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brs (phase 1b) > (dev&age) disorders of pregnancy and parturition: pre-eclampsia > Flashcards

(dev&age) disorders of pregnancy and parturition: pre-eclampsia Flashcards

1
Q

what is the epidemiology of pre-eclampsia?

A

approx in 2-4% of pregnancies in USA and Europe

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2
Q

in which part of the world is pre-eclampsia most common?

A

mostly Africa and Asia

almost 1 in 10 maternal deaths in Africa are associated with GHDs like PE

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3
Q

how many maternal deaths are caused by pre-eclampsia per year?

A

approx 50,000-60,000 maternal death per year

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4
Q

what is a GHD?

A

gestational hypertensive disorder (includes pre-eclampsia)

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5
Q

which category of people are affected by pre-eclampsia?

A

pregnant women

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6
Q

when does pre-eclampsia usually develop in pregnant women?

A

usually occurs 20 weeks post gestation

can also occur up to 6 weeks after delivery

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7
Q

what are the two cardinal features of pre-eclampsia?

A

new-onset hypertension (in a previously normotensive woman)

proteinuria

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8
Q

what protein-creatinine ratio is expected in a pre-eclamptic woman?

A

a PCR > 30 mg/mmol

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9
Q

what diastolic and systolic pressure is expected in a pre-eclamptic woman?

A

≥140 mmHg systolic

and/or

≥90 mmHg diastolic

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10
Q

what is proteinuria an indication of?

A

marker of kidney damage

can also affect the retina, brain and liver

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11
Q

differentiate between pre-eclampsia and eclampsia

A

pre-eclampsia presents with new-onset hypertension whereas the presentation of hypertension ALONGSIDE seizures occurs in eclampsia

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12
Q

in pre-eclampsia, how are fetal movements and the amniotic fluid volume affected and why?

A

reduced fetal movements

reduced amniotic fluid volume

(PE associated with placental hypoperfusion so nutrient supply reduced = intrauterine growth restriction and oligohydramnios)

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13
Q

what are the main symptoms of severe pre-eclampsia?

A

headache

oedema (cerebral, pulmonary, generalised)

abdominal pain (commonly RUQ)

visual disturbances

seizures

breathlessness

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14
Q

what are the two main subtypes of pre-eclampsia?

A

early-onset PE (<34 weeks)

late-onset PE (>34 weeks)

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15
Q

when does early-onset pre-eclampsia occur?

A

before 34 week gestation

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16
Q

when does late-onset pre-eclampsia occur?

A

after 34 week gestation

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17
Q

what are the features of early-onset pre-eclampsia?

A

associated with fetal AND maternal changes

changes in placental structure

(may experience more distress)

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18
Q

what are the features of late-onset pre-eclampsia?

A

associated with mostly maternal changes (fetus is usually unaffected)

less overt/no changes in placental structure

(more common)

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19
Q

differentiate between early and late-onset pre-eclampsia

A

while EOPE is associated w both maternal and fetal changes, LOPE is associate w only maternal changes as the fetus is unaffected

EOPE results in placental changes wheres LOPE does not usually

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20
Q

which subtype of pre-eclampsia is more common?

A

late-onset pre-eclampsia

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21
Q

which symptom of pre-eclampsia increases the risk of eclampsia?

A

the occurrence of seizures

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22
Q

what is HELLP syndrome?

A

a subtype of severe pre-eclampsia characterised by

H = haemolysis
E = elevated
L = liver enzymes
L = low
P = platelets
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23
Q

what are the cardinal features of HELLP syndrome?

A

haemolysis, elevated liver enzymes and low platelet count

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24
Q

what are the classifications of HELLP syndrome?

A

mild and severe

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25
Q

what protein measurement is expected in a pre-eclamptic woman’s 24-hour urine specimen?

A

a ≥0.3 g protein measurement in a 24-hour urine specimen

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26
Q

what maternal risk factors pre-dispose to pre-eclampsia?

A

previous pregnancy with pre-eclampsia

BMI > 30 (esp age > 35)

family history

increased maternal age (>40 or maybe even <20)

gestational/previous hypertension

pre-existing conditions: diabetes, PCOS, renal disease, subfertility, autoimmune disease

women carrying multiple babies

nulliparity

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27
Q

define nulliparity

A

first-time mother

women who have not ever given birth to children

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28
Q

what are the risks to the mother of pre-eclampsia?

A

damage to the kidneys, brain, retina, liver and other organ systems

possible progression to eclampsia (if seizures/loss of consciousness occurs)

placental abruption (separation of the placenta from the endometrium)

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29
Q

what is placental abruption?

A

separation of the placenta from the endometrium

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30
Q

what are the risks to the fetus of pre-eclampsia?

A

reduced fetal growth or movements

premature birth

pregnancy loss

stillbirth

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31
Q

what are the implications of placental abruption?

A

placenta separates from the endometrium

reduced SA as part of the area of contact with the endometrium is lost

= reduced placental efficiency

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32
Q

what does placental abruption increase the risk of and why?

A

haemorrhage

as the placenta is heavily vascularised

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33
Q

which physiological process is affected in pre-eclampsia?

A

the remodelling of the maternal spiral arteries is impaired

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34
Q

explain how the spiral arteries are remodelled in a normal maternal myometrium

A

EVT invasion downwards into the maternal spiral arteries leads to endothelial and smooth muscle breakdown

EVT becomes endovascular EVT and so the spiral arteires become high capacity, low pressure conduits

increased blood flow to the placenta and therefore to the embryo to meet increased embryonic demand

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35
Q

what is EVT?

A

extra-villus trophoblast

36
Q

why does the EVT invade the maternal spiral arteries?

A

invades down into the maternal spiral arteries to cause the breakdown of the endothelium and smooth muscle to convert them into high-capacity, low-pressure conduits for increased blood flow to the embryo

37
Q

what is the impact of EVT invasion of the maternal spiral arteries?

A

causes the breakdown of the endothelium and smooth muscle to convert the spiral arteries into high-capacity, low-pressure conduits for increased blood flow to the embryo

38
Q

why is it important that the spiral arteries are remodelled?

A

to increase blood flow to the developing fetus via the placenta in order to meet the fetal demand

39
Q

what is the pathophysiology of pre-eclampsia?

A

spiral artery remodelling does not occur as extensively as normal

as EVT does not invade the spiral arteries further down than the decidual layer, less endothelium and smooth muscle is broken down so the spiral arteries remain narrow + high-pressure, low-capacity blood vessels

restricted placental perfusion = so blood flow to the developing fetus via the placenta is impaired = oxidative stress in placenta and fetus

so the embryonic demand for development cannot be met

40
Q

how is spiral artery remodelling affected in pre-eclampsia?

A

the EVT does not invade as far down the spiral arteries and is limited to the decidual layer

so the spiral arteries are not as extensively remodelled as normal (i.e. narrower than normal)

41
Q

how does the pathophysiology of pre-eclampsia affect the developing fetus?

A

as there is reduced placental perfusion and therefore oxidative stress in the placenta

= blood flow to the developing fetus is also impaired and so fetal oxygen demand cannot be kept up with

(i.e. can cause reduced fetal growth and reduced fetal movements)

42
Q

why is restricted placental perfusion in pre-eclampsia harmful?

A

blood flow to the developing fetus is impaired and so fetal oxygen demand cannot be kept up with

(i.e. can cause reduced fetal growth and reduced fetal movements)

43
Q

why is placental perfusion restricted in pre-eclampsia?

A

the spiral arteries are not as extensively remodelled to become high-capacity, low-pressure conduits and remain narrow

= reduced blood flow to the placenta (reduced placental perfusion)

= oxidative stress

44
Q

to which uterine layer is the EVT invasion restricted in pre-eclampsia?

A

decidual layer

45
Q

differentiate between the spiral artery structure in a normal myometrium and a pre-eclamptic myometrium

A

normal myometrium = low-pressure, high-capacity, wider spiral arteries

pre-eclamptic = high-pressure, low-capacity narrower spiral arteries

46
Q

what is PLGF?

A

placental growth factor

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

47
Q

what is Flt1?

A

receptor for VEGF-like factors which is bound to the endothelial cells

which binds to soluble angiogenic factors (like PLGF and VEGF) to limit their bioavailability

48
Q

what is VEGF?

A

the main, potent angiogenic factor that stimulates placental angiogenesis

49
Q

what is sFlt-1?

A

soluble version of Flt-1 that is not bound to the endothelial cells and is freely-circulating

also binds to the same soluble pro-angiogenic factors (VEGF, PLGF) that membrane-bound Flt-1 binds to

50
Q

which receptor-substrate complexes are required for the endothelium to be healthy?

A

PLGF should bind to Flt-1
VEGF should bind to Flt-1

(some PLGF and VEGF can bind to the freely-circulating sFlt-1 = but not as a priority)

51
Q

which receptor-substrate complexes compromise the health of the endothelium?

A

when PLGF and VEGF especially bind to the freely-circulating sFlt-1 more than the membrane-bound Flt-1

(therefore cannot have the vasodilative effects or anticoagulation and instead we have vasoconstriction and pro-coagulation)

52
Q

what do healthy endothelial cells stimulate?

A

vasodilation and anticoagulation

once stimulated by VEGF and PLGF binding to endothelial membrane-bound Flt-1

53
Q

what do dysfunctional endothelial cells stimulate?

A

vasoconstriction and pro-coagulation

54
Q

why is it important especially for pregnant women that their endothelial cells are NOT dysfunctional?

A

to prevent vasoconstriction (that risks pre-eclampsia) and pro-coagulation (that risks thrombi formation)

55
Q

describe what happens with then endothelial cells, PLGF, VEGF, Flt-1 and sFlt-1 in a healthy placental environment

A

normal amounts of PLGF, VEGF, and sFlt-1 are released by a healthy placenta

most of the VEGF and the PLGF bind to the endothelial membrane-bound Flt-1 receptor

= so vasodilation and anticoagulation is stimulated

56
Q

describe what happens with then endothelial cells, PLGF, VEGF, and a Flt-1 in a dysfunctional pre-eclamptic placental environment

A

in a pre-eclamptic placenta, less PLGF is released than normal and more sFlt-1 is produced

1) with less PLGF = less binding to Flt-1

2) with more sFlt-1 = more freely-circulating receptor for VEGF and PLGF
= ‘mops up’/binds to most of the placental PLGF and prevents it from binding to the Flt-1 (membrane-bound)

!! both 1 + 2 contribute to the reduced signal for vasodilation and anticoagulation AND SO increased signal for vasoconstriction and pro-coagulation !!

57
Q

explain why endothelial cell function is impaired in pre-eclampsia

A

the pre-eclamptic placenta produces less PLGF and more sFlt-1

1) with less PLGF = less binding to Flt-1

2) with more sFlt-1 = more freely-circulating receptor for VEGF and PLGF
= ‘mops up’/binds to/sequesters most of the placental PLGF and prevents it from binding to the Flt-1 (membrane-bound)

!! both 1 + 2 contribute to the reduced signal for vasodilation and anticoagulation AND SO increased signal for vasoconstriction and pro-coagulation !!

58
Q

what is the effect of PLGF binding on the maternal endothelium?

A

causes increased vasodilation and anticoagulation

59
Q

how is placental PLGF production altered during pre-eclampsia?

A

PLGF production is reduced in a pre-eclamptic placenta

60
Q

how is placental Flt-1 production altered during pre-eclampsia?

A

Flt-1 production is increased in a pre-eclamptic placenta

61
Q

why does endothelial dysfunction occur in pre-eclampsia?

A

excess production of sFlt-1 by distressed placenta

= reduction of available pro-angiogenic factors in maternal circulation (i.e. VEGF, PLGF)

= resulting in endothelial dysfuction

62
Q

what can be used to predict pre-eclampsia?

A

1) PLGF levels alone
2) sFlt-1/PlGF ratio (Elecsys immunoassay)

can be used to predict the onset of pre-eclampsia

63
Q

how can PLGF alone be used to predict pre-eclampsia?

A

in a triage test

wherein the serum PLGF level is measured

(PLGF = pro-angiogenic + responsible for placental angiogenesis)

64
Q

what PLGF level constitutes pre-eclampsia positive and is highly abnormal?

A

PLGF < 12 pg/ml

65
Q

what PLGF level constitutes pre-eclampsia positive and is mildly abnormal?

A

PLGF between 12-100 pg/ml

66
Q

what PLGF level constitutes pre-eclampsia negative?

A

PLGF > 100 pg/ml

67
Q

how is an abnormal PLGF result interpreted in a triage test?

A

increased risk for premature delivery

68
Q

how is a normal PLGF result interpreted in a triage test?

A

unlikely to progress to pre-eclampsia within 14 days of the test

69
Q

how can the sFlt-1/PLGF ratio be used to predict pre-eclampsia?

A

elecsys immunoassay

wherein the serum PLGF and sFlt-1 levels are measures and compared

70
Q

what is a positive result for pre-eclampsia in a Elecsys immunoassay?

A

> 38

(i.e. sFlt-1 should be elevated and PLGF should be reduced = bigger ratio as ‘top number’ is increased while ‘bottom number’ is reduced)

71
Q

what is a negative result for pre-eclampsia in a Elecsys immunoassay?

A

< 38

72
Q

how is a positive Elecsys immunoassay interpreted?

A

increased risk of pre-eclampsia and premature delivery

73
Q

how is a negative Elecsys immunoassay interpreted?

A

rule out pre-eclampsia

74
Q

how is pre-eclampsia treated?

A

can only be resolved by the delivery of the fetus and placenta

75
Q

how is pre-eclampsia managed if it is before 34 weeks?

A

preferable to try and maintain the pregnancy if possible for the benefit of the fetus

76
Q

how is pre-eclampsia managed if it is after 37 weeks?

A

delivery preferable

77
Q

how is pre-eclampsia managed if it is between 34 and 37 weeks?

A

depends on the case

78
Q

how can pre-eclampsia be managed if the fetus cannot be delivered?

A

anti-hypertensive therapies

anti-platelet drugs (low dose aspirin for high-risk individuals)

regular monitoring of the mother in the hospital = blood pressure tests, urine tests, blood tests, ultrasound scans

79
Q

if the fetus is < 34 weeks and must be delivered, what precautionary measure must be taken?

A

corticosteroids must be given to promote fetal lung development before delivery

= so if the baby is born early, the respiratory system is intact so the fetus is viable outside the womb independently

80
Q

why are corticosteroids given to fetuses in pre-eclamptic women before 34 weeks?

A

to promote fetal lung development before delivery

= so if the baby is born early, the respiratory system is intact so the fetus is viable outside the womb independently

81
Q

how is pre-eclampsia prevented?

A

weight loss (esp if BMI > 35)

exercise throughout pregnancy

low dose aspirin (from week 11-14) for high-risk individuals = prevents anticoagulation

82
Q

how is the risk of seizures prevented in pre-eclamptic women and why?

A

give magnesium sulfate

mineral that reduces seizure risks in women with preeclampsia

83
Q

what are the long-term impacts of pre-eclampsia on maternal health?

A
  • elevated risk of CVD, T2DM and renal disease after pre-eclampsia
  • 1/8 risk of having PE in the next pregnancy (greater risk if early-onset type of PE)
84
Q

why is calcium supplementation given to pre-eclamptic women?

A

high-dose calcium supplementation during pregnancy reduces the risk of developing hypertension

85
Q

why is magnesium sulfate given to pre-eclamptic women?

A

reduces seizure risks in women with preeclampsia

86
Q

what are the long-term impacts of pre-eclampsia on maternal health?

A
  • elevated risk of CVD, T2DM and renal disease after pre-eclampsia
  • 1/8 risk of having pre-eclampsia in the next pregnancy (greater risk if early-onset type of PE)

brs (phase 1b) (71 decks)

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