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Physiology & Science: Reproduction > Complications of Pregnancy > Flashcards

Complications of Pregnancy Flashcards

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1
Q

The majority of pregnancies are completely straightforward and low risk. Nearly all women experience minor troublesome symptoms to some degree. What do minor symptoms include?

A
  • tiredness / nausea + vom / constipation / heartburn / breast tenderness / frequency / backache / piles / headache / heat intolerance / scramble-brain / emotional lability
  • abnormality depends on degree of symptoms
  • difficulty is spotting the pathology - “needle in a hay stack”
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2
Q

What are common complications in the first trimester?

A
  • miscarriage (15% all pregnancies)
  • ectopic pregnancy (0.5-2%)
  • hyperemesis gravidarum (2-5%)
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3
Q

What are common complications in the second and third trimesters for the mother?

A
  • UTI
  • anaemia (common)
  • pre-eclampsia (4-5%)
  • gestational diabetes (variable - 5%)
  • antepartum haemorrhage
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4
Q

What are common complications in the second and third trimesters for the foetus?

A
  • premature labour (delivery <37 completed weeks)
  • intrauterine growth restriction (IUGR) - failure to reach growth potential or <2500g at term
  • macrosomia (>4500g at term)
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5
Q

Describe and explain the risk of UTI in pregnant women

A
  • increased throughout pregnancy compared to non-preg women
  • relative urinary stasis - mass effect + progesterone leading to sm muscle relaxation (rel hydro-ureters/nephrosis)
  • immuno-suppression
  • symptoms can be mild or absent
  • UTIs associated w obstetric problems esp pre-term delivery
  • TEST urine EVERY visit!!!!
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6
Q

What is the normal range for Hb in females (non-pregnant and pregnant)?

A
  • non-pregnant females: Hb 12-16 g/dl
  • pregnant range: Hb 10.5-13 g/dl
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7
Q

Why is the normal haemoglobin range in pregnant women lower?

A
  • circulating volume increases from 4.5L -> 6L
  • increased plasma volume > inc red cell volume
  • there is physiological dilution of Hb concentration (not physiological anaemia of pregnancy!)
  • maximal dilution occurs at 28-30weeks
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8
Q

When should anaemia be investigated for in pregnant women?

A
  • when Hb <10.5g/dl
  • common causes: Fe deficiency
  • sickle cell or thalassaemia trait
  • Vit B12 + folate deficiency
  • blood dyscrasias eg. leukaemias etc.
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9
Q

How do you manage anaemia in pregnancy?

A
  • check Hb at booking / 28 / 36 weeks
  • investigate for cause of anaemia eg. serum ferritin / B12 / folate / electrophoresis
  • treat underlying cause if Hb <10.5 eg. ferrous sulphate
  • transfuse if Hb <7 or symptomatic
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10
Q

What is gestational diabetes?

A
  • diabetes mellitus diagnosed or recognised for first time >20/40 gestation
  • (true GDM + pre-existing DM)
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11
Q

How is pre-existing IDDM/NIDDM different to gestational diabetes?

A

Pre-existing - already diagnosed pre-preg or recognised <20/40

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12
Q

Why is diabetic pregnancy associated with high risk obstetrics?

A
  • increased perinatal morbidity + mortality
  • increased maternal morbidity
  • small increase maternal mortality
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13
Q

Why does gestational diabetes happen?

A
  • pregnancy
  • increased HPL, cortisol, E2, glucagon (placental)
  • leads to insulin resistance
  • there is increased ability to provide carbohydrate to feto-placental unit
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14
Q

GDM only usually occurs in already susceptible women such as..?

A
  • obese
  • family history of DM
  • previous GDM
  • previous baby >4.5kg
  • polycystic ovary syndrome
  • older
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15
Q

Who/when should be screened for GDM?

A

Screen/test high-risk groups at booking + screen everyone at 28/40

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16
Q

What is the difference between IDDM and NIDDM?

A
  • insulin dependent DM - insulin deficiency - TYPE 1
  • non-insulin dependent DM - insulin resistance - TYPE 2
17
Q

What is the link between pre-existing diabetes mellitus and risk of congenital malformation?

A
  • 2-3%
  • periconceptual:
    • HbA1c 5-8% – 4-5% inc risk
    • HbA1c 8-10% – 9% inc risk
    • HbA1c >10% – 25% inc risk!!

typical congenital malformations: can lead to sacral agenesis, CHD, skeletal/NTD

18
Q

What is the only way to alter the increased risk of malformation in pregnant women with pre-existing IDDM?

A
  • PRE-pregnancy counselling
  • not a problem for true GDM (not diabetic at conception)
  • insulin requirements x2 by term
19
Q

What is the pathophysiology following maternal hyperglycaemia?

A
  • glucose is transferred from mother to baby by facilitated diffusion
  • baby isn’t diabetic so will attempt to lower glucose by increasing insulin
  • this leads to variety of things (eg. macrosomia)
  • neonatal hypoglycaemia - baby has higher insulin levels at birth whereas glucose drops, so too much insulin!
  • fetal glycosuria will lead to polyhydramnios - bc of osmotic diuresis, there is poly-hydramnios - baby is peeing a lot as there is glucose in urine
20
Q

As a result of a pre-existing diabetic mother, there is inhibition surfactant in the fetus. What will inhibiton surfactant lead to?

A

Respiratory distress syndrome

21
Q

What can macrosomia and hyperplacentation lead to?

A
  • prolonged labour
  • operative delivery
  • shoulder dystocia
  • pre-eclampsia
  • anterpartum haemorrhage
  • postpartum haemorrhage
22
Q

Polycythaemia can lead to jaundice. What can polyhydramnios lead to?

A
  • malpresentation
  • cord prolapse
  • postpartum haemorrhage
23
Q

What are other maternal risks (for those who have pre-existing DM)?

A
  • increased infections esp UTIs
  • hypo-glycaemia (tighter regime) - type 1 usually
  • deterioration in nephropathy (reversible)
  • two fold risk of progression of retinopathy
  • if GDM = 50% lifetime risk of NIDDM
24
Q

What are the principles of management for diabetic mothers?

A
  • pre-pregnancy counselling for known DM
  • achieve normoglycaemia (fasting <5.0mmol/l, 1hr postprandial < 7-7.5 mmol/l)
  • diet +/- insulin (obstetrician PLUS diabetologist)
  • metformin - increasingly used for type 2 mothers
  • ultrasound - to detect congenital abnormalities, to assess fetal growth/polyhydramnios
  • screen for pre-eclampsia
  • timing of delivery - risk of intra-uterine demise vs resp distress
25
Q

What is pre-eclampsia (PET)?

A
  • significant rise in BP or BP 140/90
  • after 20 weeks of pregnancy
  • on 2 separate occasions
  • at least 4 hours apart
  • plus significant proteinuria
  • OR significant change from booking BP (before 20 weeks) of:
    • more than or equal to 30 (systolic)
    • more than or equal to 20 (diastolic)
26
Q

Is oedema normal in pregnant women?

A
  • normal finding in up to 80% of pregnant women
  • therefore tends to be more significant if severe or in unusual site eg. facial or sacral
27
Q

If a pregnant woman has high blood pressure, she is said to belong to one of three groups. What are these 3 groups?

A
  • pre-existing hypertension - primary or secondary to a disease
  • pregnancy induced HT - no proteinuria
  • pre-eclampsia (PET) - proteinuria (significant)

pre-existing is recognised before 20 weeks of gestation where the other 2 are after 20 weeks

28
Q

What is the physiology underlying PET in pregnant women?

A
  • BP = CO x TPR
  • pregnancy: CO increases by 40%
  • pregnancy: TPR is reduced to accomodate large placental flow
  • PET occurs when there is increased TPR secondary to systemic vasospasm
29
Q

How do BP levels differ in PET vs normal pregnancy?

A
30
Q

What is the aetoliogy of PET, although it is poorly understood?

A
  • disorder of placentation - failure of 2nd wave of trophoblastic invasion at around 15-16weeks
  • overriding pathology is systemic vasospasm
  • systemic small vessel abnormalities - inc endothelial cell wall activation of platelets + coag factors resulting in microthrombosis + infarction of end organs
  • increased capillary permeability - movement of fluid into EC Space
  • multi-system disorder involving any organ of body but particularly kidneys, liver, CNS, coag system + placenta
31
Q

What are the 3 theories of PET pathophysiology?

A
  • immunological - abnormal maternal immune rxn to trophoblast
  • vasospastic substances - NO, TNF, free-radicals, altered RAA sensitivity
  • mineral + vitamin deficiencies - selenium, vit C (ie. anti-oxidant species)

Physiology & Science: Reproduction (18 decks)

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