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3a Exam > Obstetrics > Flashcards

Obstetrics Flashcards

1
Q

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

What happens after blastocyst implantation in pregnancy?

A

The blastocyst buries (Interstitial Implantation)→ primary decidual reaction

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3
Q

What basic placental structures form after interstitial implantation in pregnancy?

A
  • Floating villi
  • Anchoring villi
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4
Q

What do Cytotrophoblast progenitor stem cells differentiate into?

A

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

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5
Q

What are the functions of extra-villous trophoblasts in pregnancy?

A

Spinal artery remodelling

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6
Q

What is spinal artery remodelling in pregnancy?

A

Endovascular invasion myometrium- optimum 02 and nutrient supply
Due to extra-villus trophoblast invasion

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7
Q

When does full placental blood flow occur in pregnancy?

A

Week 10-12

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8
Q

What may poor endovascular remodelling lead to in pregnancy?

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

What is human chorionic gonadotrophin (hCG)?

A

A hormone secreted by trophoblast cells of the blastocyst on days 6-7 that:
- Promotes maintenance of corpus luteum
- Maintains production of oestrogen and progesterone

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10
Q

Where is Progesterone produced in pegnancy?

A

Corpus Luteum makes it until 7-8 weeks
Afterwards the placenta takes over

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11
Q

What are the 4 functions 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

What does progesterone inhibit?

A

Lactation during pregnancy.
Fall in progesterone following delivery triggers milk production

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13
Q

What is the name of the breast milk that is produced at birth?

A

Colostrum

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14
Q

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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15
Q

What is the function of Prolactin?

A

Milk production

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16
Q

What is the function of Oxytocin during pregnancy?

A

Milk ejection reflex
Uterine contraction

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17
Q

What is the principle foetal nutrient during pregancy?

A

Glucose

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18
Q

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

A

Low glucose levels due to fat deposition and glycogen synthesis

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19
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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20
Q

What happens to maternal insulin levels throughout pregnancy?

A
  • Progressive rise until peak at 32 weeks.
  • hPL induces insulin resistance to ensure glucose sparing to the foetus
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21
Q

What are the initial immunity changes after fertilisation?

A

Increases in:
- GFs
- Proteolytic enzymes
- Inflammatory mediators
Facilitates implantation

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22
Q

Why is blastocyst implantation not rejected due to immunity?

A

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

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23
Q

Why are syncytiotrophoblasts and extra-villus trophoblasts not rejected due to immunity?

A

Syncytiotrophoblasts: have no self:non-self markers = no maternal immune system
Extra-Villus trophoblasts (EVT): have modified self:non-self markers = modified maternal immune response

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24
Q

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

A

Normaly = balanced Th1 and Th2

Pregnant = >Th2

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25
Q

What is the only antibody that can cross the placenta?

A

IgG

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26
Q

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: 4 subtypes and the only Ig to cross the placenta

IgM: pentameric structure (early antibody)

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27
Q

How would you describe a ‘perfect’ pregnancy?

A
  • 37-42 weeks
  • Spontaneous in onset + vertex position
    Without the use of:
  • Forceps/C-section/ventose delivery
  • Induction of labour
  • Epidural/general anaesthesia
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28
Q

What are failure to progress pregnancies 3 P’s?

A

Power
Passage
Passenger

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29
Q

Describe the pathophysiology of ‘Power’ in failure to progress pregnancy

A

Need contractions to be strong enough
Difficult in nulliparous women- may need instrumental delivery

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30
Q

Describe the pathophysiology of ‘Passage’ in failure to progress pregnancy

A

‘Pelvis’ abnormalities in:
- Anterior-posterior diameter (AP) (front to back distance)
- Transverse diameter (side to side length)

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31
Q

Describe the pathophysiology of ‘Passenger’ in failure to progress pregnancy

A

The baby needs to be in the correct position

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32
Q

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

A

Attitude: How well the babies head is flexed (well flexed is best)
- Extended 90° = brow presentation
- Hyperextended >120° = face presentation

Position: occipito anterior/ transverse/ posterior
1) OT when entering inlet
2) OA when entering outlet
3) Then turn 90° to come out facing mothers medial thigh

Size of head

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33
Q

Define moulding

A

Head compressed through the pelvis

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34
Q

Define caput

A

Swelling caused during delivery

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35
Q

How long on average is the first stage of pregnancy?

A

5-12 weeks: Multiparious
8-12 weeks: Primiparous

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36
Q

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

A

2-3 days:
- Irregular painful contractions
- Cervix is effacing and thinning
- Dilation to about 4cm
- Mucoid plug

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37
Q

What is Engagement?

A

How far above the pubic symphysis the babies head is:
3/5th of the head within pelvic brim = engaged

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38
Q

What is Presentation?

A

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

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39
Q

What is Lie?

A

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

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40
Q

What is station?

A

Relationship between lowest point of presenting part and ischial spines

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41
Q

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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42
Q

What is Entonox?
Name its side effects

A

Gas and air

SE: N+V

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43
Q

Name the maternal side effects of the most effective form of pain relief during labour

A

Epidural maternal SE:

  • 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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44
Q

Name the foetal side effects of the most effective form of pain relief during labour

A

Epidural foetal SE:
- Tachycardia: due to maternal temperature
- Diminished breast feeding behaviour

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45
Q

Name an opiate that could be used as pain relief during labour

A

Morphine

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46
Q

Name 2 foetal side effects of opiates being used as pain relief during labour

A

They cross the placenta readily:
- Respiratory depression
- Diminish breath seeking/breast feeding behaviours

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47
Q

Name 4 maternal side effects of opiates being used as pain relief during labour

A

1) Sedation
2) Euphoria/ dysphoria
3) N+V
4) Longer 1st and 2nd stage

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48
Q

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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49
Q

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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50
Q

In what timeframe should you in In primigravid and multiparous women:
- Suspect delay?
- Diagnose delay?
- Baby be born?

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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51
Q

Why is there now delayed cord clamping?

A

Early clamping doesn’t benefit baby/ mother
Improves iron intake

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52
Q

What happens to endovascular invasion after implantation in the myometrium?

A

Narrow bore high resistance vessels become wide bore low resistance vessels

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53
Q

Name some maternal CVS changes during pregnancy

A
  • Increased RBC & plasma volume
  • Increased plasma volume → decline in haematocrit
  • Increased Q due to increase Fe demand (peripheral vasodilation)
  • Hypercoagulable = increased risk of embolism
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54
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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55
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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56
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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57
Q

What is Chadwick’s Sign?

A

Early sign of pregnancy where the labia/cervix may appear blue due to increased blood flow (at 6-8 weeks)

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58
Q

Describe the function of the following hormones at birth:
Oxytocin
Prolactin
Oestrogen
Progesterone
Beta-endorphins
Adrenaline

A

Oxytocin: induces onset & labour contractions

Prolactin: begins milk production in mammary glands

Oestrogen: inhibits progesterone and prepare smooth muscle for labour

Progesterone: aids in cervical ripening

Beta-endorphins: natural pain relief

Adrenaline: energy for birth

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59
Q

What are the 9 Mechanisms of Labour?

A

DFICERIL:
- Descent
- Flexion
- Internal rotation
- Crowning
- Extension
- Restitution/External Rotation
- Internal restitution of shoulders
- Lateral flexion

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60
Q

How is haemolytic disease of a newborn caused?

A

1) Rhesus - mother and + father
2) Rhesus - mother and + baby
3) Baby has D antigen and mother does not
4) Mother produces antibody against D antigen and haemolysis of newborns RBCs

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61
Q

Which antibodies can destroy the foetal red blood cells?

A

IgG antibodies can cross the placenta and destroy foetal RBCs

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62
Q

What can haemolytic disease of a newborn do to the baby?

A
  • Anaemia
  • Jaundice
  • Brain damage
  • Fatal = miscarriage/ stillborn
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63
Q

How can you diagnose haemolytic anaemia?

A

Raised reticulocyte count, unconjugated bilirubinaemia and urinary urobilinogen
Abnormal RBC shape
Positive Coombes test
Raised red cell precursors in bone marrow

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64
Q

How can foetal RBC lysis be prevented in rhesus negative mothers?

A

Anti-D prophylaxis: destroys Rh+ IgG so no RBC are attacked

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65
Q

A rhesus- mum is having an amniocentesis.
What must you give her prior to this procedure?

A

Anti-D!

There is a risk of sensitisation

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66
Q

When is Anti-D given to rhesus negative women?

A
  • Dose 1: 28 weeks
  • Dose 2: 34 weeks
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67
Q

What are the potential consequences, if left untreated, of a rhesus - mother having a rhesus + foetus?

A

There is a risk of RBC lysis → foetal anaemia and death

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68
Q

Describe internal rotation during labour

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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69
Q

Describe crowing during labour

A

When the head pokes out

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70
Q

Describe internal restitution of the shoulders during labour

A

1) When the head is out it will turn to left/right
2) Shoulders will follow within pelvis

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71
Q

Describe the third stage of labour

A
  • Pushing out the placenta
  • Physiological management due to increased blood loss
  • 5-30mins
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72
Q

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

A
  • To create uterine contraction so that the placenta can separate
  • Prevents excessive blood loss/postpartum haemorrhage
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73
Q

Where is Relaxin released from?
What is its function in labour?

A
  • Released from placenta, membranes and lining of the uterus
  • Softens ligaments and cartilage of the pelvis, cervix + babies body so that they expand
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74
Q

What is the function of oxytocin in labour?

A
  • Stimulates uterine contractions during orgasm and childbirth
  • Triggers foetal ejection reflex when cervix fully dilated
  • Contracts uterus post birth to deliver placenta and limit bleeding
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75
Q

What is the function of prostaglandins?

A

Ripens the cervix → thinning and opening
Stimulates uterine contractions

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76
Q

Describe a breech

A

Not head first in uterus
Commonest malpresentation
Can be reversed by external cephalic version

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77
Q

What are the complications of an external cephalic version

A
  • Placenta praevia
  • APH
  • Ruptured membranes
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78
Q

What is a face presentation and the likely method of delivery?

A

Head extends rather than flexes
Forceps delivery

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79
Q

What is a brow presentation and the method of delivery?

A

Head is between full flexion and extension
LSCS delivery

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80
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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81
Q

In which malpresentation is there the highest risk of cord prolapse?
What method of delivery would you perform as a result?

A

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

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82
Q

What is a Occipitoposterior position?
What method of delivery would you perform?

A

Posterior fontanelle found to lie in posterior quadrant of pelvis
Labour is prolonged due to degree of rotation needed
Instrumental/C-section sometimes required

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83
Q

What is a Primary dysfunctional labour?

A

Most common in first labour
Due to insufficient uterine contractions

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84
Q

What is the management of Primary dysfunctional labour?

A

Hydration + Comfort + Analgesia = initial management
Syntocinon infusion after ROM

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85
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 passage)

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86
Q

What management can delay the 1st stage of labour?

A

Amniotomy (AROM)
Oxytocin (offer epidural)

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87
Q

What management can delay the 2nd stage of labour?

A

Instrumental/ LSCS delivery

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88
Q

What is quiescence?

A

There are no contractions when the myometrium is inactive

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89
Q

What are the most common reasons for inducing labour?

A
  • Prolonged pregnancy
  • Premature rupture of membranes and labour doesn’t start
  • Diabetic mother >38 weeks
  • Rhesus incompatibility
  • Pre-eclampsia
  • Diabetes
  • Growth restriction
  • Reduced foetal movements
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90
Q

What is the bishop score?

A

Assesses whether induction is required

<5 = unlikely to start without induction

> 9 = likely to start spontaneously

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91
Q

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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92
Q

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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93
Q

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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94
Q

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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95
Q

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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96
Q

What are contra-indications for induction?

A
  • Severe degree of placenta praevia
  • Transverse fetal lie
  • Severe cephalopelvic disproportion
  • Cervix <4 on bishops score
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97
Q

How is induction performed?

A

1) Membrane sweep
2) Prostaglandin gel and pessary high in vagina
3) Amniotomy: ROM
4) Oxytocin/ Syntocinon (oxytocin analogue ) (post ROM)

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98
Q

List 11 types of labour pain relief

A
  • Education (breathing, coping, birth partner)
  • Transcutaneous electrical nerve stimulation (TENS)
  • Water birth (reduces need for anaesthesia)
  • Pudendal nerve block S2,S3,S4 (for instrumental)
  • Local anaesthesia (lidocaine before epsiotomy/surturing vaginal tears)
  • Epidural (T10-S5 (performed at L3-L4))
  • Spinal anaesthesia
  • Gas and air: entonox
  • Paracetamol
  • Codeine
  • Opioids e.g. pethidine, diamorphine
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99
Q

Where is spinal anaesthesia injected into?

A

The CSF

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100
Q

Name an anaesthetic that can be given as an epidural

A

Bupivacaine

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101
Q

Give 3 indications for an epidural

A
  • Maternal request
  • Augmented labour
  • Twins
  • Existing co-morbidities
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102
Q

Give 3 contraindications for an epidural.

A
  • Maternal refusal
  • Local infection
  • Allergy
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103
Q

Describe the physiology behind a post-dural puncture headache?

A

Accidental dural puncture → CSF leakage → decreased pressure in fluid around the brain.

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104
Q

Give 3 symptoms of a post dural puncture headache

A
  • Headache is worse on sitting/standing
  • Neck stiffness
  • Photophobia
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105
Q

How would you treat a post dural puncture headache?

A
  • Lying flat
  • Analgesia
  • IV fluids
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106
Q

What is the significance of meconium liquor on the pad?

A

Foetal distress- possible breech

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107
Q

What are the 3 types of breech presentation?

A

Frank breech

Complete breech

Footling breech

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108
Q

Describe a Frank breech

A

Hips flexed
Legs extended

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109
Q

Describe a complete breech

A

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

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110
Q

Describe a footling breech

A

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

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111
Q

What is the most favourable position for vaginal delivery and why?

A

Occipito-anterior- smallest diameter comes through the pelvis

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112
Q

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.
(also true for transverse or oblique lies)

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113
Q

The mentovertical diameter is associated with what presentation?

A

Brow

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114
Q

What is the usual position of the head at engagement?

A

Occipito-transverse

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115
Q

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

A

Face presentation

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116
Q

What is hyperemesis gravidarum?

A

Persistent + excessive vomiting associated with weight loss (5% body mass), dehydration and ketosis during pregnancy

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117
Q

What placental hormone is hyperemesis gravidarum associated with?

A

B-hCG

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118
Q

What triad is found in Hyperemesis Gravidarum?

A

> 5% weight loss
Electrolyte imbalance
Dehydration

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119
Q

What is the management of Hyperemesis Gravidarum?

A

Mild:
- Avoid large volume drinks
- Small carb meals
Severe:
- Anti-emetics
- IV fluids
- Thromboprophylaxis
- Thiamine supplements

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120
Q

Give 3 types of anti-emetics and an example for each one

A

Dopamine antagonist: Metoclopramide
Phenothiazines: Prochloperazine
5HT selective serotonin antagonists: Ondansetron

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121
Q

What is Puerperal Pyrexia?

A

Maternal fever (>38°) in the first 14 days following delivery

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122
Q

What causes Puerperal Pyrexia?

A
  • Endometritis
  • UTI
  • Mastitis
  • VTE
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123
Q

What is the management of Puerperal Pyrexia?

A

Endometritis suspected = hospital admission for IV Abx (clindamycin and gentamycin) until afebrile for >24hrs

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124
Q

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

A

VTE (DVT of legs, pelvis and PE)
Preventable

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125
Q

When should you have a VTE risk assessment during pregnancy?

A
  • Booking
  • Antenatal admission
  • Labour
  • Postnatally
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126
Q

What are the risk factors for VTE during pregnancy?

A

BMI >30
Immobility
Smoking
FHx
Aged >35
Gross varicose veins
Pre-eclampsia
IVF
Multiple pregnancy
Parity >3

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127
Q

What medication can be given postnatally to reduce a woman’s risk of VTE?

A

LMWH

TED stockings

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128
Q

When is LMWH thromboprophylaxis, compression stockings and early mobilisation indicated in pregnancy?

A
  • Has any risk factor
  • If a women requires antenatal LMWH (must be given until 6 weeks postpartum)
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129
Q

If a pregnant/postpartum lady collapses what should you presume?

A

PE

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130
Q

What is anaemia during pregnancy?

A

Hb <105g/L
The fall in Hb is steepest ≈20 weeks gestation

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131
Q

What are the risk factors for anaemia?

A
  • Menorrhagia/Malaria/hookworm
  • Frequent pregnancies
  • Twins
  • Poor diet
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132
Q

How would you investigate anaemia in pregnancy?

A
  • Hb estimation at 28 weeks antenatally- test for sickle cell in black patients
  • Fe deficiency: low serum Fe, TIBC and serum ferritin
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133
Q

What causes anaemia during pregnancy?

A
  • 2x increase in iron requirements → micro-cytic aneamia (most common cause)
  • B12/folate deficiency → macrocytic anaemia
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134
Q

What is the management of iron deficiency anaemia?

A

Treat cause:
Ferrous sulphate (oral iron therapy) 2x/week
- May cause N/D/V, abdo pain and constipation
Iron rich diet
- Meat and dark green vegetables
Blood transfusion

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135
Q

What should you give to a mother with Hepatitis B?

A

All mothers should be screened
Give immunoglobulin
Vaccinate babies of carriers and infected mothers at birth

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136
Q

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

A

Give varicella immune immunoglobulin at birth + monitor for 28 days
Treat with Aciclovir if neonate develops chickenpox

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137
Q

How is Jaundice investigated?

A

LFTs
Urine dip: bile
Serology
HBsAG (Hep B surface Antigen)
Get expert help PROMPTLY: can be lethal

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138
Q

What inheritance pattern is associated with obstetric cholestasis?

A

Autosomal dominant

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139
Q

What is the clinical presentation of Obsteteric Cholestasis?

A
  • Jaundice
  • Pruritis (palms and soles)
  • Worse at night
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140
Q

What investigations would you perform for obstetric cholestasis?

A

LFTs: raised AST, ALT, GGT and bilirubin
Raised bile acid

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141
Q

Management of Obstetric Cholestasis?

A

Ursodeoxycholic acid
Emollients (i.e. calamine lotion): soothes skin
Antihistamines (e.g. chlorphenamine): sleeping
Weekly LFTs
Induced at 37 weeks

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142
Q

What are the complications of Obstetric Cholestasis?

A
  • Stillbirths
  • Preterm labour
  • Meconium
  • Foetal distress
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143
Q

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

A

3rd

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144
Q

What is the clinical presentation of Acute fatty liver of pregnancy?

A
  • Jaundice
  • Abdominal pain
  • Pre-eclampsia
  • Hypoglycaemia
  • Malaise
  • Fatigue
  • Nausea
  • Headache
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145
Q

ECTOPIC PREGNANCY

What is it?

A

A pregnancy that occurs anywhere outside the uterus

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146
Q

What is the most common place for an ectopic pregnancy

A

Ampulla of Fallopian tube

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147
Q

What are the risk factors for Ectopic Pregnancy?

A
  • IVF
  • Age
  • PID
  • Ectopic Hx
  • Smoking
  • Progesterone only pill
  • Endometriosis
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148
Q

What is the clinical presentation of Ectopic Pregnancy?

A
  • Amenorrhoea (missed period for 6-8 weeks)
  • Vaginal bleeding
  • Dizzy → fainting
  • Abdo pain/tenderness
  • Shoulder tip pain
  • Haemoperitoneum (blood in peritoneal cavity)
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149
Q

How is Ectopic Pregnancy diagnosed?

A

Positive pregnancy test (hCG)
Transvaginal USS:
- Empty uterus
- Fluid in uterus

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150
Q

How is Ectopic pregnancy managed?

A

Terminate pregnancy:
- Expectant management (awaiting natural termination)
- Medical management (methotrexate if no complication)
- Surgical management (salpingectomy or salpingotomy)

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151
Q

What is the criteria for expectant management of Ectopic Pregnancies?

A

Follow up
Unruptured
Adnexal mass <35mm
No visible heartbeat
No significant pain
HCG level < 1500 IU / l

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152
Q

What is the criteria for methotrexate management of Ectopic Pregnancies?

A

Follow up
Unruptured
Adnexal mass <35mm
No visible heartbeat
No significant pain
HCG level < 5000 IU / l
US: confirmed absence of intrauterine pregnancy

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153
Q

What is the criteria for surgical management of Ectopic Pregancies?

A

Does not fit medical or expectant management +:
Pain
Adnexal mass > 35mm
Visible heartbeat
HCG levels > 5000 IU / l

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154
Q

Name 4 side-effects of Methotrexate

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

What is gestational trophoblastic disease (GTD)?

A

A group of pregnancy related tumours

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156
Q

What is a Molar Pregnancy?

A

1) Abnormality in chr number during fertilisation
2) Non-viable fertilised egg implants into uterus
3) Will not come to term
4) Grows into uterus mass

A type of GTD

157
Q

What is a complete molar pregnancy?

A
  • Empty oocyte + one sperm (duplicates)
  • 46 chromosomes (diploid): all of paternal origin
  • No foetal tissue
158
Q

What is a partial molar pregnancy?

A
  • Normal egg + two sperm
  • 69 chromosomes (triploidy)
  • Some foetal tissue recognisable
159
Q

What is an invasive molar pregnancy?

A

When a complete mole invades the moymetrium

160
Q

What are risk factors for molar pregnancies?

A

Aged <16 or >45
Previous molar
Multiple pregnancies
Oral contraceptive
Asian
Menarche >12

161
Q

What are the complications of Molar Pregnancies?

A

Choriocarcinoma’s

162
Q

What is the clinical presentation of Molar Pregnancies?

A
  • Vaginal bleeding (early)
  • Abdominal pain (early)
  • Hyperemesis (late)
  • Hyperthyroidism (late)
  • Very high hCG levels (causes late symptoms)
  • Large uterus
  • Pre-eclampsia
  • Unexplained anaemia
163
Q

How are Molar Pregnancy investigated?

A

Urine and bloods: very high bhCG
Histology
US:
- ‘Snowstorm appearance’ in 2nd trimester
- Large

164
Q

How are molar pregnancies managed?

A

Urgent referral to specialist centre
Uterine evacuation
Suction curettage
Chemotherapy: Cisplatin (metastasise indicated by hCG is >20,000)
No pregnancy until hCG levels normal for 6 months: give contraception

165
Q

What is a miscarriage?

A

The loss of pregnancy <24 weeks gestation
Excludes ectopic or trophoblastic disease

166
Q

What is a complete miscarriage?

A

No products of conception left in uterus
TVUS: crown rump length >7mm
Gestational sack: >25mm
No foetal heartbeat

167
Q

What is crown-rump length?

A

US measures the length of foetus from the top of the head (crown) to the bottom of the buttocks (rump).
Estimates gestational age

168
Q

What is a threatened miscarriage?

A

Vaginal bleeding +/- pain + closed cervix + alive foetus

169
Q

What is an Inevitable miscarriage?

A

Vaginal bleeding +/- pain + open cervix + alive foetus

Pregnancy will not continue → complete/incomplete miscarriage

170
Q

What is an incomplete miscarriage?

A

Products of conception remain in uterus after miscarriage

Vaginal bleeding +/- pain + open cervix

171
Q

What is a missed miscarriage?

A

Foetus is dead + remains in uterus + no symptoms + closed cervix

Uterus: small for dates
No fetal HB + crown rump length is >7mm
Pregnancy test: + for weeks
Hx
Persistant dirty brown discharge

172
Q

What is recurrent miscarriage?

A

≥3 consecutive miscarriages

173
Q

What are the causes of recurrent miscarriage?

A

Abnormal foetal development
Uterine abnormality
Incompetent cervix
Placental failure
Multiple pregnancy

174
Q

What are the risk factors for miscarriage?

A

Age >30
Smoking >14 a day
Alcohol
Drug use
Uterine surgery
Uncontrolled DM
Increased parity

175
Q

What is the epidemiology of miscarriages?

A

15-20% of pregnancies
Majority: 1st trimester

176
Q

What is the clinical presentation of miscarriages?

A
  • Vaginal bleeding +/- abdominal pain following amenorrhoea
  • Cervix is open enough to admit one finger
  • Uterine size: small for dates
  • Passing products of conception
177
Q

How is a miscarriage investigated?

A

TVUS:
- Mean gestational sac diameter
- Foetal pole and crown-rump length
- Foetal heartbeat (only measured if >7mm crown-rump length)
Serum hCG (excludes ectopic)

178
Q

How are miscarriages <12 weeks managed?

A

Mifepristone (antiprogesterone to prime cervix) THEN Misoprostol 36-48hrs later

179
Q

How are miscarriages >13 weeks managed?

A

Vaginal misoprostol- bleeding may continue for 3 weeks
Manual vacuum aspiration under GA

180
Q

Until what week can a lady legally have an abortion?

A
  • 24 weeks under the Abortion Act 1967
  • > 24 weeks: illegal unless there is a substantial risk to the woman’s life OR foetal abnormalities.
181
Q

How is a termination of pregnancy carried out surgically?

A

Vacuum aspiration (adminster misoprostol before surgery to prepare cervix)

182
Q

How is a termination of pregnancy carried out medically?

A

Mifepristone (antiprogesterone to prime cervix) THEN Misoprostol 36-48hrs later

183
Q

When may a dilation and curettage procedure be performed?

A

Incomplete miscarriage
Retained placenta after delivery
Elective abortion

184
Q

What is a complication of dilatation and curettage?

A

Asherman’s Syndrome

185
Q

What are the investigations for Asherman’s Syndrome?

A

Hysterscopy
USS
Hysterosalpingogram (HSG) + dye

186
Q

What is the management of Asherman’s Syndrome?

A

Operative hysterscopy + Abx to prevent infection + oestrogen (improve quality of uterine lining)

187
Q

Define gestational hypertension

A

New high BP >20w gestation and resolves after giving birth

There is no proteinuria

188
Q

What is Pre-Eclampsia?

A

New hypertension 20 weeks post-gestation + proteinuria(>0.3g protein/24h) +/- oedema

189
Q

What is the pathophysiology of pre-eclampsia?

A

Abnormal placenta spiral arteries increase vascular resistance

190
Q

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 → vaso-constriction, clotting dysfunction and increased vascular permeability

191
Q

How is mild pre-eclampsia defined?

A

140/90-149/99 mmHg

192
Q

How is moderate pre-eclampsia defined?

A

150/100-159/109 mmHg

193
Q

How is severe pre-eclampsia defined?

A

> 160/110 mmHg

194
Q

What may happen to the foetus in severe pre-eclampsia?

A

Neurological damage due to hypoxia

195
Q

What are the moderate risk factors of pre-eclampsia?

A
  • 10 years since last pregnancy
  • 1st pregnancy
  • Aged >40yrs
  • BMI >25
  • FHx
196
Q

What are the high risk factors in pre-eclampsia?

A
  • Hx Pre-eclampsia/HTN
  • CKD
  • Autoimmune disease (SLE or antiphospholipid syndrome)
  • DM 1/2
197
Q

What is the Clinical Presentation of Pre-eclampsia?

A

New hypertension 140/90
Late signs:
- Severe headache
- Visual disturbances
- Swelling of face/hands/feet
- Liver tenderness/RUQ pain
- Vomiting
- Ankle clonus and brisk reflexes
HELLP syndrome

198
Q

How is pre-eclampsia diagnosed?

A

> 140/90 mmHg
+ 1 of:
1) Proteinuria:
- ≥1+ urine dipstick
- Urine protein:creatinine ratio (>30mg/mmol)
- Urine albumin:creatinine ratio (>8mg/mmol)
- No proteinuria= gestational hypertension
2) Organ dysfunction:
- LFT
- FBC
- Urine: MCS
3) Placental dysfunction:
- Foetal growth restriction
- Abnormal doppler

199
Q

Why would you do a urine culture in pre-eclampsia?

A

Excludes infection

200
Q

Why would you do an US of the foetus in pre-eclampsia?

A

Checks:
- Foetal growth
- Volume of amniotic fluid
- Doppler velocimetry of umbilical arteries

201
Q

What treatment can be given to women with gestational hypertension/pre-eclampsia?

A
  • Monitor BP 4x/day
  • Blood tests 2x/week
  • If not at term: labetelol (BB) to lower BP (>135/85 mmHg)
  • If no response, delivering the baby will normalise BP
  • Aspirin 75 mg OD (from 12 weeks gestation)
  • LMWH: to prevent VTE
202
Q

What antihypertensives should be avoided in pre-eclampsia?

A

ACE inhibitors

Angiotensin-II receptor antagonists

203
Q

What further monitoring should be done for pre-eclampsia?

A

USS: of foetus and amniotic fluid

CTG

Delivery once woman is stable and baby >34 weeks

204
Q

What are 4 maternal complications of pre-eclampsia?

A

Cerebrovascular haemorrhage
HELLP syndrome
Liver/renal failure
Pulmonary oedema

205
Q

What are 3 foetal complications of pre-eclampsia?

A

IUGR
Placental abruption
Preterm birth

206
Q

Define Eclampsia

A

Pre-eclampsia (gestational hypertension + proteinuria) and generalised tonic-clonic seizures

207
Q

Why does Eclampsia occur?

A

Failure to notice worsening pre-eclampsia

208
Q

When does Eclampsia occur during pregnancy?

A

Antepartum
Intrapartum
Postpartum

209
Q

What is the management of eclampsia?

A

Seizures: Magnesium sulphate
BP: IV Labetolol, nifidepine + Epidural analgesia during Labour
Deliver baby

210
Q

Why is Magnesium sulphate used in Eclampsia?

A
  • Surpresses convulsions and inhibits muscular activity
  • Reduces DIC risk by reducing platelet aggregation
211
Q

What should be monitored if using magnesium sulphate?

A

Magnesium levels: reduces reflexes and causes respiratory depression

212
Q

What is HELLP Syndrome?

A

Complication of pre-eclampsia/eclampsia at 27-37 weeks gestation

213
Q

What is the acronym of HELLP Syndrome?

A
  • Haemolysis (anaemia)
  • Elevated Liver Enzymes (ALT and AST) (blockage by fibrin)
  • Low Platelet Count (from consumption)
214
Q

What are the risk factors for HELLP Syndrome?

A

Aged >35
Nulliparity
Hx
Renal Disease/ DM
Afro-carib
Obese
HTN

215
Q

What do 10.5% of HELLP syndrome patients have?

A

Antiphospholipid syndrome

216
Q

When do the majority of HELLP patients present?

A

27-37 weeks

217
Q

In HELLP Syndrome, when do symptoms get:
Worse?
Better?

A

Worse: at night
Better: during the day

218
Q

What is the clinical presentation of HELLP Syndrome?

A

RUQ/mid-epigastric pain
Flu-like
Headache
Visual symptoms
Bruising/purpura
Oedema
Jaundice

219
Q

How is HELLP Syndrome diagnosed?

A
  • May not have hypertension or proteinuria
  • Blood film: schistocytes + haemolysis
  • FBC: anaemia + low platelets
  • Raised LDH + bilirubin
  • Raised LFTs
220
Q

Why are fragmented red cells seen on HELLP Syndrome blood films?

A

Microangiopathic haemolytic anaemia

221
Q

How is HELLP Syndrome managed?

A
  • IV magnesium sulfate
  • IV dexamethasone (foetal lung development)
  • BP control
  • Blood transfusion
  • Deliver foetus
222
Q

What is Intrauterine Growth Retardation (IUGR)?

A

Baby’s growth slows/ceases within the uterus

223
Q

What are the causes of Intrauterine Growth Retardation (IUGR)?

A
  • Maternal factors
  • Placental factors
  • Foetal factors
  • Genetic factors
224
Q

What are risk factors for Intrauterine Growth Retardation (IUGR)?

A

SHITS CRAP:
Smoking
Hypertension
IUGR previously
Twins
Still birth
Cocaine
Renal disease
Antiphospholipid syndrome
PAPP-A levels low

225
Q

What is symmetrical Intrauterine Growth Retardation (IUGR)?

A

Cause of early IUGR:
Antenatally: small head circumference, abdominal circumference and length
Postnatally: small head circumference, weight and length

226
Q

What is asymmetrical Intrauterine Growth Retardation (IUGR)?

A

Cause of late IUGR:
Antenatally: small abdominal circumference, but NORMAL head circumference and length
Postnatally: small weight, but NORMAL length and head circumference

227
Q

What adult onset diseases will IUGR babies be more susceptible to?

A
  • Metabolic syndrome
  • CHD
228
Q

How is Intrauterine Growth Retardation (IUGR) investigated?

A
  • Foetal abdominal circumference or estimated foetal weight <10th centile
  • Reduced Amniotic Fluid Index (AFI)
229
Q

What causes reduced Amniotic Fluid Index (AFI) in IUGR?

A

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

230
Q

How is Intrauterine Growth Retardation (IUGR) managed?

A

Lower segment Caesarean section (LSCS)
Corticosterioids: lung development up to 35+6 weeks

231
Q

List 4 complications of symmetrical Intrauterine Growth Retardation (IUGR)

A
  • Learning difficulties
  • Developmental delay
  • ADHD
  • Cerebral Palsy
232
Q

What is Sepsis?

A

Infection in the bloodstream + systemic symptoms

233
Q

What is Severe Sepsis?

A

Sepsis + organ dysfunction + tissue hypo-perfusion

234
Q

What is Septic shock?

A

Hypotension + hyperlactaemia + tissue hypo-perfusion despite adequate fluid replacement

235
Q

What are 9 causes of sepsis?

A
  • Pyelonephritis
  • Chorioamnionitis
  • Postpartum endometritis
  • Wound infection
  • Pneumonia
  • Acute appendicitis
  • Acute cholecystitis
  • Pancreatitis
  • Necrotising enterocolitis
236
Q

What are 10 risk factors for sepsis?

A
  • Obesity
  • Diabetes
  • Immunosuppressed
  • Anaemia
  • Vaginal discharge
  • Hx PID
  • Hx Group B Strep infection
  • Amniocentesis
  • Prolonged spontaneous rupture of membranes
  • Group A strep infection
237
Q

What is the Clinical Presentation of Sepsis?

A
  • Fever, rigors, diarrhoea and vomiting
  • Non-blanching rash (meningococcal septicaemia via Neisseria meningitidis)
  • Abdominal + pelvic pain
  • Hypoxia
  • Hypotension
  • Oliguria
  • Impaired GCS
  • Failure to respond to treatment
238
Q

Why does meningococcal septicaemia cause non-blanching rashes?

A

Meningococci release endotoxins into blood → WBCs attracted → endothelial lining damage → capillary leakage → haemorrhagic rash

239
Q

What criteria is used to identify severe sepsis?

A

Systemic Inflammatory Response Syndrome (SIRS) Criteria

240
Q

Describe the SIRS Criteria

A

3Ts White with Sugar: ≥2 points = SIRS = Severe Sepsis

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

WBC <4 or >12

Sugar >7.7mmol/L: in absence of diabetes

241
Q

What investigations would you order for Sepsis?

A
  • FBC:raised WCC
  • CRP: raised
  • U&Es:AKI common
  • ABG: raised Lactate (2° to reduced end-organ perfusion → no oxygen to use glucose → anaerobic respiration)
  • Blood cultures:identifies **causative organism
  • Urine output: reduced
242
Q

What is the management of Sepsis?

A

Blood cultures BEFORE Abx (Broad spec IV):
- Mother: piperacillin + tazobactam
- <3m= Cefotaxime + Amoxicillin + Aciclovir
Fluid resuscitation
Oxygen (94-98%)
Intubation and ventilation
Consider delivery
VTE prophylaxis

243
Q

What is Chorioamnionitis?

A

Membrane rupture → acute inflammation of amnion and chorion membranes due to an ascending bacterial infection

244
Q

What is the most common cause of Chorioamnionitis?

A

Group B streptococcus (GBS)

245
Q

What is the clinical presentation of Chorioamnionitis?

A
  • Maternal signs (pyrexia, tachycardia, leucocytosis)
  • Foul amniotic fluid
  • Maternal/foetal tachycardia
  • Uterine tenderness
  • ROM
246
Q

What is the management of Chorioamnionitis?

A

C-section delivery
IV benzyl Penicillin

247
Q

Why must Chrorioaminonitis be treated?

A

To prevent Neonatal sepsis

248
Q

What are the complications of maternal Group B Step infections?

A

Chrorioaminonitis → neonatal sepsis

249
Q

If a patient is isolated during labour, what should be given to prevent vertical Group B Step transmission to baby?

A

IV benzyl Penicillin

250
Q

Define Premature Birth

A

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

251
Q

When would a premature birth be considered non-viable?

252
Q

What organs are most likely to be affected in babies born prematurely and why?

A

Lungs and brain develop in the 3rd trimester

253
Q

What is a very low birth weight?

254
Q

What is a extremely low birth weight?

255
Q

What is an incredibly low birth weight?

256
Q

What are the risk factors for Premature Birth?

A

Unexplained
Multiple pregnancy
Cervical incompetence (e.g. surgery)
Hx
Premature rupture of membranes (PROM)

257
Q

What is the Clinical presentation of Premature Birth?

A
  • Contractions
  • Bleeding
  • Amniotic fluid loss
  • Dilation of cervix
258
Q

What are the investigations for Premature Birth?

A

Speculum examination: pooling of amniotic fluid in vagina
TVUS: cervical length
Fetal fibronectin: >50 ng/ml (indicates labour)
Insulin-like growth factor-binding protein-1 (IGFBP-1) or Placental alpha-microglobin-1 (PAMG-1): reveals ROM
Vaginal swab

259
Q

What is the management of Preterm Labour with Intact Membranes?

A

Fetal monitoring (CTG or intermittent auscultation)
Tocolysis: nifedipine (<48hr usage)
Maternal corticosteroids: <36 weeks gestation
IV magnesium sulphate: <34 weeks gestation a
Delayed cord clamping
Delivery

260
Q

What is the management of Preterm Prelabour Rupture of Membranes?

A

Prophylactic abx: erythromycin 250mg TD for ten days/until delivery (prevents chorioamnionitis)
Induction of labour: >34 weeks gestation

261
Q

What is Tocolysis?
Give 3 examples

A

Drugs that delay delivery for up to 48 hours
Work by suppressing contractions

Prostaglandin synthesis inhibitors: Indomethacin

CCBs: Nifedipine

Oxytocin antagonist: Atosiban

262
Q

How does nifedipine inhibit premature contractions?

A

Nifedipine is a CCB → muscle contraction inhibition

263
Q

Why are corticosteroids used in premature birth?

Give two examples

A

Surfactant production for foetal lung maturity

Betamethasone

Dexamethasone

264
Q

Why is magnesium sulfate used in premature births?

A

Neuroprotection: reduces risk of cerebral palsy

265
Q

What is premature rupture of membranes (PROM)?

A

Rupture of membrane <37 weeks gestation

266
Q

What are the risks of PROM?

A

Infection
>24 hours = chorioamnionitis + endometriosis
Spontaneous labour

267
Q

What is the prognosis for mid-trimester PROM (<24 weeks)?

A

Poor outcome: pulmonary hypoplasia even after steroids

268
Q

What is the treatment for PROM 24-34 weeks gestation?

A

Maternal Steroids: Dexamethasone
Erythromycin
MgSO4
Daily review for signs of infection

269
Q

What is the treatment for PROM >34 weeks gestation?

A

MgSO4
Induce labour

270
Q

What is antepartum haemorrhage?

A

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

271
Q

What are the causes of antepartum haemorrhage?

A

Majority idiopathic
Placenta praevia
Placental abruption
Vasa praevia

272
Q

What percentage of very preterm babies are born in association with APH?

273
Q

What is the clinical presentation of antepartum haemorrhage?

A
  • Bleeding +/- pain
  • Uterine contractions
  • Malpresentation or engagement failure
  • Foetal distress
  • Hypovolaemic shock
274
Q

What are the investigations of antepartum haemorrhage?

A

US: Exclude placenta praevia

275
Q

What is the management of antepartum haemorrhage?

A

Anti-D
Replacement fluids/blood
IV access
CTG
Delivery may save mothers life

276
Q

What is placental abruption?

A

Premature seperation of placenta from the uterine wall

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

277
Q

What are causes of placental abruption?

A
  • Maternal hypertension (common)
  • Maternal trauma
  • Smoking
  • Alcohol
  • Drugs
  • Short umbilical cord
  • Decompression of the uterus
278
Q

What is the clinical presentation of placental abruption?

A
  • Abdominal examination: ‘woody-hard’ and tense uterus
  • Sudden continuous abdo pain
  • DARK red vaginal bleeding
  • Uterine contractions
  • Foetal distress
279
Q

What is meant by a woody uterus in placental abruption?

A

‘Hard’ uterus due to blood invading myometrium

280
Q

How is placental abruption diagnosed?

A

Clinically

281
Q

What is the management of placental abruption?

A

Emergency!
- Induction of labour
- C-Section: if foetus in distress, vaginal if not
- Crossmatch 4 units of blood
- Fluid and blood resuscitation
- CTG monitoring of the fetus and mother
- Anti-D prophylaxis: in Rhesus-D - women

282
Q

Where should normal placenta invade into?

A

The decidua

283
Q

What is placenta praevia?

A

Placenta is inserted wholly/partly into the lower segment of the uterus

284
Q

What are the risk factors for placenta praevia?

A
  • Hx placenta praevia/ C-section / abortion
  • Increased maternal age/parity
  • Smoking
  • Cocaine
  • Deficient endometrium
  • Assisted conception
285
Q

What is the pathophysiology of placenta praevia:
Major?
Minor?

A

Major: placenta covers the entire internal cervical os (grade 3/4)

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

286
Q

What is a low-lying placenta?

A

Placenta is within 20mm of the internal cervical os

287
Q

What is the clinical Presentation of placenta praevia?

A

Normally asymptomatic
Painless bleeding >28 weeks gestation
BRIGHT RED BLEEDING
High presenting part or abnormal lie

288
Q

What are the complications of Placenta Praevia?

A

PPH
Placenta accreta or percreta

289
Q

Would a woman with a LLP complain of pain?

A

No, LLP is classically painless

290
Q

When might placenta abnormalities be detected?

A

On the 20w US anomaly scan
Placenta must be >25mm from the cervical os

291
Q

How should a LLP be managed?

A
  • Advise mum on the symptoms to look out for
  • Seek early advice.
  • If recurrent bleeds: admit until delivery
  • Elective c-section at 38 weeks
292
Q

What is the difference in blood between placenta abruption and praevia?

A

Abruption: dark red

Praevia: bright red

293
Q

What is Placenta Accreta?

A

Placenta implants on the surface of the myometrium

294
Q

What is Placenta Increta?

A

Placenta attaches deeply into the myometrium

295
Q

What is Placenta Percreta?

A

Placenta invades past the myometrium and perimetrium → other organs e.g. bladder

296
Q

What is Vasa Praevia?

A

Foetal vessels within the foetal membranes run across the internal cervical os

Risk of rupture: unsupported by the umbilical cord or placental tissue

297
Q

How to prepare for delivery with Placenta praevia, Placenta accreta and Vasa Praevia?

A

Elective LSCS 36-38 weeks
Consent to include all potential interventions e.g.
hysterectomy
Anticipate major obstetric haemorrhage
Crossmatch + Groupsave + Cell salvage
Corticosteroids: due to preterm risk

298
Q

Define puerperium

A

Period between placental delivery → 6w post-delivery

299
Q

What is postpartum haemorrhage (PPH)?

A

Bleeding after delivery of the baby and placenta

300
Q

What is the most common cause of obstetric haemorrhage?

301
Q

What is a primary postpartum haemorrhage (PPH)?

A

> 500mls vaginal bleeding in the first 24 hours post-delivery

302
Q

What is a secondary postpartum haemorrhage (PPH)?

A

> 500ml vaginal blood loss between 24 hours→ 6w post-delivery

303
Q

What is minor postpartum haemorrhage (PPH)?

A

500-1500ml vaginal blood loss + no signs of shock

304
Q

What is major postpartum haemorrhage (PPH)?

A

≥1500mls vaginal bleeding + continuing to bleed OR clinical shock

305
Q

What are the causes of postpartum haemorrhage (PPH)?

A

4 Ts:

Tone: atonic uterus (Is the uterus contracted?)

Tissue: retained placenta with prolonged 3rd stage (Is the placenta complete?)

Trauma: tears and repairs

Thrombin: pre-eclampsia/DIC (check clotting)

306
Q

What are the risk factors for postpartum haemorrhage (PPH)?

A

Hx
>40yrs
Multiple pregnancy
Polyhydramnios
Abruption or 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

307
Q

What is the conservative, medical and surgical management of postpartum haemorrhage (PPH)?

A

ABCDE
Fluid Resus
O2
Rubbing the uterus through abdominal: stimulates uterine contractions
IM Oxytocin = given with delivery of anterior shoulder
IM Ergometrine: if significant RFs (+ no HTN)
Catheterisation: give birth with empty bladder to increase uterine contraction
IM Carboprost: prostaglandin analogue stimulates uterine contraction (Consider theatre if > 2 doses required)
Misoprostol: prostaglandin analogue
IV Tranexamic acid: antifibrinolytic reduces bleeding during CS
Surgical:
Evacuation of retained products
Bi-manual uterine compression: expels clots
Balloon tamponade
B-lynch suture
Consider hysterectomy

308
Q

When must you never give Ergometrine in PPH?

A

if the patient has hypertension (vasoconstrictor)

309
Q

What are the seven cardinal movements of labour?

A

EDFIEEE
- Engagement
- Descent
- Flexion
- Internal rotation
- Extension
- External rotation/ restitution
- Expulsion

310
Q

Describe Engagement

A

Biparietal diameter (top of baby’s head) in pelvic inlet

311
Q

Describe Descent

A

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

312
Q

Describe Flexion

A

Smallest diameter of the baby’s head presents into the pelvis due to tissue resistance

313
Q

Describe Internal Rotation

A

Head rotates to accomodate the changes of pelvic diameter

Sideways → facing back of the mother (back of head against the front of the pelvis)

314
Q

Describe Extension

A

As head is born

315
Q

Describe External Rotation

A
  • Slight pause in labour after the baby’s head is born
  • Babies head rotates face down → mothers inner thigh
316
Q

Describe Expulsion

A

From symphysis pubis the following moves out:
Anterior shoulder → posterior shoulder→ rest of the body

317
Q

What is the largest diameter of the pelvic outlet?

A

Front to back

318
Q

Why is external rotation necessary?

A

So shoulders can fit

319
Q

What happens if external rotation is not successful?

A

Shoulder Dystocia

320
Q

What is shoulder dystocia?

A

Inadequate space for shoulders to pass pubic symphysis during external rotation (after head passes)
Usually the anterior shoulder

321
Q

What are the causes of shoulder dystocia?

A

3 Ps:
Power (uterus)
Passenger (foetus)
Passage (pelvis)

322
Q

What are power causes of shoulder dystocia?

A

Uncoordinated uterine activity/short infrequent contractions

323
Q

What are pasenger causes of shoulder dystocia?

A
  • Position or lie
  • Macrosomia (>4.5kg)
  • Large abdominal circumference: head circumference
324
Q

What are passage causes of shoulder dystocia?

A
  • Long and oval brim
  • Cephalopelvic disproportion: e.g. due to scoliosis, kyphosis or rickets
325
Q

What is the main risk factors for shoulder dystocia?

A
  • Gestational diabetes → macrosomia
326
Q

What is the clinical presentation of shoulder dystocia?

A
  • Difficulty 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
327
Q

What is the management of of shoulder dystocia?

A

HELPERR:
Call for Help.
Evaluate for Episiotomy: to allow Wood’s screw manoeuvre
Legs in McRoberts Manoeuvre (alters symphysis pubis)
Suprapubic Pressure
Enter pelvis
Rotational manoeuvres
Remove posterior arm

Stop pushing
Last resorts:
Symphisiotomy
Zavanelli manouvere (push baby back in→ CS)

328
Q

What are the complications of shoulder dystocia?

A

Fetal hypoxia (→ cerebral palsy)
Brachial plexus injury and Erb’s palsy
Perineal tears
Postpartum haemorrhage

329
Q

What is cord prolapse?

A

Umbilical cord descends cervix after membrane rupture
Foetal hypoxia due to cord compression

330
Q

What is the main risk factor for cord prolapse?

A

Breech presentation

331
Q

How can cord prolapse be diagnosed?

A

CTG: foetal distress CTG
Vaginal examination
Speculum examination

332
Q

What is the management of cord prolapse?

A

Tocolytics: terbutaline (reduce contractions)
DO NOT PUSH CORD BACK IN: handling causes vasospasms
Cord kept warm and wet
Patient on all 4s
CS

333
Q

Give a consequence of cord prolapse

A

Foetal hypoxia → morbidity and mortality

334
Q

What is Amniotic Fluid embolism?

A

When the liquor enters maternal circulation leading to anaphylaxis:
- Sudden dyspnoea
- Hypoxia
- Hypotension

335
Q

What are the dangers of amniotic fluid embolism?

A

80% mortality:
Membrane rupture → seizures and cardiac arrest

336
Q

Management of amniotic fluid embolism

A

Emergency management!

337
Q

What is uterine rupture?

A

Myometrium ruptures

338
Q

What is the major risk of uterine rupture?

A

Hx CS: wound dehiscence

339
Q

What is the clinical presentation of uterine rupture?

A

RUPTURE USUALLY IN LABOUR
Ceasing of uterine contractions
- Abdominal pain
- Foetal distress
- Vaginal bleeding
- Maternal shock

340
Q

What is the management of uterine rupture?

A

Resuscitation
Transfusion
Emergency CS
Hysterectomy

341
Q

What is gestational diabetes?

A

Diabetes triggered by pregnancy

342
Q

What is the pathophysiology of gestational diabetes?

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

Why does gestational diabetes cause macrosomia?

A

1) Excess glucose → excess glucose to foetus
2) Increased foetal insulin → more tissue/fatty deposits

344
Q

Why does gestational diabetes cause neonatal hypoglycaemia?

A

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

345
Q

Why does gestational diabetes cause Polyhydramnios?

A

Increase in foetal glucose → polyuria → more fluid release from the foetus

346
Q

Name 3 anti-insulin hormones produced by the placenta in gestational diabetes

A
  • Human placental lactogen (hPL)
  • Glucagon
  • Cortisol
347
Q

What are the risk factors for gestational diabetes?

A

HX of GM
Hx of macrosomic baby (≥ 4.5kg)
BMI > 30
Ethnic origin (black Caribbean, Middle Eastern and South Asian)
FHx of DM

348
Q

What is the clinical presentation of gestational diabetes?

A

Mainly during 3rd trimester
DM presentation +:
- Pre-eclampsia
- Macrosomia
- Recurrent infections
- Intrauterine death
- Polyhydramnios

349
Q

What are the complications of gestational diabetes?

A

SMASH:
Shoulder dystocia
Macrosomia
Amniotic fluid excess (polyhydramnios)
Stillbirth
Hypertension + neonatal hypoglycaemia

350
Q

What is the diagnosis of gestational diabetes?

A

OGTT at 24-28 weeks
5,6,7,8 RULE:
- Fasting: >5.6
- 2 hours: >7.8

351
Q

What is the management of gestational diabetes?

A

Lifestyle:
- BMI <27
- Low glycaemic index diet
- 30 min physical activity/day
Metformin (1st line)
Insulin (2nd line)
Deliver at TERM: CS if macrosomia/pre-eclampsia

352
Q

List 5 peripartum events that can lead to chronic infections

A
  • Prolonged ROM
  • Chorioamnionitis
  • Repeated vaginal exams
  • Catheterisation
  • Instrumental deliveries/C-sectionn
353
Q

What 10 drugs should be avoided during breastfeeding?

A

Ciprofloxacin
Tetraycline
Aspirin
Lithium
Fluoxetine
Benzodiazepines
Carbimazole
Methotrexate
Sulphonyureas
Amiodarone

354
Q

Give 3 red flag signs that a mother may be developing mental health problems postnatally

A
  • Recent change in mental state
  • Thoughts/acts of self harm
  • Estrangement from the infant
355
Q

Name the 4 types of postnatal mental illness

A
  • Baby blues
  • Postnatal depression
  • Puerperal psychosis
  • PTSD following childbirth
356
Q

What is post-natal depression?

A

Low mood post-nataly
Normally 3 months post-natal and lasts >2 weeks

357
Q

What are the risk factors for post-natal depression?

A
  • Mental health hx
  • Alcohol and drugs
  • Traumatic experience
  • Social isolation
  • Domestic/childhood maltreatment
  • Socioeconomic status
358
Q

What is the classic presentation of post-natal depression?

A

Low mood
Anhedonia (lack of pleasure in activities)
Low energy
Unable to cope
Feeling of guilt about not loving baby enough
Difficulty bonding with baby/ poor relationships with family
Tearful
Poor sleep
Poor appetite

359
Q

What is the treatment of post-natal depression?

A

SSRIs (Sertraline/paroxetine)
CBT
Reassurance and support

360
Q

How long should baby blues last?

361
Q

What is the clinical presentation of baby blues?

A

Mood swings
Low mood
Anxiety
Irritability
Tearfulness

362
Q

Does baby blues require treatment?

A

No, the majority of mothers experience this

363
Q

What is puerperal psychosis?

A

Psychosis 2-3 weeks post-nataly

364
Q

What is the clinical presentation of puerperal psychosis?

A

Delusions
Hallucinations
Depression
Mania
Confusion
Thought disorder

365
Q

What is the management of puerperal psychosis?

A

Hospital admission:mother and baby unit
CBT
Medications: antidepressants, antipsychotics or mood stabilisers
Electroconvulsive therapy (ECT)

366
Q

Name 3 neonatal screening programmes

A
  1. New born blood spot: days 5-8
  2. Hearing test: within 4 weeks
  3. New born (within 72 hours) and GP 6-8w physical examination
367
Q

When would a woman have her booking appointment?

A

8-10 weeks

368
Q

What is performed in the 8-10 week booking scan?

A

Determine location, viability and dating pregnancy
General lifestyle advice
Obstetric history and examination
Check: HIV, Hep.B, Syphillis and Rubella

369
Q

What is tested in the 11-13 week dating scan?

A

Gestational age
Crown-rump length
Risk factors for: pre-eclampsia/GDM
Proteinuria/bacteriuria

370
Q

What is the combined test in antenatal screening?

A

Screens congenital anomalies (11-14 weeks):
- PAPP-A
- bHCG
- Nuchal Translucency (fluid collection in back of neck suggests chromosomal disorder)
- Mothers age

371
Q

What is the quadruple test in antenatal screening?

A

Screens for Down’s syndrome (14-20 weeks):
- bHCG
- AFP
- Inhibin A
- Unconjugated oestradiol

372
Q

When should a foetal anomaly screening test be done?

A

Blood sample: by 14+1 weeks.
Anomaly scan: by 18-20+6 weeks.

373
Q

What diseases are screened in the foetal anomaly screening test?

A
  1. Down’s (T21)
  2. Edward’s (T18)
  3. Patau’s (T13)
374
Q

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

375
Q

What is done in the 20 week anomaly scan?

A
  • Detailed US
  • Plan delivery
  • Identify major abnormalities
376
Q

What 9 conditions are part of the new-born blood spot in the neonatal screening programme?

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)

377
Q

Name 4 things that a new born physical examination is looking for in the neonatal screening programme

A
  1. Eye problems
  2. Heart defects
  3. Dysplasia of the hips
  4. Undescended testes
378
Q

Give 2 methods to monitor foetal heart rate

A
  1. Intermittent auscultation: via pinard stethoscope or a hand held doppler
  2. Continuous monitoring: cardiotocography (CTG)
379
Q

What is the gold standard method for direct FHR monitoring?

380
Q

How do you define a normal CTG? (BraVAD)

A
  1. Baseline HR: 110-160 bpm
  2. Variability: >5
  3. Accelerations: present
  4. Decelerations: none
381
Q

What mnemonic is helpful for interpreting CTGs and determining the need for CS?

A

DR C BRAVADO

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

Contractions: 5/10 mins

BRA-Baseline rate: 110-160bpm

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

Accelerations:
- Rise by 15 beats for >15s
- 2 separate accelerations every 15 min

Decelerations :
- Reduction of 15 beats for at least 15 seconds
- Late decelerations = slow recovery hypoxia

Overall Impression:
- Terminal Bradycardia = <100bpm for >10 mins
- Terminal Deceleration = HR drops and does not recover for >3 min

382
Q

What are causes of Oligohydramnios?

A

PROM
Fetal renal problems e.g. renal agenesis
IUGR
Pre-eclampsia

383
Q

What is colour should Meconium be?

A

Green/brown

383
Q

What does meconium stained amniotic fluid
(MSAF) indicate?

A

Foetal distress from hypoxia → passing meconium whilst still inside the uterus

384
Q

What can meconium stained amniotic fluid
(MSAF) lead to?

A

Meconium aspiration syndrome: baby inhales the meconium → Respiratory Distress

385
Q

How is MSAF treated?

A

Surfactant/inhaled nitric oxide

386
Q

Define maternal death

A

The death of a woman while pregnant or within 42 days of pregnancy termination
Not due to accidental causes

387
Q

What are the 3 most common causes of maternal death?

A
  1. VTE
  2. Haemorrhage
  3. Pre-eclampsia
388
Q

Name 3 foetal emergencies

A
  1. Foetal distress
  2. Cord prolapse
  3. Shoulder dystocia

3a Exam (9 decks)

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