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Antenatal Care > Bread & Butter > Flashcards

Bread & Butter Flashcards

1
Q

What are the S/Es of methyldopa?

A

There are CNS, CVS and haematological effects:

CNS: sedation, headache, nightmares, depression/mild psychosis, Bell’s palsy, parkinsonism

CVS: postural hypotension, bradycardia, worsening of angina, myocarditis, pericarditis, oedema

Haematological: haemolytic anaemia (positive direct Coombs test); bonemarrow suppression

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2
Q

What is the increase in perinatal and neonatal mortality that is assoc with PGDM?

A

Can be increased 5-10 fold

CEMACH study showed a perinatal mortality rate of 3% (for both PGDM & GDM)

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3
Q

What is the fetal mortality rate assoc with maternal ketoacidosis?

A

10-25%

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4
Q

As pregnancy progresses, how does the mother’s body compensate for the increased insulin resistance?

A
  • Hyperplasia of the islet cells of Langerhaans in the pancreas increases insulin production.
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5
Q

What are the placental diabetogenic hormones?

A

HCG PP

Human placental lactogen
Cortisol; Corticotrophin-releasing hormone
Glucagon; growth hormone

Progesterone
Prolactin

Crh (hypothalamus)- acth( ant. Pituitary) - cortisol + sex steroids (adrenal Zona reticularis)

Glucagon (alpha pancreatic cells) - increased hepatic gluconeogenesis and glycogenolysis + growth hormone secretion

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6
Q

Target GMR during labour and delivery?

A

4-6mmol/L

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7
Q

T/F. No oral hypoglycaemic agents are licensed sedation for use in pregnancy? What FDA class is metformin? Most serious s/e of metformin?

A

True.

Metformin is Class B. No animal studies have shown harm to the fetus.

Most serious s/e of metformin is lactic acidosis - but this is a RARE complication.

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8
Q

What is the HAPO study?

A

Hyperglycemia and Adverse Pregnancy Outcome study
—- looked at >23,000 ethnically diverse women who had a 75g OGTT
–AIM: to clarify the risk of adverse outcomes assoc with degrees of glucose intolerance, that are less severe than overt diabetes.

—- the FOUR primary outcomes of the study were:
1) Macrosomia (bt>90th centile for GA, gender, Parity, ethnicity and field center)
2) Primary caesarean delivery
3) Clinical neonatal hypoglycaemia
4) Hyperinsulinaemia (cord c-peptide >90th centile for the study group

Secondary outcomes considered:
- preterm birth
- shoulder dystocia/birth injury
- skinfold thickness >90th centile for GA, gender, Parity, ethnicity, field center
- percent body fat >90th centile for GA
- admission for neonatal intensive care
- hyperbilirubinaemia
- pre-eclampsia

RESULTS:
Strong, continuous association of between maternal hyperglycemia (below levels diagnostic of diabetes) and increased birth weight, increased serum C-peptide levels and the other primary outcomes.

  • the link with secondary outcomes were present but not as strong.
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9
Q

What is the Pederson hypothesis?

A

This hypothesis states that maternal hyperglycaemia results in transplacental glucose transfer which stimulates the fetal beta islet cells of langerhaans to secrete excess insulin/Hyperinsulinaemia, which produces adiposity and macrosomia, amongst other things.

The HAPO study concluded that this hypothesis is correct.

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10
Q

What is the IADPSG criteria?

A

The International Association of Diabetes and Pregnancy Study Groups used the HAPO study as the basis for new GDM thresholds.
To diagnose GDM:
Fasting: 5.1
1hr: 10
2hr: 8.5

To diagnose overt diabetes in pregnancy:
Fasting: 7/more
HbA1C: 6.5% or more
Random blood glucose: 11/more

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11
Q

What are pre-existing factors for the development of type 2 DM?

A

3 strongest are:
1. Ethnicity!!! (South Asians very high risk, Afro-Caribbean)
2. Maternal age
3. BMI

Others include:
4. Prev GDM
5. Family h/o diabetes
6. H/o stillbirth or congenital anomaly

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12
Q

What is the increased risk of a pulmonary embolism is a pt with a BMI >30?

A

3-5 times increased

(Odds ratio 2.7-5)

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13
Q

35 y.o, 33 wks, BP 180/110. 3+ proteinuria urinalysis. Elevated BP and proteinuria are new onset. Which drug will u administer INITIALLY?
Iv betamethsone, iv mgso4, iv furosemide, iv diazepam, oral methyldopa?

A

Iv mgso4

MgSO4 is the first line anticonvulsant.
(also acts to reduce BP a little as it is a competitive inhibitor of Ca😉)

-BP every 15mins until stable then every 30mins.
- measure O2 sats continually, maintain above 95%, chart with BP
- if present measure CVP and arterial lines continuously and chart w/ bP.
- Ivf at 80cc/hr

Hourly checks:
- neurological assessment using GCS or AVPU scales.
- respiratory rate

4 HOURLY checks:
- -strict I/O charting//urine output
- clinical r/v to assess for s/e (motor paralysis, absent deep tendon reflexes, respiratory depression, cardiac artythmia).

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14
Q

What is significant proteinuria using:
1. Protein:creatinine ratio
2. Albumin:creatinine ratio
3. Dipstick
4. 24 hr urine collection?

A
  1. > 30mg/mmol
  2. > 8mg/mmol
  3. > 1g/L (1+ or more)
  4. > 300mg/24hrs
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15
Q

30 y.o, P2, 16/40, BP- 155/105 mmHg, 1mth prior was 150/100mmHg. Urinalysis 1+ protein. Spot urinary prot:creat ratio is 35mg/mmol, 24hr urine is 0.35g protein. Likely diagnosis?

A

cHTN

  • unlikely to have preeclampsia at 16 weeks, as second wave of placental invasion is only just occurring.
  • likely has chtn with renal disease (hence the proteinuria)
    —will require further renal assessment.
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16
Q

How long should pregnancy be delayed after bariatric surgery?

A

12-18mths to:
1. allow stabilisation of body weight
2. Identify and correct any nutritional deficiencies

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17
Q

What is the acceptable weight gain in obese women?

A

No acceptable weight. Focus on healthy diet instead

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18
Q

How should women with bariatric sx be managed?

A
  • Pregnancy is HIGH risk and should be managed in a consultant lead clinic.
  • Screening and surveillance for nutritional deficiencies
  • Dietician referral for advice w.r.t their specialized nutritional needs.
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19
Q

What type of nutrient deficiencies are pts at risk of post bariatric sx?

A

Folate
Vitamin B12
Iron and
Fat soluble vitamin
Macronutrients fat and protein

Can lead to an SGA fetus

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20
Q

Benefits assoc with bariatric sx?

A

Reduced risks of:
- GDM
- HTNsive disorders
- fetal macrosomia

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21
Q

T/F. 75g OGTT can provoke dumping syndrome in pts with bariatric sx?

A

True

Prevent by limiting Gestational weight gain to 5-7kg whilst doing test

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22
Q

Incidence of asthma in pregnancy?

A

10%

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23
Q

T/F. Asthma exacerbations increase postpartum?

A

False

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24
Q

Advice for patient with fasting glucose of >7.1? (OGTT)

A
  • As per the IADPSG criteria, this pt has GDM.
  • Start insulin +/- metformin
    + diet and exercise
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25
Q

Advice for patient with fasting glucose of 6.4mmol/L? (OGTT)

A
  • this patient has an Impaired fasting glucose as it is between 6.1 and <7mmol/L.
  • diet and exercise (30min walk post meals)
    – target not met after 1-2wks, add Metformin
    — target not met after 1-2 wks or metformin contraindicated, offer insulin.
26
Q

Advice for patient with fasting glucose of 6.4mmol/L on OGTT but fetus is macrosomic or u/s shows polyhydramnios?

A
  • start insulin therapy +/- metformin + diet and exercise

👆🏾Treatment for ALL pts with fetal macrosomia/polyhydramnios + fasting of 6-6.9 mmol/L!!!

27
Q

Which oral hypoglycaemic agents are safe in pregnancy?

A
  • Metformin (biguanide)
  • Glibenclamide (sulfonyurea)
28
Q

Incidence of GDM?

A

3-6%

29
Q

What are the risk factors for GDM?

A
  • ethnicity (South Asian, Afro-Caribbean, middle eastern)
  • prev gdm
  • prev macrosomic infant >4.5kg
  • Obesity (BMI>30kg/m2)
  • family h/o diabetes (1st degree relative)
30
Q

How should patients at risk for GDM be screened?

A
  • prev GDM:
    —-offer self monitoring or OGTT at 16-18wks. Repeat at 28 weeks if negative.
  • other risk factors:
    —OGTT at 24-28wks
31
Q

Risk for developing T2DM for postpartum pt with:
1. Fasting glucose between 6-6.9mmol/L?
2. HbA1C between 5.7%-6.4%?
3. Fasting glucose <6
4. Fasting glucose >7

A

High risk - 1 & 2.
Continue annual screening - 3.
Likely T2DM - 4.

32
Q

What is the recommended (NICE) postpartum diabetes screening schedule for pts with GDM?

A

Fasting blood glucose at 6-13 weeks postpartum, then screen ANNUALLY for diabetes.

*OGTT at 6wks is used by other countries.

33
Q

What postpartum advice would you give to a GDM patient?

A
  • F/U at 6-13 postpartum to screen for T2DM.
  • GDM increases the risk of developing T2DM, hence she has to be screened yearly.
  • Advise Re the symptoms of hyperglycemia (polyphagia/dipsia/uria, wt loss)
  • Continue diet and exercise to optimise her weight; reduce fat intake
  • GDM tends to recur in subsequent pregnancies however obese pts should be encouraged to lose weight. Sometimes if a woman has lost a lot of weight between pregnancies and has modified her diet substantially, she may not develop GDM.
  • Adequate contraception is important.
  • Pre-pregnancy counselling is important.
34
Q

What is the commonest cause of Monogenic diabetes?

A

aka Maturity Onset Diabetes of the Young (MODY).

  • Caused by a mutation in the glucokinase gene.
35
Q

What is the inheritance pattern for monogenic diabetes?

A

Autosomal dominant
- or maternally inherited

36
Q

Incidence of:
HTN
Pre-eclampsia
Severe pre-eclampsia
Eclampsia?

A

10-15%
3-5%
1%
0.03% (1 in 3000)

37
Q

What advice would you give to a pt @ GA 29 weeks who presents with decreased fetal movements?

A
  1. All pts >28weeks should present to the maternity unit
  2. Take the relevant hx to assess her risk for FGR and stillbirth.
    —-duration of reduced fetal movements?
    —- absent fetal movements?
    —- prev consultation for RFM, htn, dm, extremes of age, primiparity, obesity, BOH, smoking, placental insufficiency.
  3. Abdominal palpation: SFH? - to
    r/o SGA
  4. Doppler FHR assessment (to exclude fetal death. IF difficulty auscultating FHR for U/S)
  5. BP measurements + urinalysis to r/o preeclampsia.
  6. CTG for all pts > 28wks - detects fetal compromise/hypoxia
    —Reactive? RFM improve? = Reassure. 70% of pregnancies with a single episode of RFM are uncomplicated.
38
Q

What are the stillbirth rates after a reactive vs Non-reactive CTG?

A

1.9/1,000 vs

26/1,000

39
Q

Risk of stillbirth?

A

1 in 250?

40
Q

Pt presents in the early third trimester with complaints of decreased fetal movements for the first time in this pregnancy. She has no risks factors for stillbirth.
1. Next step?
2. Difference in management if risk factors for stillbirth are noted?

A
  1. Auscultate FHR. Reassure if normal.
  2. U/s assessment within 24hrs
41
Q

Advice for a patient with recurrent RFM (reduced fetal movements) and a previously normal ctg?

A

U/s assessment
— If normal, she should have consultant-led counselling on the pros and cons of IOL for her.

  • U/S is done in the semi-recumbent position.
  • Will assess efw (r/o SGA) and liquor volume.
  • BPP has a good negative predictive value i.e. fetal death is rare if the BPP is normal.
42
Q

How soon should an u/s be done in a pt with RFM (if deemed necessary)?

A

Within 24 hours

43
Q

Management of RFM;
1. Before GA 24 weeks
2. Between GA 24-28 weeks

A
  1. Ausculate FHR to check viability
    —do full antenatal checkup
  2. Auscultate FHR to check viability
    —- take hx; do stillbirth risk assessment
    —- if clinical suspicion of FGR, consider U/S
    no evidence to support routine use of ctg in this group
44
Q

What percentage of women with stillbirth experienced prior RFM?

A

55%

45
Q

What are the average number of fetal movements per hour?

A

31 [range 16 - 45]

46
Q

Briefly describe the normal pattern of fetal movements?

A
  • Fetal movements are one of the 1st signs of fetal life.
  • First felt between 18-20wks, or 16 weeks in some multipara.
  • On average 31 movements felt per hour.
  • Perception of movements before 28 weeks may be decreased in a pt with an anterior placenta.
  • Has diurnal changes, which starts at 20 weeks. Fetal activity increases in afternoons and evenings.
  • Fetal movements decrease during sleep cycles which last usu 20-40mins but can last up to 90mins.
  • Movements felt MOST when lying down, LESS when sitting and LEAST when standing.
  • Movements PLATEAU at 32 weeks
47
Q

T/F. Fetal movements decrease in late T3?

A

False

48
Q

What are some causes of RFM?

A

There are 6 causes?
Maternal:
1. Sedating drugs (opiods, alcohol, benzodiazepines)
2. Maternal hypoglycaemia
3. Cigarette Smoking
4. Corticosteroids - for 2 days after administration; decreases variability

Fetal:
5. Fetal position (feet towards maternal spine/sacrum)
6. Major Fetal anomalies (cns/skeletal/muscular dysfunction)

49
Q

What is the subjective assessment for Fetal movements?

A

Fetal kick charts- 10 movements in 2 hours

50
Q

T/F. 5-10% of chronic htn is caused by secondary causes

A

True.
Idiopathic/essential htn is makes up 90-95% of CHTN.

51
Q

What ate the stages of CKD?

A

5 stages according to the GFR in mL/min:

1: >90
2: 60 - 89
3a: 45-59
3b: 30-44
4: 15-29
5:<15

52
Q

At what degree of renal impairment is pregnancy contraindicated?

A
  1. Stages 4 &5 CKD
  2. Serum creat >250 micromol/L
  3. Pts on dialysis
53
Q

Describe the effect of pregnancy on CKD and vice versa.

A

Pregnancy on CKD
- worsening htn
- worsening proteinuria
- worsening renal function
- increased flares/relapses of glomerulonephritis

CKD on Pregnancy
- Miscarriages
- preeclampsia
- FGR
- Preterm birth
- Intrauterine death

54
Q

What is the risk of progression from PIH to preeclampsia?

A

20-30%

Increases to 50% if PIH occurs before 32 weeks.

55
Q

What is the usual Platelet count in gestational thrombocytopenia?

A

Typically >100 but usually >70

56
Q

How is antiphospholipid syndrome diagnosed?

A

By at least 1 clinical and 1 laboratory criterion:

Clinical criteria (4) include:
1. h/o thrombosis [arterial, venous, small vessel - thrombotic microangiopathy in kidney]
2. 3/more spontaneous miscarriages (<10wks)
3. At least 1 fetal death (>10wks with normal morphology)
4. At least 1 preterm birth before 34 wks w/ normal fetal morphology due to preeclampsia or severe placental insufficiency

Laboratory criteria:
- Persistent abnormality of one of the following tests measured at least twice, more than 12 weeks apart:
—–a raised titre of anti-cardiolipin antibodies OR
—–a raised titre of B2 glycoprotein 1 antibodies OR
—- presence of lupus anticoagulant

57
Q

What is the incidence of APS in the general population vs patients with SLE?

A

5% vs 30-40%

58
Q

How does APS cause fetal loss?

A
  • defective placentation due to action of anti-cardiolipin antibodies on trophoblasts
  • thrombosis of placental vasculature
  • activation of complement system
59
Q

What is Acute Fatty Liver of Pregnancy (AFLP)?

A

A rare but potentially lethal disorder associated with abnormalities in mitochondrial beta-oxidation and defects in fatty acid metabolism/LCHAD deficiency.

*Long Chain 3-Hydroxyl-acetyl-Coenzyme A Dehydrogenase

There is considerable overlap between the symptoms of this condition and HELLP syndrome and it occurs more commonly in:
- primigravidas
- male fetuses (3:1)
- low BMI (20%) and
- multiple pregnancies (20%)

60
Q

Pt with preeclampsia. What is her risk of:
1. PIH
2. Recurrent PE delivered <34wks?
3. “ “ “ “ <28wks
4. “ “ “ “ 34-37 wks?

A
  1. 12%
  2. 33%
  3. 55%
  4. 23%
61
Q

Incidence of HTnsive d/o in pregnancy?

A

8-10%

62
Q

What is eclampsia?

A

Tonic clinic seizures associated with preeclampsia

Antenatal Care (18 decks)

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