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Reproduction > Complications of Pregnancy 2 > Flashcards

Complications of Pregnancy 2 Flashcards

1
Q

Define chronic hypertension

A

HTN either pre-pregnancy or at booking (<20weeks or 20 weeks)

I.e. she’s had it before the pregnancy and they’ve just noticed now

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2
Q

Define mild HTN

A

Diastolic 90-99, systolic 140-149

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3
Q

Define moderate HTN

A

Diastolic 100-109 systolic 150-159

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4
Q

Define severe HTN

A

Diastolic >110, systolic >160

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5
Q

Define gestational hypertension

A

New HTN in pregnancy developing after 20 weeks

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6
Q

Define pre-eclampsia

A

Significant new HTN + significant proteinuria

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7
Q

What is significant proteinuria defined as?

A

Automated reagent strip urine protein estimation >1+
Spot urinary protein: creatinine ratio >30mg/mmol
24h urine protein collection >300mg/day

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8
Q

In which group of mothers is chronic HTN more common?

A

Older mothers

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9
Q

What anti-HTN can you not use in pregnancy?

A

ACEi - small risk of birth defects/impaired growth
ARBs
Antiduretics (risk of dehydration

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10
Q

Give two e.g.s of ACEis

A

Rampiril, enalopril

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11
Q

Give two e.g.s of ARBs

A

Losartan, candesartan

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12
Q

What is involved in the management of essential HTN in pregnancy?

A

Lower dietary Na
Aim for BP <150/100
Best anti-HTN drugs to use: labetabolo, nifedipine, methyldopa
Monitor for super-imposed pre-eclampsia
Monitor foetal growth
Watch out for placental abruption (higher risk)

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13
Q

What is the proper definition for pre-eclampsia diagnosis?

A

Mild HT on two occasions more than 4h apart or moderate-severe HT (one reading) AND proteinuria of more than 300mgms/24h (protein urine >+1 + protein:creatnine ratio >30mgms/mmol)

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14
Q

What systems does PET affect?

A

Multi-system disorder

Affects kidneys, liver, vascular, cerebral and pulmonary systems

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15
Q

What is the pathophysiology of PET?

A

Trophoblast invasion of spinal arterioles impaired –> placental/foetal hypoperfusion
Poorly perfused placenta releases pro-inflammatory proteins –> enter mum’s circulation and cause endothelium lining mum’s BVs to become dysfunction –> vasoconstriction

Imbalance between vasodilators (prostacyclin) and vasoconstrictors (thromboxane)

Endothelial cell dysfunction also affects kidneys causing them to retain more salt

Both –> HTN

Also localised area of vasospasm in mother’s BVs which can lead to reduced BF to certain organs

Endothelial cell dysfunction leads to BVs becoming more likely --> loss of protein from urine and increased water loss from vessels into tissues --> 
Generalised oedema (legs, hands, face)
Pulmonary oedema (cough, SoB)
Cerebral oedema (headaches, confusion, seizures (eclampsia))
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16
Q

In PET, there is vasospasm in the mother’s BVs which may lead to reduced BF to certain organs, give e.g.s of the effects of these

A

Kidneys –> glomerular damage –> oliguria & proteinuria
Retina –> blurred vision, flashing flights, scotoma
Liver –> injury and swelling –> elevation of liver enzymes, stretching of capsule –> RUQ pain (cardinal sign of severe pre-eclampsia)

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17
Q

What happens to the spiral arteries in pregnancy?

A

They are converted into the uteroplacental BF

They lose their smooth muscle and dilate by 5-10x

18
Q

What are risk factors for developing PET?

A 
First pregnancy 
Extremes of maternal age 
Pre-eclampsia in previous pregnancy 
Pregnancy interval >10y
BMI >35
FH of PET
Multiple pregnancy 
Underlying medical disorder (chronic HTN, pre-existing renal dx, pre-existing DM, autoimmune disorders (e.g. SLE)
19
Q

What are the complications of PET?

A

High BP –> haemorrhagic stroke/placental abruption
Renal failure
Pulmonary/cardiac failure (never fluid overload these patients!)
HELLP
Eclampsia
Impaired placental perfusion –> IUGR, foetal distress, prematurity

20
Q

What is HELLP?

A

Endothelial injury –> formation of tiny thrombi in microvasculature which uses up lots of platelets
Clots are hazardous to RBCs –> haemolysis
HELLP = haemolysis, elevated liver enzymes, low platelets
HELLP occurs in severe PET

21
Q

What is eclampsia?

A

Pre-eclampsia + seizures

22
Q

What are signs and symptoms of severe PET?

A

Headache, blurring of vision, epigastric pain, pain below ribs, vomiting, sudden swelling of hands/face/legs
Severe HTN >3+ urine proteinuria
Clonus/brisk reflexes, papilloedema, epigastric tenderness
Oligouria
Convulsions (eclampsia)

23
Q

What biochemical abnormalities might you get in severe PET?

A

Raised liver enzymes, bilirubin if HELLP present
Raised urea & creatinine, raised urate
Low platelets, Hb
Features of DIC

24
Q

How do you manage severe PET?

A

Frequent BP & urine protein checks
Check for symptoms/hyper-reflexia, tenderness over liver
Blood investigations - FBC, LFTs, renal function tests (serum urea, creatinine, urate), coagulation tests
Foetal investigations - scan for growth, CTG
Only cure is delivery of baby and placenta - consider induction if foetal/maternal condition deteriorates

25
Q

Why must you monitor the mother after birth if she had PET?

A

Risk of PET persist into puerperium (first 6 wks)

Most seizures occur in post-natal period

26
Q

How do you treat seizures in PET?

A

Magnesium sulphate bolus and IV infusion
Control of BP - IV labetolol, hydralazine (>160/110)
Avoid fluid overlow (aim for 80mls/hour fluid intake)

27
Q

What prophylaxis do you give for PET in subsequent pregnancies?

A

Low dose aspirin from 12 weeks till delivery

28
Q

Woman with PET have a higher risk of developing what in later life?

A

HTN

29
Q

What is gestational diabetes?

A

Carbohydrate intolerance with onset in pregnancy

Abnormal glucose tolerance reverts after delivery

30
Q

Those who have gestational diabetes during a pregnancy are more at risk of developing what in later life?

A

Type II diabetes

31
Q

What is important to remember in those with pre-existing diabetes during pregnancy (in relation to their insulin intake)?

A

Insulin requirements of the mother increase - due to human placental lactogen, progesterone, hCG & cortisol from the placenta
So will need larger dose

32
Q

What occurs to the foetus of a diabetic mother?

A

Maternal glucose crosses the placenta, induces insulin production in foetus –> macrosomia (& inc. risk of birth comps like PPH, shoulder dystocia) & risk of neonatal hypoglycaemia and IRDS

33
Q

What foetal congenital abnormalities/problems is the foetus at increased risk of if it is born to a diabetic mother?

A

Cardiac abnormalities, sacral agenesis
Miscarriage/still birth
Foetal macrosomia, polyhydramnios

34
Q

What obstetric complications are more common in diabetic mothers?

A

Shoulder dystocia

35
Q

What is shoulder dystocia?

A

Anterior shoulder of foetus impacts into maternal pubis symphysis during delivery

36
Q

How do you manage shoulder dystocia?

A

McRobert’s manuovre

37
Q

What palsy is really common with shoulder dystocia?

A

Erbs (waiters tip position due to C5/6 damage)

38
Q

What does pregnancy do to the diabetic mother?

A

Increases risk of PET, worsening of maternal nephropathy, retinopathy, hypoglycaemia, reduced awareness of hypoglycaemia, increased infections

39
Q

What should a diabetic mother do preconceptually to try and have a smooth pregnancy?

A

Achieve optimal glycaemic control (BG 4-7mmol/l and HbA1c <6.5% (<48mmol/mol)
Folic acid 5mg
Dietary advice
Retinal and renal assessment

40
Q

What should a diabetic mother do during pregnancy to have a smooth pregnancy?

A 
Optimise blood control (<5.3mmol/l fasting, <7.8 1h postprandial, <6.4 2h postprandial, <6mmol/l before bedtime)
Continue metformin/start insulin if req 
Glucagon injections incase needed
Watch out for DKA/infections/PET
Watch foetal growth
41
Q

What different precautions should be taken in the birthing process if the mother is diabetic?

A

Induce labour 38-40wk/earlier if maternal/foetal concerns
Consider C-section if macrosomia
Maintain BG in labour with insulin-dextrose infusion
Continuous CTG
Early feeding of baby to prevent neonatal hypoglycaemia

Reproduction (28 decks)

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