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Obs & Gynae > Obstetrics > Flashcards

Obstetrics Flashcards

1
Q

In what ways might a foetus lie?

A
  • Longitudinal-> fundus of uretus to lower segment
  • Transverse-> sideways
  • Oblique-> somewhere between 2
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2
Q

What is the presenting part?

A

Bit of foetus that’s 1st in the pelvic inlet-> eg cephalic or breech

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3
Q

What is the station of the foetus?

A
  • Level of presenting part compared to superior pubic rami (fixed part of mum’s pelvis)
  • Station 0-> head level with ischial spines
  • +/- 3 either side
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4
Q

What is the engagement of the foetus?

A
  • Presenting part in pelvic islet measured in 1/5ths

- Engaged-> 3/5 in pelvis + 2/5 palpable above inlet

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5
Q

What is the symphysial-fundal height?

A
  • Measurement of fundus of uterus to top of midpoint of symphysis pubis
  • From 20 weeks-> estimate size of foetus
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6
Q

What is the ‘fertilisation’ stage of early pregnancy development?

A
  • Sperm binds to zona pellucida
  • Acrosome reaction-> vesicle releases contents by exocytosis
  • Hydrolytic enzymes help sperm burrow into ZP
  • Sperm + egg plasma membranes fuse
  • Cortical reaction-> egg depolarises + ZP hardens
  • Zygote produced
  • 2 haploid nuclei of sperm + egg combine-> single diploid nucleus
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7
Q

What is the ‘cleavage’ stage of early pregnancy developement?

A
  • 2 cells divide to 8-> compaction
  • Then 16-32-> morula with 2 layers + fluid inbetween
  • Blastocyst-> ZP encases trophoblast, embryoblast + blastocyst cavity
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8
Q

What is the ‘implantation’ stage of early pregnancy development?

A
  • Blastocyst hatches from ZP + attaches to endometrium

- Trophoblast’s embryonic pole in contact with endometrium-> proliferate + fuse to form cytoplasm (synctiotrophoblast)

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9
Q

What does the blastocyst consist of at the ‘implantation’ stage of early pregnancy development?

A
  • Trophoblast-> includes synctiotrophoblast
  • Embryoblast-> inner cell mass with primary ectoderm (epiblast) + primary endoderm (hypoblast)
  • Cytotrophoblast-> cell walls + membrane
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10
Q

What happens at day 9 in early pregnancy development?

A
  • Fluid between epiblast forms amniotic cavity (cells- amnioblasts)
  • Cell migration from hypoblast to line blastocyst cavity-> form primary yolk sac
  • Placenta begins forming from synctiotrophoblast
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11
Q

What happens at day 12 of the early pregnancy development?

A

Blastocyst cavity-> now definitive yolk sac

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12
Q

What happens on day 14 of early pregnancy development?

A

Bilaminar germ disc suspended in chorionic cavity

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13
Q

What is the ‘gastrulation’ stage of early pregnancy development?

A
  • In week 3
  • Depression of epiblast (primitive streak)
  • Converts from bi- to tri-laminar disc-> epiblast cells migrate into hypoblast-> mesoderm
  • Epiblast now ‘ectoderm’ but mesoderm + endoderm derived
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14
Q

What does the mesoderm (from the trilaminar disc) develop into?

A

Early CNS

  • Notocordal process + notocord
  • Neural plate forms in epiblast
  • Lateral neural plates-> neural crest cells
  • Paraxial mesoderm-> somites-> axial skeleton + neck/trunk dermis
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15
Q

Why does fluid retention occur in pregnancy?

A
  • 30-50% increase in plasma volume
  • Increased Na+ in extracellular fluid-> increased retention
  • Influenced by capillary pressure (fluid out) + oncotic pressure (fluid in)
  • Increased osmolality-> fluid increases but not urinated-> general oedema
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16
Q

What happens to renal physiology in pregnancy?

A
  • Increases in size
  • 50-60% increased blood flow to afferent arteriole
  • Increased eGFR as increased fluids
  • UTI risks as low urethral tone
  • May get glucosuria
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17
Q

What happens to cardiovascular physiology in pregnancy?

A
  • Peripheral vasodilation
  • HR increases
  • Increased cardiac output
  • BP down in early-mid pregnancy then increases
  • Dilutional anaemia due to increased extracellular volume
  • Hypercoagulation-> increased risk of VTE
  • May see axis deviation on ECG
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18
Q

What happens to blood pressure during pregnancy?

A

Decreases in early-mid then increases to term

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19
Q

What happens to respiratory physiology in pregnancy?

A
  • Increased oxygen consumption
  • Increased diaphragm + subcostal angle-> rib cage splays
  • Increased thoracic circumference
  • Bronchial smooth muscle relaxatio
  • Subjective dyspnoea-> breathe more air per breath but not increase in RR
  • Lower pCO2-> increase gas exchange with baby
  • Foetal Hb has high oxygen affinity-> mum’s Hb gives up more O2 at same partial pressure
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20
Q

What happens to the GI and hepatic tracts in pregnancy?

A
  • Lower gastric + bowel emptying-> constipation
  • Cardiac sphinter relaxes-> heartburn
  • Gallbladder motility decreases-> increased risk of stones
  • Altered appetite
  • Excess saliva
  • Pica-> ingest non-edible substances
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21
Q

What happens to blood glucose in pregnancy?

A
  • In early pregnancy peaks lower-> storing for foetus use
  • In late pregnancy stays higher for longer-> foetal use?
  • Foetus uses from maternal circulation
  • Risk of glucosuria + gestational diabetes
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22
Q

What happens to the uterus in pregnancy?

A
  • Hyperplasia + hypertrophy
  • Natural killer cells
  • Immune privilege-> allows foreign body to grow inside
  • Endovascular remodelling ie spiral arteries infiltrated + stripped out by endovascular-> low resistance + pools of blood
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23
Q

What is Chadwick’s sign?

A

Blue tinge to the cervix due to oestrogen + increased blood flow

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24
Q

How is a pregnancy monitored in general?

A
  • US for growth-> head circumference, abdominal circumference, femur length, weight
  • Liquor volume
  • Umbillical artery doppler
  • Growth chart-> gestational age, weight, centile lines (conpared to mum’s height + weight and previous babies)
  • Intermittent auscultation
  • Cardiotocography (CTG) at >28 weeks
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25
Q

In low risk pregnancies, when do scans occur?

A
  • Dating scan-> 11-13 weeks

- Anomaly-> 20 weeks

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26
Q

When is a pregnancy considered high risk?

A

Co-morbidities, smoker, twins or more, age 35+ or <17, complications in previous pregnancy

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27
Q

When is sickle cell and thalassaemia tested for in pregnancy?

A
  • All women by 8-10 weeks
  • Dad if mum a carrier
  • Both carriers-> prenatal diagnosis + counselling by 12 weeks
  • In newborn blood spot screen
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28
Q

When are infectious diseases screened for in pregnancy and what happens if the tests are positive?

A
  • HIV, Hep B + syphilis-> recommended to all in early pregnancy
  • Offer again at 20 weeks
  • If +ve-> contact within 10 days
  • Hep B-> baby vaccinated at 24 hours then imms schedule
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29
Q

What is the foetal anomaly screening test (in general)?

A
  • Offered to all
  • For Patau’s (chromosome 13), Edward’s (18) + Down’s (21)
  • Combo test, quad test, early scan and/or non-invasive prenatal testing (NIPT)
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30
Q

What does the combination test for foetal anomaly screening entail?

A
  • At 11+2 to 14+1 weeks
  • Maternal age
  • US-> crown rump length + nuchal transluency
  • Serum PAPPA
  • Serum bHCG
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31
Q

What does the quad test for foetal anomaly screening entail?

A
  • At 14+2 to 20+0 weeks

- Serum markers-> AFP, bHCG, oestradiol + inhibin A

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32
Q

What is the ‘early scan’ and when does it occur?

A
  • At 8-12 weeks
  • To see if-> viable, single/multiple pregnancy, major anomaly
  • Check gestational age-> dating scan
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33
Q

What is non-invasive prenatal testing (NIPT)?

A
  • Can be used as foetal anomaly screening
  • From 10 weeks
  • Only private
  • Analyse foetal DNA fragments from maternal blood
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34
Q

What is the ‘anomaly scan’ and when does it occur?

A
  • For all pregnancies at 18+0 to 20+6 weeks
  • Look for-> anencephaly, exophalmos, serious cardiac defects, bilateral renal agenesis, lethal skeletal dysplasia, chromosome abnormalities
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35
Q

When is a Newborn Infant Physical Exam (NIPE) performed?

A
  • Within 72 hours of birth

- Then at 6-8 weeks after

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36
Q

What might a Newborn Infant Physical Exam (NIPE) reveal?

A

Cataracts, CHD, DDH, bilateral undescended testes

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37
Q

When would a baby by referred to a specialist after a Newborn Infant Physical Exam (NIPE) and how long would that take?

A
  • Eye problems-> within 2 weeks
  • Heart-> ASAP
  • Bilateral testes undescended-> within 24 hours
  • Unilateral testes-> 6 weeks to GP
  • DDH concerns-> 2 weeks
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38
Q

What are the risk factors for developmental dysplasia of the hip?

A
  • Breech at birth or when >36 weeks
  • 1st degree FH of hip problems
  • Twins + 1 breech
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39
Q

When is the first newborn hearing screening test done and what is it?

A
  • Within 4 weeks of birth
  • Automated otoacoustic emission test
  • Earpiece plays sound + equipment picks up response
  • Picks up permanent moderate/severe/profound deafness
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40
Q

What test is performed as part of the newborn hearing screen if the automated otoacoustic emission test detects a problem?

A
  • Automated brainstem response
  • Done within 4 weeks of AUOT
  • Sensors on head pick up response of headphones clicking
  • Referal to specialist if 1 or both ears
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41
Q

When is the newborn blood spot test performed?

A

Day 5 of life

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42
Q

What does the newborn blood spot test screen for?

A
  • Sickle cell disease
  • Congenital hypothyroidism
  • Cystic fibrosis
  • 6 metabolic disorders-> includes phenylketonuria and maple syrup urine disease
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43
Q

What is the normal circulation from the placenta to the foetus?

A
  • 500-600ml/min to allow O2 transfer via conc gradient
  • Spiral arteries respond to increased demand of blood supply to placental bed-> lower pressure + increased flow
  • 2 umbilical arteries carry oxygenated blood from foetus to chorionic plate to chorionic villi to capillaries then venous + umbilical veins-> maternal vessels alongside
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44
Q

What causes placental insufficiency?

A
  • Doesn’t develop properly
  • Damaged
  • Mum’s blood supply inadequate
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45
Q

What are the effects of placental insufficiency on the foetus?

A
  • Hypoxia-> hypoglycaemia, hypercapnia, acidaemia, hyperlactaemia
  • Hypoglycaemia but low glycogen stores so hard to get over-> growth axis downregulated (involved insulin + IGF-1)
  • Try to increase O2-carrying capacity of blood-> EPO release + polycythaemia-> increase blood viscosity + occulsions
  • Brain sparing-> blood directed to brain, adrenals + heart to increase survival but often CNS maturity delayed
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46
Q

What are the complications of placental insufficiency?

A

Foetal distress, pre-eclampsia, IUGR, stillbirth, hypothyroidism

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47
Q

What factors influence foetal growth?

A
  • Maternal-> size, weight, BMI, nutritional state, anaemia, smoking, substance abuse, environmental noise exposure, uterine blood flow, infection
  • Placental-> size, microstructure, umbilical blood flow, transporters + binding proteins, nutrition production + utilisation, transplacental glucose
  • Foetal-> genome, nutrition productio, hormone output, genetic conditions, insulin
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48
Q

What are the 3 categories of factors that influence foetal growth?

A

Maternal, placental and foetal

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49
Q

What maternal factors influence foetal growth?

A

size, weight, BMI, nutritional state, anaemia, smoking, substance abuse, environmental noise exposure, uterine blood flow, infection

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50
Q

What placental factors influence foetal growth?

A

size, microstructure, umbilical blood flow, transporters + binding proteins, nutrition production + utilisation, transplacental glucose

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51
Q

What foetal factors influence foetal growth?

A

genome, nutrition production, hormone output, genetic conditions, insulin

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52
Q

What is intra-uterine growth restriction?

A

When foetus not as big as would expect for gestational age-> symmetrical or asymmetrical

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53
Q

What is symmetrical intra-uterine growth restriction?

A

All of the baby’s body is small (30% of IUGRs)

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54
Q

What is asymmetrical intra-uterine growth restriction?

A

Baby’s head and brain is normal size but body small-> 70% of IUGRs

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55
Q

What is the definition of small for gestational age?

A
  • <10th centile for gestational age

- Height/weight <2SDs of population mean

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56
Q

What is the definition of a low birth weight?

A

<2.5kg (5 pounds 8 oz) when born

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57
Q

What are the signs and investigations for intra-uterine growth restriction?

A
  • Reduced foetal movements
  • Oligohydramnios
  • Low/absent/reversed end diastolic flow on umbilical artery doppler
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58
Q

How is intra-uterine growth restriction managed?

A
  • Monitor-> growth charts, 20 week scan measurements (abdominal + head circumference etc), umbilical artery doppler
  • Mum-> manage co-morbidities, diet advice, bed rest
  • Induction + early delivery-> when stopped growing etc
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59
Q

What are the potential consequences of intra-uterine growth restriction?

A
  • NICU admission
  • Breathing + feeding problems
  • Difficulties maintaining body temperature
  • Hypoglycaemia
  • Increased infections
  • Chronic conditions
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60
Q

What is macrosomia?

A

Weighs 4kgs (8 pounds 13 oz) at birth

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61
Q

What is the definition of large for gestational age?

A

> 90th centile for gestational age

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62
Q

How is macrosomia managed?

A
  • Prevent-> pre-conception appointment (when overweight)
  • Maternal and foetal tests for diabetes (+ manage if have)
  • Weight monitoring
  • C-section-> when over 9lb 15oz + DM or >11lb + shoulder dystocia
  • Vaginal-> inhospital as more likely forceps/ventouse
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63
Q

What are the potential complications of macrosomia?

A
  • Mum-> shoulder dystocia, GU lacerations, bleed after delivery (hypotonia + PPH risk), uterine scar rupture
  • Baby-> hypoglycaemia, obesity, metabolic syndromes, increased MI/stroke risk
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64
Q

What are the potential causes of bleeding in pregnancy?

A
  • Early-> implantation spotting, cervical changes
  • Throughout-> miscarriage, ectopic
  • Later-> infection, placenta praevia, abruption
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65
Q

What are the investigations for PV bleeding during pregnancy?

A
  • Vaginal/pelvic exam
  • TV/abdominal US
  • Serum hCG
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66
Q

What is the definition of miscarriage?

A

Loss of pregnancy before 24 weeks of gestation

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67
Q

When do most miscarriages occur?

A

Within first 12 weeks of pregnancy

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68
Q

How many pregnancies in the UK end in miscarriage?

A

20-25%

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69
Q

What are the potential causes of miscarriage?

A
  • Genetics
  • Hormones (eg irregular periods),
  • Blood clots (eg in placenta)
  • Infection (eg rubella)
  • Anatomical-> weak cervix opens as uterus grows, irregular uterus shape
  • Large fibroids
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70
Q

What are the potential causes of recurrent miscarriage?

A

Increased maternal age, low BMI, PCOS, clotting problems, abnormal karyotype, antiphospholipid syndrome, abnormal uterus

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71
Q

What are the symptoms of miscarriage?

A

Bleeding, pain, lack/loss of pregnancy symptoms

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72
Q

What are the types of miscarriage?

A
  • Complete
  • Incomplete
  • Anembryonic
  • Missed
  • Inevitable
  • Threatened
  • Recurrent
  • Septic
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73
Q

What is a complete miscarriage?

A

All products of conception expelled

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74
Q

What is an incomplete miscarriage?

A

Some products of conception remain in the uterus

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75
Q

What is an anembryonic miscarriage?

A
  • Blighted ovum/empty sac

- Gestational sac present but embryo absent or stops growing early

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76
Q

What is a missed miscarriage?

A

When the baby has passed away or not developed but has not yet been expelled from the uterus

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77
Q

What is an inevitable miscarriage?

A

Internal os open + bleeding but products of conception still in the uterus

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78
Q

What is a threatened miscarriage?

A

Some bleeding + pain but os closed + viable pregnancy

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79
Q

What is recurrent miscarriage?

A

3+ consecutive miscarriages

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80
Q

What is septic miscarriage?

A

Tissue from missed/incomplete miscarriage gets infected

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81
Q

How is miscarriage diagnosed?

A
  • US-> no heartbeat, crown rump length >7mm
  • Expelled contents examination
  • hCG-> rule out ectopic
  • Clotting screen + cytogenics
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82
Q

How is miscarriage managed?

A
  • Oral/vaginal prostaglandin analogues

- Surgical-> evacuation of retained products (ERPC) if bleeding/infection

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83
Q

What is an ectopic pregnancy?

A

Pregnancy that implants + develops outside the uterine cavity (usually fallopian tubes)

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84
Q

What are the risk factors for ectopic pregnancy?

A

IVF + assisted conception, PID, endometriosis, previous ectopic, smoking, IUD, fallopian tube/cilia damage

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85
Q

How does ectopic pregnancy present?

A
  • Unilateral abdominal pain
  • Bleeding
  • Amenorrhoea-> if don’t know pregnant
  • Shoulder tip pain-> intraabdominal blood irritates diaphragm
  • Collapse
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86
Q

How is ectopic pregnancy investigated?

A
  • Serum hCG + repeat in 24 hours-> rise but not as much as would expect
  • TV US> locate
  • Serum progesterone-> <20nmol/L suggests failing
  • Laparoscopy
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87
Q

How is ectopic pregnancy managed?

A
  • Expectant + monitoring as may dissolve by self
  • IM single dose MTX-> stop growth
  • Laparoscopic partial or total fallopian tube removal
  • Laparotomy if ruptured
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88
Q

When does ectopic pregnancy usually rupture?

A

At 14-16 weeks

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89
Q

What is pregnancy of unknown location (PUL)?

A

Positive pregnancy test but doesn’t appear as intrauterine, ectopic or retained products of conception

90
Q

How does pregnancy of unknown location (PUL) present?

A

Asymptomatic, abdominal pain, bleeding

91
Q

How is pregnancy of unknown location (PUL) investigated?

A
  • Progesterone
  • hCG
  • Laparoscopy
92
Q

What are the potential outcomes of pregnancy of unknown location (PUL)?

A

Intrauterine pregnancy, ectopic, failing pregnant, persistent PUL, ovarian/CNS tumour

93
Q

What is a molar pregnancy?

A

Hydatidiform mole-> unusual + rapid growth of placenta, cysts burrow in uterine wall, complete or partial

94
Q

What is complete molar pregnancy?

A

Sperm fertilises empty ovum + foetus doesn’t develop

95
Q

What is partial molar pregnancy?

A

2 sperms fertilise the ovum + foetus might be present

96
Q

How does molar pregnancy present?

A
  • Irregular bleeding
  • Uterus large for dates
  • Pain
  • Exaggerated pregnancy symptoms-> hyperemesis gravidarum
97
Q

What is the characteristic US appearance of molar pregnancy?

A

Snowstorm appearance

98
Q

How is molar pregnancy managed?

A

Surgical/medical evacuation

99
Q

What is hyperemesis gradivarum and how does it present?

A

Symptoms due to excess b-hCG

  • Vomiting
  • Weight loss
  • Muscle wasting
  • Dehydration
  • Electrolyte imbalances
100
Q

How is hyperemesis gradivarum investigated?

A
  • Urinalysis + MSU
  • FBC, U+E, LFT
  • US-> molar pregnancy
101
Q

How is hyperemesis gradivarum managed?

A

Oral/IV fluids, monitoring, antiemetics, thiamine, thromboprophylaxis

102
Q

What is pre-eclampsia?

A

Hypertension + proteinuria at 20+ weeks of pregnancy

103
Q

What is the pathophysiology of pre-eclampsia?

A
  • Incomplete trophoblast invasion into spiral arteries-> not lower resistance
  • Decreased blood flow to placenta-> ischaemia + growth prevention
  • Affect RAAS-> vasoconstriction + DIC
104
Q

What are the risk factors for pre-eclampsia?

A

Primigravida, young, BAME, multipregnancy, hypertension, renal disease

105
Q

How is pre-eclampsia investigated?

A
  • BP-> 140/90-149/99 (mild), 150/100-159/109 (moderate), 160/110+ (severe)
  • Urine-> proteinuria
  • May have oligouria
  • Bloods-> deranged LFTs, low platelets
  • IUGR
106
Q

How is pre-eclampsia treated?

A
  • Labetolol or nifedipine
  • MgSO4-> pre-seizure management
  • Delivery+ anti-hypertensives
  • NOT push in labour if >160 systolic-> intracerebral bleeding risk
107
Q

How is pre-eclampsia prevented?

A

Aspirin 75mg-> at 12-28 weeks of pregnancy

108
Q

What is eclampsia?

A

Tonic clonic seizures

109
Q

What is the definition of hypertension in pregnancy?

A
  • Gestational-> new, 20+ weeks, no proteinuria

- Chronic-> before pregnancy or <20 weeks

110
Q

How is hypertension managed in pregnancy?

A

Aspirin 150mg from 12 weeks-> reduce pre-eclampsia risk

111
Q

What is placenta praevia?

A
  • Placenta inserted wholly or partially into the lower segment of the uterus
  • Usually called ‘low-lying placenta’ until >37 weeks as often moves
112
Q

What are the different grades of placenta praevia?

A
  • Minor (I/II)-> close to/encroaching on cervical os (<2cm)

- Major (III/IV)-> lies over os, can cause cervical effacement + dilation, bleeding + death

113
Q

How does placenta praevia present?

A
  • Asymptomatic

- Painless bleeding triggered by sex or injury

114
Q

How is placenta praevia monitored?

A
  • 20 weeks-> US + TVUS
  • 32 weeks-> check position + may measure cervix (assess early labour risk)
  • 36 weeks-> check again
115
Q

How is placenta praevia managed?

A
  • Regular monitoring
  • Stay home-> asymptomatic + close to hospital etc
  • Symptoms-> admit from 34+ weeks
  • Steroid injections-> at 34-36 weeks
  • Magnesium sulphate-> if <32 weeks
  • C-section likely at 36-37 weeks
  • Irons supplements + regular Hb measurements
116
Q

What is placental abruption?

A

Placenta separates from uterine wall-> concealed or revealed

117
Q

How does placental abruption present?

A

Pain, PV bleeding, hard/woody uterus, haemodynamic instability

118
Q

How is placental abruption managed?

A
  • Watch + wait if small
  • Induction at 37+ weeks
  • C-section
119
Q

What is placental accreta?

A

When the placental villi grows into deeper tissues + makes delivery more difficult

  • Accreta-> attached to myometrium
  • Increta-> into the myometrium
  • Percreta-> through myometrium to serosa + other structures
120
Q

What causes placental accreta?

A

Previous C-section (into scar), uterus surgery, fibroids, bicornate uterus, 35+, IVF, previous childbirth

121
Q

How is placental accreta diagnosed?

A
  • Suspected via US or MRI

- Confirm in delivery-> placenta not delivered in 30 minutes or 1 hour

122
Q

What are the risks/implications of placental accreta?

A
  • Severe bleed (PPH) especially if retained-> DIC, RDS, kidney failure
  • Damage other organs-> bladder
  • Occult blood loss-> behind placenta
123
Q

How is placental accreta managed?

A
  • FBCs, group save + crossmatch
  • IV access
  • Oxytocin into umbilical vein + wait
  • Manual removal of placenta (MROP)-> take out with hands in 1 piece then give oxytocin for 4 hours + IV antibiotics
  • Often need delivery at 32 weeks ish
124
Q

What is vasa previa?

A
  • Foetal vessels through membranes over internal cervical os

- Unprotected by placental tissue + umbilical cord-> prone to bleeding

125
Q

How does vasa previa present?

A
  • Moderate PV bleed
  • Foetal distress
  • Especially after membrane rupture
126
Q

How is vasa previa managed?

A
  • TV US

- Emergency C-section

127
Q

What are the risk factors for uterine rupture?

A

Previous C-section

128
Q

How does uterine rupture present?

A
  • CTG abnormalities
  • Feel foetal parts on abdomen
  • Severe pain between contractions
  • Maternal shock
129
Q

What is antepartum haemorrhage?

A

A bleed at any point up to 24 weeks of pregnancy

130
Q

What can cause antepartum haemorrhage?

A

Placental abruption

  • Placenta praevia
  • Severe chorioamnionitis
  • Sepsis
  • Severe pre-eclampsia-> hepatic rupture
  • Retained deceased foetus
  • Ectopic
131
Q

How is antepartum haemorrhage managed?

A
  • Admit for 24 hours-> high risk of rebleed
  • Maternal-> FBC, coagulation screen, Kleinhaur test (see if rhesus change from negative + need anti-D)
  • Foetal-> US, umbilical artery doppler, increase monitoring
  • Resus if need
  • Left lateral tilt-> reduce VC compression + increase return
132
Q

What is the definition of primary post-partum haemorrhage?

A

Blood loss of >500ml in first 24 hours after delivery

133
Q

What is the definition of secondary post-partum haemorrhage?

A

Excess vaginal bleeding from 24 hours to 12 weeks after delivery

134
Q

What is the definition of minor post-partum haemorrhage?

A

<1500ml blood loss + no shock

135
Q

What is the definition of major post-partum haemorrhage?

A

> 1500ml blood loss + shock

136
Q

Why can post-partum haemorrhage progress quickly?

A
  • Uterus blood flow at term is 500-800ml/min-> potential to lose lots
  • Can tolerate 10-15% but lose CV compensation if 30-40+%
137
Q

What causes primary post-partum haemorrhage?

A

4T’s…

  • Tone-> uterine atony
  • Tissue-> retained products
  • Trauma-> to genital tract
  • Thrombin-> coagulopathy
138
Q

What causes secondary post-partum haemorrhage?

A
  • Infection of retained products
  • Gestational trophoblastic disease
  • Uterine AV malformation
139
Q

How does CMV present in pregnancy?

A

Asymptomatic or infective mononucleosis picture in mum

140
Q

How is CMV in pregnancy managed?

A
  • Antibodies-> IgG
  • Avidity index-> low means 1st infection
  • Amniocentesis
  • 4 weeks of acyclovir
141
Q

What are the complications of CMV in pregnancy?

A

Sensorineural hearing loss, microcephaly, SGA, large ventricles, calcifications, hepatosplenomegaly

142
Q

How are chronic diseases managed in pregnancy (generally)?

A
  • Preconception counselling-> consider effect of pregnancy on condition
  • Optimise disease control
  • Contraception if defer pregnancy
  • Joint obstetric-medical clinics
143
Q

What are the cardiac risks in pregnancy and what should be considered?

A

IHD risk 3-4x higher

  • Postural hypotension
  • If have stenosis-> pulmonary oedema + HF
  • Manage-> echo/ECGs, monitor foetal growth, no ACE-i’s
144
Q

What are the cardiac risks in pregnancy and what should be considered?

A

IHD risk 3-4x higher

  • Postural hypotension
  • If have stenosis-> pulmonary oedema + HF
  • Manage-> echo/ECGs, monitor foetal growth, no ACE-i’s
145
Q

What effects might being pregnant have on a person with asthma?

A
  • If not controlled likely to worsen in 3rd trimester
  • Safe to use-> SABA, LABA, ICS, LTAs, steroids etc
  • Affect on foetus-> IUGR (eg poor placental perfusion), prematurity, neonatal hypoxia
146
Q

How is hyperthyroidism managed in pregnancy?

A
  • Usually improves in 1st trimester
  • Measure thyroid antibodies + baby growth
  • Risks-> thyroid crisis + thyrotoxicosis in baby
  • Give propylthiouracil in 1st trimester then carbimazole later (can cause foetal anomalies)
147
Q

How is hypothyroidism managed in pregnancy?

A
  • Complications of foetal loss + neurodevelopmental problems

- Increase thyroxine in 1st trimester

148
Q

How might CKD affect pregnancy?

A
  • Renal blood flow usually increases by 50% (healthy)
  • Investigate-> BP, creatinine, proteinuria
  • Maternal risks-> severe HTN, pre-eclampsia
  • Baby risks-> prematurity, stillbirth, microsomia
149
Q

What neuro conditions are common in pregnancy?

A
  • Migraine
  • Epilepsy
  • Spina bifida in baby-> epilepsy + meds etc
150
Q

How is epilepsy managed in pregnancy?

A
  • Folic acid 5mg (high dose)
  • Screen for abnormalities
  • Delivery plan-> exhaustion + pain can predispose to seizures
  • NOT sodium valproate
151
Q

What are the risks associated with epilepsy in pregnancy?

A
  • Foetal abnormalities-> eg valproate SEs
  • Inheritance
  • Seizure in labour-> foetal hypoxia
152
Q

What effect might pulmonary hypertension have in pregnancy?

A
  • Baby-> IUGR, premature, drug SEs

- Need anaesthetic input in birth

153
Q

What is the pathophysiology of obstetric cholestasis?

A
  • Changes to bowels-> increased transit times, decreased emptying, peristalsis, low oesophageal sphincter pressure
  • Bile moves slower-> can stasis
154
Q

How does obstetric cholestasis present?

A

Itching without rash

155
Q

How is obstetric cholestasis investigated?

A
  • AST + ALT raised
  • Liver scan
  • Bile acids increased
156
Q

How is obstetric cholestasis managed?

A
  • Ursodeoxycholic acid

- Resolves after delivery

157
Q

What are the complications of obstetric cholestasis?

A
  • Premature labour
  • Stillbirth
  • Recurs in future pregnancy in 80%
158
Q

What are the definitions of anaemia in pregnancy?

A
  • 1st trimester-> <110 Hb
  • 2nd + 3rd-> <105
  • Post-delivery-> <100
159
Q

What happens to the blood in pregnancy?

A
  • Increased volume-> dilutional anaemia
  • WCC, clotting and fibrinogen up
  • Haematocrit, Hb, antithrombin, platelets down
  • Iron requirements increase by 2-3x
  • Folate requirements up by 10-20x
160
Q

What complications might iron deficiency anaemia in pregnancy cause?

A
  • PPH
  • Post-natal depression
  • Prematurity
  • Low birthweight
161
Q

How is iron deficiency anaemia in pregnancy managed?

A

Supplements-> ferrous sulphate 200mg TDS for a month then check again

162
Q

How is B12/folate deficiency anaemia in pregnancy managed?

A

5mg folic acid OD then recheck in 4 weeks

163
Q

What is gestational diabetes?

A

Carbohydrate intolerance first recognised in pregnancy-> increases chance of T2DM

164
Q

How is pre-existing diabetes managed in pregnancy?

A
  • Aim for HbA1c of <48mmol/l
  • Folic acid 5mg
  • Stop ACEis and statins
  • Retinal + renal screening
  • If pre-conception HbA1c >68mmol/L-> advise against pregnancy (likely abnormalities)
165
Q

What are the potential complications of diabetes in pregnancy?

A
  • Baby-> sencondary foetal hyperinsulinaemia, excess glucose, macrosomia, IUGR, miscarriage, stillbirth, shoulder dystocia + Erb’s palsy)
  • Mum-> DKA, hypos, retinopathy, pre-eclampsia, prematurity
166
Q

What is the definition of labour?

A

Regular uterine contractions with progressive cervical effacement + dilation

167
Q

What are the stages of labour?

A
  • Stage 1-> latent (cervix <4cm) + active (4-10cm)
  • Stage 2-> giving birth
  • Stage 3-> from baby delivery to delivery of placenta
  • After-> increased oxytocin for bonding + uterus contraction
168
Q

What are the features of labour?

A
  • Membrane rupture + amniotic fluid leakage
  • Foetus through pelvis-> engage + descent, internal rotation, crowning, restitution, external rotation, anterior the posterior shoulder delivery
  • Contractions-> from fundus down to expel baby
  • Effacement-> soften + thinning of uterus
169
Q

What is the most common shape of the female pelvis?

A

Gynaecoid

170
Q

What are the different stages of the foetus moving through the pelvis during birth?

A
  • engage + descent-> head occipital-transverse
  • internal rotation at ischial spine-> head occipital anterior
  • crowning ie head extends
  • restitution-> head rotates so in line with foetal spine
  • external rotation
  • anterior then posterior shoulder delivery
171
Q

What are the 3Ps of successful labour?

A
  • Passageway (pelvis)
  • Passenger
  • Power
172
Q

What is the modified Bishop’s score of the cervix?

A
  • Looks for if labour is likely to start spontaenously
  • If 8+ then is likely
  • If lower may need to induce
173
Q

What is the role of prostaglandins in induction of labour?

A
  • Into posterior fornix via gel/pessary
  • Prep cervix + helps opening in response to contractions
  • SEs of prolonged contractions + pain + diarrhoea
174
Q

What is the role of oxytocin (eg syntocinon) in labour?

A
  • Via infusion
  • 6 hours after prostaglandins used
  • Initiate uterine contractions via myometrium contractions
  • When membranes ruptured
175
Q

What pain management options are available in labour?

A
  • Non-medical-> pool birth, upright, slow breaths, aromatherapy
  • Medical-> paracetamol, codeine, entonox, opioids, epidural (eg fentanyl + bupivacaine)
176
Q

What is delayed cord clamping?

A
  • Allow 1 minute of blood transfusion

- Benefits-> increases RBCs, iron and stem cells

177
Q

What are some options for management of 3rd stage of labour?

A
  • IV oxytocin
  • Controlled cord traction-> risk of cord snapping or uterus inversion
  • Examination
178
Q

How is the foetus monitored in labour?

A
  • Intermittent auscultation-> Pinnard/doppler every 15 mins for 1 min
  • Cardiotocography (CTG)-> intermittent or continuous depending on risk level
  • Foetal ECG-> on scalp or abdomen
  • Foetal blood sample-> when abnormal CTG + >4cm dilation
179
Q

What is monitored on cardiotocography (CTG)?

A

DR C BRaVADO

  • DR-> define risk
  • Contractions-> worry if >5 every 10 mins
  • Bradycardia-> >3 mins (definite), 6 (think about theatre), 9 mins (theatre), 12 (born)
  • Variability-> 5-25bpm normal + baseline 110-160bpm
  • Accelerations
  • Decelerations-> normal in contractions as compressed but variable or after contraction may be worrying
  • Overall-> normal (all OK), suspicious (1+ abnormal), abnormal (2+)
180
Q

How does foetal blood samples be interpretted?

A

Look at pH

  • > 7.25 is normal
  • 7.21-7.24 is borderline + should repeat in 30 mins
  • <7.2 should consider delivery
181
Q

What are the different types of rupture of membranes?

A
  • Spontaneous
  • Artificial
  • Premature
182
Q

What is the definition of failure to progress (in 1st stage of labour)?

A
  • <2cm dilation in 4 hours or slowing of dilation
  • Primary dysfunctional labour-> from early active phase
  • Secondary arrest-> slowing when previously adequate
183
Q

What causes failure to progress (in 1st stage of labour)?

A
  • Insufficient uterine power/activity
  • Malposition/malpresentation
  • Large baby
  • Inadequate pelvis eg too small
184
Q

What is failure to progress (in 2nd stage of labour)?

A

When baby not delivered within 1 hour of active pushing (multiparous) or 2 hours (nulliparous)

185
Q

What are the risk factors for failure to progress (in 2nd stage of labour)?

A

Epidural, amniotic sac problems, diabetes, PROM

186
Q

What are the consequences of failure to progress in labour?

A

Foetal distress, foetal intracranial haemorrhage, increased chance of needing operative delivery, injury (CP, HIE), foetal infection, birth canal damage, PPH, post-partum infection

187
Q

What is a malpresentation?

A

Baby in any position other than vertex/cephalic lying near internal os

188
Q

What is the best presentation for baby to be in?

A

Cephalic-> left occipital anterior

189
Q

What can cause malpresentation?

A
  • Maternal-> multiparous, pelvic tumours, contracted pelvis
  • Foetal-> premature, multipregnancy, macrosomia, death
  • Placenta-> previa etc
190
Q

What are the types of breech presentation?

A
  • Extended/Frank-> feet by head
  • Flexed/complete-> bum + feet
  • Footling-> 1 foot
191
Q

How is breech presentation managed?

A

Try ECV at 36 weeks

192
Q

What are the types of malpresentation?

A
  • Breech
  • Face-> hyperextension of neck
  • Brow-> midway between flex + extension
  • Cord-> emergency as risk of cord prolapse
193
Q

What is cord prolapse?

A
  • Cord presents after rupture of membranes

- Exposure leads to vasospasm + compression-> hypoxia in baby

194
Q

What are the risk factors for developing cord prolapse?

A

PROM, malpresentation, polyhydramnios, multiparity, multipregnancy

195
Q

How is cord prolapse managed?

A
  • Emergency-> want to deliver in a few minutes
  • Elevate foetal head so not pushing
  • Trendelenburg-> mum on all 4s, feet higher than head etc
196
Q

What is shoulder dystocia?

A

Failure to deliver the anterior shoulder

197
Q

What are the risk factors for shoulder dystocia?

A

Diabetes, previous shoulder dystocia, macrosomia, obesity, prolonged labour, instrumental delivery

198
Q

What are the complications of shoulder dystocia?

A
  • Mum-> PPH, vaginal tears, PTSD

- Neonate-> hypoxia, fits, CP, Erb’s palsy (C5-6 nerves)

199
Q

How might Erb’s palsy be prevented in shoulder dystocia?

A
  • Breaking bones eg clavicle or humerus

- Episiotomy

200
Q

How is shoulder dystocia managed?

A

HELPERRR

  • Help
  • Evaluate for episiotomy
  • Legs in McRobert’s ie full flexion
  • Suprapubic pressure
  • Enter pelvis
  • Rotational manouvre
  • Remove posterior arm
  • Replace head + CS
201
Q

What is the puerperium?

A

Time from delivering the placenta to 6 weeks after

202
Q

What is involution in the puerperium?

A

Shrinking of the uterus + genital, muscle changes + decidua (mucous membrane lining the uterus)

203
Q

What are the different stages of lochia expulsion during involution in the puerperium?

A
  • Lochia rubra-> day 0-4, blood, discharge, decidua, foetal membrane, vernix (protective layer on baby), meconium
  • Lochia serosa-> day 4-10, WBCs, mucous, exudate, foetal membrane
  • Lochia alba-> day 10-28, cholesterol, epithelial fat, mucous, leukocytes
204
Q

What is the role of prolactin in the puerperium?

A
  • Produced during suckle-> sensory input from nipple to brain
  • Secreted from anterior pituitary-> blood
  • Lactocytes-> produce milk + suppress ovulation
  • Increases at night + during feeds
205
Q

What is the role of oxytocin in the puerperium?

A
  • Suckle causes sensory input to brain
  • Secreted from posterior pitutary
  • Causes myoepithelial contraction + expulsion of milk
  • Increased when sees baby
  • Decreases when stressed
206
Q

What is the role of lactoferrin in breastfeeding?

A
  • Protein-> 7x more in colostrum (early milk)
  • Regulate iron absorption to cells
  • Protects from infection
207
Q

What are the risk factors for developing maternal sepsis?

A

Obesity, diabetes, BAME, anaemia, amniocentesis, prolonged SROM, vaginal trauma

208
Q

What can cause maternal sepsis?

A
  • Endometriosis
  • Skin + soft tissue infections
  • Mastitis
  • UTI
  • Pneumonia
  • GE
  • Pharyngitis
  • Epidural/spinal
209
Q

How does maternal sepsis present?

A

3Ts white with sugar

  • Temperature <36 or >38
  • Tachycardia (90+)
  • Tachypneoa (20+)
  • WCC >12 or <4
  • Hyperglycaemia (>7.7)
  • Clues for source-> PROM, offensive liquor/lochia, dysuria, meningism, D+V, breast
210
Q

What are the risk factors for developing VTE in pregnancy?

A
  • Increased age
  • High BMI
  • Operative delivery
  • Previous VTE
  • Thrombophilia
  • After birth-> 5x risk
211
Q

How is VTE managed in pregnancy?

A
  • Doppler US, VQ scan, CTPA
  • High risk-> 6+ weeks postnatal LMWH
  • Intermediate risk-> 10+ days LMWH
212
Q

What is the baby blues?

A

Emotional or tearful for 3-10 days after birth-> affects 85%

213
Q

What are some signs of postnatal depression?

A
  • Low mood
  • Irritability
  • Bonding with baby affected
  • 10% affected
214
Q

What are some signs of postpartum psychosis?

A
  • Depression
  • Mania
  • Psychosis-> delusions + hallucinations
215
Q

What are some signs of post-natal PTSD?

A
  • Anger, dissociating, flashbacks
  • Avoiding intimacy with partner
  • Requesting C-section for next birth
216
Q

What are th risk factors for developing post-natal PTSD?

A

Perceived lack of care, poor communications, feeling unsafe, focus on outcome not mum

217
Q

What is the definition of a maternal death?

A
  • Death whilst pregnant or within 42 days of TOP
  • Irrespective of duration of pregnancy + site
  • For any caused related to or aggravated by pregnancy or its management
  • Not from an accident or incident
218
Q

When do maternal deaths usually take place?

A

Postnatal (70%)

219
Q

What is a direct maternal death?

A
  • Directly related to pregnancy
  • VTE, haemorrhage, pre-eclampsia
  • 1/3 deaths
220
Q

What is an indirect maternal death?

A
  • Not directly due to pregnancy
  • Pre-existing medical disorder (75%), cardiac disease, neuro, MH problem
  • Includes suicide
  • 2/3 maternal deaths

Obs & Gynae (5 decks)

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