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Danny's Phase 3A Medicine > Obstetrics > Flashcards

Obstetrics Flashcards

1
Q

PREGNANCY PHYSIOLOGY

When is the window of blastocyst implantation and why?

A

Cycle day 20-24 due to the perfect balance of hormones.

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2
Q

PREGNANCY PHYSIOLOGY

what happens after blastocyst implantation?

A

the blastocyst buries which is called ‘Interstitial Implantation’

This starts the primary decidual reaction

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3
Q

PREGNANCY PHYSIOLOGY

What basic placental structures form after interstitial implantation

A
  • floating villi

- Anchoring villi

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4
Q

PREGNANCY PHYSIOLOGY

What do Cytotrophoblast progenitor stem cells differentiate into?

A

1) Terminal differentiation into syncytiotrophoblast
2) Extra-villus trophoblasts
3) Regenerate new CTBs

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5
Q

PREGNANCY PHYSIOLOGY

What are the functions of extra-villous trophoblasts?

A
  • Spinal artery remodelling
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6
Q

PREGNANCY PHYSIOLOGY

what is spinal artery remodelling?

A

Endovascular invasion myometrium where there is optimum 02 and nutrient supply.

(Due to extra-villus trophoblast invasion)

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7
Q

PREGNANCY PHYSIOLOGY

When does full placental blood flow occur?

A

week 10-12

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8
Q

PREGNANCY PHYSIOLOGY

What may poor endovascular remodelling lead to?

A

reduced fetal 02 and nutrient supply and subsequently =

Pre- eclampsia

Intrauterine growth restriction (IUGR)

Preterm birth

Recurrent miscarriage

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9
Q

PREGNANCY PHYSIOLOGY

what is human chorionic gonadotrophin (hCG)?

A

a hormone that is secreted from day 6-7 trophoblast cells of the blastocyst that:

Promotes maintenance of corpus luteum

Maintains production of oestrogen and progesterone

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10
Q

PREGNANCY PHYSIOLOGY

Where is Progesterone produced?

A

Corpus Luteum makes it until 7-8 weeks when the placenta makes it

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11
Q

PREGNANCY PHYSIOLOGY

Function of Progesterone?

A
  • Prepares uterus for implantation
  • makes the cervical mucous thick and impenetrable to sperm after fertilisation
  • Decreases immune response to allow pregnancy to happen
  • Decreases contractility of uterine smooth muscle to prevent pre-term labour
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12
Q

PREGNANCY PHYSIOLOGY

What does progesterone inhibit?

A

progesterone inhibits lactation during pregnancy. The fall in progesterone levels following delivery is one of the triggers for milk production.

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13
Q

PREGNANCY PHYSIOLOGY

What is the function of Hyman Placental Lactogen (hPL)

A
  • Mobilises glucose from fat reserves
  • Insulin antagonist to facilitate energy supply to foetus
  • Converts mammory glands into milk-secreting tissue
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14
Q

PREGNANCY PHYSIOLOGY

What is the function of Prolactin?

A
  • Milk production
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15
Q

PREGNANCY PHYSIOLOGY

What is the function of Oxytocin?

A

Milk ejection reflex

Uterine contraction

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16
Q

What happens to maternal glucose levels at the early stages of pregnancy?

A

Low glucose levels due to fat depositioon and glycogen synthesis

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17
Q

What happens to maternal glucose levels at the late stages of pregnancy?

A

High glucose levels and maternal insulin resistance to ensure glucose sparing for the foetus

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18
Q

What happens to maternal insulin levels throughout pregnancy?

A

progressive rise until the peak at 32 weeks. hPL induces insulin resistance to ensure glucose sparing to the foetus

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19
Q

IMMUNITY

What are the initial immunity changes after fertilisation?

A

Increases in:
GFs,
proteolytic enzymes
inflammatory mediators

facilitates implantation

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20
Q

IMMUNITY

Why is the blastocyst implantation not rejected?

A

Change in self:non self pattern recognition molecules (HLA and MHC proteins)

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21
Q

IMMUNITY

Why are syncytiotrophoblasts and extra-villus trophoblasts not rejected?

A

➢Syncytiotrophoblast -has no self:non-self markers = no maternal immune system

➢ Extra-Villus trophoblast (EVT) - has modified self:non-self markers = modified maternal immune response

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22
Q

IMMUNITY

What happens to T helper subtype ratio when you’re pregnant?

A

normal people = balanced Th1 and Th2

Pregnant = more Th2 (more antibody production involved in humoral response)

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23
Q

IMMUNITY

Name the relevance of the following Antibodies to pregnancy

IgA
IgD
IgE
IgG
IgM
A

IgA- Secreted in breast milk

IgD- on b-cell membranes

IgE- mast cells (anaphylaxis)

IgG - has 4 subtypes and the only Ig to cross the placenta

IgM - pentameric structure ‘early antibody’

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24
Q

NORMAL LABOUR

How would you describe a ‘perfect’ pregnancy?

A
  • 37-42 weeks
  • Spontaneous in onset in vertex position

Without the use of:

  • Forceps/ C-section/ ventose delivery
  • Induction of labour
  • Epidural/ general anaesthesia
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25
Q

FAILURE TO PROGRESS

What are the 3 Ps?

A

power
passage
passenger

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26
Q

FAILURE TO PROGRESS

Describe the ‘Power’ of the 3 P’s to think about before birth

A

Need contractions to be strong enough. in nulliparous women this may be difficult and need instrumental delivery (4 every 10 min)

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27
Q

FAILURE TO PROGRESS

Describe the ‘Passage’ of the 3 P’s to think about before birth

A

‘Pelvis’

Anterior-posterior diameter (AP) -front to back distance

Transverse diameter- side to side length

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28
Q

FAILURE TO PROGRESS

Describe the ‘Passenger’ of the 3 P’s to think about before birth

A

The baby needs to be in the correct position

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29
Q

NORMAL LABOUR

Describe the baby head landmarks felt on vaginal examination to assess baby position

A

Attitude:
How well the babys head is flexed (well flexed is best)
extended 90 = brow presentation
Hyperextended >120 = face presentation

Position:
either occipito anterior/ transverse/ posterior
OT when entering inlet
OA when entering outlet
then turn 90 to come out facing mothers medial thigh

Size of head

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30
Q

NORMAL LABOUR

Define the words:

Moulding

Caput

A

Moulding = head compressed through the pelvis

Caput = Swelling caused during delivery

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31
Q

NORMAL LABOUR

How long on average is the first stage of pregnancy?

A

5-12 Multiparious

8-12 Primiparous

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32
Q

NORMAL LABOUR

Describe the early/latent phase of the first part of labour

A
  • Irregular painful contractions
  • Cervix is effacing and thinning
  • Dilation to about 4cm
  • Mucoid plug

(2-3 days)

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33
Q

NORMAL LABOUR

What is Engagement?

A

How far above the pubic symphysis the babies head is

3/5 of the head within pelvic brim is classed as engaged

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34
Q

NORMAL LABOUR

What is Presentation

A

anatomical part of the foetus that presents itself first through the birth canal

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35
Q

NORMAL LABOUR

What is Lie?

A

Relationship between long axis of the foetus and long axis of the uterus

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36
Q

NORMAL LABOUR

What is Station?

A

Relationship between lowest point of presenting part and ischial spines

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37
Q

NORMAL LABOUR

Describe the Active Phase of Labour (2nd)

A
  • further dilation from 4cm. (0.5cm every hour)
  • regular contractions (3-4 an hour)
  • Vaginal exam every 4 hours to assess degree of dilation
  • Role of oxytocin/ syntocinon inducing labour
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38
Q

PAIN

What is Entonox and name the side effects

A

gas and air

SE: N+V

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39
Q

PAIN

Name the maternal side effects of the most effective form of pain relief: epidural

A

Maternal Side effects:

  • Increase length of 1st and 2nd stage
  • Loss of mobility
  • Loss of bladder control
  • Need for more oxytocin
  • Increase incidence of malposition
  • Increase instrumental rate
  • hypotension & pyrexia
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40
Q

PAIN

Name the foetal side effects of the most effective form of pain relief: epidural

A

Tachycardia due to maternal temperature

Can diminish breast feeding behaviour

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41
Q

PAIN

Name an opiate that could be used as pain relief?

A

Morphine

Pethidine

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42
Q

PAIN

Name some foetal side effects of opiates being used as pain relief during labour

A

Respiratory depression

Diminish breath seeking/ breast feeding behaviours

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43
Q

PAIN

Name some maternal side effects of opiates being used as pain relief during labour

A
  • euphoria/ dysphoria
  • N+V
  • Longer 1st and 2nd stage
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44
Q

NORMAL LABOUR

Describe the initial Transition stage of the second stage of labour

A

Spontaneous rupture of membranes (SROM)

  • Start to feel pressure (anxious and distressed)
  • Contractions can slow/stop
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45
Q

NORMAL LABOUR

Describe the second part of the Transition stage of the second stage of labour

A
  • full dilation (10cm)
  • external signs (head visible)
  • check baby head landmarks to assess if correct position
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46
Q

NORMAL LABOUR

In what timeframe should you

  • Suspect delay
  • Diagnose delay
  • baby be born

in primigravid and multiparous women

A

Primigravid:

Suspect delay - 1hr
Diagnose delay - 2hr
baby born - within 3 hours of pushing

multiparous:

Suspect delay - 30mins
Diagnose delay - 1hr
baby born - within 2 hours of pushing

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47
Q

Why is there now delayed cord clamping?

A

Evidence that early clamping doesn’t benefit baby/ mother and improves iron intake

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48
Q

PREGNANCY PHYSIOLOGY

What happens to the appearance of the endovascular invasion after implantation in the myometrium

A

Narrow bore high resistance vessels become

WIDE BORE LOW RESISTANCE vessels

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49
Q

PREGNANCY PHYSIOLOGY

Name some maternal CVS changes

A
  • increased RBC & plasma volume
  • Increase plasma volume means overall decline in haematocrit
  • increase Q due to increase Fe demand (peripheral vasodilation)
  • Hypercoagulable = increased risk of embolism
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50
Q

Name the 4 forces that determine fluid movement in/out of a capillary

A

Out of the capillary :

Capillary pressure
Interstitial fluid colloid oncotic pressure

Into the capillary :

Interstitial fluid pressure
Plasma colloid oncotic pressure (albumin)

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51
Q

Why is there an increased risk of UTIs in pregnancy

A

Kidney dilation

Decreased uretal tone and peristalsis = urinary stasis

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52
Q

What is the effect of delayed gastric emptying in pregnancy

A

Increased heartburn

Increased nutrient uptake

Increase water reabsorption May cause constipation

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53
Q

What is Chadwick’s Sign?

A

Early sign of pregnancy where the labia/cervix may appear blue due to increased blood flow

(6-8 weeks it is visible)

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54
Q

HORMONES OF BIRTH

Describe the function of the following hormones at birth:

Oxytocin
Prolactin 
Oestrogen
Progesterone
Beta-endorphins
Adrenaline
A

Oxytocin: induce onset & labour contractions

Prolactin: begin milk production in mammary glands

Oestrogen: inhibit progesterone and prepare smooth muscle for labour

Progesterone: aid cervical ripening

Beta-endorphins: natural pain relief

Adrenaline: energy for birth

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55
Q

What are the Mechanisms of Labour?

A
  • Descent
  • Flexion
  • internal rotation
  • crowning
  • Extension
  • Restitution / External Rotation
  • Internal restitution of shoulders
  • Lateral flexion

DFICERIL

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56
Q

How is haemolytic disease of a newborn caused?

A

Rhesus negative mother and rhesus positive father.

If the mothers negative blood crosses with the positive fetal blood the mother can make antibodies against the fetal red blood cells

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57
Q

Which antibodies can destroy the fetal red blood cells?

A

IgG antibodies can cross the placenta and start to destroy the fetal RBCs

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58
Q

What can haemolytic disease of a newborn cause for a baby?

A
  • Anaemia
  • jaundice
  • Brain damage
  • Fatal = miscarriage/ stillborn
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59
Q

MECHANISMS OF LABOUR

What is meant by the following term:

Internal rotation

A

when the babies head hits the pelvic floor, it turns straight again

(has to go through pelvis at an angle to fit!)

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60
Q

MECHANISMS OF LABOUR

What is meant by the following term

Crowning

A

When the head pokes out

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61
Q

MECHANISMS OF LABOUR

What is meant by the following term

internal restitution of the shoulders

A

When the head is out it will turn to left or the right;

shoulders will follow within pelvis

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62
Q

NORMAL LABOUR

Describe the third stage of labour

A
  • Pushing out the placenta
  • Physiological management due to increased blood loss
  • 5-30mins
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63
Q

NORMAL LABOUR

Why may oxytocin be given in the 3rd stage of labour

A
  • to create uterine contraction so that the placenta can separate
  • prevent excessive blood loss/ postpartum haemorrhage
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64
Q

Where is Relaxin released from and what is its function in labour?

A
  • released from placenta, membranes and lining of the uterus
  • Softens ligaments and cartilage of the pelvis so that it can expand

softens (cervix, vaginal tissues, babies body, perineum)

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65
Q

Function of oxytocin in labour?

A
  • Stimulates uterine contractions during orgasm and childbirth
  • Triggers fetal ejection reflex when cervix fully dilated
  • Contracts uterus post birth to deliver placenta and limit bleeding
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66
Q

Function of prostaglandins

A

ripens the cervix and causes it to begin process of thinning and opening

Stimulates uterine contractions

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67
Q

MALPRESENTATIONS

Describe a breech

SEARCH DIAGRAM FOR MALPRESENTATION APPEARANCES

A

commonest malpresentation diagnosed by ultrasound. Can be reversed by external cephalic version

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68
Q

What are the complications of an external cephalic version

A
  • Placenta praevia
  • APH
  • ruptured membranes
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69
Q

MALPRESENTATIONS

Describe a face/brow presentation and the likely method of delivery

SEARCH DIAGRAM FOR MALPRESENTATION APPEARANCES

A

Face- head extends rather than flexes = FORCEPS delivery

Brow - head is between full flexion and extension= LSCS delivery

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70
Q

How is a transverse lie antenatally diagnosed

A
  • ovoid uterus wider at the sides
  • lower pole is empty
  • head lies in one flank
  • foetal heart heard in variable positions
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71
Q

In which malpresentation is there the highest risk of cord prolapse

A

Tranverse lie- if persists at 37 weeks and ECV fails = C-section

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72
Q

MALPRESENTATIONS

Describe an Occipitoposterior position

SEARCH DIAGRAM FOR MALPRESENTATION APPEARANCES

A

Posterior fontanelle found to lie in posterior quadrant of pelvis

labour is prolonged due to degree of rotation needed

some require INSTRUMENTAL/C-SECTION delivery

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73
Q

What is a Primary dysfunctional labour and what is the treatment

A

Most common in first labour this is likely due to insufficient uterine contractions.

Hydration, comfort and analgesia is the initial management + syntocinon infusion after ROM

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74
Q

What is secondary dysfunctional labour and what is the likely cause?

A

Labour progresses to full dilation and then stops.

Likely due to cephalopelvic disproportion (passenger or passge)

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75
Q

Management to a delay in the 1st stage?

A

Amniotomy (AROM)

Oxytocin (offer epidural)

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76
Q

Management to a delay in the 2nd stage?

A

Instrumental/ LSCS delivery

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77
Q

INDUCTION

Most common reasons for inducing labour?

A
  • Prolonged pregnancy (70% induced after 41 weeks)
  • Premature rupture of membranes and labour doesnt start
  • Diabetic mother >38 weeks
  • Rhesus incompatibility
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78
Q

INDUCTION

What is the bishop score?

A

score to assess whether induction is required

<5 = unlikely to start without induction

> 9 = likely to start spontaneously

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79
Q

INDUCTION

Describe the 5 parts of the bishop score

A
  • Cervical dilation (cm)
  • Length of cervix (cm)
  • Station of head (cm above ischial spines)
  • Cervical consistency
  • Position of cervix
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80
Q

INDUCTION

In the bishops score you can either get 0,1 or 2.

For each of the 5 parts state what would give a score of 0

A
  • Cervical dilation (0cm)
  • Length of cervix (>2cm)
  • Station of head (3cm above ischial spines)
  • Cervical consistency (firm)
  • Position of cervix (posterior)
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81
Q

INDUCTION

In the bishops score you can either get 0,1 or 2.

For each of the 5 parts state what would give a score of 1

A
  • Cervical dilation (1-2cm)
  • Length of cervix (1-2cm)
  • Station of head (2cm above ischial spines)
  • Cervical consistency (medium)
  • Position of cervix (middle)
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82
Q

INDUCTION

In the bishops score you can either get 0,1 or 2.

For each of the 5 parts state what would give a score of 2

A
  • Cervical dilation (3-4cm)
  • Length of cervix (<1cm)
  • Station of head (1cm above ischial spines)
  • Cervical consistency (soft)
  • Position of cervix (anterior)
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83
Q

INDUCTION

What should be checked prior to induction?

A
  • Lie and position of foetus
  • volume of amniotic fluid
  • tone of uterus
  • ripeness of cervix (using bishops system)
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84
Q

INDUCTION

Contra-indications of induction?

A
  • Severe degree of placenta praevia
  • transverse fetal lie
  • Severe cephalopelvic disproportion
  • Cervix <4 on bishops score
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85
Q

INDUCTION

Induction procedure?

A

1) membrane sweep
2) Prostaglandin gel and pessary high in vagina
3) Amniotomy - ROM
4) Oxytocin/ Syntocinon (post ROM)

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86
Q

List types of labour pain relief

A
  • Education (breathing, coping, birth partner)
  • Transcutaneous electrical nerve stimulation (TENS)
  • water birth (reduces need for regional anaesthesia)
  • Entonox
  • Narcotics (diamorphine/ pethidine)
  • Pudendal nerve block S2,S3,S4 (for instrumental)
  • Local anaesthesia (lidocaine before epsiotomy/ surturing vaginal tears)
  • Epidural (regional- T10 to S5- normally inserted at L3-L4)
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87
Q

Describe a normal Cardiotography (CTG)

A

HR 110-160

Variability >5bpm

No decelerations

Accelerations present (reassuring feature as it shows baby moving)

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88
Q

Cardiotography (CTG)

Possible indications for a HR of >160

A
  • Maternal pyrexia
  • Chorioamnionitis
  • Hypoxia
  • Prematurity
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89
Q

Cardiotography (CTG)

Possible indications for a HR of <100

A
  • Increased foetal vagal tone

- Maternal beta blocker use

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90
Q

Cardiotography (CTG)

Possible indications for
loss of baseline variability (<5bpm)

A
  • Prematurity

- Hypoxia

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91
Q

Cardiotography (CTG)

Possible indications for early deceleration

A

usually innocuous- comes with normal contractions

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92
Q

Cardiotography (CTG)

Possible indications for late deceleration

A

foetal distress- asphyxia / placental insufficiency

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93
Q

Cardiotography (CTG)

Possible indications for variable decelerations

A

cord compression

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94
Q

Significance of meconium liquor on the pad?

A

Foetal distress, possible breech

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95
Q

What are the 3 types of breech presentation?

A

Frank breech

Complete breech

Footling breech

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96
Q

Describe a Frank breech

A

where the hips are flexed and the legs extended

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97
Q

Describe a complete breech

A

Hips and knees are flexed and the feet are below the level of the foetal buttocks

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98
Q

Describe a footling breech

A

Where one of both feet are presenting as the lowest part of the foetus (dangling legs)

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99
Q

Mos favourable position for vaginal delivery and why?

A

Occipito-anterior. this allows for the smallest diameter to come through the pelvis

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100
Q
  1. Which breech presentation is associated with highest-risk of cord prolapse?
A

Footling breech
There is nothing to act as a plug over the cervix if the membranes rupture. This is also the case with transverse or oblique lies.

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101
Q

the mentovertical diameter is associated with what presentation

A

brow

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102
Q

The usual position of the head at engagement

A

Occipito transverse

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103
Q

The presenting diameter is submento-bregmatic what does this mean?

A

Face presentation

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104
Q

The presenting diameter is submento-bregmatic what does this mean?

A

Face presentation

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105
Q

HYPEREMESIS GRAVIDARUM

What is it?

A

Persistent pregnancy-related vomiting associated with weight loss (5% body mass) and ketosis

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106
Q

HYPEREMESIS GRAVIDARUM

Triad?

A

> 5% weight loss

Electrolyte imbalance

Dehydration

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107
Q

HYPEREMESIS GRAVIDARUM

Management?

A

mild: avoid large volume drinks, small carb meals

Severe: 
Anti-emetics
IV fluids
thromboprophylaxis 
Thiamine supplements
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108
Q

give 3 types of anti-emetics and an example drug for each type

A

Dopamine antagonist:
Metoclopramide

Phenothiazines: Prochloperazine

5HT selective serotonin antagonists: Ondansetron

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109
Q

PUERPERAL PYREXIA

What is it?

A

A temperature of >38 degrees in the first 14 days following delivery

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110
Q

PUERPERAL PYREXIA

Causes?

A
  • Endometritis
  • UTI
  • Mastitis
  • VTE
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111
Q

PUERPERAL PYREXIA

Management?

A

If endometritis suspected the patient should be referred to hospital for IV Abx (clindamycin and gentamycin) until afebrile for greater than 24hrs

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112
Q

What is the leading cause of morbidity and mortality in pregnancy in developed countries?

A

VTE-

preventable (includes DVT of legs, pelvis and PE)

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113
Q

VTE IN PREGNANCY

When should you have a VTE risk assessment?

A
  • Booking
  • Antenatal admission
  • Labour
  • Postnatally
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114
Q

VTE IN PREGNANCY

Risk factors?

Modifiable and non modifiable

A

Non-Modifiable:

BMI >30
Immobility
Smoking

Family Hx of VTE
Age >35
Gross varicose veins

Pre-eclampsia
IVF
Multiple pregnancy
Parity >3

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115
Q

VTE IN PREGNANCY

Indications for LMWH thromboprophylaxis?

+ compression stockings and early mobilisation

A

If the women has any risk factors

If a women requires antenatal LMWH, this must be given until 6 weeks postpartum

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116
Q

How many more times common are DVTs than PEs and what percentage of DVTs lead to PE?

A

DVT 3x more common

16% of DVTs lead to PE in untreated patients

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117
Q

VTE IN PREGNANCY

Symptoms of DVT

A
  • Leg swelling
  • Pain
  • Redness
  • Pitting oedema
  • Distended veins
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118
Q

VTE IN PREGNANCY

Symptoms of PE

A
  • SOB
  • Pleuritic chest pain
  • Haemoptysis
  • Tachycardia

Severe: cyanosis, increased JVP

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119
Q

If a pregnant/postpartum lady collapses what should you presume

A

PE

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120
Q

VTE IN PREGNANCY

Investigations?

A

FBC, U&E, LFTs, clotting screen

D-dimer

PE-
ABG - Type 1 respiratory failure (O2 <8kPa)
ECG- (inverted T in V1-V6 and RBBB)
CXR

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121
Q

VTE IN PREGNANCY

Imaging investigation?

PE and DVT

A

DVT: Compression or duplex US of deep veins

PE: CXR and duplex US of deep veins (can assume PE if positive alongside respiratory symptoms)

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122
Q

VTE IN PREGNANCY

Treatment?

A

should start as soon as clinical suspicion and only stopped once ruled out.

LMWH.
Dalteparin
Warfarin/ NOAC

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123
Q

VTE IN PREGNANCY

How do you monitor dosage of treatment and how does treatment work?

A

Anti-Xa

  • Activation of anti-thrombin III which inhibits factor Xa and stops coagulation cascade
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124
Q

Gold standard imaging of PE?

A

CTPA - CT pulmonary angiogram

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125
Q

ANAEMIA IN PREGNANCY

Definition?

A

Hb <105g/L.

The fall in Hb is steepest around 20 weeks gestation

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126
Q

ANAEMIA IN PREGNANCY

Risk factors?

A
  • Menorrhagia/Malaria/hookworm
  • Frequent pregnancies
  • twins
  • Poor diet
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127
Q

ANAEMIA IN PREGNANCY

Investigations?

A
  • Hb estimation at 28 weeks antenatally, test for sickle cell in black patients
  • Serum iron, TIBC and serum ferritin are low in Fe deficiency
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128
Q

ANAEMIA IN PREGNANCY

causes?

A

Commonest- Iron deficiency

  • Folate deficiency
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129
Q

ANAEMIA IN PREGNANCY

Treatment?

A

Oral iron. once every 2/3 days

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130
Q

GROUP B STREP INFECTION

Risk factors?

A
  • Prematurity
  • Prolonged ROM
  • Previous GBS sibling
  • Maternal pyrexia
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131
Q

GROUP B STREP INFECTION

IF a patient is isolated during labour what should be given?

A

IV benzyl Penicillin to reduce neonatal transmission

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132
Q

GROUP B STREP INFECTION

Features of Chorioamnionitis?

A
  • Fevers
  • Lower abdo tenderness
  • foul discharge
  • Maternal/foetal tachycardia
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133
Q

Symptoms of measles?

A
  • Fever
  • Generalised maculopapular erythematous rash
  • Koplik’s spots
  • Cough
  • Coryza
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134
Q

Features of Rubella?

A

Cataracts 8-9 weeks
Deafness 5-7 weeks
Cardiac lesions 5-10 weeks

  • Cerebral Palsy
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135
Q

Congenital defects associated with Cytomegalovirus?

A
  • IUGR
  • Microcephaly
  • Hepatosplenoegaly
  • Jaundice
  • Chorioretinitis

LATER = motor and cognitive impairment

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136
Q

Symptoms and treatment of Toxoplasmosis

A

Similar to glandular fever (fever, rash, eosinophilia)

FLU LIKE

Caused by raw meat/ cat faeces

Tx= Pyrimethamine + Sulphadiazine + Spiramycin

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137
Q

What should you give to a mother with Hepatitis B?

A

all mothers should be screened.

  • Give immunoglobulin and vaccinate babies of carriers and infected mothers at birth
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138
Q

If mother develops Varicella Zoster (Chickenpox) near delivery what should be done to the baby?

A

give varicella immune immunoglobulin at birth and monitor for 28 days

Treat with ACICLOVIR if neonate develops chickenpox

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139
Q

Signs of Parvovirus B19?

A

often no symtpoms but slapped cheek syndrome may occur

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140
Q

JAUNDICE

Investigations?

A

LFTs
Urine dip- bile
Serology
HBsAG (Hep B surface Antigen)

Get expert help PROMPTLY- can be lethal

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141
Q

Features of Obsteteric Cholestasis?

A
  • Jaundice
  • Pruritis (palms and soles)
  • Worse at night
  • raised bilirubin
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142
Q

Management of Obstetric Cholestasis?

A

Ursodeoxycholic acid

Weekly LFTs
Induced at 37 weeks typically

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143
Q

Complications of Obstetric Cholestasis

A
  • Stillbirths

- Preterm labour, meconium, foetal distress

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144
Q

In which trimester is Intrahepatic cholestasis and acute fatty liver of pregnancy generally seen?

A

3rd trimester

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145
Q

features of Acute fatty liver of pregnancy?

A
  • Jaundice
  • Abdominal pain
  • Pre-eclampsia (30-60%)
  • Hypoglycaemia

non specific- Malaise, fatigue, nausea, headache

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146
Q

ECTOPIC PREGNANCY

What is it?

A

A pregnancy that occurs anywhere outside the uterus

97% in fallopian tubes

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147
Q

ECTOPIC PREGNANCY

What is the most common place for an ectopic pregnancy

A

Ampulla of Fallopian tube

isthmic after

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148
Q

ECTOPIC PREGNANCY

Risk factors?

A
  • IVF
  • Age
  • PID
  • previous ectopic
  • smoking
  • progesterone only pill
  • Endometriosis
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149
Q

ECTOPIC PREGNANCY

Clinical presentation?

A

Symptoms:

  • Amenorrhoea (missed period for 6-8 weeks)
  • Vaginal bleeding
  • dizzy, fainting

Signs:

Abdo pain/tenderness
Shoulder tip pain

Possible haemoperitoneum

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150
Q

ECTOPIC PREGNANCY

Ddx?

A
  • threatened miscarriage
  • Appendicitis
  • Bowel Ischaemia
151
Q

ECTOPIC PREGNANCY

Diagnostic tests?

A
  • Transvaginal USS

- Empty uterus & positive pregnancy test

152
Q

ECTOPIC PREGNANCY

Medical treatment?

A

If no complications= single dose methotrexate (no haemoperitoneum on TVS)

  • FBC
  • IV fluids
153
Q

ECTOPIC PREGNANCY

Surgical treatment?

A
  • Salpingectomy

- Salpingotomy

154
Q

Side effects of Methotrexate?

A
  • Conjunctivitis
  • Stomatitis
  • Diarrhoea
  • Abdominal pain
155
Q

MOLAR PREGNANCY

What is it?

A

Non-viable fertilised egg= implants into uterus -> will not come to term

156
Q

MOLAR PREGNANCY

What is a complete molar pregnancy?

A
  • empty oocyte is fertilised

Sperm + empty egg

no foetal tissue

157
Q

MOLAR PREGNANCY

What is a partial molar pregnancy?

A
  • Triploid

2 sperm + 1 egg

some foetal tissue recognisable

158
Q

MOLAR PREGNANCY

What is an invasive mole?

A

When a complete mole invades the moymetrium

159
Q

MOLAR PREGNANCY

Risk factor?

A 
Age <16  or >45
Previous molar
Multiple pregnancies 
Oral contraceptive 
Asian
Menarche >12
160
Q

MOLAR PREGNANCY

Malignant complications?

A

Choriocarcinoma (2-3%)

Placental site trophoblastic tumours

161
Q

MOLAR PREGNANCY

Clinical presentation

A
  • Vaginal bleeding
  • very high hCG levels
  • Large uterus
  • Pre-eclampsia
  • Unexplained anaemia
162
Q

MOLAR PREGNANCY

Diagnostic tests and results?

A
  • Urine and blood levels very high bhCG
  • histology
  • USS ‘snowstorm appearance’ in 2nd trimester + Large
163
Q

MOLAR PREGNANCY

Treatment?

A

Uterine evacuation
Suction curettage

  • Urgent referral to specialist centre
  • No pregnancy until hCG levels have been normal for 6 months- give effective contraception
164
Q

MOLAR PREGNANCY

What is given if the hCG is >20,000

A

Chemo - Cisplatin

165
Q

MISCARRIAGE

Definition?

A

The loss of pregnancy before 24 weeks gestation

doesn’t include ectopic or trophoblastic disease

166
Q

MISCARRIAGE

What is a complete miscarriage

A

TVUS shows crown rump length >7mm

gestational sack >25mm

no foetal heartbeat

167
Q

What is meant by crown rump length

A

Crown-rump length (CRL) is the measurement of the length of human embryos and fetuses from the top of the head (crown) to the bottom of the buttocks (rump). It is typically determined from ultrasound imagery and can be used to estimate gestational age.

168
Q

MISCARRIAGE

What is a threatened miscarriage?

A

Mild symptoms of bleeding with little or no pain,

cervical os is closed

169
Q

MISCARRIAGE

What is an Inevitable miscarriage?

A

Heavy bleeding with clots and pain,

cervical os is open.

the pregnancy will not continue, proceed to complete/incomplete miscarriage

170
Q

MISCARRIAGE

What is an incomplete miscarriage

A

Occurs when the products of conception are partially expelled.

Cervical os open.

Pain + vaginal bleeding

171
Q

MISCARRIAGE

What is a missed miscarriage?

A

foetus is dead but retained.

Uterus is small for dates

Pregnancy test can remain positive for several weeks.

History of threatened miscarriage with PERSISTENT DIRTY BROWN DISCHARGE

Closed os

172
Q

MISCARRIAGE

What is recurrent miscarriage?

A

Three or more consecutive miscarriages

173
Q

MISCARRIAGE

Causes?

A 
Abnormality to: 
foetal development
cervix
uterus
Placenta

PCOS
Previous miscarriage
BV infection

174
Q

MISCARRIAGE

risk factors?

A 
Age >30 
Smoking >14 a day 
Excess alcohol
Drug use
Uterine surgery 
Uncontrolled DM

Incidence increases with parity

175
Q

MISCARRIAGE

Epidemiology?

A

15-20% of recognised pregnancies

85% in first trimester

176
Q

MISCARRIAGE

Clinical presentation?

A

Vaginal bleeding with/without abdominal pain

Cervical os is open enough to admit one finger

uterine size small for dates

Passing products of conception

177
Q

MISCARRIAGE

Ddx?

A
  • Ectopic pregnancy
  • Neoplasia
  • Hydatiform mole
  • Chorionic cyst
  • Sub chorionic haemorrhage
178
Q

MISCARRIAGE

Diagnostic tests and results?

A

transvaginal USS

Serium hCG (to exclude ectopic)

179
Q

MISCARRIAGE

Medical treatment before 12 weeks?

A

<12 weeks :

Mifepristone (antiprogesterone to prime cervix) THEN

Misoprostol 36-48hrs later

180
Q

MISCARRIAGE

Medical treatment after 12 weeks?

A

Vaginal misoprostol

bleeding may continue for 3 weeks following medical treatment

181
Q

MISCARRIAGE

Surgical treatment?

A

Suction evacuation under GA if under 13 weeks

182
Q

MISCARRIAGE

Causes for recurrent miscarriages?

A

APS/ DM/ thyroid disorders/ PCOS

Smoking

Uterine abnormality (uterine septum e.g.)

183
Q

Under what circumstances can a termination of pregnancy occur after 24 weeks?

A
  • Risk to mothers life

- Substantial risk that if the baby was born it would be seriously handicapped

184
Q

How is a termination of pregnancy carried out surgically?

A

Vacuum aspiration (adminster misoprostol before surgery to prepare cervix)

185
Q

How is a termination of pregnancy carried out medically?

A

regimes of Mifepristone- to prime CERVIX

then Misoprostol (prostaglandin)

186
Q

PRE-ECLAMPSIA

What is it?

A

pregnany induced hypertension in association with:

  • Proteinuria (>0.3g in 24hrs)

with or without oedema

187
Q

PRE-ECLAMPSIA

How is severe pre-eclampsia defined?

A

diastolic BP of 110 +
systolic BP of 160

AND symptoms/haemotological/biochemical impairment

188
Q

PRE-ECLAMPSIA

What may happen to the foetus in severe pre-eclampsia

A

Foetus may have neurological damage due to hypoxia

189
Q

PRE-ECLAMPSIA

Describe the two stages of pre-eclampsia

A

Stage 1: incomplete trophoblastic invasion of spiral arterioles = decreased uteroplacental blood flow

Stage 2 : Ischaemic placenta induces endothelial cell damage which leads to vaso-constriction, clotting dysfunction and increased vascular permeability

190
Q

PRE-ECLAMPSIA

What are the high risk factors? and what should be done in response?

A
  • Pre-eclampsia/HTN in previous pregnancy
  • CKD
  • Autoimmune disease (SLE, Antiphospholipid syndrome)
  • DM 1/2

START ON ASPIRIN AT 12 WEEKS

191
Q

PRE-ECLAMPSIA

What are the moderate risk factors? and what should be done in response?

A
  • 10 years since last pregnancy
  • first pregnancy
  • > 40 years or more
  • BMI over 25
  • Family history of pre-eclampsia
192
Q

When may a dilation and curettage procedure be performed?

A

incomplete miscarriage,
retained placenta after delivery,
an elective abortion.

193
Q

Diagnosis and treatment of Asherman’s Syndrome?

A

Hysterscopy
USS
Hysterosalpingogram (HSG- dye inserted)

Tx= Operative hysterscopy + Abx to prevent infection + oestrogen to improve quality of uterine lining

194
Q

Diagnosis and treatment of Asherman’s Syndrome?

A

Hysterscopy
USS
Hysterosalpingogram (HSG- dye inserted)

Tx= Operative hysterscopy + Abx to prevent infection + oestrogen to improve quality of uterine lining

195
Q

PRE-ECLAMPSIA

Clinical presentation?

A

New hypertension 140/90

Late signs:

  • Severe headache
  • Visual disturbances
  • Swelling of face/hands/feet
  • Liver tenderness/RUQ pain
  • vomiting

HELLP syndrome

Small for gestational age infant

196
Q

PRE-ECLAMPSIA

Diagnostic tests?

A

Urinalysis - Dipstick for proteinuria

No proteinuria =Gestational pre-eclampsia

HTN

Frequent monitoring of FBC, LFTs, Renal function

197
Q

PRE-ECLAMPSIA

Why would you do a urine culture

A

Exclude infection

198
Q

PRE-ECLAMPSIA

Why would you do an USS of foetus

A

CHECK:

  • Foetal growth
  • Volume of amniotic fluid
  • Doppler velocimetry of umbilical arteries
199
Q

PRE-ECLAMPSIA

How is mild pre-eclampsia defined and what is the treatment?

A

140-149/90-99

  • Monitor BP 4 times a day
  • blood tests 2 times a week
200
Q

PRE-ECLAMPSIA

How is severe pre-eclampsia defined and what is the treatment?

A

> 160/110

  • Monitor BP 4 times a day
  • blood tests 2 times a week

Start antihypertensive e.g Labetolol

Magnesium sulphate to reduce risk of eclampsia

201
Q

PRE-ECLAMPSIA

How is moderate pre-eclampsia defined and what is the treatment?

A

150-159/100-109

  • Monitor BP 4 times a day
  • blood tests 2 times a week

Start antihypertensive e.g Labetolol

202
Q

PRE-ECLAMPSIA

What antihypertensives should be avoideed?

A

ACE inhibitors

Angiotensin-II receptor antagonists

203
Q

PRE-ECLAMPSIA

What antihypertensives should be avoideed?

A

ACE inhibitors

Angiotensin-II receptor antagonists

204
Q

PRE-ECLAMPSIA

What further monitoring should be done?

A

USS of foetus and amniotic fluid

CTG

Delivery once woman is stable and baby >34 weeks

205
Q

PRE-ECLAMPSIA

Maternal complications?

A

Cerebrovascular haemorrhage

HELLP syndrome

Liver/renal failure

Pulmonary oedema

206
Q

PRE-ECLAMPSIA

Foetal complications?

A

IUGR
Placental abruption
Preterm birth

207
Q

Definiton of ECLAMPSIA?

A

Onset of convulsion in a pregnancy complicated with pre-eclampsia

208
Q

Why does Eclampsia occur and when can it happen?

A

Failure to notice worsening pre-eclampsia

Can occur antepartum, intrapartum and postpartum

209
Q

Treatment of ECLAMPSIA

A

Control fits: Magnesium sulphate

Control BP: IV Labetolol, nifidepine, Epidural analgesia during labour

210
Q

Why is Magnesium sulphate used in Eclampsia treatment

A
  • Suppresses convulsions and inhibits muscular activity

- Reduces DIC risk as it reduces platelet aggregation

211
Q

What should be monitored if using magnesium sulphate

A

Magnesium levels: Can cause reduced reflexes and respiratory depression

212
Q

What should be monitored if using magnesium sulphate

A

Magnesium levels: Can cause reduced reflexes and respiratory depression

213
Q

HELLP SYNDROME

What is it?

A

A complication of pregnancy which usually present in women who have pre-eclampsi or eclampsia

214
Q

HELLP SYNDROME

What is it characterised by?

A
  • Haemolysis
  • Elevated liver enzymes
  • Low platelet count
215
Q

HELLP SYNDROME

What do affected women show

A

Signs of liver damage and abnormalities of blood clotting

216
Q

HELLP SYNDROME

Risk factors?

A 
Age >35
nulliparity 
previous hx of HELLP, pre-eclampsia
Renal Disease/ DM
Afro- carib 
Obese
HTN
217
Q

HELLP SYNDROME

What do 10.5% of HELLP syndrome patients have?

A

Antiphospholipid syndrome

218
Q

HELLP SYNDROME

when do symptoms present?

A

70% before pregnancy 27-37 weeks

30% post partum

219
Q

HELLP SYNDROME

Symptoms?

A

Usually non specific: Malaise, fatigue, RUQ/epigastric pain, flu-like

Headache and visual symptoms

Bruising/purpura
Oedema/hypertension/proteinuria
Jaundice

220
Q

HELLP SYNDROME

When do symptoms get worse / better?

A

Worse at night

better during the day

221
Q

HELLP SYNDROME

Ddx?

A
  • Acute fatty liver of Pregnancy
  • thrombotic thrombocytopenic purpura (TTP)
  • Immune thrombocytopenia (ITP)
  • Haemolytic uraemic syndrome
  • Acute exacerbation of SLE
  • Viral hepatitis
  • Cholangitis
222
Q

HELLP SYNDROME

Diagnostic tests and results

A
  • haemolysis with fragmented red cells on blood film
  • riased LDH with raised bilirubin
  • Raised liver enzymes
  • low platelets
223
Q

HELLP SYNDROME

Treatment?

A
  • Delivery of foetus
  • Magnesium sulphate
  • blood transfusion
  • Control BP
224
Q

HELLP SYNDROME

Symptoms?

A

Usually non specific: Malaise, fatigue, RUQ/epigastric pain, flu-like

Headache and visual symptoms

Bruising/purpura
Oedema/hypertension/proteinuria
Jaundice

225
Q

HELLP SYNDROME

When do symptoms get worse better?

A

Worse at night

better during the day

226
Q

HELLP SYNDROME

Why are fragmented red cells seen on blood film?

A

Microangiopathic haemolytic anaemia

227
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

What is it?

A

When a baby’s growth slows or ceases when it is in the uterus

228
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

What are the contributing factors/ causes?

A
  • Maternal factors
  • Placental factors
  • Foetal factors
  • Genetic factors
229
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Name some maternal factors

A 
Age >40
Smoker
cocaine use
previous SGA baby
Diabetes
Antiphospholipid
HTN
230
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Name some placental factors

A

Abnormal trophoblastic implantation e.g pre-eclampsia

Placental dysfunction

placental abruption

231
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Name some foetal factors

A

Genetic abnormalities:

Trisomy 13,18,21
Turner’s

Congential heart disease

232
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Name some genetic factors

A

Placental genes
Foetal genes
Materna; genes

233
Q

What is Trisomy 18

A

Edwards Syndrome

234
Q

What is Trisomy 13

A

Patau Syndrome (most die within 7-10 days)

235
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Name some high risk factors?

A 
S moking
H ypertension
I UGR previously
T wins
S till birth

SHITS

236
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Name some rarer high risk factors?

A

C ocaine
R enal disease
A ntiphospholipid syndrome
P APP-A levels low

CRAP

237
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Describe symmetrical IUGR

A

cause of IUGR EARLIER in pregnancy

Antenatally: small head, abdomen and foetal length

Postnatally: weight, length and head circumference all reduced

238
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Describe asymmetrical IUGR

A

cause of IUGR LATER in pregnancy

Antenatally: small abdominal circumference but head and femur length normal

Postnatally: reduced weight but length and head circumference normal

239
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

List some long term complications

A
  • Lower scores on cognitive tests
  • Learning difficulties
  • Developmental delay
  • ADHD
  • Poor perceptual performance
  • CEREBRAL PALSY
240
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

What adult onset diseases will the baby be more susceptible too

A
  • Diabetes
  • Hypertension
  • Obesity
  • Metabolic syndrome
  • CHD
241
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Diagnostic tests and results

A
  • Foetal abdominal circumference or estimated foetal weight <10th centile
  • Reduced Amniotic Fluid Index (AFI)
242
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

How is a reduced Amniotic Fluid Index (AFI) caused

A

1) Reduced O2 to baby leads to redistribution of blood away from organs e.g. kidneys
2) reduced urine output and smaller amniotic fluid volume

243
Q

SEPSIS

What is it?

A

Infection + systemic manifestations of infection

244
Q

INTRAUTERINE GROWTH RETARDATION (IUGR)

Treatment?

A
  • LSCS

Offer corticosterioids- Lung development up to 35+6

245
Q

SEPSIS

What is severe Sepsis?

A

Sepsis with sepsis-induced organ dysfunction or evidence of tissue hypo-perfusion

246
Q

SEPSIS

What is Septic shock

A

Persistent tissue hypo-perfusion despite adequate fluid replacement

247
Q

SEPSIS

Causes?

A
  • Pyelonephritis
  • Chorioamnionitis
  • Postpartum endometritis
  • Wound infection
  • Pneumonia
  • Acute appendicitis
  • Acute cholecystitis
  • Pancreatitis
  • Necrotising enterocolitis
248
Q

SEPSIS

Risk factors?

A
  • Obesity
  • Diabetes
  • Impaired immunity/immunosuppressant medication
  • Anaemia
  • Vaginal discharge
  • History of pelvic infection
  • History of group B streptococcal infection
  • Amniocentesis and other invasive procedures
  • Cervical cerclage
  • Prolonged spontaneous rupture of membranes
  • Group A strep infection in close contacts / family members
249
Q

SEPSIS

Signs and symptoms?

A
  • Fever, rigors, diarrhoea, vomiting
  • Rash
  • Abdominal + pelvic pain
  • Hypoxia
  • Hypotension
  • Oliguria
  • Impaired consciousness
  • Failure to respond to treatment
250
Q

SEPSIS

Describe 3Ts white with Sugar to describe Sepsis clinical signs

A

SIRS CRITERIA:

Temperature >38 or <36
Tachycardia >90bpm
Tachypnoea >20bpm

WBC <4 or >12

Sugar >7.7 in absence of diabetes

251
Q

SEPSIS

Management? (involve experts early)

A 
Blood cultures
Urine output
Fluid resuscitation 
Antibiotics (broad spec IV)
Lactate, Hb, Glucose
Oxygen

+2 -
Consider delivery and VTE prophylaxis

252
Q

CHORIOAMNIONITIS

What is it and why is it caused?

A

Acute inflammation of amnion and chorion membranes due to ascending bacterial infection in setting of membrane rupture

253
Q

CHORIOAMNIONITIS

Clinical features and management?

A
  • Uterine tenderness
  • ROM
  • Foul odour of amniotic fluid
  • Maternal signs (pyrexia, tachycardia, leucocytosis)

Management- C-section delivery & IV Abx

254
Q

PREMATURE BIRTH

Definiton?

A

Presence of contractions of sufficient strength and frequency to effect progressive effacement and dilation of the cervix before 37 weeks gestation

255
Q

PREMATURE BIRTH

Risk factors?

A 
30% unexplained
30% multiple pregnancy
- Cervical incompetence (e.g. surgery)
- Previous preterm/ miscarriage after 14weeks
- Preterm prelabour rupture of membranes
256
Q

PREMATURE BIRTH

How many births take place before 32 weeks gestation?

A

1.4% of U.K births but this 1.4% accounts for 51% of infant deaths

257
Q

PREMATURE BIRTH

Clinical presentation?

A
  • Contractions
  • Bleeding or amniotic fluid loss
  • Dilation of cervix
258
Q

PREMATURE BIRTH

Diagnostic tests and results?

A

Screening & +ve risk factors

  • transvaginal USS - measurement of cervical
    length
  • Vaginal swab
259
Q

PREMATURE BIRTH

Treatment?

A

TOCOLYTICS

  • Corticosteroids
  • Magnesium sulfate
  • Cervical stitch
  • Delivery
260
Q

PREMATURE BIRTH

What is tocolysis and give some examples

A

Drugs that delay delivery up to 48 hours

Prostaglandin synthesis inhibitors- Indomethacin

CCBs- Nifedipine

Atosiban if cant use CCB

261
Q

PREMATURE BIRTH

Why are corticosteroids used?

Give examples

A

To help with foetal surfactant production

Betamethasone

Dexamethasone

262
Q

PREMATURE BIRTH

Why is magnesium sulfate used?

A

For neuroprotection

Reduced risk of cerebral palsy

263
Q

PREMATURE RUPTURE OF MEMBRANES

What is it?

A

Rupture of mebranrd <37 weeks

264
Q

PREMATURE RUPTURE OF MEMBRANES

What are the risks?

A

Risk of serious infection.

After 24 hours = chorioamnionitis + endometriosis

60% will go into spontaneous labour

265
Q

PREMATURE RUPTURE OF MEMBRANES

What is the treatment for mid-trimester PROM <24 weeks

A

Normally poor outcome- pulmonary hypoplasia even after steroids

266
Q

PREMATURE RUPTURE OF MEMBRANES

What is the treatment for 24-34 weeks gestation PROM

A

Maternal Steroids- Dexamethasone

Erythromycin

Daily review for signs of infection

267
Q

PREMATURE RUPTURE OF MEMBRANES

What is the treatment for >34 weeks gestation

A

Induce labour

268
Q

ANTEPARTUM HAEMORRHAGE

What is it?

A

Bleeding from the birth canal after 24 weeks gestation (before is a miscarriage)

269
Q

ANTEPARTUM HAEMORRHAGE

Causes?

A
  • 50% idiopathic

Placenta praevia (low lying placenta)

Placental abruption

Vasa praevia

Lower genital tract causes:

Cervical polyps/erosions/ carcinoma
Cervicitis/Vaginitis

270
Q

ANTEPARTUM HAEMORRHAGE

Epidemiology?

A

3-5% of all pregnancies

Up to 20% of very preterm babies are born in association with APH

271
Q

ANTEPARTUM HAEMORRHAGE

Clinical signs and symptoms

A
  • Bleeding with/without pain
  • Uterine contractions
  • Malpresentation or failure for foetal head to engage
  • Foetal distrss
  • Signs of hypovolaemic shock
272
Q

ANTEPARTUM HAEMORRHAGE

Diagnostic tests and results

A

Exclude placenta praevia with USS

273
Q

ANTEPARTUM HAEMORRHAGE

Treatment

A

Anti-D

Replacement fluids/blood

IV access
CTG
Delivery may save mothers life

274
Q

PLACENTAL ABRUPTION

What is it?

A

Premature seperation of placenta from the uterus

Significant cause of third-trimester bleeding associated with foetal and maternal morbidity and mortality

275
Q

PLACENTAL ABRUPTION

Cause?

A
  • Maternal hypertension (common)
  • Maternal trauma
  • Smoking,alcohol,drugs
  • Short umbilical cord
  • decompression of the uterus
276
Q

PLACENTAL ABRUPTION

Risk factors?

A
  • Smoking
  • Previous abruption
  • HTN/ pre-eclampsia
  • Thrombophilia
  • Cocaine
  • Trauma
277
Q

PLACENTAL ABRUPTION

Clinical presentation?

A
  • Pain
  • DARK red vaginal bleeding
  • uterine contractions
  • Foetal distress
278
Q

PLACENTAL ABRUPTION

What is meant by a woody uterus

A

‘Hard’ uterus due to blood invading myometrium

279
Q

PLACENTA PRAEVIA

What is it?

A

When the placenta is inserted wholly or in part into the lower segment of the uterus

280
Q

PLACENTA PRAEVIA

Risk factors?

A
  • Previous placenta praevia/ C-section / abortion
  • Increased maternal age/ parity
  • Smoking/ Cocaine
  • Deficient endometrium
  • Assisted conception
281
Q

PLACENTA PRAEVIA

What is the pathophysiology of Major/Minor placenta praevia

A

Major: Placenta covers the entire internal os of the cervix (grade 3/4)

Minor/Partial: If the leading edge is in the lower segment but not covering the os (grade 1/2)

282
Q

PLACENTA PRAEVIA

Clinical Presentation?

A

Painless bleeding after the 28th week

BRIGHT RED BLEEDING

  • High presenting part or abnormal lie
283
Q

Methods of assisted conception?

A

intrauterine insemination (IUI)

in vitro fertilisation (IVF).

284
Q

What is Vasa Praevia and what are the risks?

A

when fetal blood vessels cross or run near the internal opening of the uterus. These vessels are at risk of rupture when the supporting membranes rupture, as they are unsupported by the umbilical cord or placental tissue

285
Q

PLACENTA PRAEVIA

Complications?

A

PPH

Placenta accreta or percreta

286
Q

What is Vasa Praevia and what are the risks?

A

when fetal blood vessels cross or run near the internal opening of the uterus. These vessels are at risk of rupture when the supporting membranes rupture, as they are unsupported by the umbilical cord or placental tissue

287
Q

PLACENTA PRAEVIA

How is a placenta defined ‘low lying’

A

IF within 2cm of the cervix before 26 weeks

288
Q

Difference in blood between placenta abruption and praevia?

A

Abruption tends to be darker red

Praevia tends to be bright red

289
Q

Difference in blood between placenta abruption and praevia?

A

Abruption tends to be darker red

Praevia tends to be bright red

290
Q

What is Placenta Accreta?

A

chorionic villi attach to the myometrium,

rather than being restricted within the decidua basalis

291
Q

What is Placenta Increta?

A

Chorionic villi invade the myometrium

292
Q

What is Placenta Percreta?

A

Chorionic villi invades THROUGH the myometrium

293
Q

How to prepare for delivery with Placenta praevia and accreta

A

Elective LSCS 36-38 weeks

Consent to include all potential interventions including
hysterectomy

Consultant obstetric/anaesthetic input

Anticipate major obstetric haemorrhage

Blood available + consider cell salvage

Ensure critical care bed available

294
Q

POSTPARTUM HAEMORRHAGE (PPH)

What is a primary PPH?

A

Bleeding from the genital tract in excess of 500mls in the first 24 hours after delivery of the baby

295
Q

POSTPARTUM HAEMORRHAGE (PPH)

What is a secondary PPH?

A

Abnormal vaginal bleeding any time between 24 hours and 6 weeks

296
Q

POSTPARTUM HAEMORRHAGE (PPH)

What is a minor PPH

A

Estimated blood loss >500mls but less than 1500 and no signs of shock

297
Q

POSTPARTUM HAEMORRHAGE (PPH)

What is a major PPH

A

Estimated blood loss of 1500mls or moreand continuing to bleed OR clinical shock

298
Q

POSTPARTUM HAEMORRHAGE (PPH)

Causes?

A

4 Ts

Tone (70%) - atonic uterus

Tissue (10%) - Retained placenta with prolonged 3rd stage

Trauma (20%) - tears and repairs

Thrombin (<1%) - pre-eclampsia/ DIC

299
Q

POSTPARTUM HAEMORRHAGE (PPH)

Risk factors?

A

Past history of postpartum haemorrhage

Grand multiparity

Maternal age >40 years

Multiple pregnancy

Polyhydramnios

Abruption Placenta praevia

Pre-eclampsia/gestational hypertension

BMI>35

Pre-existing anaemia

Operative Delivery (LSCS or instrumental)

Induction of labour

Retained placenta

Big baby

Pyrexia in labour

Prolonged labour

Fibroids

300
Q

POSTPARTUM HAEMORRHAGE (PPH)

Prophylaxis?

A

IM Oxytocin = given with delivery of anterior shoulder

If significant RFs (+ no HTN) then consider adding: Ergometrine

301
Q

POSTPARTUM HAEMORRHAGE (PPH)

Medical Treatment?

A

Fluid Resus + ABC, O2

IV Oxytocin or Ergometrine

Misoprostol

IM Carboprost

(Consider theatre if > 2 doses required)

IV Tranexamic acid

302
Q

POSTPARTUM HAEMORRHAGE (PPH)

Surgical treatment?

A

Evacuation of retained products

Bi-manual uterine compression to expel clots (massage and compress)

Balloon tamponade

B-lynch suture

Consider hysterectomy

303
Q

POSTPARTUM HAEMORRHAGE (PPH)

When must you never give Ergometrine?

A

if the patient has hypertension (vasoconstrictor)

304
Q

What are the seven cardinal movements?

A
  • Engagement
  • Descent
  • Flexion
  • Internal rotation
  • Extension
  • External rotation/ restitution
  • Expulsion

EDFIEEE

305
Q

Describe Engagement

Cardinal Movement 1

A

Entering the biparietal diameter (ear tip to ear tip across the top of baby’s head) into the pelvic inlet

306
Q

Describe Descent

Cardinal Movement 2

A

Baby’s head deep into the pelvic cavity (Lightening)

When the occiput is at the level of the ischial spines it can be assumed that the biparietal diameter is engaged and then descends into the pelvic inlet

307
Q

Describe Flexion

Cardinal Movement 3

A
  • Occurs during descent, the resistance from the tissues of the pelvis brings about flexion to the baby’s head
  • Smallest diameter of the baby’s head presents into the pelvis
308
Q

Describe Internal Rotation

Cardinal Movement 4

A

Head rotates to accomodate the changes of pelvic diameter because:

Pelvic inlet: diameter widest from right to left

Pelvic outlet: diameter widest from front to back

Therefore baby must go from sideways to facing back of the mother (back of head against the front of the pelvis)

309
Q

Describe Extension

Cardinal Movement 5

A

After internal rotation extension occurs as the head is born

310
Q

Describe External Rotation

Cardinal Movement 6

A
  • Slight pause in labour after the baby’s head is born

- Babies head must rotate from face down to facing one of the mothers inner thigh

311
Q

Describe Expulsion

Cardinal Movement 7

A

Immediately after external rotation, the anterior shoulder moves out from under the symphysis pubis.

The perineum become distended by the posterior shoulder which is then also born, followed by the rest of the body.

(upward motion by midwife)

312
Q

What is the largest diameter of the pelvic outlet?

A

Front to back

313
Q

Describe internal rotation

A

baby moves from a sideways position (inlet) to one where the sagittal suture is in the anteropsoterior diameter of the outlet

314
Q

Describe internal rotation

A

baby moves from a sideways position (inlet) to one where the sagittal suture is in the anteropsoterior diameter of the outlet

315
Q

Why is external rotation necessary

A

‘Restitution’ is necessary for the shoulders to fit around and under the pubic arch

316
Q

Why is external rotation necessary

A

‘Restitution’ is necessary for the shoulders to fit around and under the pubic arch

317
Q

What happens if external rotation is not successful

A

Shoulder Dystocia

318
Q

SHOULDER DYSTOCIA

What is it?

A

When the baby’s shoulders are halted at the pelvic outlet due to inadequate space through to which to pass

  • Usually the anterior shoulder which impacts on the maternal symphysis
319
Q

SHOULDER DYSTOCIA

What is it?

A

When the baby’s shoulders are halted at the pelvic outlet due to inadequate space through to which to pass

  • Usually the anterior shoulder which impacts on the maternal symphysis
320
Q

SHOULDER DYSTOCIA

Cause?

A

3 Ps

Power (uterus)
Passenger (foetus)
Passage (pelvis)

321
Q

SHOULDER DYSTOCIA

Uterine causal factors?

A
  • Uncoordinated uterine activity/ short infrequent contractions.

Oxytocin can enhance and co-ordinate uterine contractions

322
Q

SHOULDER DYSTOCIA

Foetal causal factors?

A
  • Position or lie
  • Macrosomia (>4.5kg)
    Large AC compared to HC ratio

(AC= abdominal circumference, HC = head circumference)

323
Q

SHOULDER DYSTOCIA

Pelvic passage causal factors?

A
  • Long and oval brim

- Scoliosis, kyphosis and rickets can lead to cephalopelvic disproportion

324
Q

SHOULDER DYSTOCIA

Risk factors?

A
  • Diabetes
  • Macrosomia
  • Obesity
  • Induction of labour
  • Assisted vaginal delivery (forceps/vacuum)
  • Oxytocin use
  • Prolonged labour
  • Previous shoulder dystocia
325
Q

SHOULDER DYSTOCIA

Clinical presentation?

A
  • difficulty when delivering the face
  • head remaining tightly applied to the vulva or retracting: ‘Turtle-neck Sign’
  • failure of head to restitute
  • Failure of shoulders to descend
326
Q

SHOULDER DYSTOCIA

Management?

A
  • Stop pushing
  • McRobert’s Manoeuvre
  • Epsiotomy to allow Wood’s screw manoeuvre

Last resorts include symphisiotomy and the Zavanelli manouvere (which includes Caesarean section)

327
Q

SHOULDER DYSTOCIA

Foetal complications?

A
  • Brachial Plexus injury (10% permanent damage)
    (upper = Erbs Palsy, lower = Klumpke’s Palsy)
  • hypoxia and acidosis can lead to perinatal morbidity/mortality
  • Fractured humerus/clavicle (4%)
  • pneumothorax
328
Q

SHOULDER DYSTOCIA

Maternal complications?

A
  • PPH
  • third and fourth degree tears
  • Vaginal lacerations
  • Cervical tear
  • Bladder/uterine rupture
329
Q

What is Zavenelli’s Manoeuvre?

A

returning the head to the occiput anterior or occiput posterior position if the head has rotated from either position. The second step is to flex the head and slowly push it back into the vagina, following which cesarean delivery is performed

330
Q

What is Zavenelli’s Manoeuvre?

A

returning the head to the occiput anterior or occiput posterior position if the head has rotated from either position. The second step is to flex the head and slowly push it back into the vagina, following which cesarean delivery is performed

331
Q

CORD PROLAPSE

What is it?

A

When the umbilical cord descends below the presenting part and causes hypoxia for the baby due to compression or spasm

332
Q

CORD PROLAPSE

Risk factors?

A
  • Pre-term labour/ ROM
  • Breech presentation
  • Polyhydraminos
  • Twins
333
Q

CORD PROLAPSE

Management?

A

Tocolytics to reduce compression (Terbutaline)

  • Presenting part pushed back into uterus for C-section
  • Patient on all 4s
334
Q

What is Amniotic Fluid embolism?

A

When the liquor enters maternal circulation leading to Anaphylaxis:

  • Sudden dyspnoea
  • Hypoxia
  • Hypotension
335
Q

Dangers of amniotic fluid embolism

A

80% mortality

Associated with seizures and cardiac arrest- usually occurs when membranes rupture

336
Q

Management of amniotic fluid embolism

A

Resus
O2, fluids, bloods etc

ABC

337
Q

UTERINE RUPTURE

Causes?

A
  • New

- Old scar from previous C-section - wound dehiscence

338
Q

UTERINE RUPTURE

Signs?

A

RUPTURE USUALLY IN LABOUR

  • Foetal HR abnormality
  • Abdominal pain
  • Foetal distress
  • Maternal shock
  • Cessation of contractions
339
Q

UTERINE RUPTURE

Risk factors?

A
  • Labours with scarred uterus
    (c-section or deep myomectomy/previous uterine surgery or cervical surgery)
  • Breech extraction
340
Q

UTERINE RUPTURE

Management?

A

Maternal resus

Emergency C/S if suspected in labour
Repair if small

341
Q

What is Bishops score?

A

A pre scoring system to assist in prediciting whether induction will be required

Used to assess the odds of spontaneous preterm delivery

342
Q

GESTATIONAL DIABETES

Cause?

A

1) Increased resistance to insulin due to the placental production of anti-insulin hormones
2) If maternal pancreas cannot increase insulin production to combat = GM

343
Q

GESTATIONAL DIABETES

Risk factors?

A
  • Previous GD
  • Obesity
  • FH of DM
  • Ethnic background
  • Glycosuria
  • Macrosomia (previously)
  • Hx of PCOS
  • Polyhydraminios
344
Q

GESTATIONAL DIABETES

Clinical features?

A
  • May be asymptomatic
  • Polydipsia
  • Polyuria
  • Dry mouth
  • Tiredness
345
Q

GESTATIONAL DIABETES

Implications in 1st trimester?

A

Rarely seen

346
Q

GESTATIONAL DIABETES

Implications in 2nd trimester?

A

Pre-eclampsia

Macrosomia

347
Q

GESTATIONAL DIABETES

Name some anti-insulin hormones produced by the placenta

A
  • Human placental lactogen (hPL)
  • Glucagon
  • Cortisol
348
Q

GESTATIONAL DIABETES

Implications in 3rd trimester?

A
  • Pre-eclampsia
  • Macrosomia
  • Recurrent infections
  • Intrauterine death
  • Polyhydramnios
349
Q

GESTATIONAL DIABETES

Implications at delivery?

A
  • Poor progress/ stillbirth (especially if pre-existing diabetes)
  • Traumatic (C-section/ instrumental)
  • Shoulder dystocia
350
Q

GESTATIONAL DIABETES

Implications postnatally?

A
  • Neonatal hypoglycaemia
  • Respiratory distress syndrome
  • Jaundice
351
Q

GESTATIONAL DIABETES

Long term implications?

A
  • Type 2 DM later in life

- Childhood obesity

352
Q

GESTATIONAL DIABETES

Complications and risks from GD?

A

SMASH

Shoulder dystocia

Macrosomia

Amniotic fluid excess (polyhydramnios)

Stillbirth

Hypertension + neonatal hypoglycaemia

353
Q

GESTATIONAL DIABETES

Diagnosis?

Management?

A

OGTT at 24-28 weeks

5,6,7,8 RULE

Fasting = >5.6
2 hours = >7.8

  • Glucose control
  • Deliver at TERM unless macrosomia/pre-eclampsia
354
Q

GESTATIONAL DIABETES

Name some anti-insulin hormones produced by the placenta

A
  • Human placental lactogen (hPL)
  • Glucagon
  • Cortisol
355
Q

GESTATIONAL DIABETES

Why does this cause macrosomia?

A

1) Excess glucose leads to excess glucose transferred to foetus.
2) Foetus produces increased amounts of insulin and therefore more tissue/fatty deposits.

356
Q

GESTATIONAL DIABETES

Why is Polyhydramnios caused?

A

Increase in fetal glucose = polyuria and more fluid release from the foetus

357
Q

GESTATIONAL DIABETES

Why is neonatal hypoglycaemia caused?

A

Increased fetal insulin- lower glucose intake after birth compared to intra-uterine

358
Q

GESTATIONAL DIABETES

Methods of glucose control?

A
  • Diet (Avoid glucose fluctuations) + Exercise
  • Metformin &
  • Glibenclamide
  • Insulin (Short acting before meals)
359
Q

List some peripartum events that can lead to chronic infections

A
  • Prolonged ROM
  • Chorioamnionitis
  • Repeated vaginal exams
  • Catheterisation
  • Instrumental deliveries/ C-sectionn
360
Q

What drugs should be avoided during breastfeeding?

A

Ciprofloxacin, Sulphonamides, tetraycline

Aspirin,
Lithium
Fluoxetine
Benzodiazepines
Carbimazole
Methotrexate
Sulphonyureas
Amiodarone
361
Q

Name the 4 classifications of Postnatal mental illness

A
  • Baby blues
  • Postnatal depression
  • Puerperal psychosis
  • Post traumatic stress sydnrome following childbirth
362
Q

Risk factors of PND?

A
  • Mental health hx
  • Alcohol and drugs
  • Traumatic experience
  • Social isolation
  • Domestic/childhood maltreatment
  • Socioeconomic status
363
Q

Clinical features of PND?

A
  • Low mood
  • Low energy/libido
  • Irritable
  • Unable to cope
  • Feeling of guilt about not loving baby enough
  • Tearful
  • Poor sleep
  • Poor appetite
  • Difficulty bonding with baby/ poor relationships with family
364
Q

Treatment of PND?

10% of women

A

SSRIs (Sertraline/paroxetine)

Reassurance and support

365
Q

Features of puerperal psychosis?

A

Severe mood swings and disordered perception

Needing hospital admission and long acting benzodiazepine

366
Q

ANTENATAL SCREENING

Describe the Combined test (for Down’s syndrome)

A

Scans for:

1) Nuchal translucency (fluid collection in back of neck suggests chromosomal disorder)
2) Beta-hCG
3) PAPP-A

Detection rate 85%, must be done in 1st trimester to allow TOP

367
Q

ANTENATAL SCREENING

What is Non-invasive prenatal testing

A

Tests for T21, T13 and T18

only be done in private sector, analyses fragments of fetal DNA in maternal blood

368
Q

ANTENATAL SCREENING

What is tested in the 8-10 week booking scan

A

Determine location, viability, dating of pregnancy

369
Q

ANTENATAL SCREENING

What is tested in the 11-13 week dating scan

A

Gestational age

crown- rump length

risk factors for pre-eclampsia / Gestational DM

Test for proteinuria/ bacteriuria

370
Q

ANTENATAL SCREENING

What is done in the 20 week anomaly scan

A
  • Detailed US
  • Plan delivery
  • Identify major abnormalities
371
Q

ANTENATAL SCREENING

What are the 9 conditions that are part of the new-born blood spot?

A

1) CF
2) Hypothyroidism
3) Sickle cell

INHERITED METABOLIC DISEASES

1) phenylketouria (PKU)
2) Medium chain acyl-coA dehydrogenase deficiency (MCADD)
3) Maple syrup urine disease (MSUD)
4) Isovaleric acidaemia (IVA)
5) Glutaric aciduria tye 1 (GA1)
6) Hymocystinuria (HCU)

3-6 are 1 in 100,000 RARE

372
Q

When is Anti-D given to rhesus negative women?

A

28 weeks Dose 1

34 weeks Dose 2

373
Q

What mnemonic is helpful for interpreting CTGs?

Describe it

A

DR C BRAVADO

DR- Define risk- why are they having it? (e.g pre-eclampsia)

C- Contractions (5 in 10 mins)

BRA- Baseline rate should be 110-160bpm

V- Baseline variability
Normal = 5-25 bpm
Reduced = <5bpm

A- Accelerations
Rise by 15 beats for more than 15 seconds. Should be 2 separate accelerations every 15 mins

D- Decelerations
Reduction of 15 beats for at least 15 seconds

Late decelerations = sign of slow recovery hypoxia

O- Overall Impression

Terminal Bradycardia = <100bpm for >10 mins

Terminal Deceleration = HR drops and does not recover for more than 3 minutes

These make up a ‘pre-terminal’ CTG and indicators of emergency C-section

374
Q

Causes of Oligohydramnios?

A 
premature rupture of membranes
fetal renal problems e.g. renal agenesis
intrauterine growth restriction
post-term gestation
pre-eclampsia

Danny's Phase 3A Medicine (10 decks)

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