Disorders of Pregnancy Flashcards

1
Q

How common is Pre-Eclampsia?

A

Occurs in around 2-4% of pregnancies in USA and Europe (incidence rising?)

More common in Africa and Asia (8% to as high as 16%?)

~1/10 maternal deaths in Africa and up to 1/4 in South America are associated with gestational hypertensive disorders (including PE).

Estimated to cause 50,000-60,000 maternal deaths per year

Precise underlying causes remain a mystery

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2
Q

What are the symptoms of Pre-Eclampsia?

A

New onset hypertension (in a previously normotensive woman) BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic
Occurring after 20 weeks’ gestation

Reduced fetal movement and/or amniotic fluid volume (by ultrasound) in 30% cases

Oedema common but not discriminatory for PE
Headache (in around 40% of severe PE patients)
Abdominal pain (in around 15% of severe PE patients)
Visual disturbances, seizures and breathlessness associated with severe PE and risk of eclampsia (seizures)

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3
Q

What happens in Early onset PE?

A

Early onset: <34 weeks
Associated with fetal and maternal symptoms
Changes in placental structure

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4
Q

What happens in late onset PE?

A
Late onset: >34 weeks
More common (90%)
Mostly maternal symptoms
Fetus generally OK
Less overt/no placental changes
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5
Q

What are the risk factors for PE?

A

Previous pregnancy with pre-eclampsia
BMI >30 (esp >35)
Family history
Increased maternal age (>40, <20?)
Gestational hypertension or previous hypertension
Pre-existing conditions: diabetes, PCOS, renal disease, subfertility, autoimmune disease.
Non-natural cycle IVF?

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6
Q

What are the risks to the mother and foetus in PE?

A

Mother: damage to kidneys, liver, brain and other organ systems
Possible progression to eclampsia (seizures, loss of consciousness)

Placental abruption (separation of the placenta from the endometrium)

Fetus: reduced fetal growth, preterm birth, pregnancy loss/stillbirth

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7
Q

What goes wrong in the Placenta in PE?

A

EVT invasion of maternal spiral arteries is limited to decidual layer. Spiral arteries are not extensively remodelled, thus placental perfusion is restricted.

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8
Q

What is PLGF?

A

Placental Growth Factor

VEGF related, pro-angiogenic factor released in large amounts by the placenta.

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9
Q

What is Flt1?

A

Flt1 (soluble VEGFR1)

Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailabliltiy.

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10
Q

What happens in PE with Flt1?

A

excess production of Flt-1 by distressed placenta leads to reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfuction.

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11
Q

How can you predict onset of PE?

A

PLGR levels alone or Flt-1/PlGR ratio can be used to predict onset of PE

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12
Q

How is PE managed?

A

PE can only be resolved by delivery of the placenta

If <34 weeks, preferable to try and maintain the pregnancy if possible for benefit of the fetus
If >37 weeks, delivery preferable
In between – case by case basis.

Anti-hypertensive therapies.
Corticosteroids for <34 weeks to promote fetal lung development before delivery.

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13
Q

What are the 3 ways to prevent PE?

A

Weight loss (esp if BMI >35)

Exercise throughout pregnancy (seems to work independent of BMI)

Low-dose asprin (from 11-14 weeks) for high risk groups – but may only prevent early onset.

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14
Q

What are the long term effects of PE on the mothers health?

A

Elevated risk of cardiovascular disease, type 2 diabetes and renal disease after PE

Roughly 1/8 risk of having pre-eclampsia in next pregnancy (greater if early onset)

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