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Prog test revision MBCHB > O&G Cases 5, 7 & 20 > Flashcards

O&G Cases 5, 7 & 20 Flashcards

1
Q

What factors should be taken into account in a discussion on contraceptive choices?

A

● Contraindications → aura, DVT risk, smoking etc
● Family completion
○ Ease of reversal
● Previous contraceptives that have/have not worked
● Cross tx i.e acne. bleeding
● Ability to take medications reliably

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2
Q

Discuss sterilisation:

A

● “irreversible”
○ Expensive if you do reverse
○ Requires GA
- Wound inf. risks with surgery
- Only 99% effective
- No further preg.

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3
Q

How should you approach discussing contraception?

A
  • How
  • Further preg?
  • SE
  • Efficacy -> optimum, realistic
  • Risk/Benefits
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4
Q

What are the Pill options for contraception?

A

POP: Progesterone only pill
COC: Combined oral contraceptive

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5
Q

How does low dose POP work? What are some examples. When is a woman not contraceptively safe?

A

● Low dose
○ Works by thickening the cervical mucus thus decreasing sperm penetration

○ Woman is not contraceptively safe if she is > 27 hours since the last pill was taken (3
hours late)

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6
Q

How does high dose POP work? Example? When is a woman not contraceptively safe?

A

● High dose
○ Stop ovulation
○ Cerazette (desogestrel) ***(not subsidised)
○ Woman is not contraceptively safe if she is >36 hours since the last pill was taken (12
hours late)

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7
Q

What contraception can an antenatal woman go on?

A

Breastfeeding (first 3-6 weeks after birth) we would not normally prescribe the COC but can
prescribe POP, injection, barriers or IUD

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8
Q

What are some considerations for POP?

A
  • Safe in pregnancy
  • Still have period.
  • Good for woman who cannot tolerate oestrogen (e.g. migraine with aura, history of VTE)
  • ● Main concern: Short window:

○ Noriday and Microlut must be taken within the same 3 hours every day
○ Cerazette has a longer window- it must be taken within 12 hours every day.

● If a pill is missed or taken late = take the pill as soon as she remembers, but will need another
form of contraception for 2 days

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9
Q

What are the interactions of the POP?

A

○ Not affected by antibacterials that do not induce liver enzymes
○ Reduced by enzyme-inducing drugs → use additional method and continue for at least 4 weeks after

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10
Q

How does the COC work? What happens with the placebo pills?

A

Prevents ovulation. and endometrial mucous.

Hormone withdrawal bleed when taking the placebo pills

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11
Q

What COC do we prescribe in NZ?

A

In NZ we will usually start with prescribing pills which are low dose pills (ie estrogen dose of
35 micrograms of ethinyl estradiol or less) and which contain a second generation
progestogen (levonorgestrel or norethisterone)

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12
Q

What is needed when prescribing the COC?

A

Full medical and family history + BP and BMI

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13
Q

When does the COC not work?

A

COC taken 21/7, a woman is not contraceptively safe if she is >48 hours since the last pill
was taken (2 missed pills)

If they miss one then use other contraception for seven days

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14
Q

Whats some general advice if you miss the COC?

A

● 7+ Hormone pills to be safe again. Thus NEED another form of contraception
● Need ECP if that method breaks / fails
● If there are less than 7 hormone pills left in the pack, finish the hormone pills and start your
new pack immediately (miss the 7 inactive pills or the 7 day break)

● Note → these are important during the week before or after inactive pill use
○ If she has taken 7 active pills already ovaries “asleep” so if misses 2-3 pills is OK → does not need 7 day rule or ecp if unprotected sex

○ The same is true if she misses pills in week 3 of hormone pills – AS LONG AS she does not take her placebos but goes straight to the hormone pills in the next packet

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15
Q

What is the DEPO provera? How does it work? How is it adminsitered?

A
  • Intramuscular injectable (bottom), Progesterone only.
  • 12 weeks (evidence suggests up to 16)
  • Prevents ovulation
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16
Q

What are the side effects of DEPO provera?

A
  • Irregular bleeding or no period
  • Weight gain
  • Fertility can take up to 18 months to return
  • Immediately effective if given on day 1-5 of cycle
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17
Q

What is the benefit of an IUCD or IUS with patient selection?

A

● No restriction related to age, nulliparity, or past history of pelvic infection or ectopic pregnancy
● No restriction on weight
● No interaction with any medication
● No restriction for women with CVD

Must not be pregnant…

Merina not recommended int hose with hx of breast Ca

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18
Q

When does the marine or copper IUD become effective?

A

Copper = immediate
Mirena = 7 days protection unless day 1-7 of cycle.

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19
Q

What are the side effects of IUD?

A

● Mirena
○ Irregular bleeding is common
○ May cause systemic progestogenic side effects (10%); breast tenderness, acne

● Copper
○ Prolonged, heavier bleeding
○ Dysmenorrhea

● Both
○ Risk of pregnancy low BUT if get pregnant higher chance of ectopic
○ Expulsion rate → 5%
○ Perforation on exertion rate 1/1000

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20
Q

How does the mirena work?

A

● Reservoir on the stem which slowly releases levonorgestrel (LNG) directly to the endometrium

● Prevents fertilisation and thins endometrium, also prevents ovulation 25% of cycles

○ Within 3-6 months many women are amenorrhoeic, 2/3 experience irregular bleeding before this.
○ Irregular bleeding may be alleviated by a trial of the OCP used either cyclically or continuously

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21
Q

Whats a non-contraceptive use of mirena?

A

○ Due to effect on endometrium = effective treatment for HMB (reduced menstrual blood loss by 90% per year

○ Other beneficial effects include improvement in dysmenorrhoea and the symptoms of endometriosis

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22
Q

How does the Copper IUD work?

A

○ Copper is directly toxic to sperm and ova
○ Endometrial inflammatory effect prevents implantation should fertilisation occur

Thus

● Has pre- and post-fertilisation effects → main effect is to prevent fertilisation

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23
Q

What else can copper IUD do?

A

Be used as an emergency contraceptive up to five days post ovulation

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24
Q

What is a side effect of the copper IUD?

A

May increase bleeding and pain during periods

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25
Q

What are some implant options for contraception?

A

● Jadelle = 2 rod implant releasing levonorgestrel

● Nexplanon = 1 rod implant releasing etonogestrel

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26
Q

How does the Jadelle work?

A

● 2 main modes of action are:
○ Suppression of ovulation - in year 1 less than 10% of cycles are ovulatory
○ Effects on mucus (decreased penetrability) - by 48 hours after insertion cervical
mucus production is decreased and the mucus itself is thick and almost impenetrable
to sperm

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27
Q

What are some other effects of the jadelle?

A

● Other actions
○ Decreased natural progesterone production by the ovary during the postovulatory (luteal) phase even when ovulation occurs.
○ Suppression of endometrial growth (hypoplasia)

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28
Q

What reduces the efficacy of the jadelle?

A

● Hepatic enzyme inducing drugs decrease efficacy during their use and for 28 days
afterwards
○ Antibiotics; rifampicin
○ Anti epileptics; phenytoin, carbamazepine and topiramate
○ Antiretroviral therapy
○ St John’s Wort

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29
Q

What are some absolute contraindications to the jadelle?

A

● Absolute contraindications (MEC 4)
○ Pregnancy
○ Current breast cancer (past history = UKMEC 3)
○ Unexplained vaginal bleeding
○ Sensitivity to LNG
○ Current or past liver tumour (benign or malignant)

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30
Q

What is the target blood glucose for someone with gestational diabetes?

A

Treatment targets for capillary glucose are:
● fasting glucose ≤ 5.0 mmol/L
● one-hour postprandial ≤ 7.4 mmol/L
● two-hour postprandial ≤ 6.7 mmol/L

31
Q

Who is involved in the care of someone with GDM?

A

Care team to include either; specialist diabetes midwife, diabetic nurse specialist, midwife, obstetrician, or a multidisciplinary team

32
Q

What is the diet and lifestyle advice for someone with GDM?

A

○ Avoid excessive weight gain in pregnancy
■ Energy intake should be no less than 1800 kcal/day and should include a distribution of macronutrients. Have smaller, more frequent nutrient dense meals
■ Develop individualised meal plans with a dietician, incorporating lifestyle and cultural factors

33
Q

Why is diet and lifetstyle advice important in someone with GDM?

A

■ Can reduce risk of preeclampsia
■ Reduced risk of cesarean
■ Reduced gestational weight gain
■ Reduced risk for LGA babies
■ Reduced risk of hyperbilirubinemia
■ Reduced risk of shoulder dystocia

34
Q

What is the role of oral hypoglyceamics and insulin with GDM?

A
  • Offer oral hypoglycemics (metformin or glibenclamide) and/or insulin therapy (women’s preferences and her ability to adhere to medication and self monitoring) for poor diet and lifestyle control.

○ Metformin appears to be as effective as insulin

○ Glibenclamide is more likely to result in a LGA baby and there is an increased risk of neonatal hypoglycaemia.

○ Some women with gestational diabetes may prefer the option of oral hypoglycemics to insulin therapy

35
Q

What is the management for GDM?

A
  • Diet and lifestyle
  • +/- Oral hypoglyceamics or insulin
  • Growth scan at 28 + 36 weeks.
36
Q

What are the risk factors for GDM?

A

● Ethnicity
● Maternal age >/=40 years
● BMI >/=35kgm2
● Family history
● PCOS
● Previous GDM
● Impaired glucose tolerance
● Medications: corticosteroids, antipsychotics

37
Q

What is important in the obstetric history for GDM?

A

● Previous LGA babies
● Previous birth complications
○ Previous shoulder dystocia
○ PPH
○ 3rd/4th degree tears
○ Wound infection (c-section, episiotomy)
○ Postnatal infections

38
Q

Whats the relevant hx if already diagnosed with GDM?

A

1) How was it diagnosed? HbA1c, Polycose, OGTT
2) Gestation at Dx
3) Management i.e drugs or lifestyle
4) Current sugars
5) Growth scan

39
Q

What is the relevant exam and investigations for GDM?

A

● General appearance
● BP, HR, urine dipstick
● BMI
○ Note the pattern of weight distribution (truncal or general)
○ Can make USS and CTG more difficult
● Abdominal examination
○ Tenderness
○ Symphysiofundal height
○ Fetal lie
○ Presentation
○ Position
● Fetal HR
● Urine dipstick

40
Q

What makes pregnancy diabetogenic?

A

Maternal hormones mobilises macronutrients for the developing fetus. i.e Estro, Prog, Prolactin, cortisol

Human placental lactogen creates a transient insulin insensitivity on the maternal side.

Gestational diabetes occurs when the maternal pancreas cannot overcome these counter regulatory measures.

41
Q

What is the diagnostic criteria for gestational diabetes in NZ?

A

Hyperglycaemia first detected in pregnancy should be either considered
● Diabetes mellitus in pregnancy
● Gestational diabetes mellitus

Diagnostic lab criteria for diabetes mellitus in pregnancy
● Fasting plasma glucose >/= 7mmol/L
● 2hour plasma glucose >/= 11.1 mmol/l following a 75 g oral glucose load
● A random plasma glucose >/= 11.1 mmol/l in the presence of diabetes symptoms.

Diagnostic lab criteria for gestational diabetes mellitus (GDM)
● Booking HbA1c >40mmol/mol
i. If >/= 50mmol/L → undiagnosed pre-existing type 2 diabetes
ii. If 41 to 49 mmol/mol only the two hour GTT is required.
● Polycose >/= 7.8mmol/L → requires OGTT
● Polycose >/= 11mmol/L → diabetes referral
● OGTT fasting >/= 5.5.mmol/L or 2hour >/= 9mmol/L → diabetes referral

42
Q

4)What is the difference between a screening test and a diagnostic test?

A

A screening test = given to those without symptoms of a condition
A diagnostic test = used to confirm a suspected condition (based on initial testing/screening or high risk)

43
Q

What is the screening test for GDM?

A

SCREENING (Polycose test)
● Low risk women → polycose test (50g glucose load given at any time of day, followed up by
blood test 1 hour later)
○ If negative and no other signs of diabetes → no other resting required
○ If positive (7.8-11mmol/L) → move on to diagnostic testing ( high risk woman)
■ Note → if >/= 11.1mmol/L refer to diabetes services without further testing

44
Q

What is the diagnostic test for GDM?

A

DIAGNOSTIC (OGGT)
● High risk women (positive polycose test or risk factors for diabetes) → fasting blood test (fast 8 hours prior to test) and then given 75g glucose load, blood test taken at 2 hours.
○ If negative → no other testing required unless sx develop
○ If positive → confirmed diagnosis of GDM and referral to specialist
■ Fasting >/= 5.5mmol/L
■ 2hr postprandial >/=9mmol/L

45
Q

What are the potential short term maternal consequences of DM?

A

Short term → antenatal
● Vasculopathies → not enough blood to placenta
● Hypertension
● Preeclampsia
● Infection
● Polyhydramnios
Short term → during birth
● Increased chance of needing induction of labour due to infant size
● Increased chance of instrumental or caesarean section
● PPH
● Perineal tear

46
Q

What are the potential long term maternal consequences of GDM?

A

Long term
● Higher risk of developing diabetes later in life
● Increased risk of another GDM birth
● Infection postpartum
● Increased risk of cardiovascular and metabolic disease
● Pregnancy can aggravate existing diabetes

47
Q

What are the short term fetal consequences of gestational diabetes?

A

Short term → antenatal
● Miscarriage
● Congenital malformations (usually in pre-existing diabetes) → particularly cardiovascular
● IUGR or LGA or Macrosomia
● Sudden intrauterine death

Short term → birth
● Birth trauma (#, dystocia, brachial pal, hypocia ischemic encephalopathy)
● Stillbirth

48
Q

What are the post natal consequences of gestational diabetes for fetus?

A

● Respiratory distress
● Neonatal hypoglycaemia
● Polycythaemia (may be secondary to fetal hypoxia) → hyperbilirubinemia, jaundice, feeding difficulties, respiratory distress, lethargy
● Prematurity
Long term
● Development of diabetes or metabolic syndrome later in life

49
Q

What are the methods to reduce the risk of pre-gestational diabetes?

A

● Control blood sugars pre-pregnancy (and during conception and organogenesis)
● Monitor woman during pregnancy for development of diabetes complications
● Suggest diet and exercise plan
● Delivery → 40+ weeks or 38-39weeks depending on fetal growth
○ Insulin→ 38 weeks or even earlier for poorly controlled
● HbA1c follow up
● Follow up for child

50
Q

Under what circumstances might you consider testing glucose tolerance prior to pregnancy?

A

● If you are concerned that the woman may have undiagnosed diabetes (signs, symptoms, risks of diabetes) and she is planning to become pregnant
● Previous GDM → concern she may have developed diabetes following last GDM pregnancy
● Family history, ethnicity, age risk factors, PCOS

51
Q

How would you counsel a woman who has Type II diabetes and wishes to become pregnant?

A

● Inform her about the risks to herself and baby and how these may be mitigated through good glucose control and blood glucose monitoring, exercise and diet modification
● Consider waiting until she has good control
● Still advise about folic acid and iodine
● Assess for her own diabetic complications → retinopathy etc

52
Q

Do you get a doppler done for a normally grown baby?

A

No, no one knows the relevance

53
Q

What does the customised growth chart relate to?

A

Estimated fetal weight

54
Q

What are fetal movements?

A
  • Begins 16-22 weeks.
  • Pattern of movements develops by week 28.
  • Develop sleep/wake cycles
  • More likely to notice movements when static
    ● >36 weeks gestation → change to the ‘type’ of movement = more rolling, squirming, pressing movements (more forceful), may notice their arms and legs moving
55
Q

What affects sensation of fetal movements?

A

● Things affecting sensation of fetal movements;
○ Maternal BMI
○ Placental position
○ Whether is is mothers first baby
■ First baby - feel first movements later

56
Q

What is the importance of reduced fetal movements?

A

● RFM important because they can proceed stillbirth - often mothers notice a period of reduced fetal movement prior to a stillbirth
● Baby that is struggling in utero → reduces movements so it can conserve energy
● Usually in the days before it dies
● Can be a clue of IUGR/SGA, placental insufficiency, feto-maternal transfusion

57
Q

What are pregnancy factors associated with reduced fetal movements?

A
  • Fetal growth restriction
  • SGA
  • Placental insufficiency → can’t deliver
    sufficient nutrients to the baby through the placenta → could be reason why baby is smaller
  • Oligohydramnios → too little fluid for gestational age
  • Threatened preterm labour
  • Fetomaternal transfusion → fetal blood
    in maternal circulation, normally a barrier is formed, can be spontaneous or trauma/placental abruption
  • Intrauterine infections
58
Q

What outcomes are associated with reduced fetal movements?

A
  • Congenital malformations
  • Preterm birth
  • Perinatal brain injury
  • Disturbed neurodevelopment
  • Low birth weight
  • Low apgar score
  • Hypoglycaemia
  • Caesarean section
  • IOL
  • Fetal death
  • Neonatal death
59
Q

What is SGA? How is it different to IUGR?

A

SGA is based on personalised growth chart. Less than 10% centile.

IUGR is based on population based centiles.

60
Q

What defines SGA compared to IUGR?

A

● The birth weight/ estimated fetal weight being below a certain point defines SGA, whereas a reduction in fetal growth rate is what defines IUGR. So, a baby can be born SGA but not be IUGR (the baby would have been small throughout the pregnancy but stuck to the growth rate that we expected, and then been born at an SGA birth weight).
○ If the baby is born with a normal weight, or even large but been IUGR, it would have had a reduced growth rate throughout pregnancy, but it was not so reduced that the birth weight is below <10th centile at birth

61
Q

What are the type of growth patterns seen in SGA?

A

Symmetric and assymetric growth restriction

62
Q

What constitutes assymetric growth restriction?

A

● Abdominal growth is disproportionate to the head
● Results from the capacity of the fetus to adapt to a pathological environment late in gestation
● Suggests a situation where fetus is lacking nutrients and therefore blood is redistributed to the vital organs = poor uteroplacental circulation and reduced nutrient supply to fetus

63
Q

What constitutes symmetric growth restriction?

A

● All measurements are small
● Less common
● Global impairment of cellular
hyperplasia early in gestation
● Fetal infection, chromosomal anomaly
● Early onset placental disease e.g.
preeclampsia

64
Q

What are customised fetal growth charts and why is their use now considered best practice?

A

● Computer generated for individual mothers Takes into account (maternal)
● Age
● Ethnicity
● Parity
● Height
● Weight at booking
● EDD
● If has had previous pregnancies → takes into account birth weight, infant sex, gestation at
delivery
● Improve SGA detection and thus prevent perinatal death/stillbirths

65
Q

What does a customised growth chart take into account and what is it used for?

A

● Unique to the woman and this pregnancy
● To work out babies that are truly growth restricted and small (rather than constitutionally
small)
● Use fundal height (FH) and estimated fetal weight (abdominal circumference (AC)) to plot on
chart

66
Q

What is a population growth chart based off and used for?

A

● Tracking all parameters → rather than focusing on SGA/LGA
● How are biometrics tracking along
● Placental insufficiency → tracking along normally until growth drops off late in 3rd trimester
(baby tries to spare brain); BPD and head grow normally, as does femur length, but abdominal circumference drops (determined by glycogen stores in liver)
○ Asymmetrical growth reduction

67
Q

What does fetal US scans measure?

A

Measures:
○ BPD
○ HC
○ AC
○ FL
○ EFW

68
Q

How does USS measure liquor volume and what does it measure?

A

● Assesses liquor volume (amniotic fluid volume)
○ Indicator of fetal wellbeing and health
○ Looking for Oligohydramnios = largest pocket of amniotic fluid measuring <2cm
vertical depth
■ Can be an indicator of blood flow being shunted to vital organs and therefore
renal blood flow is reduced and as AF is largely fetal urine from 14 weeks+ it is a good indicator of renal function/renal blood flow (i.e. placental insufficiency)

69
Q

What does fetal doppler sound show?

A

● Doppler studies = umbilical, middle cerebral artery (MCA), cerebroplacental ratio (CPR)
○ Doppler → using US to look at blood flow velocity in certain vessels (fetal and
maternal) and resistance to flow
○ In growth restricted fetus circulatory adaptations occur to make sure there is blood flow to vital organs (brain, heart, adrenals, placenta)
○ PI (pulsatility index)
■ Low PI = sign of redistribution of blood flow to the brain in response to
hypoxia

70
Q

What are the common causes of SGA?

A

● 5-10% = intrinsic fetal factors
○ Trisomies, congenital infection, congenital anomalies
● 20-30% = factors that make them constitutionally small ○ Small mother, ethnicity
● 60% = placental insufficiency
○ Reduced utero-placental perfusion, abnormal placental villi and vessels. Abnormal
placental transfer ● Smoking, alcohol, drugs

71
Q

What is the significance of SGA, both for the pregnancy and the long term health of the baby?

A

● SGA = major risk for stillbirths (50% of stillborns are SGA)
● Lifetime consequences = ↑ risk of perinatal mortality, cerebral palsy, developmental delay
● Later = increased risk of diabetes and CVD

72
Q

What are the risk factors for SGA?

A
  • Age 40<
  • Ethnicity
  • Smoking
  • Drug use
  • Preeclampsia
  • Previous SGA
  • Antiphospholipid syndrome
  • Hypertension
73
Q

What would you advise a woman smoking in pregnancy?

A

○ Increases risk of most pregnancy complications → miscarriage, ectopic, cleft lip baby,
placental abruption/placenta praevia, preterm labour, SGA, stillbirth
○ After birth → increased risk SUDI
○ Preterm or small babies → increased risk of infections, heart problems etc
○ Risks are dose dependent, if woman stop smoking before 15weeks their risks of
preterm birth, stillbirth and SGA babies are same as for non-smokers

74
Q
A

Prog test revision MBCHB (6 decks)

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