasia

Slide 16 · Timing helps organize the differential

First / early second

Spontaneous abortion

Ectopic pregnancy

Mid second

Fetal vascular malperfusion

Infection • placental hypoplasia

Third / peripartum

Cord lesions • malperfusion

Implantation disorders • preeclampsia

Timing is a diagnostic framework, not an exclusive or rigid boundary.

Slide 17 · Spontaneous abortion: Definition and distribution

The textbook defines miscarriage as pregnancy loss before 20 weeks of gestation.

Most reported miscarriages occur before 12 weeks.

An important proportion of clinically recognized gestations end in miscarriage.

Sensitive HCG testing reveals additional very early pregnancy losses.

Definition and frequency follow Robbins; Local clinical terminology and legal cutoffs may differ.

Slide 18 · Etiologic framework for pregnancy loss

Fetal genetics

Aneuploidy

Polyploidy

Rearrangements

Maternal endocrine

Luteal-phase defect

Uncontrolled diabetes

Uterine structure

Submucosal leiomyoma

Polyp • malformation

Vascular / immune / infectious

Antiphospholipid syndrome

Infection • immune dysregulation

Slide 19 · Chromosomal abnormalities drive many early losses

Aneuploidy, polyploidy, and chromosomal translocations are major fetal factors.

Chromosomal anomalies in approximately half of early abortuses.

Additional subtle genetic defects may evade routine testing.

A detected fetal chromosome anomaly identifies a mechanism, not necessarily a maternal disorder.

Slide 20 · Maternal factors may disrupt implantation

Endocrine

Hormonal / metabolic support

Structural

Uterine implantation site

Vascular

Maternal placental perfusion

Impaired establishment or maintenance of pregnancy

Slide 21 · Pregnancy loss: Vascular, infectious, immune factors

Antiphospholipid syndrome, coagulopathy, and hypertension may compromise maternal vessels.

Pathogens can ascend from the cervicovaginal tract or spread hematogenously.

Ascending infection is particularly relevant to second-trimester losses.

Disturbed maternal tolerance of fetal trophoblast may contribute to recurrent loss.

Slide 22 · Maternal immune tolerance protects the hemi-allograft

The fetoplacental unit carries paternal genetic material.

The maternal immune system must support extravillous trophoblast invasion without destructive rejection.

Robbins implicates disturbances in innate and adaptive immunity in some recurrent miscarriages.

Defective regulatory T-cell activity is discussed as a possible mechanism, not a universal explanation.

Slide 23 · Ectopic pregnancy: Implantation outside the uterine cavity

Normal site

Endometrial uterine cavity

Most frequent ectopic site

Fallopian tube

Other sites

Ovary • abdomen • scar • interstitial region

An extrauterine location cannot accommodate normal placental invasion and growth.

Fallopian tube as the dominant site (~90%).

Slide 24 · Tubal scarring is a major ectopic risk factor

Chronic salpingitis from pelvic inflammatory disease can scar the tubal lumen.

Peritubal adhesions can follow endometriosis, appendicitis, or abdominal/pelvic surgery.

Prior surgery and abnormal tubal transport can impair passage toward the uterine cavity.

Some ectopic pregnancies occur in tubes without recognizable lesions.

Slide 25 · Tubal pregnancy progresses from implantation to rupture

Tubal implantation

Trophoblast invades wall

Tubal distension

Wall thinning / rupture

Rupture can cause massive intraperitoneal hemorrhage and shock.

Slide 26 · Morphology of tubal ectopic gestation

Immature villi and trophoblast implant within the tubal lumen.

Trophoblast and villi invade the tubal wall as gestation develops.

The tube becomes distended; Hematosalpinx is an important morphologic clue.

Rupture produces hemorrhage into the peritoneal cavity.

Slide 27 · Ruptured ectopic pregnancy is an emergency

Abdominal pain and vaginal bleeding may occur after several weeks of amenorrhea.

Rapid intraperitoneal blood loss can cause an acute abdomen and hemorrhagic shock.

Investigation may use serial HCG assessment and pelvic ultrasonography.

Endometrial decidual change without villi may support—but alone does not prove—extrauterine implantation.

Clinical pathway is source-derived; It does not replace urgent patient-specific care.

Slide 28 · Miscarriage versus ectopic pregnancy

Feature

Spontaneous abortion

Tubal ectopic pregnancy

Primary process

Loss of an intrauterine gestation

Implantation within fallopian tube

Key mechanisms

Fetal genetic and maternal factors

Scarring / altered tubal passage

Morphologic clue

Products of conception may be present

Hematosalpinx; Villi invade tube

Immediate hazard

Bleeding; Retained gestational tissue

Tubal rupture; Intraperitoneal hemorrhage

Slide 29 · Second trimester: Demand exceeds placental reserve

Fetal metabolic and nutritional needs rise rapidly during the second trimester.

An immature placenta has relatively limited reserve for exchange.

Infection, placental hypoplasia, and diminished fetal vascular perfusion may precipitate loss.

The same lesions may cause fetal demise earlier than they would at term.

Slide 30 · Fetal vascular malperfusion: Mechanism

Cord or fetal vessel obstruction

Fetal blood-flow reduction

Villous thrombosis / ischemia

Avascular villi

Cord compression or thrombosis may produce a pattern of fetal-side villous injury.

Slide 31 · Umbilical cord pathology compromises fetal blood flow

True knots, kinking, prolapse, and compression can obstruct umbilical vessels.

Acute obstruction may cause fetal death while leaving few specific placental changes.

Chronic or intermittent compromise can produce fetal vascular thrombi and avascular villi.

Fetal vascular lesions should be interpreted with cord and clinical findings.

Slide 32 · Maternal versus fetal vascular malperfusion

Maternal vascular malperfusion

Fetal vascular malperfusion

Primary circulation

Uteroplacental / spiral arteries

Umbilical or fetal placental vessels

Proximal defect

Poor maternal supply to intervillous space

Impaired flow within fetal circulation

Typical findings

Infarcts; Distal villous hypoplasia

Thrombi; Avascular villi

Clinical associations

Growth restriction; Preeclampsia

Cord lesions; Fetal compromise

Slide 33 · Twin placentation determines shared vascular risk

Dichorionic diamniotic

Chorionic compartments: 2

Amniotic sacs: 2

Monochorionic diamniotic

Chorionic compartments: 1

Amniotic sacs: 2

Monochorionic monoamniotic

Chorionic compartments: 1

Amniotic sacs: 1

Slide 34 · Twin-to-twin transfusion follows unequal shunting

Shared monochorionic placenta

Placental vascular anastomoses

Donor twin

Relative underperfusion

Recipient twin

Fluid overload

Slide 35 · Third-trimester placental pathology: A clinical map

Fetal-side flow

Umbilical cord lesions • thrombi

Maternal-side flow

Placental infarction • malperfusion

Implantation

Previa • accreta spectrum

Inflammation

Membrane or villous infection

Slide 36 · Maternal vascular malperfusion: Core mechanism

Inadequate maternal delivery of blood to the intervillous space produces placental ischemia.

Causes include abnormal implantation/remodeling and maternal vascular disease.

Consequences range from fetal growth restriction to severe uteroplacental injury.

The pathologic diagnosis is based on a constellation of findings rather than one isolated lesion.

Slide 37 · Morphologic pattern of maternal vascular malperfusion

Placental hypoplasia

Weight below gestational-age expectation

Infarcts

Ischemic parenchymal injury

Decidual vasculopathy

Abnormal spiral vessel remodeling

Villous ischemia

Distal villous hypoplasia / syncytial knots

Slide 38 · Placental infarcts reflect reduced maternal supply

Infarction is one recognized component of maternal vascular malperfusion.

An ischemic placenta may show numerous or extensive infarcts.

Placental weight and infarct burden require interpretation relative to gestational age.

Infarction and impaired flow help explain uteroplacental insufficiency and restricted fetal growth.

Slide 39 · Abnormal implantation: Two distinct clinical hazards

Placenta previa

Implantation over / near internal cervical opening

May cause severe bleeding in late pregnancy

Placental location is the principal abnormality

Placenta accreta spectrum

Decidua deficient at implantation site

Villi appose or extend into myometrium

Failure of separation may cause postpartum hemorrhage

These disorders may coexist but are not synonyms.

Slide 40 · Placenta previa: Malpositioned implantation

Placental tissue lies in the lower uterine segment and covers the cervical region.

May be associated with significant third-trimester hemorrhage.

Bleeding risk arises from placental attachment at the site of cervical change.

Placental site and obstetric context determine management.

Slide 41 · Placenta accreta spectrum: Loss of the decidual plane

Normal separation plane

Placental villi

Decidua

Myometrium

Decidual interface between villi and myometrium

Accreta spectrum

Placental villi

Myometrium

Focally absent decidua: Direct villous–myometrial contact

Slide 42 · Placental infection: Two routes, different tissues

Ascending route

Microbes ascend from the cervicovaginal canal

Usually involve membranes and amniotic fluid

Acute chorioamnionitis with neutrophils

Hematogenous route

Bloodstream transmission from maternal infection

Microbes reach placental villi

Often associated with chronic villitis

The route of infection predicts the predominant inflammatory compartment.

Slide 43 · Acute chorioamnionitis: Maternal response

Ascending bacterial infection can inflame amnion and chorion.

Amniotic fluid may appear cloudy or purulent.

Maternal neutrophils infiltrate placental membranes.

Local inflammation may accompany premature rupture of membranes or preterm delivery.

Slide 44 · Maternal and fetal inflammatory responses differ

Response

Principal site

Interpretation

Maternal acute chorioamnionitis

Chorion-amnion membranes

Maternal neutrophilic response

Fetal inflammatory response

Umbilical vessels / chorionic plate vessels

Fetal vasculitic response

Hematogenous villitis

Chorionic villi

Inflammation in exchange parenchyma

Slide 45 · Hematogenous infection predominantly affects villi

Maternal sepsis, viremia, or parasitemia can seed the placenta.

Transplacental infections may cause chronic villitis.

Infectious villitis is associated with impaired fetal growth and infection risk.

Pathogen identification requires clinicopathologic correlation; A pattern alone is not species-specific.

Slide 46 · Placental infectious patterns: Diagnostic comparison

Process

Main compartment

Usual pattern

Ascending infection

Membranes / amniotic fluid

Neutrophilic chorioamnionitis

Fetal response

Umbilical / chorionic vessels

Inflammation of fetal vessels

Transplacental infection

Villi

Villitis; Often chronic

Uncommon bloodborne bacteria

Villi / intervillous region

May elicit acute inflammation

Slide 47 · Preeclampsia: Placental disease with systemic effects

A maternal syndrome with new-onset hypertension after 20 weeks and evidence of organ involvement.

Maternal endothelial dysfunction is central to its manifestations.

Renal, hepatic, hematologic, pulmonary, and neurologic complications may occur.

Eclampsia denotes seizures complicating the syndrome.

Textbook clinical description is retained; No separate external guideline criteria are asserted.

Slide 48 · Preeclampsia complications follow endothelial injury

Placenta-derived endothelial disturbances

Vasoconstriction

Hypertension

Leaky endothelium

Edema / proteinuria

Prothrombotic state

Organ microthrombi

Slide 49 · Preeclampsia begins with defective placentation

Shallow trophoblast invasion

Failed spiral artery remodeling

Placental ischemia

Late maternal syndrome

The vascular defect begins early; Clinical manifestations commonly appear later.

Slide 50 · Normal remodeling versus preeclamptic placentation

Normal

Extravillous trophoblast enters vessel walls

Smooth-muscle media reduced

Large-caliber, low-resistance uteroplacental vessel

Preeclampsia

Invasion and remodeling are incomplete

Spiral arteries retain resistance-vessel character

Placental supply may become inadequate as fetal demands grow

Shallow implantation is an initiating lesion, not merely a consequence of late hypertension.

Slide 51 · Antiangiogenic mediators link placenta to maternal vessels

Ischemic placental tissue

↑ sFlt-1 + ↑ soluble endoglin

Reduced VEGF activity

Reduced TGF-β signaling

These pathways converge on endothelial dysfunction and impaired vasodilator/antithrombotic signaling.

Slide 52 · Endothelial dysfunction explains systemic injury

Maternal endothelial dysfunction

Vascular tone

Vasoconstriction • hypertension

Permeability

Proteinuria • edema

Hemostasis

Microthrombi • ischemia

Slide 53 · Preeclampsia generates a prothrombotic state

Widespread endothelial injury favors microvascular thrombus formation.

Placenta, kidneys, liver, brain, and pituitary may be affected.

Reduced VEGF signaling may lower endothelial prostacyclin (PGI₂) activity.

The resulting imbalance promotes coagulation and tissue hypoperfusion.

Slide 54 · Placental lesions associated with preeclampsia

Placental hypoplasia

Low placental mass for gestation

Infarction

Extensive ischemic foci

Distal villous hypoplasia

Small, shrunken villi; Syncytial knots

Decidual arteriopathy

Acute atherosis / fibrinoid necrosis

Slide 55 · Renal and hepatic pathology in severe preeclampsia

Kidney

Glomerular endothelial swelling

Endothelial-side dense material / fibrin

In severe cases, glomerular and cortical thrombosis

Liver

Subcapsular or intraparenchymal hemorrhage

Microvascular fibrin thrombi

Focal hemorrhagic necrosis

Clinical pathology includes proteinuria, renal failure, and hepatic complications.

Slide 56 · Gestational hypertension, preeclampsia, eclampsia, HELLP

Term

Defining feature context

Gestational hypertension

New pregnancy-associated hypertension without preeclampsia features

Preeclampsia

New hypertension plus evidence of maternal systemic involvement

Eclampsia

Seizures complicating preeclampsia

HELLP syndrome

Hemolysis • elevated liver enzymes • low platelets

Slide 57 · Gestational trophoblastic disease: A spectrum

Gestational trophoblastic disease

Hydatidiform mole

Complete • partial • invasive

Choriocarcinoma

Highly malignant, villi absent

Extravillous tumors

PSTT • ETT

Slide 58 · Complete mole: Androgenetic diploid concept

Ovum without maternal nuclear genome

Sperm genetic contribution

Paternal-only diploid nuclear genome

Commonly: One sperm genome duplicates → 46,XX.

Less commonly: Dispermy of an empty ovum → 46,XX or 46,XY.

Embryonic development is absent in typical complete mole.

Slide 59 · Partial mole: Usually diandric triploidy

Normal maternal haploid genome

Two sperm contribute paternal genomes

Triploid conceptus

Typical triploid constitutions include 69,XXY and 69,XXX.

Some fetal development may occur but is abnormal.

Persistent molar disease is possible; Postmolar choriocarcinoma is uncommon.

Slide 60 · Complete versus partial mole: Diagnostic morphology

Feature

Complete mole

Partial mole

Villi

Diffuse enlarged, hydropic villi

Subset enlarged, often scalloped

Trophoblast

Marked circumferential proliferation

More focal / mild proliferation

Villous outline

Typically smooth, rounded

Irregular; Trophoblastic inclusions

Embryonic tissue

Absent

May be present

Typical genetics

Paternal-only diploid

Usually triploid

Slide 61 · Hydatidiform mole: Clinical recognition and follow-up

Abnormal ultrasound appearance or early miscarriage may prompt evacuation.

HCG levels in complete mole can substantially exceed those in normal pregnancy.

Molar villi are hydropic; Histologic assessment distinguishes complete and partial patterns.

Serial HCG follow-up after evacuation detects persistent trophoblastic disease.

Slide 62 · Persistent HCG after molar evacuation is a warning

Evacuation of molar tissue

Serial HCG monitoring

Failure to normalize

Evaluate persistent trophoblastic disease

Persistent HCG warrants assessment for invasive mole or choriocarcinoma; No patient-specific protocol is depicted.

Slide 63 · Invasive mole: Villi extend into myometrium

Hydropic villi with trophoblastic proliferation penetrate the uterine wall.

Myometrial infiltration may cause persistent bleeding and uterine enlargement.

HCG may remain elevated following evacuation.

Villi may extend into vessels and extrauterine sites; Unlike choriocarcinoma, villi are present.

Slide 64 · Choriocarcinoma: Malignant trophoblast without villi

The lesion comprises proliferating malignant cytotrophoblast and syncytiotrophoblast.

Chorionic villi are absent, a decisive morphologic distinction from invasive mole.

Gross tumors show extensive hemorrhage and necrosis.

Destructive vascular invasion permits early hematogenous metastasis.

Slide 65 · Three major malignant trophoblastic patterns

Entity

Distinguishing morphology

Clinical tendency

Invasive mole

Hydropic chorionic villi invading myometrium

Persistent HCG; Occasional emboli

Choriocarcinoma

Malignant biphasic trophoblast; Villi absent

Hemorrhagic invasion and metastases

Placental site trophoblastic tumor

Mononuclear extravillous trophoblast; Vessel tropism

Uterine mass; Variable HCG

Epithelioid trophoblastic tumor

Mononuclear epithelioid cells; Hyaline material

Mass lesion; Metastatic potential

Slide 66 · Gestational choriocarcinoma: Clinical behavior

May arise after molar pregnancy, miscarriage, or apparently normal gestation.

Bleeding can present during or after pregnancy; Diagnosis may be delayed.

Common metastatic destinations include lung and vagina.

Gestational choriocarcinoma is highly chemosensitive, unlike its nongestational counterpart.

Slide 67 · Extravillous trophoblast tumors: PSTT and ETT

Placental site trophoblastic tumor (PSTT) is composed of invasive mononuclear extravillous trophoblast.

PSTT may infiltrate myometrium and show affinity for maternal vessels.

Epithelioid trophoblastic tumor (ETT) comprises epithelioid mononuclear trophoblast and hyaline material.

Both lesions can be malignant; Their morphology differs from biphasic choriocarcinoma.

Slide 68 · Pathologic interpretation: Integrate location and lesion

Site of gestation

Intrauterine versus ectopic

Compartment

Villi • membranes • cord • decidua

Pattern

Ischemia • inflammation • trophoblast

Clinical context

Gestational age • fetal growth • maternal disease

Slide 69 · Applied case: Early pregnancy with shock

A patient with amenorrhea, pelvic pain and vaginal bleeding develops hypotension. At surgery, a distended fallopian tube and hemoperitoneum are found.

What is the most likely lesion?

What histologic structures establish gestational implantation?

Why can the lesion become immediately life-threatening?

Slide 70 · Case interpretation: Ruptured tubal pregnancy

The combination of a tubal gestation and intraperitoneal bleeding supports ruptured ectopic pregnancy.

Chorionic villi and trophoblast within tubal tissue demonstrate implantation.

Invasion and distension may thin and rupture the tubal wall.

Massive blood loss is the immediate mechanism of hemodynamic collapse.

Slide 71 · Applied case: Hypertension with fetal growth restriction

After midgestation, new maternal hypertension and proteinuria accompany fetal growth restriction. Placental examination shows infarcts, small distal villi and abnormal decidual arteries.

Which placental vascular process explains the findings?

How does abnormal early implantation produce a late maternal syndrome?

What maternal organs may be damaged by endothelial dysfunction?

Slide 72 · Case interpretation: Preeclampsia with malperfusion

The placental pattern supports maternal vascular malperfusion.

Defective spiral artery remodeling can limit placental perfusion.

Placenta-derived antiangiogenic mediators contribute to widespread endothelial dysfunction.

Maternal renal, hepatic, cerebral and hematologic complications may follow.

Slide 73 · Applied case: Enlarged hydropic chorionic villi

After evacuation of an abnormal early gestation, pathology shows enlarged hydropic villi and trophoblast proliferation. The clinician asks whether this is complete or partial mole and whether surveillance is needed.

What microscopic patterns distinguish the mole types?

What genetic origin supports complete mole?

Why does persistently elevated HCG matter after evacuation?

Slide 74 · Case interpretation: Hydatidiform mole

Complete mole has diffuse villous hydropic enlargement with circumferential trophoblast hyperplasia.

Partial mole shows heterogeneous scalloped villi, inclusions, and more focal proliferation.

Complete mole usually has a paternal-only diploid nuclear genome.

Persistent postevacuation HCG can indicate invasive/persistent trophoblastic disease.

Slide 75 · Synthesis: Lesion → compartment → clinical consequence

Pathology

Diagnostic compartment

Principal consequence

Tubal ectopic pregnancy

Fallopian tube villi / trophoblast

Rupture, hemorrhage

Fetal malperfusion

Cord / fetal villous vessels

Fetal ischemia; Avascular villi

Maternal malperfusion

Decidua / intervillous supply

Growth restriction; Infarcts

Ascending infection

Membranes / fetal vessels

Preterm delivery / perinatal injury

Preeclampsia

Placental bed plus maternal endothelium

Hypertension and organ dysfunction

Gestational trophoblastic disease

Villous / extravillous trophoblast

Persistent disease or malignancy

Slide 76 · Selected reference

Robbins, Cotran & Kumar

Pathologic Basis of Disease

11th edition (2026)

Foundational pathology reference