Labour and Delivery Flashcards

1
Q

What are the stages of labour?

A

First stage = creation of birth canal

Second stage = descent, rotation, delivery

Third stage = placental delivery

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2
Q

Outline the first stage of labour

A

Contractions begin

Descent of fetal head into birth canal

Creation of birth canal

1) latent phase = slow cervical softening, shortening, opening
2) active phase = faster rate of change, regular contractions

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3
Q

Outline the second stage of labour

A

Fetal head descent and rotation through the dilated cervix, birth canal and delivery

1) passive phase = descent and rotation
2) active phase = maternal effort to expel the fetus and achieve birth

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4
Q

Outline the third stage of labour

A

Delivery of placenta

Usually 5-15 mins

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5
Q

How does labour get initiated?

A

Rise in oestrogen:progesterone ratio

Prostaglandins = initiate softening of cervix, maintain/initiate uterine contractions

Oxytocin = uterine contractions

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6
Q

Outline the functions of prostaglandins

A

Induce cervical ripening

Induce cervical contractions

Increase myometrial sensitivity to oxytocin

Raise intracellular Ca = myometrial cell contract

Enhance myometrial gap junctions = strengthen contractions

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7
Q

What is cervical ripening?

A

The changes in the cervix when labour is being initiated

1) reduction in collagen
2) increases in GAGs
3) increase in hyaluronic acid
4) reduced aggregation of collagen fibres

Due to oestrogen, relaxin and prostaglandins breaking down the connective tissue

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8
Q

Where are prostaglandins produced?

A

Mainly in myometrium and decidua

Increased synthesis by amnion in third trimester

Released from cervical stretching

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9
Q

How does progesterone effect contractions?

A

Inhibits

Relative fall in progesterone = facilitates myometral excitability

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10
Q

Where is oxytocin secreted from and how is it controlled?

A

Secreted by posterior pituitary

Controlled by hypothalamus = +ve feedback from cervix and vagina (Ferguson reflex)

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11
Q

What is the role of oxytocin?

A

Initiates uterine contractions

Increases prod of prostaglandins which increase the contractions further

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12
Q

What increases the number of oxytocin receptors?

A

Oestrogen

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13
Q

Define cervical effacement

A

Thinning of the cervix = cervical ripening

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14
Q

What is the normal diameter of the birth canal?

A

9.5/10cm

Max size determined by the pelvis but softening of ligs may increase it

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15
Q

Describe the contraction of myometrium during labour

A

Contracts but only partially relaxes = doesn’t return to original size

Contraction from 2 poles – then fundus – then lower segment

Forces in upper segment more powerful than lower segment

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16
Q

How is labour induced?

A

Stimulate release of prostaglandins – membrane rupture

Artificial prostaglandins

Synthetic oxytocin

Anti-progesterone agents

17
Q

How can the physiology be monitored during labour?

A

Maternal

  • HR, P, T
  • contractions
  • cervical dilation

Fetal

  • colour and amount of amniotic fluid
  • scalp capillary pH, acid/base balance

Partogram - fetal HR, cervical dilation (1cm/h), station, contractions, maternal obs

18
Q

Outline the mechanism of labour

A

Head flexes = present minimum diameter

Head rotates internally = hits levator ani which contracts and rotates it (head tucked under and facing backwards)

Head crowns = stretches perineal muscle and skin

Extension of head and external rotation

Shoulder rotate, shoulders delivery – followed rapidly by body

19
Q

How can delivery be facilitated?

A

Cesarean section

Forceps

Vacuum extraction

20
Q

Describe the separation and descent of the placenta

A

Baby born = reduced uterus size

Inelastic placenta squeezed by contraction

21
Q

How is bleeding controlled?

A

Powerful contractions of uterus = constrict blood vessels through myometrium

Pressure on placental site by wall of contracted uterus

Blood clotting

22
Q

Describe the control of milk let down

A

Suckling = activation of mechanoreceptors = up spinal cord to hypothalamus = 1) on signal to PP to prod oxytocin, 2) off signal to AP to stop prod dopamine, which allows prolactin to be secreted

Prolactin = milk fat synthesis

Oxytocin = stim myoepithelial cell = milk ejection

23
Q

Order the cardinal movement of labour

A
engage
flexion of the neck
rotation
extension of the neck
restitution
delivery of anterior shoulder
delivery of posterior shouder
24
Q

What does the first stage of labour end with?

A

Ripening = pull dilation of the cervix

25
Q

What is the most common cause of post-partum haemorrhage?

A

uterine atony = uterus fails to contract after delivery

26
Q

What hormonal change is responsible for secretion of milk after delivery?

A

decreased progesterone and oestrogen

27
Q

Outline ‘failure to progress’

A

Delay in 1st or 2nd stage

Causes = inadequate contractions, malposition/malpresentation, cephalopelvic disproportion, obstructed labour, maternal exhaustion

Inadequate contractions = oxytocin

28
Q

What are the causes of fetal compromise and how should it be managed?

A

Causes:

  • uterine hyperstimulation (?iatrogenic)
  • hypotension
  • poor tolerance of labour
  • cord compression
  • infection
  • maternal disease

Mx

  • rectify reversible causes
  • L lateral position
  • stop oxytocics
  • confirm comprise by FBS
  • deliver by speediest route
29
Q

Discuss operative delivery

A

Ventouse, forceps

Indications = failure to progress in 2nd stage, fetal distress in 2nd stage, maternal reasons

Requirements = fully dilated, absent membranes, cephalic presentation, empty bladder

Comp = failure, maternal/fetal trauma, postpartum haemorrhage, urinary retention, cephalhaematoma (forceps)

30
Q

What is the Bishop score?

A

Assessment of cervical ripeness which predicts whether induction of labour will be required

Score <4 – labour is unlikely to progress naturally

Factors = cervical feature, dilation, length, station, consistency, position

31
Q

Briefly outline abnormal fetal HR patterns and the causes

A

Tachy (>160) = Fetal hypoxia, Chorioamnionitis – if maternal fever also present, Hyperthyroidism, Fetal or maternal anaemia, Fetal tachyarrhythmia

Brady (<100) = Prolonged cord compression, Cord prolapse, Epidural and spinal anaesthesia, Maternal seizures, Rapid fetal descent

Normal variability is between 5-25 bpm

Reduced variability =

  • Fetal sleeping: should last no longer than 40 minutes (most common cause)
  • Fetal acidosis (due to hypoxia) – more likely if late decelerations are also present
  • Fetal tachycardia
  • Drugs – opiates / benzodiazepines / methyldopa / magnesium sulphate
  • Prematurity – variability is reduced at earlier gestation (<28 weeks)
  • Congenital heart abnormalities

Early deceleration = normal
Late deceleration = insufficient blood flow to the uterus and placenta (hypotension, pre-eclampsia, uterine hyperstimulation)