Pre-eclampsia & Gestational diabetes Flashcards

1
Q

Gestational diabetes (GDM)

A

Impaired glucose tolerance resulting in hyperglycaemia diagnosed in pregnancy – may be pre-existing or undiagnosed – significant risk of subsequent type II DM

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2
Q

Risk to fetus from GDM

A

Macrosomia and related birth complications
Neonatal hypoglycaemia and late pregnancy loss
Increased life time risk of obesity and diabetes

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3
Q

Epidemiology of GDM

A

Recurrent of GDM between pregnancies is about 60% – greater if they required insulin
South asian have an 7-11 fold risk and afrocaribbean 3x risk
50% risk of developing type II DM in the next 10yrs.

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4
Q

Risk factors for GDM

A
BMI over 30
Previous macrosomic baby (>4.5kg) or GDM
FHx of diabetes
Non-white (Nor africans but afro-caribbean)
Advanced maternal age
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5
Q

Diagnosing GDM

A

Fasting of over 6.1mmol/L or >6.7mmol/L 2hrs after 75gs of glucose - higher cut-offs if capillary blood or plasma

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6
Q

Pathogenesis of GDM

A

Placental hormones including progesterone, cortisol, hPL, growth hormone and prolactin reduce insulin sensitivity
In healthy women this countered by increased insulin production – if this is not possible GDM develops

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7
Q

Cogenital malformations in GDM

A

Rare as GDM develops mainly in the 3rd trimester – unless there is pre-existing, uncontrolled diabetes leading to hyperglycaemia during organogenesis

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8
Q

Treatment of GDM

A

Women with GDM should be treated as it reduces the chance of complications –> can use diet, BM & fetal monitoring, oral hypoglycaemics and in 20% insulin

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9
Q

Labour in GDM

A

If well controlled may not need any special interventions but all should be offered elective birth after 38wks as this reduces the risk of shoulder dystocia and C-section
Aim to keep BM between 4-7mmol/L

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10
Q

Post natal care

A

Women with GDM should not require treatment after birth for the GDM –> monitoring should be continued until glucose returns to normal because of the risk of developing subsequent diabetes (6month then yearly diabetes checks after this)

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11
Q

Medication for GDM

A

Same as for DM (oral hypoglycaemic agents or insulin) but 80-90% of women are able to control it using diet and exercise

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12
Q

Target blood sugars for GDM

A

Before food – 3.4-5.9mmol/L
After Food – <7.8mmol/L
These measures are more closely associated with good outcomes than HbA1c

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13
Q

Fetal monitoring

A

Should be offered but there is little evidence this reduces the chance of stillbirth or macrosomia

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14
Q

Forms of Hypertension in Pregnancy

A

May be pre-existing chronic hypertension

Pregnancy induced hypertension (PIH) - Non-proteinuric PIH and pre-eclampsia

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15
Q

Pre-existing hypertension in pregnancy

A

Will develop before the 20th wk
If there is pre-existing proteinuria as well it is chronic renal disease
If there is new onset proteinuria then there is superimposed pre-eclampsia

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16
Q

Criteria for hypertension in pregnancy

A

Mild –>Diastolic 90–99, systolic 140–149
Moderate –> Diastolic 100–109 , systolic 150–159.
Severe –> Diastolic ≥ 110, systolic ≥ 160.

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17
Q

Criteria for proteinuria in pregnancy

A

> 300mg of protein/24hrs
OR
two properly collected samples over 4hrs apart with >2+s of protein
Albumin/creatinine ratio is a newer method which is very sensitive and specific

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18
Q

Pregnancy induced hypertension

A

Isolated Gestational hypertension or Proteinuria

Pre-eclampsia - gestational proteinuria hypertension

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19
Q

Eclampsia

A

A convulsive condition of malignant hypertension with proteinuria which can develop from pre-eclampsia
BUT only 50% of eclampsic women will have had previous hypertension and proteinuria

20
Q

Maternal mortality from pre-eclampsia

A

Eclampsia occurs in 26.8/100,000 pregnancies
60,000 deaths per year worldwide –
1/4 admissions for monitoring are due to concerns over hypertension/proteinuria

21
Q

Complications associated with pre-eclampsia

A

IUGR and placental abruption –> one of the commonest causes of iatrogenic preterm birth (15%) –25% of V. low birth weight infants – with associated adult health/IQ implications

22
Q

Epidemiology of Pre-eclampsia

A

2-5% of antenatal cases will develop PE while PIH is about 3x higher (6-15%)
With one risk factor incidence increases to 15%

23
Q

Risk factors for pre-eclampsia (5)

A

Likely genetic factors/FHx of pre-eclampsia
Link to paternal genetics - 2x risk if father has previously fathered an affected pregnancy
First pregnancy or young mothers
Increased exposure to spermatic antigens reduces risk
Underlying medical conditions increase risk

24
Q

Pathogenesis of Pre-eclampsia

A

Likely genetic factor –> faulty interaction between trophoblast and decidua (failure of physiological vasodilation) –> decreased blood supply to placenta –> oxidative stress and release of inflammatory/endothelial activating factors –> widespread disease

25
Q

Clinical Features of Pre-eclampsia

A

Hypertension and proteinuria developing after 20wks
Multisystem disorder –> risk of progressing to eclampsia and death due to convulsions, cerebral haemorrhage and respiratory distress

26
Q

Management of Pre-eclampsia

A

Survalience, early delivery and prophylaxis are mainstays of treatment

27
Q

Doppler artery waveform

A

Cheap and easy – if reduced or reversed end diastolic flow it is a sign of future PE – the later it is performed the greater the predictive strength – at 20wks abnormal waveform indicates 6 times increased risk

28
Q

Angiotensin II test

A

measure response of BP to infusion of Angiotensin II – poor predictor and costly

29
Q

Prophylaxis in PE

A

Low-dose aspirin has a 10% reduction in pre-eclampsia and associated complications and is recommended for high risk women
Calcium supplementation has also been investigated with promising results

30
Q

Treatment of Eclamptic fits

A
Magnesium sulphate (up to 8gs) is 1st line, 2nd is diazepam (10mg) -- usually will self limit unless of brain pathology is present (bleed)
MgSO4 reduces chance of further fits and need for ventilation/ITC admission
31
Q

Magnesium sulphate

A

1st line anticonvulsant/prophylaxis –> 2g loading dose with 1-2g/hr infusion –> renally excreted so care must be taken in oligouria
Membrane stabilizer vasodilator which reduces ischemia

32
Q

Time of onset of hypertension in pregnancy

A

Occuring after 37wks rarely results in morbidity
Before 20wks is likely pre-existing HTN but must still be monitored
Before 28wks is a bad signs and 50% will go on to develop pre-eclampsia

33
Q

Clinical Signs of eclampsia

A

Nausea, vomiting, headaches, visual disturbance may precede convulsions - 1/3 are post-partum (can be 3-4days)
Also abdominal pain, liver failure, HELLP syndrome, pulmonary edema, and oliguria.

34
Q

HELLP syndrome

A

Haemolysis, Elevated Liver enzymes and Low platelets
A complication of Pre-eclampsia which usually occurs in the 3rd trimester and 8% after birth
Will present with malaise (90%), nausea/vomiting (50%) and epigastric/upper right quadrant pain (90%)
30% will have neurological symptoms and 20% DIC
There must be some hypertension

35
Q

Treatment of HELLP syndrome

A

The only definite treatment is delivery but antihypertensives and transfusion may be needed as well
The usefulness of MgSO4 is debated but may help to prevent the development of eclampsia

36
Q

Management of hypertension

A

Mild –> monitor BP and urine multiple times/day

Moderate –>monitor and give oral labetalol (aim Oral/IV labetalol or IV hydralazine

37
Q

Timing of birth in pre-eclampsia

A

Only in severe refractory hypertension consider birth before 34wks – attempt to complete steroid maturation)
34-37wks – necessary if severe but controlled hypertension and offer if mild/moderate and appropriate facilities are available
Aftre 37wks – recommend with 24-48hrs if mild/moderate hypertension

38
Q

Obstetric Cholestasis

A

Whole body pruritis (palms and soles) which presents 30-32 wks gestation –> linked to mass effect of gravid uterus and cholestatic effects of oestrogens – > Usually have mildly elevated transaminases (AST, ALT) but these can be normal with only raised bile salts or GGT – may have dark urine, pale stools etc

39
Q

Epidemiology of OC

A

0.7% prevalence in the uk - higher in south america, indian and Scandinavian women
1/3 of suffers have a positive family history

40
Q

Risks of OC

A

PPH due to low Vit k due to malabsorption
preterm labour, MEC stained liquor, fetal distress and fetal death
Risk of fetal death correlates with bile salt levels and increases with gestational age

41
Q

Management of OC

A

antihistamines and emollients for the itching –> ursodeoxycholic acid (UDCA) has been shown to improve itching and liver function but impact on fetal risk is unclear
Fetal surveillance and early delivery are the only measures –> usually aiming for delivery by 37/38 wks but the evidence is conflicted

42
Q

Use of syntometrine IM in HTN

A

Contraindicated. Oxytocin alone is preferred

43
Q

How many pregnant women are diabetic?

A

2-5% – 60-65% are gestational. 40% pre-existing.

44
Q

Risk of congential abnormalities if mother is poorly controlled diabetic?

A

If HbA1c is over 10% the risk of congenital abnormalities is 25%, women in this situation should use contraception until better control is reached.

45
Q

If there is very poorly controlled diabetes and/or evidence of complications how do you treat?

A

If complications (macrosomnia) then start on insulin straight away.