Obstetrics Flashcards

1
Q

Define Gravidity (1)

A

Total number of pregnancies she has had, including the current one

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2
Q

Define Parity (1)

A

Pregnancies that resulted in delivery beyond 24 weeks

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3
Q

What does it mean if she is para 2+1?

A

She has had 2 deliveries after 24 weeks and 1 pregnancy which ended before 24 weeks

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4
Q

What is the gravidity of a para 1+2 who is currently pregnant?

A

4

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5
Q

What is the gravidity and parity of a first time Mum who has had one abortion?

A

gravidity 2

para 0+1

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6
Q

Dating a Pregnancy (1)

A

Expected delivery date = 1 year and 7 days after the LMP minus 3 months

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7
Q

If LMP was 09/04/20, what is due date?

A

16/01/21

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8
Q

Antenatal Booking Visit (5)

A

8-12 weeks
General info + advice (including folic acid until 13 weeks)
Routine care: BP, urine dipstick, BMI
Booking bloods: FBC, blood group, rhesus status, HIV, hep B, syphilis serology
Booking urine culture for asymptomatic bacteriuria

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9
Q

General Changes in Pregnancy (3)

A

Ligamentous laxity: ligaments relax to soften symphysis pubis but this can cause SP joint dysfunction, back and joint pain
Linea nigra
Spider naevi

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10
Q

Endocrine Changes in Pregnancy (3)

A

Breasts: increased oestrogen increases size and vascularity, leading to tenderness and colostrum
Thyroid: BhCG mimics T4 leading to reduced TSH, mimicking hyperthyroidism
Placenta: BhCG causes morning sickness, progesterone produced by placenta increases body temperature

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11
Q

GI Changes in Pregnancy (2)

A

Stomach: progesterone mediates pyloric sphincter relaxation, increased bile in stomach, reduced peristalsis
Large bowel: increased progesterone and reduced motilin cause constipation

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12
Q

Cardiovascular Changes in Pregnancy (4)

A

Antenatal cardiac output: circulating volume increases by 50-70%, high CO, high SV, low VR, high HR when supine due to IVC
Intrapartum cardiac output: 100% increase in CO2 due to autotransfusion of contractions and catecholamine release
Postnatal cardiac output: VR high above pre-pregnancy levels in first 2 weeks, HR normal after 2 weeks, CO2 normal by 24 weeks
BP: reduced in first trimester and continues to fall until 20-24 weeks, then increases to pre-pregnancy levels at term

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13
Q

Respiratory Changes in Pregnancy (2)

A

Increased O2 demand: increased ventilation, increased RR, increased TV (can cause SOB), peak flow + FEV1 unchanged
Progesterone acts centrally to reduce PCO2 leading to physiological respiratory acidosis

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14
Q

Renal Changes in Pregnancy (3)

A

Dilation of collecting system: increased blood flow to kidneys, high gFR and creatinine clearance
Increased renin and angiotensin in response to hypotension
Increased protein excretion causing oedema

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15
Q

Haematological Changes in Pregnancy (4)

A

Increased plasma volume: low Hb, MCV normal, low platelets
Increased iron and folate requirements
Increased WCC
Hypercoagulability (DVT + PE)

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16
Q

Sonography

Early Pregnancy USS (<11w) (3)

A

Not routine
Purpose: date pregnancy/determine location
Indications: hyperemesis gravidarum, bleeding, pain

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17
Q
Sonography 
Early USS (10-13+6w) (2)
A

Purpose: viability, multiples, anomalies incompatible with life
Calculate gestational age: crown rump length (or BPD if 12-20w)

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18
Q
Sonography 
Anomaly scan (18-20+6w) (1)
A

Purpose: identify structural problems

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19
Q
Sonography 
Fetal echocardiography (5)
A
If high risk of cardiac abnormality 
Maternal/family history 
Increased nuchal translucency 
Drugs in pregnancy 
Pre-existing DM
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20
Q

Sonography

Fetal growth scans (2)

A

If require accurate gestational age: SGA/LGA
Abdominal circumference + head circumference + femur length used to calculate estimated fetal weight, as well as liquour volume

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21
Q
Sonography 
Doppler ultrasound (3)
A

Blood flow to uterus, placenta and fetus
Uterine artery Doppler: high resistance indicates PET, IUGR
Umbilical artery Doppler: high resistance indicates placental failure + risk of intrauterine death

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22
Q

Down Syndrome Screening

Risk (2)

A

1:700

Increased with maternal age

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23
Q
Down Syndrome Screening 
Normal screening (4)
A

Offered to all
Only provides estimation of risk (need further tests to confirm)
Combined test at 11-13+6w: high serum BhCG and low PAPP-A (pregnancy associated plasma protein A) + increased ultrasound fetal nuchal translucency
Triple/quadruple test if 15-20w: reduced alpha-fetoprotein + unconjugated oestriol + high BhCG (+inhibin A)

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24
Q
Down Syndrome Screening 
Prenatal Diagnosis (2)
A

Chorionic villus sampling at 10-14w

Amniocentesis if >15w

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25
Q

Testing for Neural Tube Defects (4)

A

Screening not routine, offered if personal/family history
1st trimester USS: anencephaly and spina bifida detectable
2nd trimester biochemical screening: maternal AFP >2 warrant further testing
Anomaly scan detects 90% (lemon shaped skull and curved cerebellum)

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26
Q

Pre-Existing Hypertension in Pregnancy

Epidemiology (1)

A

3-5% of pregnancies

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27
Q

Pre-Existing Hypertension in Pregnancy

Investigations (2)

A

Urinalysis (no proteinuria, but these women are at a high risk of pre-eclampsia)
Investigate for an underlying cause if a new finding (eg. CKD, aortic coarctation)

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28
Q
Pre-Existing Hypertension in Pregnancy 
Preconception Management (2)
A

Stop ACE-i, ARB, thiazides as risk congenital abnormality

Labetalol (combined alpha/beta blocker) or methyldopa

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29
Q
Pre-Existing Hypertension in Pregnancy 
Antenatal Management (3)
A

Aim BP <150/90 or 140/90 if end-organ damage
Labetalol/methyldopa
Fetal US every 4 weeks from 28 weeks to assess fetal growth, amniotic fluid volume and umbilical artery dopplers

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30
Q
Pre-Existing Hypertension in Pregnancy 
Intrapartum Management (3)
A

Monitor BP hourly if <159/109 or continuously if >160/100
Continue drugs
Give oxytocin alone for 3rd stage because ergometrine causes severe hypertension, risking stroke

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31
Q
Pre-Existing Hypertension in Pregnancy 
Postnatal Management (3)
A

Check BP on days 1,2 and once between days 3-5 and then at 2 weeks
Change methyldopa after delivery as risks postnatal depression
Avoid diuretics if breastfeeding

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32
Q

Pre-Existing Hypertension in Pregnancy

Complications (3)

A

Pre-eclampsia
IUGR
Placental abruption

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33
Q

Gestational Hypertension

Epidemiology (1)

A

6-7% of pregnancies

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34
Q

Gestational Hypertension

Definition (1)

A

Hypertension (>140/90) in 2nd half of pregnancy in the absence of proteinuria or other features of pre-eclampsia (although at higher risk of developing it)

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35
Q

Gestational Hypertension

Investigations (3)

A

Urinalysis: no proteinuria
Bloods: FBC, U&E, AST/ALT and bilirubin if high BP (at presentation and weekly)
USS: 4-weekly growth scans

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36
Q
Gestational Hypertension 
Antenatal Treatment (2)
A

140-159/90-109: labetalol or methyldopa

>160/110: admit, if can’t stabilise on anti-hypertensives then deliver

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37
Q
Gestational Hypertension 
Intrapartum Treatment (2)
A

Continue anti-hypertensives

BP measured hourly (continuously if >160/110), do operative delivery if won’t settle

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38
Q
Gestational Hypertension 
Postnatal Treatment (2)
A

Reduce when 130/80

Stop methyldopa

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39
Q

Pre-Eclampsia

Epidemiology (1)

A

5% of pregnancies

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40
Q

Pre-Eclampsia

Pathology (2)

A

Failure of trophoblastic invasion of spiral arteries leaving them vasoactive (when they are properly invaded they can’t clamp down in response to vasoconstrictors and thus protects placental flow)
Increase in BP to compensate

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41
Q
Pre-Eclampsia 
Risk factors (10)
A
Previous severe or early (<20 weeks) onset pre-eclampsia 
Chronic hypertension or previous gestational hyperetension 
CKD 
Diabetes 
1st pregnancy 
Pregnancy interval >10 years 
Increasing maternal age 
High BMI 
Multiple pregnancy 
Family history of pre-eclampsia
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42
Q

Pre-Eclampsia

Symptoms (5)

A
Headache 
Flashing lights 
Epigastric/right upper quadrant pain 
Nausea and vomiting 
Facial/finger/lower limb swelling
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43
Q

Pre-Eclampsia

Investigations (7)

A

Urinalysis: proteinuria
Protein:Creatinine ratio >30
FBC + LFT: HELLP syndrome (Haemolysis= +bilirubin, Elevated liver enzymes= high AST + ALT, Low Platelets)
Clotting: prolonged PT + APTT
U&E + creatinine: high creatinine
CTG
Growth scan with umbilical artery Doppler (may have IUGR + polyhydramnios)

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44
Q
Pre-Eclampsia 
Traget BP (1)
A

135/85

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45
Q
Pre-Eclampsia 
Antenatal Management (6)
A

1st labetalol
2nd nifedipine
3rd methyldopa
Induction at 37 weeks
Admit if severe (>160/110), IV labetalol
If very severe, give magnesium sulphate for seizure prophylaxis

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46
Q
Pre-Eclampsia 
Intrapartum Management (4)
A

If planned and uncomplicated just continue anti-hypertensives and monitor BP hourly or every 15-30mins if severe
Early C-section (<37 weeks) if unable to control BP, low sats, HELLP, eclampsia, abruption, worrying fetal monitoring
Deliver at 37 weeks onwards in emergency- induction if not severe, otherwise C-section
3rd stage only use oxytocin because Synto/Ergometrine contraindicated due to high risk of severe hypertension –> stroke

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47
Q

Pre-Eclampsia

Complications (8)

A
Eclampsia
HELLP syndrome 
Microaneurysms develop in arteries (contributing to DIC) 
Cerebral haemorrhages 
IUGR 
Renal failure 
Placental abruption 
Stillbirth
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48
Q

Eclampsia

Definition (2)

A

Tonic-clonic seizure and pre-eclampsia (occurs in 1% of pregnancies with pre-eclampsia)
Most fits occur postnatally

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49
Q

Eclampsia

Treatment (4)

A

Magnesium sulfate for prevention and treatment (IV bolus 4g over 5-10min then 1g/h for 24h)
For repeated seizures: diazepam
If antenatal/intrapartum then C-section once stable
Manage 3rd stage with oxytocin as Synto/Ergometrine are contraindicated as risk severe hypertension + stroke

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50
Q

HELLP Syndrome

3

A

Haemolysis, Elevated Liver enzymes, Low Platelets
Symptoms: epigastric/RUQ pain, nausea and vomiting, dark urine due to haemolysis
Treatment: delivery and same treatment as eclampsia§§

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51
Q

Pre-Existing Diabetes

Pathology (3)

A

Maternal insulin requirements increase
Because placental lactogen, beta hCG, progesterone and cortisol are anti-insulin
Maternal glucose crosses the placenta leading to fetal hyperinsulinaemia and macrosomia

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52
Q

Pre-Existing Diabetes

Pre-pregnancy management (4)

A

Optimise control (aim glucose 4-7mmol/l and HbA1c <48mmol/l)
5mg folic acid daily
Stop oral hypoglycaemics except metformin
Stop ACE-i, ARBs and statins

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53
Q
Pre-Existing Diabetes
Antenatal management (2)
A

Continue insulin type 1 and metformin type 2 (although may require insulin for tighter control)
Growth scans every 4 weeks from 28 weeks

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54
Q
Pre-Existing Diabetes
Intrapartum Management (4)
A

Induction/C-section at 38 weeks
Corticosteroids to promote fetal lung maturity if premature
Continuous fetal monitoring
Sliding scale infusion of insulin (halve rate of infusion after placental delivery in type 1 and stop in type 2)

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55
Q
Pre-Existing Diabetes
Postnatal Management (1)
A

Metformin and insulin fine for breastfeeding

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56
Q
Pre-Existing Diabetes
Maternal complications (3)
A

Hypoglycaemia unawareness (especially 1st trimester)
Increased risk of pre-eclampsia
Increased risk of infection

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57
Q
Pre-Existing Diabetes
Fetal complications (7)
A
Miscarriage 
Increased risk of malformation 
Macrosomia (risk of shoulder dystocia) 
Polyhydrammnios 
Growth restriction 
Preterm labour 
Stillbirth
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58
Q
Gestational Diabetes
Risk Factors (6)
A
BMI >30 
1st degree relative 
Previous baby >4.5kg
Previous gestational diabetes 
Increasing age 
Ethnicity
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59
Q

Gestational Diabetes

Investigations (2)

A

OGTT (if any risk factors) >7.8

HbA1c to exclude undetected pre-pregnancy type 2 diabetes

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60
Q

Gestational Diabetes

Treatment (2)

A

Diet and exercise for 1-2 weeks (after this start medical therapy)
Metformin/insulin

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61
Q

Gestational Diabetes

Complications (7)

A
Type 2 DM (50%- so give lifelong dietary advice and follow up) 
Macrosomia 
Birth trauma 
Shoulder dystocia 
Polyhydramnios 
Prematurity 
Stillbirth
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62
Q

Hyperemesis Gravidarum

Definition (1)

A

Persisting vomiting in pregnancy which causes weight loss (>5% of pre-pregnancy weight) and ketosis

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63
Q
Hyperemesis Gravidarum 
Risk factors (3)
A

Multiple pregnancy (due to high BhCG)
Molar pregnancy
History of hyperemesis

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64
Q

Hyperemesis Gravidarum

Signs + symptoms (5)

A
Inability to keep food/fluids down 
Weight loss 
Dehydration 
Electrolyte disturbance with hypokalaemia and hyponatraemic shock 
Haematemesis from Mallory-Weiss tear
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65
Q

Hyperemesis Gravidarum

Investigations (4)

A

Urinalysis: ketones
U&E: hypokalaemia, hyponatraemia
FBC: raised haematocrit
US: diagnose multiple pregnancy and exclude a mole

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66
Q

Hyperemesis Gravidarum

Treatment (5)

A

Admit for rehydration and correction of metabolic disturbance if unable to keep anything down despite oral anti-emetics
Fluids: 0.9% NaCl + K or Hartmann’s (maintenance fluids)
Folic acid
Anti-emetics eg. promethazine, cyclizine, metoclopramide
Thiamine (eg. pabrinex) to avoid Wernicke’s encephalopathy

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67
Q

Hyperemesis Gravidarum

Complications (5)

A
Wernicke encephalopathy 
Mallory-Weiss tear 
VTE 
SGA 
Pre-term birth
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68
Q

Venous Thromboembolism in Pregnancy

Pathology (3)

A

Increased venous stasis
Trauma to pelvic vessels at delivery
In factors X, VIII and fibrinogen

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69
Q
Venous Thromboembolism in Pregnancy 
Risk factors (7)
A
Increasing age
High BMI 
Increasing parity 
Smoking 
Pre-eclampsia 
Family history of unprovoked DVT 
Multiple pregnancy
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70
Q

Venous Thromboembolism in Pregnancy

Signs + symptoms (2)

A

DVT: swelling, pain, redness
PE: SOB, chest pain, haemoptysis

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71
Q

Venous Thromboembolism in Pregnancy

Investigations (3)

A

Compression/duplex US for suspected DVT
D-dimer inaccurate in pregnancy as they are raised anyway due to changes in the coagulation system
For suspected PE: duplex USS then CXR + V/Q scan

72
Q

Venous Thromboembolism in Pregnancy

Treatment (2)

A

LMWH for 3 months

Stop during labour and resume after delivery (if too high risk to stop anticoagulants consider unfractionated heparin)

73
Q

Small for Gestational Age

Definition (1)

A

Estimated fetal weight <10th centile for their gestational age or abdominal circumference <10th centile

74
Q

Small for Gestational Age

Aetiology (2)

A

Placental: abnormal trophoblast invasion eg. pre-eclampsia, infarction, abruption (tends to cause a symmetrical growth restriction with head sparing + reduced abdo circumference) OR poor nutrient transfer (low pre-pregnancy weight, undernutrition, cocaine, alcohol, smoking)
Fetal: genetic abnormalities eg. trisomy 21 and Turner syndrome OR congenital abnormalities OR infection eg. CMV, rubella OR multiple pregnancy

75
Q

Small for Gestational Age

Major risk factors (9)

A
Age >40 
Smoking 
Cocaine 
Previous SGA baby 
Previous stillbirth 
Family history of SGA 
Diabetes 
Chronic hypertension 
Pre-eclampsia
76
Q

Small for Gestational Age

Minor risk factors (5)

A
Age >35
Nulliparity 
BMI >20 
IVF 
Gestational hypertension
77
Q

Small for Gestational Age

Investigations (2)

A

Serum growth scans

Umbilical artery Doppler

78
Q

Small for Gestational Age

Complications (6)

A

Higher mortality
Higher incidence of cerebral palsy
More likely to have intrapartum fetal distress, meconium aspiration and emergency C-section
Neonatal hypothermia
Neonatal hypoglycaemia
As adults, higher risk of hypertension, type 2 DM

79
Q

Twin Pregnancies

Epidemiology (1)

A

1 in 65

80
Q

Twin Pregnancies

Classification (2)

A

Monozygotic: identical, develop from single ovum which has divided to form 2 embryos
Dizygotic: non-identical, develop from 2 separate ova fertilised at same time

81
Q
Twin Pregnancies
Predisposing factors (4)
A

Induced ovulation and IVF
Previous twins
Family history of twins
Increasing maternal age

82
Q

Twin Pregnancies

Complications during pregnancy (5)

A
Polyhydramnios 
Pre-eclampsia (30% in twins) 
Anaemia more common 
APH 
Gestational diabetes
83
Q
Twin Pregnancies
Fetal complications (5)
A

Increased perinatal mortality
Prematurity (mean gestation 37 weeks)
Growth restriction
Increased malformation rates (especially if monozygotic)
Twin to twin transfusion syndrome: monochorionic twins share a chorion and blood vessels that anastomose so donor twins blood supply disproportionately goes to recipient so donor gets IUGR + oligohydramnios and recipient is larger + polyhydramnios

84
Q

Twin Pregnancies

Complications of Labour (4)

A

PPH
Malpresentation
Vasa praevia rupture
Cord prolapse

85
Q
Rhesus Disease (Isoimmunisation) 
Aetiology (1)
A

Mother Rh-ve and Father Rh+ve

86
Q
Rhesus Disease (Isoimmunisation) 
Pathology (2)
A

Rh-ve mother carrying Rh+ve fetus in her 1st pregnancy develops anti-D antibodies when fetal RBCs enter maternal circulation
In subsequent pregnancies with a Rh+ve fetus, anti-D crosses the placenta leading to fetal RBC destruction and haemolytic disease of the newborn

87
Q
Rhesus Disease (Isoimmunisation) 
Investigations (1)
A

Screen at 8-12 weeks for rhesus status

88
Q
Rhesus Disease (Isoimmunisation) 
Treatment (1)
A

Prophylactic anti-D IgG at 28 + 34 weeks to prevent woman making her own anti-D

89
Q
Rhesus Disease (Isoimmunisation) 
Additional indications for anti-D (5)
A
Miscarriage >12 weeks 
Threatened miscarriage 
Ectopic pregnancy 
APH 
At delivery if baby is Rh+ve
90
Q

Antepartum Haemorrhage

Definition (1)

A

Genital tract bleeding from 24 weeks gestation

91
Q

Antepartum Haemorrhage

Aetiology (9)

A
Placental abruption 
Placenta praevia 
Vasa praevia 
Circumvallate placenta 
Cervical polyps 
Cervical erosions 
Cervical cancer 
Cervicitis 
Vaginitis
92
Q

Antepartum Haemorrhage

Treatment (5)

A

Admit (unless spotting has stopped and the placenta is not low-lying)
If bleeding severe, IV fluids, take bloods, raise legs and give O2
If shocked, give transfusion until BP >100
C-section for placenta praevia (sometimes for abruption or induction) and beware PPH (manage 3rd stage with Syntometrine)
If bleeding mild: for placenta praevia keep in hospital until delivery (C-section at 37-38 weeks), for abruption can go home if settles then treat as high risk

93
Q

Placental Abruption

Associations (8)

A
Pre-eclampsia 
Smoking 
IUGR 
Preterm rupture of membranes 
Multiple pregnancy 
Polyhydramnios 
High maternal age 
Cocaine use
94
Q

Placental Abruption

Signs + symptoms (5)

A
Shock out of keeping with visible loss (bleeding maybe well localised to one placental area and there may be delay before bleeding is revealed) 
Pain constant 
Tender, tense uterus 
Normal lie and presentation 
Fetal heart: absent/distressed
95
Q

Placental Abruption

Consequences (5)

A

Placental insufficiency may cause fetal anoxia/death
Compression of uterine muscles by blood causes tenderness and may prevent good contractions
Posterior abruptions may present with backache
Thromboplastin release may cause DIC
Concealed bleeding may cause maternal shock after which beware renal failure + Sheehan’s syndrome

96
Q

Placenta Praevia

Associations (6)

A
C-section 
Multiparity 
Multiple pregnancy 
Mother >40 
Assisted conception 
Fibroids
97
Q

Placenta Praevia

Signs + symptoms (6)

A
Shock in proportion to visible loss 
No pain 
Uterus not tender 
Abnormal lie and/or abnormal presentation 
Fetal heart usually normal 
Small bleeds before large
98
Q

Placenta Praevia

Investigations (3)

A

US at <24 weeks shows low-lying placenta in many women but by term only 3% lie low (TVUS superior to TAUS)
Combine US with Doppler/MRI to diagnose vasa praevia/placenta accreta
Avoid digital PV examination but speculum is safe, avoid penetrative intercourse

99
Q

Placenta Praevia

Grading (4)

A

Grade I- encroaches lower segment but doesn’t reach the os
Grade II- reaches os but doesn’t cover it
Grade III- partially covers os
Grade IV- completely covers os

100
Q

Placenta Praevia

Treatment (2)

A

Major (III + IV) requires C-section

Minor (I + II) aim for normal delivery unless within 2cm of internal os

101
Q

Vasa Praevia

Definition (3)

A

Fetal vessels from velamentous insertion or between lobes risks damage at membrane rupture causing fetal haemorrhage
Velamentous insertion: umbilical vessels go within the membranes before placental insertion
Placenta succenturia: separate lobe forms away from main placenta which may fail to separate normally and cause a pPH

102
Q

Placental Accreta

Definition (1)

A

There is abnormal adherence of all or part of the placenta to the uterus (placenta increta if myometrium infiltrated, placenta percreta if reaches serosa), predisposing to PPH

103
Q

Retained Placenta

Associations (7)

A
Previous retained placentauterine surgery 
Preterm delivery 
Maternal age >35 
Placental weight is low 
Parity >5 
Induced labour 
Pethidine used in labour
104
Q

Retained Placenta

Treatment (5)

A

Avoid excessive cord traction as it may snap
Put baby to breast to stimulate oxytocin production
Give oxytocin into umbilical vein and clamp cord
If placenta still not delivered 30 min after oxytocin, do manual removal
If fails to transfer to theatre for removal

105
Q

Normal Labour

Definition (1)

A

After 37 weeks and results in spontaneous vaginal delivery of baby within 24h of the onset of regular spontaneous contractions, often follows a ‘show’- plug of cervical mucus and blood as the membranes strip from the os

106
Q

Normal Labour

First stage- latent phase (2)

A

Painful, irregular contractions

Cervix initially effaces (becomes shorter and softer) then dilates to 4cm

107
Q

Normal Labour

First stage- established phase (6)

A

Regular contractions with dilation from 4cm
Rate of dilation should be 0.5cm/h
Takes 8-18h in primip, 5-12 in multip
Check maternal BP + temp every 4h
Assess contractions every 30 min (ideally up to 3-4 per 10 min, lasting up to 1 min)
Vaginal exam every 4h

108
Q

Normal Labour

Second stage- passive stage (2)

A

Complete cervical dilatation but no pushing

Seen particularly in epidurals, where you should allow 1-2 hours to reduce instrumental delivery rate

109
Q

Normal Labour

Second stage- active stage (4)

A

Maternal pushing
Within 3h if primip, 2h if multip
Prevent precipitate delivery (and so intracranial bleeding) by putting pressure over perineum
1 min delay in clamping cord in vigorous term babies, 3 min delay in prematurity (reduces anaemia)

110
Q
Normal Labour
Third stage (3)
A

Delivery of placenta
Physiological management takes less than 1 h
Use of syntometrine (ergometrine + oxytocin) as anterior shoulder is born decreases 3rd stage time to 5min

111
Q

Induction of Labour

Epidemiology (1)

A

20% of UK labours

112
Q

Induction of Labour

Indications (8)

A
Hypertension
Pre-eclampsia
Prolonged pregnancy
Rhesus disease
Diabetes
Placental abruption
Fetal death in utero 
Placental insufficiency
113
Q

Induction of Labour

Contraindications (5)

A
Malpresentation
Fetal distress
Placenta praevia
Cord presentation
Vasa praevia
114
Q

Induction of Labour

Bishop’s Score (6)

A
Cervical dilation 
Length of cervix 
Station of head (cm above spines) 
Cervical consistency 
Position of cervix 
Score >5 favourable and if >7, induction with artificial rupture is possible, avoiding prostaglandins
115
Q

Induction of Labour

Method (3)

A

Prostaglandin PGE2 in pessary or gel form OR misoprostol
Artificial rupture of membranes
After 2-4hours if no contractions start oxytocin infusion

116
Q

Induction of Labour

Complications (5)

A
Failed induction 
Uterine hyperstimulation
Infection
Cord prolapse
C-section (20%) and instrumental delivery (15%) rates are higher
117
Q

Delay in Labour

Causes (3)

A

Power: poor uterine contractions
Passenger: malpresentation, malposition, large fetus
Passage: inadequate pelvis

118
Q
Pain Relief in Labour 
Nitrous oxide (2)
A

Contraindications: pneumothorax

Side effects: nausea, vomiting, faintness

119
Q
Pain Relief in Labour
Narcotic agents (3)
A

Eg. pethidine, diamorphine
Side effects: maternal drowsiness, nausea, vomiting, fetal short term respiratory depression and drowsiness
Give with an anti-emetic

120
Q

Pain Relief in Labour

Pudendal nerve block (1)

A

Sacral nerve roots 2,3 + 4

121
Q

Pain Relief in Labour

Epidural (4)

A

Anaesthetising pain fibres carried by T10-S5
Reduced maternal catecholamine secretion
Helps to lower BP in pre-eclampsia
Complications: patchy block, hypotension, dural puncture

122
Q
Malpresentations
Breech presentation (6)
A

Commonest malpresentation
Causes/associations: idiopathic, uterine abnormalities (bicornuate uterus, fibroids), prematurity, placenta praevia oligohydramnios
30% present undiagnosed in labour
Mother may present with pain under ribs
On palpation the tie is longitudinal, no head felt in pelvis
Most delivered by C-section

123
Q
Malpresentations
Face presentation (3)
A

Many are due to congenital abnormality such as anencephaly
Most occur by chance as head extends rather than flexes as it engages
Almost all rotate so head can be born by flexion but if not then do C-section

124
Q
Malpresentations
Brow presentation (2)
A

Head is between full flexion and full extension and may revert to either
If it persists, vaginal delivery not possible

125
Q
Malpresentations
Shoulder presentation (3)
A

Lie is transverse
Causes: multiparity, multiple pregnancy, polyhydramnios, placenta praevia
High risk of cord prolapse

126
Q
Fetal Monitoring in Labour 
Intermittent auscultation (3)
A

For low risk women
Every 15 min in 1st stage
Every 5 min in 2nd stage

127
Q

Fetal Monitoring in Labour

Indications for CTG (10)

A
Induction of labour 
Postmaturity 
Previous C-section
Pre-eclampsia/hypertension 
Prematurity 
Prolonged rupture of membranes (>24h) 
Diabetes 
Oxytocin 
Epidural 
Pyrexia
128
Q

Fetal Monitoring in Labour

Describing a CTG

A

DRCBRAVADO
DR: determine risk, why is she having CTG?
C: contractions, how many in 10 mins?
BRA: baseline rate (reassuring 100-160)
V: variability
A: accelerations
D: decelerations (downward spikes of >15bpm for >15seconds, late decels = peak decel after contraction passed and are a sign of acidosis)
O: overall (normal, non-reassuring, abnormal)

129
Q

Fetal Monitoring in Labour

Improving a CTG (3)

A

Left lateral position to shift weight off maternal vessels and correct cord compression
IV fluids if hypotensive
Reduce/stop oxytocin

130
Q

Fetal Monitoring in Labour

Fetal blood sampling (2)

A

Take when trace abnormal, unless immediate delivery required
Normal: pH >7.25

131
Q

Cord Prolapse

Definition (2)

A

Descent of cord through the cervix, below presenting part, after rupture of membranes
An emergency because cord compression and vasospasm from exposure of the cord causes fetal asphyxia

132
Q

Cord Prolapse

Associations (5)

A
2nd twin 
Prematurity
Polyhydramnios
Transverse/unstable lie 
Male
133
Q

Cord Prolapse

Treatmetn (4)

A

Deliver fetus immediately (C-section or instrumental if operative delivery)
Displace presenting part by putting a hand in the vagina, push it back up during contractions
Knee-to-chest position so that her bottom is higher than her head
Tocolysis (terbutaline) reduces contractions and helps bradycardia

134
Q

Shoulder Dystocia

Definition (1)

A

Delivery requiring additional obstetric manoeuvres to release the shoulders after gentle downward traction has failed

135
Q

Shoulder Dystocia

Associations (5)

A
Large fetus 
High maternal BMI 
Induction/oxytocin 
Prolonged 1st/2nd stage 
Assisted vaginal delivery
136
Q

Shoulder Dystocia

Complications (4)

A

Increased rate of fetal mortality (asphyxia)
Brachial plexus injuries
PPH
4th degree perineal tears

137
Q

Shoulder Dystocia

Treatment (7)

A

May need episiotomy for space for internal manoeuvres
(1) McRoberts position (hyperflexed lithotomy)
(2) Suprapubic pressure
(3) Internal manoeuvres: rotate baby by 180 degrees and deliver posterior arm
(4) Roll mother onto all fours
Maternal symphysiotomy
C-section after replacement of head by firm pressure of hand to reverse movements of labour

138
Q

Operative Vaginal Delivery

Epidemiology (1)

A

10-15% of UK births

139
Q

Operative Vaginal Delivery

Criteria for use (8)

A
Consent 
1/5th or less head palpable per abdomen 
Ruptured membranes 
Adequate analgesia: epidural/pudendal block 
Adequate contractions 
Full dilatation 
Cephalic presentation 
Neonatal doctor in attendance
140
Q

Operative Vaginal Delivery

Indications (4)

A

Prolonged 2nd stage
Fetal distress
Cord prolapse in 2nd stage
Maternal exhaustion

141
Q

Operative Vaginal Delivery

Forceps vs Ventouse (3)

A

Forceps safer for baby
Forceps cause significant maternal genital tract trauma
Ventouse more likely to fail

142
Q

Operative Vaginal Delivery

Complications (3)

A

Maternal genital tract trauma
Fetal injuries with forceps (rare): facial nerve palsy, skull fractures, orbital injury, intracranial haemorrhage
Fetal injuries with ventouse: cephalhaematoma (most common), retinal haemorrhage

143
Q

Operative Vaginal Delivery

When to Abandon (3)

A

No descent with each subsequent pull
Delivery not imminent after 3 pulls
Head impacted in pelvis

144
Q

Caesarean Section

Layers (7)

A

Skin -> fat -> rectus sheath -> rectus abdominis -> parietal peritoneum -> visceral peritoneum -> uterus

145
Q

Caesarean Section

Indications (7)

A

Repeat CS
Fetal compromise eg. cord prolapse, scalp pH <7.2
Failure to progress/failed induction
Malpresentation
Severe pre-eclampsia
Twin pregnancy with non-cephalic presenting twin
Placenta praevia

146
Q

Caesarean Section

Complications (3)

A

Intraoperative: blood loss, uterine lacerations, bladder laceration
Post-op: wound infection, endometritis, VTE (all emergency C patients get 7 days LMWH)
Higher risk of placenta praevia/accreta in subsequent pregnancies

147
Q

Postpartum Haemorrhage

Primary PPH definition (1)

A

Loss of >500ml in first 24h after deliverry

148
Q

Postpartum Haemorrhage

Primary PPH causes (4)

A

Tone: uterine atony (most common cause)
Tissue: retained products of conception
Trauma: genital tract trauma
Thrombin: clotting disorders

149
Q

Postpartum Haemorrhage

Secondary PPH definition (2)

A

Excessive blood loss from the genital tract after 24h from delivery
Usually occurs between 5-12 days and usually due to retained placental tissue or clot, often with infection

150
Q

Postpartum Haemorrhage

Antenatal risk factors (8)

A
Previous PPH/retained placenta 
High BMI 
Low Hb in mother 
APH 
Multiparity 
Increasing maternal age 
Large placental site (eg. twins, rhesus disease, large baby) 
Low placenta
151
Q

Postpartum Haemorrhage

Intrapartum risk factors (3)

A

Prolonged labour
Induction/oxytocin
Operative birth/C-section

152
Q

Postpartum Haemorrhage

Treatment (10)

A

IV fluids
Deliver placenta and empty the uterus
Massage uterus to generate contraction or perform bimanual compression
Give drugs to contract uterus eg. Syntometrine, oxytocin, ergometrine, misoprostol, carboprost
Repair tears
If bleeding after 2 carboprost doses or suspect retained tissue, theatre for examination under anaesthesia
In theatre, Rusch balloon
Then B-lynch suture
If still ongoing, internal iliac/uterine artery ligation
Then uterine artery embolisation/hysterectomy

153
Q
Tears
First degree (3)
A

Superficial
Don’t damage muscle
Suture

154
Q
Tears
Second degree (1)
A

Involve perineal muscle

155
Q
Tears
Third degree (4)
A

Damage involves anal sphincter

3a: external anal sphincter thickness <50% torn
3b: external anal sphincter thickness >50% torn
3c: both external and internal anal sphincters torn

156
Q
Tears
Fourth degree (1)
A

Anal/rectal mucosa involved

157
Q

Episiotomy

Indications (3)

A

To hasten birth of a distressed baby
For instrumental/breech delivery
To prevent 3rd degree tears

158
Q
Postnatal Mental Health 
Baby blues (3)
A

75% of new mums
Most often 3-5 days after delivery
Commonly lasts 1-2 days but may persist for up to 2 weeks

159
Q
Postnatal Mental Health 
Postnatal depression (3)
A

10% if no psychiatric history
Most resolves within 6 months
Short-term antidepressants (tricyclics/SSRIs)

160
Q
Postnatal Mental Health 
Postpartum psychosis (2)
A

Peak onset 2 weeks

Previous postpartum psychosis has 30% recurrence rate

161
Q

Miscarriage

Definition (1)

A

Loss of a pregnancy before 24 weeks gestation

162
Q

Miscarriage

Epidemiology (1)

A

15-20% of pregnancies

163
Q

Miscarriage

Aetiology (8)

A

Abnormal conceptus (chromosomal or structural)
Uterine abnormality (fibroids or congenital)
Cervical incompetence
Maternal factors (high age, DM, high/low weight)
Bacterial vaginosis (particularly 2nd trimester loss)
Antiphospholipid syndrome present in many women with recurrent miscarriage
Thrombophilia
Unknown

164
Q
Miscarriage 
Threatened Miscarriage (4)
A

Viable pregnancy
Cervical os closed
Symptoms mild
Treatment: conservative, often settles and progresses as normal pregnancy

165
Q
Miscarriage 
Inevitable miscarriage (3)
A

Symptoms severe
Cervical os open
Treatment: conservative, ergometrine IM if profuse bleeding, surgical management if unacceptable bleeding (>2 weeks) or pain or retained products

166
Q
Miscarriage 
Incomplete miscarriage (3)
A

Most products of conception expelled
Remaining tissue may lead to infection
Treatment: conservative, ergometrine IM if profuse bleeding, surgical management if unacceptable bleeding (>2 weeks) or pain or retained products

167
Q
Miscarriage 
Complete miscarriage (3)
A

All products of conception expelled
Os closed
Bleeding stopped

168
Q
Miscarriage 
Missed miscarriage (4)
A

Fetus dead but remains in utero
Cervix closed
Ultrasound: fetal pole >7mm with no fetal heart activity, or mean gestation sac diameter >25mm with no fetal pole or yolk sac
Treatment: expectant (wait 7-14 days for spontaneous completion), 1st vaginal misoprostol, mifepristone, surgical management

169
Q
Ectopic Pregnancy 
Risk factors (7)
A
Damage to the tubes (pelvic inflammatory disease, previous surgery) 
Previous ectopic 
Endometriosis 
IUCD
POP
IVF
Smoking
170
Q

Ectopic Pregnancy

Site (2)

A

97% tubal, most in ampulla, risk of rupture greatest in isthmus
3% implant on ovary, cervix, peritoneum

171
Q

Ectopic Pregnancy

Signs + Symptoms (8)

A
Abdominal pain 
Bleeding 
Fainting 
Diarrhoea and/or vomiting 
Amenorrhoea and +ve urine BhCG 
Referred shoulder tip pain: haemoperitoneum causes diaphragmatic irritation 
Normal sized uterus 
Cervical excitation +/- adnexal tenderness
172
Q

Ectopic Pregnancy

Investigations (5)

A

FBC
Group and save
Serum BhCG (if >1500 a uterine pregnancy would be visible on USS)
Serum progesterone (<20 indicates failing pregnancy)
TVUSS: adnexal mass, no visible intrauterine pregnancy

173
Q

Ectopic Pregnancy

Treatment (5)

A

Conservative: closely monitor, if BhCG levels rise or if become symptomatic then intervene (strict criteria for conservative management- no heartbeat, <30mm, BhCG <2000 and declining)
IM methotrexate
Laparoscopic salpingectomy if other tube healthy, if not then do salpingotomy

174
Q

Gestational Trophoblastic Disorders

Definition (1)

A

Spectrum of disorders ranging from premalignant hydatidiform mole to choriocarcinoma

175
Q

Gestational Trophoblastic Disorders

Pathology (3)

A

Large chorionic villi with overgrowth of trophoblastic cells
Complete mole: empty egg fertilised by sperm that duplicates its own DNA
Partial mole: normal egg fertilised by 2 sperm and are triploid (2 sets of paternal haploid genes, 1 haploid maternal set), may have fetal parts or red cells, much commoner

176
Q
Gestational Trophoblastic Disorders
Hydatidiform moles (3)
A

Signs + symptoms: heavy bleeding, molar tissue like frogspawn, severe morning sickness, large uterus
Investigations: serum BhCG very high
Treatment: evacuation of uterus, anti-D if rhesus -ve, monitor hCG for 6 months and if they don’t drop then give methotrexate

177
Q

Gestational Trophoblastic Disorders

Choriocarcinoma (3)

A

Pathology: from following a benign mole, miscarriage or normal pregnancy
Signs + symptoms: may be years after pregnancy, general malaise, uterine bleeding, signs of metastases
Treatment: methotrexate