Gestational Disorders Flashcards

1
Q

Spontaneous Abortion/Miscarriage

A

Loss of pregnancy before 20 weeks gestation

Occurs in 10-20% of recognized pregnancies, and as many as 40% of hCG positive pregnancies

Signs include vaginal bleeding, lower abdominal pain, cramping with a positive test

May pass products of contraception (placental tissue, fetal fragments, amniotic sac remnants, endometrium pieces)

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2
Q

What are the causes of spontaneous abortion?

A

FIRST SEMESTER - mainly chromosomal malformations (Trisomy 21, 18, 13, 16; Triploidy - 69 chromosomes; Turner’s Syndrome - 45 XO - only disorder associated with bilateral cystic hygroma

2nd Trimester –> organ specific malformations (13-19 weeks) are the main cause (anencephaly, congenital heart defects) - also associated with inflammatory conditions

3rd Trimerster – vascular pathologies such as pre-eclampsia/eclampsia

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3
Q

Hydrops Fetalis

A

Characterized by a MARKEDLY EDEMATOUS FETUS (esp face and abdomen)

95% of the time it is NON-IMMUNE cause (Turner’s, Trisomies, fetal anemia, infections, CV defects), but 5% of the time it is due to Rh INCOMPATIBILITY

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4
Q

Pre-Eclampsia/Eclampsia

A

Pre-eclampsia = pregnancy induced HTN, proteinuria, edema; Eclampsia = pre-eclampsia + seizures!

5-10% of pregnancies get pre-eclampsia, usually in the THIRD TRIMESTER in women OLDER THAN 35

Deliver baby as early as possible (safely) to prevent thrombi from entering CNS and causing full fledged eclampsia

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5
Q

Causes of Pre-Eclampsia

A

Vascular etiology

NORMAL –> fetal extravillous trophoblastic cells (those not associated with chorionic villi) at the implantation site invade the maternal decidua and decidual vessels, destroy the vascular smooth muscle and replace the maternal endothelial cells with fetal trophoblastic cells) –> this process converts the spiral arteries from SMALL CALIBER to LARGER CAPACITY urteroplacental vessels lacking a smooth muscle coat

IN PRE-ECLAMPSIA –> there is a failure of the trophoblasts to invade the walls of the vessels, resulting in DECREASED BF THROUGH THE PLACENTA and an ABNORMALLY SMALL and INFARCTED PLACENTA (the above remodeling DOES NOT happen, so the placenta is ILL-EQUIPPED to meet the needs of late-gestation –> placental ischemia!)

Results in fetal growth retardation, spontaneous abortion can result

Anti-angiogenic substance release in UNREGULATED and the result is VASOCONSTRICTION –> HTN! Endothelial dysfunction or injury could result in THROMBI FORMATION (DIC) –> kidney damage and proteinuria in mom

IF THROMBI ENTER THE CNS –> SEIZURES –> ECLAMPSIA!!!!!!

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6
Q

Histology of Pre-Eclampsia

A

FIBRINOID NECROSIS and INTRAINTIMAL LIPID DEPOSITION –> ACUTE ATHEROSIS –> Diagnostic of the disease!

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7
Q

Intrauterine Infections

A

Two mechanisms –> ASCENDING and HEMATOGENOUS

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8
Q

Ascending Intrauterine Infections

A

Organisms of the vagina move through the cervix and pass through intact or rupture membranes into the AMNIOTIC FLUID and then to the FETUS

Group B Strep –> colonize the vagina in 15-25% of preggos –> bacteria infect membranes (CHORIOAMNIONITIS) and pass to the amniotic fluid

Inflammation of the umbilical cord (funisitis) indicates fetal response to infection

Infected amniotic fluid enters lungs –> Congenital PNEUMONIA –> 3/1000 births

Other common infections –> E. Coli, Staph, Haemophilus, Proteus, Klebsiella, Pseudomonas

Chorioamnionitis is characterized by EXTRA-PLACENTAL MEMBRANE INFECTION –> normally the membranes are THIN AND CLEAR at delivery, but THICK AND YELLOW MEMBRANES are a clue

Histology –> acute inflammation (neutrophils) and the fetus may have neuro deficits

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9
Q

Hematogenous Infections

A

From the MATERNAL CIRCULATION across the TROPHOBLAST CELLS into the FETAL CIRCULATION

Occurs with TORCHS organisms (Toxo, other, Rubella, CMV, Herpes, Syphilis) –> associated with HYDROPS, HEPATOSPLENOMEGALY, GROWTH RETARDATION, CNS DAMAGE, PETECHIAE, PLACENTAL VILLITIS, DIC

Listeria –> can cause abscess formation in the placenta and result in RECURRENT PREGNANCY LOSS

Parvovirus –> Infects RBCs and can cause HYDROPS; anemia occurs that can result in HEART FAILURE and MARKED FETAL EDEMA; inclusions would be seen in RBCs

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10
Q

What can fetal alcohol syndrome present as?

A

Fetal growth retardation, small jaw, joint anomalies, small palpebral fissures (separation between eyelids), cardiac and CNS effects

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11
Q

Ecotopic Pregnancy

A

Implantation of the fetus in ANY OTHER site than a normal intrauterine location –> 1/150 pregnancies

Most common site is the FALLOPIAN TUBE (ampulla, isthmus) but can also implant in the OVARY or ABDOMEN

Risk factors –> inflammation or scarring of the tubes (salpingitis in 35-50%), prior ectopic pregnancy, surgery, developmental abnormalities –> HOWEVER, most of the time, none of these are present

Clinical Features –> Severe abdominal pain about 6 weeks after a previously normal menstrual period, abnormal bleeding, amenorrhea, adnexal tenderness (fallopian tube/ovary tenderness), lack of uterine enlargement

If detected early, the fetus may not be visible, but ectopic chorionic villi will be noted

Later, a small fetus may be seen

Rupture of a tubal pregnancy can occur, causing hemorrhage into the peritoneum

Often clinically misdiagnosed as appendicitis!!!

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12
Q

Abruptio Placentae

A

Occurs when normal implantation takes place, but the PLACENTA SEPARATES FROM THE UTERUS PREMATURELY in the 3rd trimester

Results in vaginal bleeding and several potential mother/fetal complications

If there is ONLY PARTIAL SEPARATION of the placenta, then concealed hemorrhage can occur, resulting in DECREASED FETAL PERFUSION and DEATH

1/120 live births

Associated with maternal HTN, chorioamnionitis, increased age, smoking, cocaine use

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13
Q

Placental Accreta

A

Occurs when the placenta/chorionic villi is ABNORMALLY ADHERENT to the MYOMETRIUM, making it difficult to deliver the placenta (due to an absence of the DECIDUA, the uterine lining during pregnancy)

If bleeding is too severe –> hysterectomy

Uterine perforation is also possible

Important cause of post-partum bleeding

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14
Q

Placenta Previa

A

Condition in which the placenta IMPLANTS IN THE LOWER UTERINE SEGMENT OR CERVIX, often with serious 3rd trimester bleeding

Blocks the cervical os, indication for a C-section

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15
Q

Umbilical cord problems

A

Strictures (abnormally narrowing), torsion, knots, nuchal cord, cord prolapse, single umbilical artery (usually 2 arteries and a vein)

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16
Q

Gestational Trophoblastic Disease

A

Characterized by ABNORMAL PROLIFERATION OF TROPHOBLASTIC CELLS in pregnancy

In a normal placenta, there are VILLI filled with FETAL RBCS and trophoblasts, surrounded by MATERNAL RBCs

Abnormalities in this makeup indicate gestational trophoblastic disease

Constitutes a spectrum of tumors and tumor-like conditions characterized by proliferation of placental tissue, either villous or trophoblastic

17
Q

HYDATIDIFORM MOLES (overview)

A

Represent a defect in fertilization and are characterized by VILLOUS SWELLING and TROPHOBLASTIC HYPERPLASIA (1/2000 pregnancies)

Can be COMPLETE or PARTIAL

Present commonly with abnormal vaginal bleeding and is the most common precursor of CHORIOCARCINOMA; Can lead to uterine rupture

18
Q

COMPLETE Moles

A

80%

Presents with HTN, molar tissue passage, uterine size greater than it should be (at time of checkups)

HCG is elevated

DIPLOID KARYOTYPE –> 90% have 46 XX with both sets paternally derived –> can occur from 1 sperm fertilizing an empty ovum, or 2 sperm fertilizing an empty ovum

GROSSLY –> diffuse swelling of ALL CHORIONIC VILLI (grape-like clusters) with an ABSENT FETUS

Histology –> UNIFORM DILATION of VILLI with clear fluid, trophoblast hyperplasia, absent villous capillaries

After evacuation, 80% spontaneously regress –> of the remaining 20%, 2% develop choriocarcinoma, 18% an invasive mole

19
Q

PARTIAL Moles

A

20%

Usually present with a MISSED ABORTION (HCG levels slightly elevated/normal)

Molar villi have a TRIPLOID KARYOTYPE –> Majority are XXY (2 sperm in one normal ovum)

Uterus will be NORMAL or SMALLER than it should be at the time of checkup

Grossly –> mass of thin-walled, translucent, custic, GRAPE-LIKE structures consisting of sweollen edematous villi; FETAL PARTS frequently seen!!!!

Histology –> DILATED EDEMATOUS VILLI with NORMAL VILLI

20
Q

Treatment of Hydatidiform Moles

A

BOTH begin with UTERINE CURETTAGE to remove the products of conception

Monitor HCG levels

If HCG returns to normal, no further treatment is needed (note: normal = undetectable)

Increase/Plateau in HCG –> may indicate INCOMPLETE EVACUATION of the mole – persistent disease!

In rare cases it could be INVASIVE! Myometrium has been invaded (uterine rupture, hemoperitoneum, much like an ectopic pregnancy)

Could be CHORIOCARCINOMA –> can occur DURING or FOLLOWING a normal pregnancy, or COMPLETE molar pregnancy (2% of the time) and is GENERALLY WELL CONTROLLED WITH CHEMO

PARTIAL moles RARELY DEVELOP INTO CHORIOCARCINOMA!!!!