Women's Health

Question 1

What is the menstrual cycle?

Answer 1

Monthly bleeding from the female reproductive tract induced by cyclical hormonal changes

Defined as the interval between 1st day of last period and the 1st day of next period

Question 2

Is bleeding between taking the OCP a period?

Answer 2

Occurs due to the drop in oestrogen + progesterone

= withdrawal bleed
It is not induced by cyclical hormonal changes so is not a period

Question 3

When is the last menstrual period (LMP) defined as?

Answer 3

1st day of last period

Question 4

What is menarche? When does it occur?

Answer 4

onset of menstruation

occurs 12-13yrs but age is decreasing (95% between 11-14.5yrs)

Question 5

What are the 4 stages of the menstrual cycle? Which days do they occur?

Answer 5

Menstruation (day 1-5) > proliferation (day 6-15) > ovulation (day 14) > secretion (day 16-28)

Question 6

What hormones cause the onset of menses and secondary sexual characteristics?

Answer 6

from 8yrs:
GnRH pulses increase in amplitude and frequency > FSH and LH release increases > stimulate oestrogen release from ovaries > development of secondary sexual characteristics

Question 7

What is thelarche? When does it occur?

Answer 7

breast development

9-11yrs

Question 8

What is adrenarche? When does it occur?

Answer 8

growth of pubic hair

11-12yrs

Question 9

How regular is the menstrual cycle shortly after menarche? How does it change?

Answer 9

initial cycles often irregular > as oestrogen secretion rises > become more regular + pregnancy is then possible

Question 10

When does growth in a female usually finish by?

Answer 10

By 16yrs most growth has finished and epiphyses fuse

Question 11

What is primary amenorrhea?

Answer 11

Failure to menstruate by the age of 16

OR failure to menstruate by the age of 14 in someone with no secondary sexual characteristics

Question 12

What happens to hormone levels in the follicular phase of the ovarian cycle? What do these changes result in?

Answer 12

Day 1:

• low oestrogen (after menses) + progesterone > stimulate pulses of GnRH from the hypothalamus
• GnRH acts on the anterior pituitary to stimulate LH and FSH release
• FSH and LH act on ovarian follicles > induce follicular enlargement and production of oestrogen
• Follicles produce oestradiol (E2) + inhibit > suppress FSH in -ve feedback loop = only one follicle and oocyte mature

Question 13

What cells produce oestrogen?

Answer 13

granulosa cells

Question 14

What happens to hormone levels on day 14 of the ovarian cycle?

Answer 14

• oestrogen levels reach their peak as the follicle matures > (FSH release inhibited) LH surge > triggers ovulation 18hrs post surge

18hrs + day 14 is quite concrete in most women no matter how long their cycle is

Question 15

What happens in the luteal phase of the ovarian cycle IF the egg is fertilised?

Answer 15

If the egg is fertilised:

• syncytiotrophoblast produces bHCG > acts in the same way as LH to keep the corpus luteum going and producing progesterone
• corpus luteum persists for 6mo
• function taken over by the placenta by 3mo

Question 16

What happens in the luteal phase of the ovarian cycle if the egg ISN’T fertilised?

Answer 16

Initially: follicle from which the egg was released becomes the corpus luteum > produces more oestrogen than progesterones (peaks later at day 21)
Towards the end:
corpus luteum breaks down > progesterone + oestrogen levels fall > lining of the womb sheds in a period = menstruation > cycle restarts

Question 17

How can contraception prevent menstruation?

Answer 17

continuous administration of exogenous progesterones maintains a secondary endometrium
it’s the FALL in progesterone that triggers menstruation

Question 18

How does contraception prevent ovulation?

Answer 18

oestrogen suppresses LH until it reaches a certain level at which points it triggers LH
steady state oestrogen inhibits LH + FSH > prevents the surge of LH which triggers ovulation

Question 19

What medication can be taken when needing to delay a period e.g. a holiday?

Answer 19

noresthisterone - stop taking when acceptable to have a period again

Question 20

What is the first phase of the uterine cycle?

Answer 20

Menstrual phase - day 1-4ish

• spiral arteries contract in response to decreasing progesterone (as the corpus luteum is dying off due to decreasing LH)
• functional endometrium becomes necrotic + is shed as a period
• myometrial contraction occurs = can be painful

Question 21

What is the second phase of the uterine cycle?

Answer 21

Proliferative phase - day 5-13

• regrowth of the functional endometrium in response to rising oestrogen = thickens as the stroll cells proliferate
• development of endometrial glands (elongate) and spiral arteries

Question 22

What is the 3rd phase of the uterine cycle?

Answer 22

Secretary phase (aka luteal) - day 14-28

• driven by progesterone post ovulation - peaks at day 21 (oestrogen also produced)
• stroll cell enlarge
• endometrial glands swell + deepen and become entwined with the spiral arteries (increases blood supply to facilitate transfer of glucose between mum + foetus)
• endometrial glands produce glycogen (role in implantation)

Question 23

How do oestrogen levels change throughout the menstrual cycle?

Answer 23

increase up to day 14 (peak) and then decrease until menses with a small rise at the beginning of the secretory phase

Question 24

How do progesterone levels change throughout the menstrual cycle?

Answer 24

increase more slowly than oestrogen, peak at secretory phase (day 21ish) and then decrease until menses

Question 25

When is labour diagnosed?

Answer 25

painful uterine contractions accompany dilatation and effacement of the cervix

Question 26

Define a normal birth

Answer 26

low-risk at the start of labour and throughout born spontaneously in the vertex position between 37 and 42 weeks of pregnancy after birth, mother and infant are in good condition

Question 27

What are the 3 mechanical factors that affect labour?

Answer 27

1. power - degree of force expelling the foetus 2. passage - dimensions of the pelvis and resistance of soft tissues 3. passenger - diameters of the foetal head

Question 28

Where do contractions originate from?

Answer 28

arise in one of the pacemakers at each cornua of the fundus of the uterus

Question 29

What happens to the uterus in a contraction?

Answer 29

retraction/shortening of muscle fibres > pulls lower segment towards the fundus = cervix dilates (aided by the pressure of the head as the uterus pushes the head down onto the pelvis)

Question 30

What is the expected frequency of contractions once labour is established?

Answer 30

build in amplitude as labour progresses | contracts for 45-60 seconds every 2-4 minutes

Question 31

What is the cervix like before labour?

Answer 31

hard close tube, around 4cm long | tightly closed throughout pregnancy, protected by a plug of mucus

Question 32

What is cervical effacement? When does it occur during labour?

Answer 32

ripening > thinning/softening of the cervix in primiparous women > completed by time active 1st stage of labour begins in multiparous > can take place at the same time as dilatation

Question 33

What factors allow cervical dilatation?

Answer 33

caused by contracting muscle + pressure on the cervical opening + ability of cervix to soften and allow distension measured in cm by vaginal examination

Question 34

What are the features of the latent phase of labour?

Answer 34

contractions - often irregular so can be a difficult stage mucoid plug (show) comes away as a sticky pink mucus, before labour starts ROM may occur cervix begins to efface and dilate up to 4cm

Question 35

How long does the latent phase of labour usually last?

Answer 35

can be the longest stage | especially in primiparous women - can last 2-3 days

Question 36

What is SROM?

Answer 36

spontaneous rupture of membranes - can happen any point prior to/during labour

Question 37

What is ARM?

Answer 37

artificial rupture of membranes > can speed up/augment process/induce labour

Question 38

Where is the amniotic fluid? What does it do?

Answer 38

fluid between the baby and the amnion (sac) acts as a cushion around the foetus to protect it against any bumps to mother’s abdomen foetus can swallow the fluid > helps create urine and meconium rich in stem cells

Question 39

How much amniotic fluid should there be at term?

Answer 39

500-800mls

Question 40

What is the term for when a foetus is born within the amniotic sac?

Answer 40

en caul = very rare

Question 41

When is the 1st stage of labour defined as?

Answer 41

from 4cm to full dilatation (10cm) | = active/established labour

Question 42

What happens in the 1st stage of labour?

Answer 42

stronger uterine contractions cervix continues to efface and dilate up to 10cm ROM if not already occurred, or ARM will need to happen Descent, flexion and internal rotation of foetal head may start to happen

Question 43

What rate of dilatation is normal in the first stage of labour?

Answer 43

``` Nulliparous = 0.5cm/hr Multiparous = 1cm/hr (normal progression) ```

Question 44

How long does the 1st stage of labour usually last?

Answer 44

no longer than 16hrs average = 8hrs in nulliparous, 5h in multiparous

Question 45

When is the 2nd stage of labour defined as?

Answer 45

from full dilatation to the birth of the foetus

Question 46

How long does the 2nd stage of labour last?

Answer 46

from 5 mins (multiparous) to 2-3hrs

Question 47

What is a passive stage in the 2nd stage of labour?

Answer 47

woman is fully dilated but does not have urge to push yet can slow down contractions before pushing starts

Question 48

What happens in the active stage in the 2nd stage of labour? How long does it last?

Answer 48

when pushing is happening pressure on the pelvic floor produces an irresistible desire to push delivered on average after 40 mins (nulliparous) or 20 mins (multiparous) head descends, flexes further, rotation usually completed

Question 49

After how long pushing does spontaneous delivery become increasingly unlikely?

Answer 49

>1hr

Question 50

What are the steps of the delivery of the foetal head?

Answer 50

1. descent 2. flexion 3. internal rotation 4. extension 5. restitution/external rotation 6. delivery of the body

Question 51

What happens in descent of the foetal head?

Answer 51

foetus descends into the pelvis occurs from 37wks but might not happen until established labour measured by comparison with the level of the ischial spines (station)

Question 52

What happens in flexion of the foetal head?

Answer 52

foetal neck flexes, foetal skull has a smaller diameter in this position = aids passage through pelvis flexion increases throughout labour > reaches vertex position

Question 53

What happens in internal rotation of the foetal head?

Answer 53

With each contraction, the foetal head is pushed onto the pelvic floor Following each contraction, a rebound effect causes slight rotation Regular contractions eventually > complete 90 degree turn of foetal head = faces mum’s sacrum

Question 54

What happens in extension of the foetal head?

Answer 54

Occiput slips beneath the suprapubic arch, allowing the head to extend Foetal head is now born, usually facing mum’s back depending on position

Question 55

What happens in restitution/external rotation of the foetal head?

Answer 55

May see head externally rotate to face mum’s right/left thigh to align with the shoulders = restitution Perineum stretches and often tears - can be cut (episiotomy) if progress if slow/foetal distress

Question 56

What happens in delivery of the body? How can delivery of the shoulders be assisted?

Answer 56

Gentle axial traction can assist with the delivery of the shoulder below the suprapubic arch May be followed by gentle upwards traction to assist delivery of the posterior shoulder

Question 57

What injury can occur if force applied during delivery of the shoulders is too excessive?

Answer 57

brachial plexus damage

Question 58

What is delayed cord clamping?

Answer 58

Umbilical cord not immediately clamped and cut at point of birth to allow at least 1 minute to transfuse blood to the baby Baby can receive up to 214g of blood if this happens (average term newborn has 80mls/kg so 214 = significant)

Question 59

What are the potential advantages of delayed cord clamping?

Answer 59

- allows baby time to transition to extrauterine life - increase in rbcs, iron + stem cells = aid with growth and development initially - reduced need for inotropic support Very beneficial for preterm babies

Question 60

When is the 3rd stage of labour defined as?

Answer 60

from the birth of the foetus to the expulsion of the placenta usually lasts about 15 mins

Question 61

How is the placenta expelled by the uterus?

Answer 61

Uterine muscle fibres contract to compress the vessels formerly supplying the placenta which shears away from the uterine wall

Question 62

What are the two ways the placenta can be delivered?

Answer 62

1. physiological - body expels it without intervention 2. active - mum given an IM oxytocin drug > uterus contracts and expels the placenta > delivered using controlled cord traction

Question 63

What are the risks when a placenta is delivered using cord traction?

Answer 63

excessive force > snapped cord, inverted uterus

Question 64

Why is it important to check the placenta and membranes once they are delivered?

Answer 64

must check if any is left in the uterus | = risk of serious PPH

Question 65

What membranes should be delivered with the placenta?

Answer 65

amnion (bag around baby) | chorion (membranes around placenta)

Question 66

What is the role of the placenta?

Answer 66

- O2, nutrients + maternal abs passed to foetus - waste products from the foetus are passed back to the maternal blood for disposal - produces hormones that assist with foetal growth and development however alcohol + nicotine can also be passed on

Question 67

Some midwives describe a 4th stage of labour, what is this?

Answer 67

early postnatal phase skin to skin contact increases oxytocin for mum and baby = bonding, uterus contracts, regulates baby’s HR and breathing

Question 68

What role does oxytocin have in labour?

Answer 68

a surge in oxytocin at the onset of labour contracts the uterus

Question 69

What role does prolactin have in labour?

Answer 69

begins the process of milk PRODUCTION in the mammary glands

Question 70

What role does oestrogen have in labour?

Answer 70

surge at onset of labour to inhibit progesterone to prepare the smooth muscles for labour

Question 71

What role do prostaglandins have in labour?

Answer 71

aid with cervical ripening

Question 72

What role do beta-endorphins have in labour?

Answer 72

natural pain relief

Question 73

What role does adrenaline have in labour?

Answer 73

released as birth is imminent to give woman the energy to give birth

Question 74

What damage occurs in a 1st degree perineal tear?

Answer 74

minor damage to the fourchette

Question 75

What damage occurs in a 2nd degree perineal tear or an episiotomy?

Answer 75

involves the perineal muscle

Question 76

What damage occurs in a 3rd degree perineal tear?

Answer 76

involves the anal sphincter (1% of deliveries)

Question 77

What damage occurs in a 4th degree perineal tear?

Answer 77

also involves the anal mucosa

Question 78

Define malpresentation

Answer 78

when the foetus is not presenting by the vertex

Question 79

What term describes a normal lie of the foetus?

Answer 79

cephalic (94% of deliveries)

Question 80

Define breech presentation

Answer 80

presenting part of the foetus is not the head - foetus is in a longitudinal lie with buttocks or feet closest to the cervix

Question 81

What is the most common type of breech presentation?

Answer 81

extended breech - presenting part is the bottom

Question 82

What are some causes of breech presentation?

Answer 82

Idiopathic Uterine abnormalities (bicornuate uterus, fibroids) Prematurity (baby hasn’t turned around yet) Placenta praevia Oligohydramnios Foetal abnormalities eg hydrocephalus

Question 83

How are breech babies identified?

Answer 83

Try to dx antenatally on USS 30% present undiagnosed in labour - identify by palpation via abdo exam or feeling breech vaginally + mum may complain of pain under ribs

Question 84

How are breech babies managed?

Answer 84

1. External cephalic version (ECV) - manoeuvring baby to correct the breech, can be done at 37 wks 2. If unsuccessful/CI > LSCS

Question 85

When might external cephalic version be contraindicated for a breech baby?

Answer 85

placenta praevia multiple pregnancies (except delivery of 2nd twin) uterine abnormalities/scars eg previous LSCS pre-eclampsia/HTN (increased risk of abruption) APH in last 7/7 rupture membranes growth restricted babies abnormal CTG foetal abnormality

Question 86

What is the most ideal lie of a foetus?

Answer 86

LOA - left occiput anterior | back of foetus is on mother's left side and towards the front so the occiput leads in delivery

Question 87

What is the most common pelvis type in females?

Answer 87

gynecoid > lots of adaptation for childbirth e.g. wide subpubic arch, transverse oval inlet

Question 88

What bones and fontanelles is the foetal skull made up of? How does the foetal skull aid passage through the pelvis?

Answer 88

frontal, parietal, temporal bones sagittal suture runs down the middle with an anterior and posterior fontanelle Bones are not fully formed or fused at birth = allows movement and overlapping as baby travels through the birth canal

Question 89

What general care should be provided to support a women's physical health during labour?

Answer 89

- obs (temp and BP every 4hrs, pulse every hr and then every 15 mins in the 2nd stage) - contraction frequency recorded every 30mins - foetal HR monitoring - ACTIVE process - mum in control - hydration - IV fluids may be needed in prolonged labour - bladder care - encourage to micturate frequently (catheterisation may be needed if she has an epidural)

Question 90

What positions are most ideal for giving birth in?

Answer 90

all fours > increases diameter of pelvic inlet, less compression on aorta, gravity squatting, kneeling, left-lateral position also

Question 91

Why is the supine position avoided during birth?

Answer 91

1. has to push the baby around a u-bend 2. uterus compresses vessels > reduced CO > hypotension (aortocaval compression) combine with left-lateral tilt to improve position

Question 92

How and why should pyrexia in labour be managed?

Answer 92

increased risk of neonatal illness more common with epidurals, prolonged labour vaginal, blood + urine cultures give paracetamol if 38: IV abx + CTG monitoring

Question 93

Why is bladder care important during labour?

Answer 93

dehydration can interrupt labour full bladder can prevent head descending pushing with a full bladder can cause bruising/damage to bladder in 3rd stage: increases risk of uterus not contracting > PPH risk

Question 94

What general care should be provided to support a women's psychological health during labour?

Answer 94

environment - music, privacy, home/water birth partner present breathing/sighing (holding breath/hyperventilation affects O2 delivery to mum and baby) 1:1 support during labour mum in control - have a birth plan

Question 95

What non-invasive, holistic methods can be used for pain management during labour?

Answer 95

``` water immersion comfortable positions/environment aromatherapy massage hypnobirthing TENS machine ```

Question 96

What pharmacological methods can be used for pain management during labour?

Answer 96

Paracetamol/codeine - esp effective in early/latent phases Entonox (gas &air - 50% O2, 50% nitrous oxide) opioids IV or single shot IM - diamorphine = most common, pethidine, remifentanil epidural

Question 97

What are the advantages of entonox?

Answer 97

``` fast acting (20-30 seconds to take effect) short half-life (some women don't like the feeling but it doesn't last long) does not require further foetal monitoring can be used alongside other analgesia good distraction therapy ```

Question 98

What are the disadvantages of entonox?

Answer 98

nausea, light-headedness | wears off quickly

Question 99

What are the advantages of opioids as pain management in labour?

Answer 99

can be given by a midwife still able to mobilise does not slow labour drowsiness - can sleep between contractions

Question 100

What are the disadvantages of opioids as pain management in labour?

Answer 100

maternal SE: N&V, eu/dysphoria, can prolong 1st/2nd stages, resp depression, pruritus foetal SE: resp depression, diminishes breast seeking and feeding behaviour

Question 101

What medication does an epidural contain?

Answer 101

mixture of bupivacaine and fentanyl (i.e. a local anaesthetic and an opioid)

Question 102

Where is an epidural inserted? How does it work?

Answer 102

epidural catheter inserted into the epidural space at L3/4 by an anaesthetist drugs administered through this via a pump

Question 103

When is an epidural indicated?

Answer 103

``` maternal request HTN/pre-eclampsia cardiac disease induced labour multiple births ``` Used in long/difficult labours, baby in awkward position, mum exhausted, augmented labour with syntocinon

Question 104

CI to an epidural?

Answer 104

local infection | allergy to local anaesthetics

Question 105

What are the advantages of an epidural?

Answer 105

total pain relief in 90% of ptients | effect lasts until baby is born

Question 106

What are the disadvantages of an epidural?

Answer 106

Maternal SE: can slow labour if not established (1st/2nd stages), need for more oxytocin, increased need for instrumental/LSCS, reduced mobility, can take up to an hr to take effect, will need a catheter, pyrexia Foetal SE: tachycardia, diminishes breast-feeding behaviour

Question 107

What are the potential complications of an epidural?

Answer 107

damage to spinal cord, hypotension + bradycardia, haematoma/abscess at injection site, anaphylaxis, post dural puncture headache

Question 108

How is progress in labour recorded and monitored?

Answer 108

partogram

Question 109

What is the NICE definition of slow progress labour?

Answer 109

<2cm dilatation in 4hrs

Question 110

What on the partogram indicates slow progress?

Answer 110

alert and action lines an action line = ACTION must be taken point at which progression stops may indicate a cause

Question 111

What factors does the partogram assess?

Answer 111

``` FHR cervical dilatation contractions per 10mins drugs + fluids given maternal pulse + BP urine ```

Question 112

When is progression of labour abnormal?

Answer 112

slow from beginning = dysfunctional labour | sudden slowing of labour = secondary arrest

Question 113

What are the RFs for failure to progress in labour?

Answer 113

``` large baby breech baby 1st time mother previous delayed labour premature ROM ```

Question 114

How is failure to progress in labour assessed?

Answer 114

Palpate abdomen for lie, head and contractions CTG Colour of amniotic fluid Vaginal examination

Question 115

What are the 3 main causes of slow progress in labour?

Answer 115

power passenger passage or a combination

Question 116

What is the most common cause of slow progress in labour? Who is it most common in?

Answer 116

inefficient uterine action | common in nulliparous women (+ induced labour)

Question 117

What are the power causes of slow progress of labour?

Answer 117

inefficient uterine action hyperactive uterine action maternal exhaustion

Question 118

How can hyperactive uterine action be managed?

Answer 118

excessively strong/frequent/prolonged contractions depends on cause if no abruption > tocolytic e.g. salbutamol IV/SC LSCS often indicated due to foetal distress

Question 119

What are the passenger causes of slow progress of labour?

Answer 119

malpresentation malposition of large baby (presenting part is in the right place but wrong position e.g. occipital-transverse/posterior, brow)

Question 120

What are the passage causes of slow progress of labour?

Answer 120

``` inadequate pelvis cephalopelvic disproportion (big baby, small pelvis) ```

Question 121

What is augmentation vs induction of labour?

Answer 121

augmentation: artificial strengthening of contractions in established labour induction: artificial initiation of labour

Question 122

How is failure to progress in the 1st stage of labour managed?

Answer 122

augmentation by ARM/amniotomy CTG monitoring, FBS if concerns if membranes already ruptured/fails to dilate further > oxytocin infusion then consider LSCS

Question 123

How is failure to progress in the 2nd stage of labour managed?

Answer 123

Allow to push for 2hrs if primp, 1hr if multip If not breech - oxytocin and keep assessing If breech - try ECV first, no point giving oxytocin > LSCS If no imminent delivery > obstetric review for instrumental delivery/LSCS

Question 124

What factors is the mode of delivery influenced by?

Answer 124

size + presentation of baby well-being of both, length of labour, maternal exhaustion adequacy of pelvis

Question 125

What are the foetal consequences of slow progress in labour?

Answer 125

foetal distress foetal hypoxia > hypoxic-ischaemic encephalopathy increased morbidity/mortality

Question 126

What are the maternal consequences of slow progress in labour?

Answer 126

bleeding | tears

Question 127

Which drug can stop the effect of oxytocin by blocking its receptor?

Answer 127

atosiban can inhibit myometrial contractions by blocking oxytocin > used to prevent premature birth

Question 128

What are some causes of meconium stained liqour?

Answer 128

foetal distress | foetal maturity - late baby ready to be born

Question 129

What can meconium aspiration result in?

Answer 129

severe pneumonitis

Question 130

Define APH

Answer 130

any bleeding from the genital tract after 24 weeks

Question 131

What are the possible causes of an APH?

Answer 131

placenta praevia + vasa praevia + placental abruption less common: - placental adhesive disorder - uterine rupture of a LSCS scar - incidental genital tract pathology e.g. cervical carcinoma, polyps, cervical ectropion - trophoblastic disease

Question 132

How is an APH investigated and diagnosed?

Answer 132

ABCDE assessment, vitals Bloods: FBC, U&Es, clotting, CRP, cross match/G&S Kleinbauer test, consider anti-d prophylaxis CTG USS to rule out LLP/abruption

Question 133

What must you avoid before confirming the position of the placenta?

Answer 133

NO INTERNAL EXAM ESP VAGINAL IF YOU HAVEN’T CONFIRMED POSITION OF PLACENTA = risk you may put your fingers through it

Question 134

How is an APH managed?

Answer 134

ABCDE management Consider blood transfusion, fluids Depends on the cause: - placenta praevia > admit, steroids if <34wks, LSCS at 39wks or before if bleeding heavily - abruption > may be able to manage expectantly if minor, if in foetal distress - LSCS, if not distressed - after 37wks induce labour - accreta - deliver, caesarean hysterectomy (removing placenta can cause catastrophic bleeding)

Question 135

Define a primary PPH

Answer 135

Primary = within 24hrs of delivery | AND >500ml blood loss (or >1000ml after caesarean)

Question 136

How is major bleeding in a PPH defined?

Answer 136

>1500ml/signs of clinical shock

Question 137

What are the causes of PPH?

Answer 137

Tone - uterine atony (most common) Thrombin - bleeding disorders Trauma - eg perineal tear Tissue - retained products

Question 138

What are the 4T's of causes of PPH?

Answer 138

Tone (70%) - uterine atony Trauma (20%) - perineal/vaginal tear Tissue (10%) - retained placental/membrane tissue Thrombin (<1%) - coagulopathy e.g. anticoagulants, DIC, inherited e.g. haemophilia/VWD, acquired e.g. HELPP syndrome

Question 139

What makes uterine atony more likely?

Answer 139

prolonged labour grand multiparity over distension of the uterus e.g. polyhydramnios, multiple pregnancy fibroids

Question 140

When should antenatal thromboprophylaxis be stopped?

Answer 140

at least 12hrs before labour/delivery to reduce chances of a PPH

Question 141

What are the RFs for a PPH?

Answer 141

Tone - multiple pregnancy, polyhydramnios, prolonged/very short labour, grand multiparity Thrombin - coagulation defect/anticoagulant therapy Tissue - retained placenta APH, Previous PPH Previous c-section C-section/instrumental delivery, augmentation/induction of labour Obesity

Question 142

How should a primary PPH be investigated?

Answer 142

ABCDE assessment IV access with 2 large bore grey cannulas - Bloods - FBC< U&Es, coag, LFT, G&S, cross match Examination - abdo - is uterus contracted? - vaginal - trauma?

Question 143

What will an atonic uterus feel like on palpation?

Answer 143

uterus impalpable (would normally be palpable after delivery)

Question 144

What medication in the 3rd stage of labour can reduce incidence of a PPH?

Answer 144

oxytocin

Question 145

How should a primary PPH be immediately managed?

Answer 145

ABCDE - O2, IV access, lots of fluids +/- blood transfusion Find the source of the bleeding! Tx coagulopathy if present - fresh frozen plasma and cryoprecipitate may be required If >1L of bleeding - give tranexamic acid Remove retained placenta manually if bleeding and not expelled within 1hr of delivery If blood loss is >1500ml and ongoing > MPH protocol

Question 146

What interventions can be taken in a PPH if the uterus is atonic?

Answer 146

Empty bladder Massage uterus/rub abdomen Bimanual compression of uterus Then pharmacological > IV syntocinon > IM carboprost > surgery

Question 147

After immediate management, how should a PPH be treated?

Answer 147

1. Uterine massage + catheter 2. oxytocin/syntocinon IV infusion 3. ergometrin (CI = HTN) 4. carboprost (must be IM/inject directly into uterus) = prostaglandin (PGF2a) 5. misoprostol PR > long lasting uterine contraction 6. surgery

Question 148

What surgical options are there for the tx of a PPH?

Answer 148

- Bleeding from a placental bed (well-contracted uterus with no trauma) > Rusch balloon (least invasive option) - inflates in uterus, fill with warm saline, exerts hydrostatic pressure onto bleeding vessels + meds to stop bleeding - B-linch/brace suture - 2 big brace sutures around uterus = mechanical compression - Uterine artery embolisation - Ligation of internal iliac/uterine artery Catheterisation Hysterectomy if other options fail

Question 149

Define a secondary PPH

Answer 149

excessive blood loss >24hrs and <12wks after delivery

Question 150

What are the possible causes of a secondary PPH?

Answer 150

Most common = endometritis or retained placental tissue

Question 151

Investigations for a secondary PPH?

Answer 151

high vaginal swabs (endometritis) - look for CT/GC USS - retained products

Question 152

How to manage a secondary PPH?

Answer 152

Depending on cause: endometritis: abx RPC: evacuation of retained products of conception (ERPC)

Question 153

What is synctocinon?

Answer 153

combination of ergometrine and oxytocin to help uterus contract

Question 154

What are the 4 types of HTN that can occur in pregnancy?

Answer 154

1. Gestational HTN = only during pregnancy and occurs for the 1st time during pregnancy 2. Preeclampsia-eclampsia 3. Chronic HTN = occurs prior to pregnancy 4. Preeclampsia superimposed upon chronic HTN/renal disease

Question 155

How are spiral arteries different in a pregnant woman with preeclampsia?

Answer 155

In pregnancy they are more dilated and have less tortuosity and should become less spiral to supply placenta In pre-eclampsia they don’t dilate and stay tortuous > less blood flow to the trophoblast/placenta

Question 156

RFs for developing preeclampsia?

Answer 156

Young teenagers + >37yrs Black women Obesity Primigravidity Multifoetal pregnancies, polyhydramnios ie large placenta Long interpregnancy interval Previous/family hx Chronic HTN Renal disease/other PMH - diabetes, AI disease

Question 157

Define gestational HTN

Answer 157

After 20wks Systolic >140 or Diastolic >90 or increase above booking levels of >30 systolic or >15 diastolic no proteinuria resolves following birth

Question 158

When is HTN chronic rather than gestational in a pregnant female?

Answer 158

HTN diagnosed before pregnancy/before 20th wk of gestation if not checked before pregnancy/during pregnancy and not resolved postpartum

Question 159

Define preeclampsia

Answer 159

New HTN after 20th wk (earlier with trophoblastic disease) with proteinuria +/- oedema

Question 160

What is eclampsia?

Answer 160

features of pre-eclampsia + generalised tonic-clonic seizures

Question 161

What are the 2 criteria for preeclampsia superimposed upon chronic HTN?

Answer 161

A. HTN + no proteinuria <20wks + new onset proteinuria after 20wks B. HTN + proteinuria <20 wks + sudden increase in proteinuria/BP that was well controlled/thrombocytopenia (<100,000), abnormal (raised) ALT/AST

Question 162

What are the sx of preeclampsia?

Answer 162

usually asymptomatic Oligouria Visual disturbances Headache (similar to migraine) Epigastric pain - hepatic swelling/inflammation, stretch of liver capsule +/e oedema Rapid weight gain (fluid retention)

Question 163

What signs does preeclampsia present with?

Answer 163

HTN = 1st sign Proteinuria Oedema - incl facial oedema Retinal vasospasm/oedema (hypertensive retinopathy) RUQ tenderness (suggests impending complications) Brisk reflexes common in pregnancy but ankle clonus = sign of neuromuscular irritability > concerning of imminent eclampsia

Question 164

How should preeclampsia be investigated?

Answer 164

- Hb, platelets - both decreased in severe pre-eclampsia - Raised serum uric acid - LFTs (raised ALT > impending liver damage/HELPP) - If 1+ protein by clean catch dipstick > timed collection for protein and creatinine - Accurate dating and assessment of foetal growth

Question 165

Define the criteria for diagnosis of preeclampsia

Answer 165

1. Gestational HTN = systolic >140, diastolic >90 (repeat measurement 6hrs after 1st to see if still exceeded) 2. Proteinuria = If 2+ = significant proteinuria likely > quantify for confirmed significant: Protein:creatinine - >30mg/nmol Or 24hr collection - >0.3g/24hr Repeat as may be absent in early disease

Question 166

What indicates a patient's preeclampsia is severe?

Answer 166

BP: >160 systolic, >100 diastolic +/- sx | +/- biochemical/haematological impairment

Question 167

What is the cure for preeclampsia?

Answer 167

delivery = always beneficial for mum, sometimes not for foetus

Question 168

How is mild/moderate preeclampsia managed?

Answer 168

oral labetalol (nifedipine if asthmatic, methyldopa) bp monitoring every 48hrs FBC, LFT, renal function 2x wk

Question 169

Which patients should be given MgSO4 with caution?

Answer 169

renal failure | Mg toxicity > cardiac arrest

Question 170

Which antihypertensives are teratogenic? How is pre-existing HTN managed in pregnancy?

Answer 170

ACEi are teratogenic 1st line = labetalol 2nd = nifedipine

Question 171

How is acute severe preeclampsia treated? When is it severe?

Answer 171

BP = 160/110+ lV hydralazine/oral or IV labetalol (CI in asthma, CHF)/oral nifedipine Hospital admission for close monitoring consider birth if no response to tx

Question 172

When should baby be delivered if the mother has preeclampsia?

Answer 172

<34wks: continue surveillance, offer MgSO4 + corticosteroids 36-37: continue surveillance, corticosteroids, decision based on risk if needed early 37: initiate birth within 24-48hrs

Question 173

What mode of delivery is preferable in women with preeclampsia? What can be given during delivery to reduce HTN

Answer 173

vaginal hydrazine/labetalol (only in severe HTN as can also reduce supply to placenta)

Question 174

What postpartum care will the mother need after having preeclampsia?

Answer 174

continue monitoring bloods, BP and fluid balance Continue htn tx for 2 weeks then review, 1st line = enalipril (2nd = nifedipine - 1st in afro-caribbean) Refer if HTN persists after 6wks

Question 175

What are the maternal complications that can occur due to preeclampsia?

Answer 175

``` CVA eclampsia pulmonary oedema liver complications renal failure ```

Question 176

What are the foetal complications that can occur due to preeclampsia?

Answer 176

IUGR preterm birth placental abruption hypoxia

Question 177

For how long after delivery/last seizure should MgSO4 be continued in a woman with eclampsia?

Answer 177

24hrs

Question 178

What is HELPP syndrome?

Answer 178

``` H = haemolysis EL = elevated liver enzymes LP = low platelets ```

Question 179

What S&S does HELPP syndrome cause?

Answer 179

haemolysis > dark urine, raised lactic dehydrogenase elevated liver enzymes > epigastric pain, liver failure, abnormal clotting low platelets

Question 180

How is HELPP syndrome managed?

Answer 180

supportive tx magnesium sulphate prophylaxis against eclampsia immediate delivery depending on gestation

Question 181

Why is anaemia more common in pregnant women?

Answer 181

40% increase in blood volume in pregnancy is relatively greater than the increase in red cell mass > net fall in Hb concentration Iron and folic acid requirements increase Iron absorption increases 3fold

Question 182

High Hb is a/w with that risks in pregnancy?

Answer 182

preterm delivery | IUGR

Question 183

What are the causes of anaemia in pregnancy?

Answer 183

``` inadequate intake poor absorption haemolytic e.g. sickle cell excessive demands e.g. twins vaginal loss/preexisting haemorrhage ```

Question 184

When does IDA become symptomatic in a pregnant woman?

Answer 184

hb <9g/dL

Question 185

How does IDA present on blood tests?

Answer 185

MCV reduced, ferritin reduced

Question 186

How is IDA treated in pregnant women?

Answer 186

``` oral iron (can cause GI upset) if severe > IV iron is quicker, may prevent need for blood transfusion ```

Question 187

If a pregnant woman present with anaemia without microcytosis what should the cause be assumed to be?

Answer 187

folic acid deficiency - more common than vit b12

Question 188

How does folic acid and vit B12 deficiency present on blood tests?

Answer 188

MCV usually increased | red cell folic acid/vit B12 levels low

Question 189

How can anaemia be prevented in pregnancy?

Answer 189

Routine iron supplements - often poorly tolerated Dietary advice Hb checked at booking, 28 and 34 wks Iron +/- folic acid given if Hb is <11g/dL Routine preconceptual and 1st trimester folic acid 0.4mg supplement recommended to all women (reduces incidence of NTDs)

Question 190

What is the difference between adult and foetal Hb?

Answer 190

Adult Hb: 2 alpha and 2 beta | Foetal Hb: 2 alpha and 2 gamma

Question 191

What happens to Hb in sickle cell disease?

Answer 191

abnormal beta-chain formation (S chain) in Hb > made up of 2 alpha an 2 S chains (or C chains)

Question 192

How is sickle cell disease inherited?

Answer 192

autosomal recessive

Question 193

What routine test is done on all pregnant women to identify if a woman is a carrier for sickle cell disease? What is done if she is a heterozygote?

Answer 193

Hb electrophoresis If a heterozygote > partner is tested > if +ve > prenatal dx for homozygosity is offered

Question 194

What are the sx of sickle cell disease?

Answer 194

Crises of bone pain and pulmonary sx Lifetime chronic haemolytic anaemia Pulmonary HTN, proliferative retinopathy possible

Question 195

What are the possible maternal and foetal complications of sickle cell disease?

Answer 195

Maternal complications: acute painful crises, pre-eclampsia, thrombosis Foetal complications: miscarriage, IUGR, preterm labour, death

Question 196

Which medication used to tx sickle cell disease is teratogenic?

Answer 196

hydroxycarbamide = should be stopped

Question 197

How is sickle cell disease managed during pregnancy? And during crises?

Answer 197

Avoid dehydration, seek early help advice Penicillin V continued, high-dose 5mg folic acid supplements, aspirin (for preeclampsia prophylaxis) + LMWH often indicated ``` Monthly urine culture Avoid iron (due to overload) USS used 4wkly for foetal growth, delivery indicated by 38wks ``` Crises: Exchange transfusions may be required Hydration, analgesia + often abx, anticoagulation

Question 198

Define endometriosis

Answer 198

The presence of endometrial tissue outside the endometrial cavity

Question 199

Where can endometriosis occur? What are the most common locations?

Answer 199

most common = pelvis (particularly uterosacral ligaments, pouch of Douglas, on/behind ovaries) can be anywhere eg abdominal wound scars - appendectomy, rectum, even the lungs, umbilicus

Question 200

When in a women's lifetime might endometrial sx regress?

Answer 200

oestrogen dependant = starts after puberty regresses during pregnancy, after menopause, if on androgens

Question 201

What does changes can the bleeding in endometriosis cause in the uterus ?

Answer 201

accumulated altered blood (dark brown) > inflammation > progressive fibrosis and adhesions if blood has no exit > nerve entrapment, peritoneal irritation etc can form a 'chocolate cyst' = endometrioma in the ovaries

Question 202

What can happen in severe grade 4 endometriosis?

Answer 202

frozen pelvis > uterus adhered to bowel so can’t have a hysterectomy in case of perforation

Question 203

What are the 3 theories behind the pathophysiology of endometriosis?

Answer 203

1. Sampson’s theory - retrograde menstruation > shedded endometrial tissue in a period goes back through the fallopian tubes and implants elsewhere 2. Halban’s theory - more distant tissue > mechanical, lymphatic, blood-borne spread 3. Meyers theory > metaplasia of mesothelial cells

Question 204

Retrograde menstruation is very common. Why doesn't everyone with it have endometriosis?

Answer 204

individual factors determine whether the endometrial tissue implants and grows (eg impaired immunity, genetics)

Question 205

Why do endometrial sx increase towards a women's period?

Answer 205

oestrogen increases during the menstrual cycle > endometrial tissue gets bigger and bleeds when menses occurs (triggered by progesterone) + becomes painful so depending location may have cyclical haemoptysis, nosebleeds, haematuria (uncommon)

Question 206

Who is more likely to be affected by endometriosis?

Answer 206

low parity women (the more someone is pregnant > more exposed to progesterone > endometrium shrinks) usually dx in younger women (30-45yrs)

Question 207

Differential diagnoses of endometriosis?

Answer 207

1 = adenomyosis Chronic PID Chronic pelvic pain Pelvis masses IBS

Question 208

What are the key sx of endometriosis?

Answer 208

often asymptomatic ``` cyclical chronic pelvic pain dysmenorrhea deep dyspareunia dychezia/dysuria during menses sub fertility may have bleeding from other places during periods e.g. nosebleeds ```

Question 209

What is the pattern of pain in endometriosis? What other painful sx is it a/w?

Answer 209

- cyclical (builds up 2-3 days before a periods and stops afterwards, pain not related to periods is unlikely to be endometriosis) - dysmenorrhea (NOT a/w heavy periods) - deep dyspareunia (pouch of Douglas = site of trauma during sex) - dyschezia/dysuria during menses

Question 210

Why can endometriosis affect fertility?

Answer 210

Due to immune factors (cytokines released by areas of endometriosis), oocyte toxicity, adhesions, tubal/ovarian dysfunction

Question 211

How might endometriosis present O/E?

Answer 211

tenderness/thickening behind uterus/in adnexa | in mild disease = often normal

Question 212

What is the gold standard investigation for endometriosis?

Answer 212

laparoscopy

Question 213

What would be seen on laparoscopy in a women with endometriosis?

Answer 213

Red vesicles/punctate marks = acute lesions white scars/brown spots = less active Ovarian endometriomas/extensive adhesions = severe can be graded from 1-4

Question 214

Investigations for endometriosis?

Answer 214

laparoscopy +/- biopsy transvaginal USS can exclude an endometrioma (mottled white) very extensive disease > MRI

Question 215

How can endometriosis be managed?

Answer 215

Sometimes it regresses/doesn't progress > asymptomatic endometriosis doesn't need tx 1. analgesia (may be enough if pt doesn't wan't hormonal therapy) 2. hormonal therapy to either abolish cyclicity or do glandular atrophy 3. surgery

Question 216

What is the aim behind medical management of endometriosis?

Answer 216

oestrogen dependant | tx either mimics pregnancy or menopause

Question 217

What are the hormonal therapy options for endometriosis?

Answer 217

abolish cyclicality a. COCP b. GnRH agonists glandular atrophy (give progesterone) = work well if patient doesn't want to get pregnant a. oral prostagens/depot provera in cyclical/continuous basis b. mirena coil (progestogen releasing device)

Question 218

How does the COCP treat endometriosis? How is it given?

Answer 218

Mimics pregnancy Give continuously > atrophy and thinning of endometrium Give back to back for 3mo = triphasic - then allow to have a period or will eventually have breakthrough bleeds anyway, this way increases compliance

Question 219

How do GnRH agonists work in the treatment of endometriosis?

Answer 219

Overstimulation of the pituitary > down regulation of its GnRH receptors > FSH/LH inhibited > ovarian hormone production inhibited = induces temporary menopause without affecting the ovaries

Question 220

What are the downsides to GnRH agonists?

Answer 220

cause menopausal sx = risk of osteoporosis so can only be given short term add HRT add back therapy (combined o+p) = takes away hot flushes without rebuilding endometrium > reduces risk of osteoporosis so can be given a bit longer term

Question 221

What are the downsides of oral prostagens/depot provera as a tx for endometriosis? How do they work?

Answer 221

= mimics pregnancy SEs: poor cycle control, erratic bleeding, PMS like sx, fluid retention, weight gain

Question 222

Why is the mirena coil an effective tx for endometriosis?

Answer 222

effective progesterone delivery, contraception + lightens periods especially good if pt gets SEs from COCP/POP as progesterone directly to the uterus reduces SEs

Question 223

What are the surgical options for treating endometriosis?

Answer 223

If fertility is desired: - scissors (excision), laser, bipolar diathermy (ablation) laparoscopically at time of dx +/- adhesiolysis (removal of adhesions/endometriomas) = may be better than medical tx if struggling to concieve If severe/likely to be infertile/finished having a family > oophorectomy, consider pelvic clearance (hysterectomy with bilateral sapling-oophorectomy) (HRT may be required if ovaries are removed)

Question 224

What can unopposed oestrogen put a women at risk of?

Answer 224

endometrial carcinoma

Question 225

Define stillbirth

Answer 225

a baby delivered with no signs of life known to have died after 24 completed weeks of pregnancy

Question 226

Define intra-uterine foetal death

Answer 226

the death is diagnosed when the baby is still inside eg on scan

Question 227

Epidemiology of stillbirth?

Answer 227

1/3rd are SGA 50% unexplained Suboptimal care identified in half of cases

Question 228

Why have the rates of stillbirth remained constant?

Answer 228

rising obesity rates | average maternal age

Question 229

What factors make a women's pregnancy high risk?

Answer 229

Underlying medical conditions - HTN, diabetes, epilepsy, RA, asthma, IBD, any almost anything else Raised/low BMI, smoking/alcohol/drugs, old/young mothers Complications in previous pregnancies eg c-section, 3rd/4th degree tear, traumatic delivery, pre-eclampsia, PPH, small baby, preterm, stillbirth Complications in current pregnancy eg pre-eclampsia, breech, gestational diabetes, multiple pregnancy, placenta praevia

Question 230

How are high and low risk pregnancies managed differently?

Answer 230

low risk can just be managed in the community | high risk managed by hospital and community

Question 231

How is the foetus monitored in the antenatal period?

Answer 231

USS + umbilical artery doppler Intermittent auscultation with hand-help doppler/pinard stethoscope CTG

Question 232

What does an USS assess during the antenatal period?

Answer 232

- growth - HC, AC, FL + these 3 give estimated foetal weight > plot on customised growth chart - liquor volume

Question 233

What does an umbilical artery doppler measure? How is it read? What should it show?

Answer 233

blood flow to baby Pressure in vessels during systole increases > peaks are systole, troughs are diastole Want to see flow even in diastole (positive EDF)

Question 234

What are the red flag signs on umbilical artery doppler?

Answer 234

no flow (absent EDF/ADEF) or reversed flow (REDF) compared to systole = evidence of high (rather than low) resistance circulation

Question 235

Define IUGR?

Answer 235

EFW <10th centile

Question 236

What are the causes of asymmetrical IUGR? When does it usually happen? What happens to the measurements?

Answer 236

due to extrinsic factors e.g. placental insufficiency Maternal conditions eg smoking, diabetes, HTN Pregnancy conditions eg pre-eclampsia Usually in later stages - 3rd trimester Normal HC, small body and limbs

Question 237

When is US used for foetal monitoring in pregnancy?

Answer 237

after the 1st trimester

Question 238

What can low pregnancy-associated plasma protein A indicate?

Answer 238

chromosomal abnormalities (screening for Down’s), high risk of IUGR, placental abruption, stillbirth

Question 239

What are the causes of symmetrical IUGR? What happens to the measurements?

Answer 239

Intrinsic factors eg early infections (TORCH), aneuploidy (chromosomal) Shows global growth restriction Increased risk neurological sequelae

Question 240

What are the TORCH infections?

Answer 240

toxoplasmosis, other agents, rubella, CMV, HSV

Question 241

What signs of IUGR may show on US?

Answer 241

- EFW <10th centile - Oligohydramnios - too little amniotic fluid - Reduced FM possible due to reduced O2

Question 242

How is the amount of amniotic fluid measured?

Answer 242

Either look at single deepest pocket they can see | Or measure amniotic fluid index (AFI) by scanning the 4 quadrants of the stomach

Question 243

What are the possible causes of oligohydramnios?

Answer 243

reduced excretion - urinary tract problem? leakage ruptured membrane reduced production e.g. reduced renal perfusion

Question 244

How is the foetus monitored intrapartum? Which is used for low vs high risk pregnancy?

Answer 244

``` intermittent auscultation (for low risk) continuous monitoring (for high risk) e.g. CTG ``` Pts should classified into low/high risk at the beginning of labour with continual risk assessment

Question 245

What are the NICE guidelines for intermittent auscultation of low risk pregnancies during labour?

Answer 245

offer pinard stethoscope or hand-held doppler 1st stage: IA immediately after a contraction for at least 1 minute, at least every 15 minutes 2nd stage: at least every 5 minutes

Question 246

What does the foetal HR vs placenta sound like on intermittent ausculation?

Answer 246

foetal HR = clip clop sound, much faster than mum's | placenta = whoosh sound

Question 247

What are the drawbacks of intermittent auscultation?

Answer 247

Can’t measure variability/decelerations long-term monitoring not possible quality of FHR affected by maternal HR and movement = listen for at least a minute

Question 248

What is the most common method to continuous monitoring? When is it used?

Answer 248

CTG 2 straps over the abdomen - one over foetus, one to pick up contractions not useful it patient it low risk from 26wks gestation

Question 249

What are the advantages of CTG?

Answer 249

shows FHR and uterine contractions long-term monitoring average variability can be determined

Question 250

What are the disadvantages of CTG?

Answer 250

can only be done in hospital number of contractions not strength some foetal exposure to US insonation not true beat to beat info

Question 251

What is an acronym to help interpret a CTG?

Answer 251

Dr C Bravado ``` Dr = define risk C = contractions (bottom line shows no of contractions) Bra = baseline rate (should be 110-160bpm) V = variability (how wiggly the line is - should vary between 5 and 25bpm) A = accelerations (rise form baseline of at least 15 beats for 15secs+ - should be at least 2 every 15 mins, often with contractions) D = decelerations (drop from baseline for 15 beats for at least 15secs, generally abnormal) O = overall assessment ``` Can be reassuring, non-reassuring or abnormal

Question 252

What is the ideal number of contractions during labour? How many is too many?

Answer 252

ideally 4 in 10, regular and strong with each squeeze, potentially reduce blood supply so baby needs time to recover tachysystole = >5 in 10

Question 253

What is a reassuring CTG?

Answer 253

Baseline: 110-160 Variability: >5bpm Accelerations present No or early decelerations

Question 254

What is a normal amount of variability on CTG? How long can it be abnormal for?

Answer 254

5-25bpm reduced level of variability acceptable for 40 mins (baby may be sleeping)

Question 255

What are the 3 types of deceleration? What do they indicate?

Answer 255

Early: peak of contraction corresponds with trough of deceleration (common cause = head compression due to a contraction > not concerning) Variable: vary in shape and timing (common cause = cord compression > non-reassuring) Late: deceleration after contraction (sign of distress, suggests hypoxia = abnormal)

Question 256

What are the concerning features of variable decelerations?

Answer 256

last >60 secs, reduced variability within the deceleration, biphasic W (taking longer to recover), loss of shouldering, failure to return to baseline

Question 257

What is the gold standard for FHR monitoring? Why is it the gold standard?

Answer 257

direct foetal ECG by scalp ECG | = gives true beat to beat information

Question 258

What are the downsides to a scalp ECG?

Answer 258

Invasive, only in labour, must be >2cm dilated/membranes absent, a/w scalp injury and perinatal infection

Question 259

What is a method of obtaining an indirect foetal ECG? What are the advantages of this method?

Answer 259

abdominal foetal ECG - only used in high risk patients only ambulatory method and can be done at home, non-invasive, true beat to beat FHR (shows short term variability) and morphological analysis not rly used in general practise

Question 260

What is foetal blood sampling used? When is it used?

Answer 260

analyses like an ABG | cervix must be 4cm dilated

Question 261

What is a normal and abnormal foetal blood sampling result?

Answer 261

7. 25+ pH = normal, repeat after 1hr if CTG remains the same | 7. 20 or less = abnormal, consider delivery

Question 262

Other than umbilical artery, what other methods of doppler are sometimes used?

Answer 262

foetal cerebral circulation (resistance/velocity of MCA) - develops low resistance pattern compared to the thoracic aorta/renal vessels in foetal compromise foetal venous circulation - measures ductus venous as a measure of cardiac function, useful in extremely preterm foetuses

Question 263

Define placenta praevia/LLP

Answer 263

Any part of the placenta that has implanted into the lower segment

Question 264

What is the difference between a major and minor placenta praevia?

Answer 264

``` Major = covering/partially covering os = obstructs head Minor = in lower segment, not cover os ```

Question 265

Why do LLPs found at the 20wk scan usually resolve by term?

Answer 265

Can often be low lying at 20wks but most move up as the pregnancy progresses Formation of the lower segment of the uterus occurs in the 3rd trimester > the myometrium where the placenta implants moves away from the internal cervical os

Question 266

What examinations should be avoided if the patient has a LLP?

Answer 266

Vaginal exams and penetrative intercourse should be avoided = can go through placenta > risk of massive bleeding Speculum exam safe

Question 267

What are the RFs for placenta praevia?

Answer 267

``` Previous c-section Previous termination of pregnancy (uterine evacuation) Multiparity Multiple pregnancy Mother >40yrs Assisted conception Manual removal of previous placenta Fibroids Endometriosis ```

Question 268

How does placenta praevia present?

Answer 268

Intermittent painless bleeds - increase in frequency/intensity over several weeks O/E: abnormal lie (transverse and breech positions common), foetal head high and not engaged

Question 269

How does the bleeding differ in placenta praevia vs abruption?

Answer 269

``` abruption = painful and smaller amount of blood praevia = painless, lots of blood ```

Question 270

How is placenta praevia diagnosed? When are scans repeated to confirm?

Answer 270

on USS at the 20wk anomaly scan Minor praevia: repeat scan at 36wks Major praevia: repeat scan at 32wks If <2cm from the internal os = likely to be praevia at term If anterior and under a c-section scar > may need 3-D power US to exclude accreta/MRI

Question 271

How is a placenta praevia managed?

Answer 271

Advise sx to watch for - any bleeding even if just spotting OP mx if asymptomatic Placenta must be >2cm from cervical os to deliver If minor aim for normal delivery <2cm = elective c-section at 38-39wks by a senior or before if bleeding doesn’t settle

Question 272

How is a bleeding placenta praevia managed?

Answer 272

If recurrent bleeds, may need adx until delivery with weekly x match + anti-D is rhesus -ve If major: ABCDE mx - two 14/16G cannulas, IV fluids (crystalloid), X match 6 units, inform senior team and paeds FBC, clotting Exam: general, abdo USS? Check 20wk scan Foetal monitoring (CTG) +/- delivery Steroids if <34 wks gestation (ideally 2 doses 12/24hrs apart)

Question 273

What is a key complication of placenta praevia?

Answer 273

severe APH bleeding commonly continues during and after delivery (PPH) as lower segment is less able to contract and constrict the maternal blood supply

Question 274

What can happen if a LLP implants into a previous c-section scar?

Answer 274

``` placenta accreta (> can't separate) or can penetrate through uterine wall to other structures e.g. bladder = placenta percreta > can lead to massive haemorrhage and may require a hysterectomy ```

Question 275

Define placental abruption

Answer 275

Premature separation of part of all of the placenta from the uterine wall

Question 276

What are the 2 types of placental abruption?

Answer 276

1. concealed (blood fluids up behind placenta and can't drain) 2. revealed (blood can drain > vaginal bleeding)

Question 277

What are the RFs for a placental abruption?

Answer 277

``` IUGR Pre-eclampsia Pre-existing HTN Maternal smoking, cocaine use Previous abruption ``` AI disease, multiple pregnancy, high parity, trauma

Question 278

What sx does a placental abruption present with?

Answer 278

``` Painful bleeding (usually constant with exacerbations, dark blood) - degree of bleed doesn’t reflect severity of abruption as some may not escape uterus Posterior abruption > backache ```

Question 279

How can you tell if a placental abruption is concealed or revealed by the patient's sx?

Answer 279

If pain occurs alone = concealed, if there is bleeding = revealed

Question 280

What are the signs of a placental abruption?

Answer 280

woody-hard (in severe cases), tense uterus so foetus is hard to feel - often contracting and labour ensues Maternal shock eg tachycardia, hypotension, pallor (may be out of proportion to blood loss if concealed) Foetal heart tones often abnormal/absent, possible foetal distress eg bradycardia

Question 281

What are the signs of a major placental abruption?

Answer 281

maternal collapse, coagulopathy, foetal distress, woody hard uterus, poor urine output/renal failure

Question 282

How is a placental abruption diagnosed?

Answer 282

Usually clinically - investigate to determine severity Establish foetal well-being: CTG - foetal distress, may see very frequent uterine activity USS - EFW at preterm gestation, exclude placenta praevia, but abruption may not be visible Establish maternal well-being: Regular FBC, coag, U&Es + x-match Catheterization with hourly urine output

Question 283

How are small abruptions managed? Do they need admission?

Answer 283

Adx required even without bleeding if there is pain and uterine tenderness Small abruptions may be managed conservatively If there is no foetal distress and pregnancy is preterm > steroids given if <34wks, pt monitored on ward, if sx settle > discharged but monitored as pregnancy is now high risk

Question 284

How are large placental abruptions managed?

Answer 284

need resuscitation and delivery! ``` CTG fluid balance, U&Es, FBC, clotting Iv fluids to replace loss early delivery blood transfusion +/- blood products, anti-D for rhesus -ve steroids if <34wks opiate analgesia ```

Question 285

When is a foetus delivered if the mother has a placental abruption?

Answer 285

mother must be stable for delivery If foetal distress > urgent c-section If no foetal distress and gestation 37+wks > induction of labour with amniotomy, close monitoring, c-section if goes into distress if dead > coagulopathy likely, give blood products, labour induced

Question 286

What are the possible complications of a placental abruption?

Answer 286

foetal death common (30%) APH/PPH (> sheehan's syndrome) uterine hyper-contractibility DIC, renal failure

Question 287

What is Sheehan's syndrome?

Answer 287

pituitary necrosis following PPH

Question 288

Describe the key differences between placental abruption and placental praevia? In terms of pain, bleeding, tenderness, foetus, on USS?

Answer 288

pain: a = severe, constant with exacerbations p = usually none bleeding: a = may be absent, often dark p = red and often profuse, often smaller previous APHs tenderness: a = often severe, uterus may be hard p = rare foetus: a = lie normal, often engaged, may be dead/distressed p = lie often abnormal, head high, FHR usually normal USS: a = often normal p = placenta low

Question 289

Define rhesus disease

Answer 289

Rbc isoimmunisation occurs when the mother mounts at immune response against antigens on foetal red cells that enter her circulation Resulting antibodies cross the placenta > foetal rbc destruction

Question 290

How is blood classified?

Answer 290

ABO and rhesus genotype

Question 291

How many gene pairs are there in the Rhesus system? How are they inherited?

Answer 291

Rhesus system consists of 3 linked gene pairs - one allele of each is dominant to the other (Cc, Dd, Ee) An individual inherits 1 allele from each pair from each parent

Question 292

What genetics of the parents make a baby most at risk of developing rhesus disease?

Answer 292

mother is rh -ve and father is rh +ve > baby has 50-100% of being rh +ve if father is rh -ve there is no problem

Question 293

Why doesn't rhesus disease occur in the first pregnancy? As opposed to subsequent pregnancies?

Answer 293

- When sensitisation occurs > maternal immune responses > produces IgM abs which can’t cross the placenta - Memory cells are produced - If the mother's immune system is exposed to the antigen again (e.g. another pregnancy) > memory cells means IgG can be rapidly produced - IgG can cross the placenta and affect the pregnancy Worsens with each successive pregnancy as maternal ab production increases

Question 294

What are some example of sensitising events?

Answer 294

termination of pregnancy/evacuation of retained products of conception after miscarriage ectopic vaginal bleeding >12wks/<12wks if heavy ECV invasive uterine procedure eg amniocentesis/chorionic villus sampling intrauterine death delivery

Question 295

What method of prophylaxis can be used to prevent rhesus disease?

Answer 295

Production of maternal anti-D can be prevented by the administration of exogenous anti-D to the mother = mops up foetal red cells that have crossed the placenta by binding to their antigens > prevents recognition by the mother’s immune system

Question 296

Can you give anti-D if sensitisation has already occurred?

Answer 296

Anti-D is pointless if maternal anti-D is already present > sensitization has already occurred

Question 297

What is the only antibody that can cross the placenta?

Answer 297

IgG

Question 298

How does rhesus disease present in mild and severe disease?

Answer 298

Haemolysis causes: - in mild cases: neonatal jaundice only - more haemolysis: neonatal anaemia (haemolytic disease of the newborn) - more severe disease: in utero anaemia (as this worsens > cardiac failure, ascites, oedema (hydrous) > foetal death)

Question 299

How is the risk of rhesus disease identified?

Answer 299

Unsensitized women screened for antibodies at booking and 28wks - If abs found > foetal genotype should be determined: If father is homozygous (DD) > foetus = Dd and at risk If father is heterozygous (Dd)/can’t be tested > maternal blood sampled for free foetal DNA (non-invasive prenatal testing - NIPT) to assess foetal Rh status If foetus is rh-ve = no risk Ab testing fortnightly - above 4IU/ml = needs to be investigated for anaemia

Question 300

How is the severity of foetal anaemia investigated in a foetus with rhesus disease?

Answer 300

a. USS - doppler US of peak velocity in systole of the foetal MCA = used fortnightly in at risk pregnancies Very severe anaemia will show as foetal hydrops/excessive foetal fluid b. if anaemia is suspected > foetal blood sampling

Question 301

How is foetal anaemia due to rhesus disease treated?

Answer 301

transfuse blood | deliver if >36wks

Question 302

How is rhesus disease managed postnatally?

Answer 302

- Blood transfusion - top-up for anaemia and exchange for hyperbilirubinemia due to haemolysis - rh -ve women: babies have rhesus group + FBC, blood film, bilirubin - If rh +ve: anti-D given to the mother within 72hrs of delivery - Kleihauer test - higher dose of anti-D needed?

Question 303

What are the RFs for GD?

Answer 303

``` previous GD previous macrosomic baby BMI >30 ethnic origin FHx diabetes ```

Question 304

How is pre-existing diabetes managed during pregnancy?

Answer 304

weight loss stop hypoglycaemic agents except metformin + commence insulin 5mg folic acid/day until 12 wks

Question 305

How is GD managed depending on fasting glucose level?

Answer 305

<7: trial of diet + exercise target not met within 1-2wks > start metformin still not met > + insulin (short-acting) 7+: insulin 6-6.9 + complications eg hydramnios, macrosomia = insulin glibenclamide if cannot tolerate metformin/fail on metformin and decline insulin

Question 306

What is the screening test for GD? Who has it? Whata re the cut-off scores?

Answer 306

OGTT - women with RFs or a large fetus/polyhydramnios/glucose on urine dipstick cut-offs: fasting: <5.6 at 2hrs after glucose drink: <7.8 (think 5 6 7 8)

Question 307

How is antenatal care different for women with GD?

Answer 307

- monitor blood sugar - 4wkly US to monitor fetal growth/AFV after 28wks fasting >7 or >6 and macrosomic or diet and exercise not helped: insulin + metformin

Question 308

How much folic acid should diabetic women take until 12wks?

Answer 308

5mg

Question 309

Do pregnant women with pre-existing diabetes need extra antenatal care?

Answer 309

retinopathy screening at booking + 28wks planned delivery between 37-39wks continue managing diabetes as before pregnancy

Question 310

When can women with GD stop their diabetic medication?

Answer 310

should improve immediately after birth = stop meds test fasting glucose for 6wks after existing diabetes - lower insulin = higher risk of hypoglycaemia

Question 311

What events decrease and increase insulin sensitivity?

Answer 311

decrease = pregnancy increase = after birth, breastfeeding

Question 312

What are the 2 key complications of GD?

Answer 312

macrosomia > shoulder dystocia neonatal hypoglycaemia - accustomed to large supply of glucose in pregnancy > cannot maintain usual supply with oral feeding

Question 313

How is neonatal hypoglycaemia managed? What is the target blood sugar?

Answer 313

>2mmol/L IV dextrose + NG feeding

Question 314

What is obstetric cholestasis?

Answer 314

reduced outflow of bile acids from liver which resolves after delivery

Question 315

When is obstetric cholestasis likely to occur during pregnancy?

Answer 315

usually after 28wks

Question 316

How does obstetric cholestasis present?

Answer 316

ITCHING (build up of bile in blood) - esp palms of hands/soles of feet fatigue, dark urine, pale/greasy stools, jaundice NO rash

Question 317

What are causes of pruritus and deranged LFTs during pregnancy?

Answer 317

obstetric cholestasis gallstones acute fatty liver AI or viral hepatitis

Question 318

How will obstetric cholestasis present in bloods?

Answer 318

abnormal LFTs - esp ALT, AST, GGT | raised bile acids

Question 319

A rise of which LFT with otherwise normal LFTs is normal during pregnancy?

Answer 319

ALP - produced by placenta

Question 320

How is obstetric cholestasis treated?

Answer 320

ursodeoxycholic acid itching mx with emollients + antihistamines water-sol vit K if clotting deranged

Question 321

Obstetric cholestasis is a/w with what risk to fetus?

Answer 321

still birth monitor LFTs consider planned delivery after 37wks depending on severity

Question 322

Define monozygotic versus dizygotic twins

Answer 322

``` mono = identical twins from single zygote di = non-identical from two zygotes ```

Question 323

Define mono versus dichorionic twins?

Answer 323

``` mono = share single placenta di = two separate placentas ```

Question 324

What type of twin pregnancy have the best outcome?

Answer 324

diamniotic dichorionic

Question 325

How can each type of twin pregnancy be determined on US?

Answer 325

dichorionic diamniotic = lambda sign (triangular) monochorionic diamnoitic = T sign monochorionic monoamniotic = no membrane between twins

Question 326

What are the risks of multiple pregnancy to the mother?

Answer 326

``` anaemia polyhydramnios HTN malpresentation preterm birth/instrumental delivery/c-section PPH ```

Question 327

What are the risks of multiple pregnancy to the fetus?

Answer 327

``` miscarriage/stillbirth growth restriction prematurity twin-twin transfusion syndrome twin anaemia polycythaemia sequence congenital abnormalities ```

Question 328

What is twin-twin transfusion syndrome? Which type of twin pregnancy can it occur in?

Answer 328

monochorionic pregnancies one fetus receives the majority of the blood from the placenta

Question 329

What are the different risks to the recipient and donor fetus in twin-twin transfusion syndrome?

Answer 329

recipient: fluid overload > HF, polyhydramnios donor: growth restriction, anaemia, oligohydramnios

Question 330

What is twin anaemia polycythaemia sequence?

Answer 330

less acute than twin-twin transfusion syndrome | one twin becomes anaemic + one becomes polycythaemic

Question 331

How are women with multiple pregnancy managed differently?

Answer 331

extra anaemia monitoring - FBC @ booking, 20 + 28wks additional USs for growth monitoring early planned birth depending on type of twin pregnancy

Question 332

When/what type of delivery is aimed for in mono versus diamniotic twins?

Answer 332

mono = elective LSCS at 32-34wks di = 37-39wks vaginal if 1st baby is cephalic/LSCS may be needed for 2nd baby/elective LSCS if presenting twin not cephalic

Question 333

How is prematurity classified?

Answer 333

<23: non-viable <28: extreme preterm 28-32: very preterm 32-37: mod-late preterm

Question 334

What are 2 methods of preventing preterm labour?

Answer 334

1. vaginal progesterone - maintains pregnancy, decreases activity of myometrium + prevents cervix remodelling 2. cervical cerclage - stitch in cervix to keep it closed rescue one can be offered later if there is dilatation without ROM = offered to women with cervical length <25mm on US between 16-24wks + previous premature birth or cervical trauma for cerclage

Question 335

What needs to be given after preterm prelabour ROM?

Answer 335

prophylatic abx for chorioamnionitis - erythromycin induction from 34wks

Question 336

What tests can check the likelihood of preterm labour if unsure/intact membranes?

Answer 336

``` TVUS - cervical length >15mm = unlikely fetal fibronectin (glue between chorion + uterus = in vagina during labour) <50ng/ml = unlikely ```

Question 337

What measures are used to improve outcomes in preterm labour?

Answer 337

fetal monitoring tocolysis (nifedipine, suppresses labour) maternal corticosteroids (<35 wks, for lung maturation) IV MgSO4 (<34wks, protects brain) delayed cord clamping (increases circulating blood vol + Hb)

Question 338

What is tocolysis? What is the medication of choice?

Answer 338

stop uterine contractions to delay delivery can be given between 24 + 34 wks nidefipine

Question 339

Why are antenatal steroids given in suspected preterm labour? What is an example regime?

Answer 339

develop fetal lungs > reduce RDS postnatally can be given <36wks 2x dose IM betamethasone 24hrs apart

Question 340

Why is MgSO4 given in suspected preterm labour? When must it be given?

Answer 340

help protect fetal brain > reduces risk of cerebral palsy given within 24hrs of delivery in babies <34weeks require monitoring for Mg toxicity

Question 341

What causes a neural tube defect?

Answer 341

incomplete closure of the neural tube within 28 days of conception > birth defect of brain/spinal cord

Question 342

What are the 3 most common NTDs?

Answer 342

anencephaly spina bifida encephalocele

Question 343

What are the RFs for NTDs?

Answer 343

``` maternal folate/vit B12 deficiency previous hx of infant with NTD smoking diabetes obesity antiepileptic drugs ```

Question 344

What is an important preventative method for NTDs?

Answer 344

400mcg daily folic acid before conception + until week 12 5mg daily for women at higher risk

Question 345

When is the first prenatal US? What does it check for?

Answer 345

11-13 weeks number of fetuses, heartbreat, crown rump length, nucha translucency, ovaries

Question 346

What is the miscarriage risk in amniocentesis and CVS?

Answer 346

amnio: 1% CVS: 1-2%

Question 347

What can amniocentesis detect?

Answer 347

chromosomal abnormalities, infections eg CF, CMV, SCD, toxoplasmosis

Question 348

How long does amniocentesis take compared to CVS?

Answer 348

3 weeks versus 2 days

Question 349

What is CVS?

Answer 349

biopsy of trophoblast

Question 350

What is hydrops fetalis?

Answer 350

abnormal fluid accumuldation in 2+ fetal compartments eg ascites, pleural effusion, pericardial effusion, skin oedema

Question 351

What are the 2 types of hydrops fetalis and the main causes of each?

Answer 351

1. immune - complication of severe Rh incompatability 2. nonimmune (90%) - cadiac abnormalities, severe anaemia (congenital parvovirus, alpha thalassaemia major, massive materno-fetal haemorrhage), trisomy 13/18/21/turner's, infection (CMV, toxoplasmosis, rubella, varicella, TTTS, chorioangioma

Question 352

How can hydrops fetalis be detected antenatally?

Answer 352

high AFV abnormally large placenta fluid causing swelling in/around organs - liver, spleen, heart, lungs amniocentesis/frequent US to monitor severity

Question 353

How is hydrops fetalis managed? What is the prognosis?

Answer 353

antenatal: early delivery intrauterine blood transfusion ``` postnatal: often results in death immune - exchange transfusion, transfusion of matched rbcs remove extra fluid with needle control HF ventilation ```

Question 354

What is the difference between SGA and IUGR?

Answer 354

sga = baby is small for dates without stating why eg may be constitutionally small and growing appropriately which = no increased risks IUGR = small/not growing as expected fetus due to pathology reducing the amount of nutrients/O2 delivered to the fetus

Question 355

What are the causes of placenta mediated growth restriction?

Answer 355

``` idiopathic pre-eclampsia maternal smoking/alcohol anaemia malnutrition infection maternal health conditions ```

Question 356

What are the causes of placenta mediated growth restriction?

Answer 356

ie pathology of fetus genetic or structural abnormalities fetal infection errors of metabolism

Question 357

What signs would indicate IUGR as the cause for a baby SGA?

Answer 357

reduced AFV abnormal doppled reduced movement abnormal CTG

Question 358

What are the short term complications of IUGR?

Answer 358

fetal death/stillbirth birth asphyxia neonatal hypothermia or hypoglycaemia

Question 359

What are the long term complications of IUGR?

Answer 359

CVD, esp HTN T2DM obesity mood/behavioural problems

Question 360

Define SGA + severe SGA

Answer 360

<10th centile for their GA severe = <3rd centile based on estimated fetal weight + fetal abdo circumference

Question 361

What factors are considered in a customised growth chart?

Answer 361

with women's weight, height, ethnicity, parity

Question 362

Define low birth weight

Answer 362

<2500g

Question 363

What are the 2 causes of SGA?

Answer 363

1. constitutionally small - match mothers/family, growing appropriately 2. IUGR

Question 364

What are the RFs for having a baby SGA?

Answer 364

previous SGA baby ``` obesity smoking diabetes existing HTN >35yrs antiphospholipid syndrome ``` pre-eclampsia multiple pregnancy low PAPPA APH

Question 365

Which women require serial growth scans for SGA monitoring?

Answer 365

symphisis fundal height fallen <10th centile from 24wks 3+ minor or 1+ major RFs issues measuring SFH eg fibroids, high BMI

Question 366

What is measured in serial growth scans of women with/at risk of a SGA baby?

Answer 366

serial US scans with umbilical artery doppler measuring: EFW + AC umbilical arterial pulsatility index AFV

Question 367

How is an SGA baby managed antenatally?

Answer 367

identify underlying cause tx modifiable RFs aspirin if risk of pre-eclampsia serial growth scans early delivery if growth static/other concerns + corticosteroids before

Question 368

What ix are done to explore an underlying cause of SGA babies?

Answer 368

``` BP + urine dipstick (pre-eclampsia) uterine artery doppler scanning fetal anatomy scan karyotyping (chromosomal abnormalities) test for infections ```

Question 369

Can pregnant women have the MMR vaccine?

Answer 369

NO - live vaccine | given before if planned/offer after giving birth

Question 370

What window of pregnancy can congenital rubella syndrome occur?

Answer 370

maternal infection in 1st 20wks | risk highest <10wks

Question 371

Why is chickenpox dangerous during pregnancy?

Answer 371

more severe case in mother eg varicella pneumonitis/heptitis/encephalitis fetal varicella syndrome severe neonatal varicella syndrome

Question 372

If a pregnant woman is exposed to chickenpox during pregnancy and are not immune, what can they be treated with?

Answer 372

IV varicella IGs as prophylaxis within 10 days of exposure

Question 373

How is chickenpox during pregnancy treated? When can it be?

Answer 373

oral aciclovir if present within 24hrs + >20wks

Question 374

How does congenital varicella syndrome present? When does the infection have to occur?

Answer 374

<28wks IUGR microcephaly, hydrocephalus, LDs scars/sig skin changes in specific dermatomes limb hypoplasia cataracts + inflammation in eye (chorioretinitis)

Question 375

What type of bacteria is listeria? How is it transmitted?

Answer 375

gram +ve bact transmitted by unpasteurised dairy products, processed meat, contaminated food = AVOID in pregnancy eg blue cheese + good food hygiene

Question 376

How does listeriosis present in a pregnant woman?

Answer 376

much more likely in pregnant women may be asymptomatic flu-like illness possibly pneumonia/meningoencephalitis

Question 377

Why is listeriosis dangerous in pregnant women?

Answer 377

high rate of miscarriage/fetal death | severe neonatal infection

Question 378

How is CMV transmitted?

Answer 378

via infected saliva/urine of asymptomatic children

Question 379

How does congenital CMV present? How common is it?

Answer 379

most CMV in pregnancy don't cause congenital CMV IUGR microcephaly, hearing/vision loss, LDs, seizures

Question 380

How is toxoplasmosis transmitted?

Answer 380

usually contamination with faeces from a cat that is host of the parasite

Question 381

How does toxoplasmosis present in a pregnant woman?

Answer 381

usually asymptomatic

Question 382

What is the classic triad of congenital toxoplasmosis? When is the risk highest?

Answer 382

risk higher later in pregnancy intracranial calcification hydrocephalus chorioretinitis

Question 383

How does congenital parvovirus B19 present? When does parvovirus in pregnancy cause the most complications?

Answer 383

1st + 2nd trimesters miscarriage/fetal death severe fetal anaemia hydrops fetalis maternal pre-eclampsia-like syndrome (hydrops + placental oedema + maternal oedema)

Question 384

Define cord prolapse

Answer 384

umbilical cord descends below presenting part of fetus into vagina, after ROM

Question 385

What is the main danger in cord prolapse?

Answer 385

presenting part of fetus compresses cord = feta hypoxia

Question 386

What is the most significant RF for cord prolapse?

Answer 386

abnormal lie after 37 wks - provides space for cord to prolapse below presenting part

Question 387

When should cord prolapse be suspected?

Answer 387

fetal distress on CTG confirm by vaginal exam

Question 388

How is cord prolapse managed?

Answer 388

emergency c-section (normal = high risk of cord compression) while waiting: keep cord warm, wet + minimal handling (risk of vasospasm) lie in left lateral with pillow under hip/all fours to draw fetus away from pelvis tocolytics to minimise contractions

Question 389

What is recommended after instrumental delivery to reduce risk of infection?

Answer 389

co-amoxiclav single dose

Question 390

When is an instrumental delivery indicated?

Answer 390

failure to progress fetal distress maternal exhaustion control of head in various fetal positions

Question 391

What type of pain management during labor increases the risk of needing an instrumental delivery?

Answer 391

epidural

Question 392

What are the increased risks to mother during an instrumental delivery?

Answer 392

PPH episiotomy, perineal tears, injury to anal sphincter incontinence temporary nerve injury (obturator/femoral nerve)

Question 393

What is the key risk to baby during a ventous delivery?

Answer 393

cephalohaematoma

Question 394

What are the risks to baby during a forceps delivery?

Answer 394

key risk = facial nerve palsy ``` bruising on face fat necrosis (hardened lumps on cheeks) ```

Question 395

What are the indications for an elective caesarean?

Answer 395

``` previous caesarean symptomatic after previous sig perineal tear placenta/vasa praevia breech multiple pregnancy uncontrolled HIV cervical Ca ```

Question 396

What is a category 1 emergency caesarean? How long must the time to delivery be?

Answer 396

immediate threat to life of mother/baby | 30 mins

Question 397

What is a category 2 emergency caesarean? How long must the time to delivery be?

Answer 397

not an imminent threat to life but ceasarean required urgently due to compromise 75 mins

Question 398

What is a category 3 emergency caesarean?

Answer 398

delivery required by mum/baby are stable

Question 399

What is a category 4 emergency caesarean?

Answer 399

elective

Question 400

What medications can be given before/during to reduce risks during a c-section?

Answer 400

H2 receptor antagonists (eg ranitidine) or PPI: for aspiration pneumonitis caused by acid reflux/aspiration during prolonged lying flat prophylactic abx: infection oxytocin: PPH LMWH: VTE

Question 401

What are the increased risks for future pregnancies caesarean?

Answer 401

repeat caeserean uterine rupture placenta praevia stillbirth

Question 402

What are the possible complications in the postpartum period after a caeserean?

Answer 402

PPH wound infection/dehiscence endometritis

Question 403

What VTE prophylaxis methods should be considered for women post-caeserean?

Answer 403

early mobilisation anti-embolism stockings LMWH eg enoxaparin

Question 404

What is the most common cause of shoulder dystocia?

Answer 404

macrosomia 2ndary to gestational diabetes

Question 405

What are 2 key signs that failure to deliver the body is due to shoulder dystocia?

Answer 405

failure of restitution - head remains face down and doesn't turn sideways turtle neck sign - head delivered but retracts back into vagina

Question 406

What techniques can be used to manage shoulder dystocia?

Answer 406

obstetric emergency episiotomy pressure to anterior shoulder mcroberts manoeuvre - hyper flexion of mother at hip > posterior pelvic tilt to lift pubic symphysis out of way rubins manoeuvre - reach into vagina and put pressure on posterior aspect of baby's anterior shoulder wood's screw manoeuvre - during rubins, other hand used to put pressure on anterior aspect of posterior shoulder (or vice versa) zavanelli manoeuvre - push head back in to do emergency c-section

Question 407

What are the 4 key complications of shoulder dystocia?

Answer 407

fetal hypoxia brachial plexus injury + Erb's palsy perineal tears PPH

Question 408

What are the RFs for VTE in pregnancy?

Answer 408

``` smoking parity 3+ age >35 BMI >30 reduced mobility multiple pregnancy pre-eclampsia gross varicose veins family hx thrombophilia IVF ```

Question 409

When should VTE prophylaxis be started from, in which women?

Answer 409

4+ RFs > 1st trimester 3 RFs > 28 wks risk assessed at booking + after birth + extra if admission/surgery etc

Question 410

What VTE prophylaxis is given to women at higher risk?

Answer 410

LMWH eg enoxaparin, dalteparin (continued until 6wks postnatally, temporarily stopped during labour) if CI: intermittent pneumatic compression anti-embolic compression stockings

Question 411

What are the key sx to look out for in a DVT?

Answer 411

UNILATERAL calf/leg swelling + tenderness + oedema + colour change dilated superficial veins

Question 412

How is leg swelling defined in a suspected DVT?

Answer 412

measure calf 10cm below tibial tuberosity >3cm difference between legs = significant

Question 413

What are the key sx to look out for in a PE?

Answer 413

``` SoB cough +/- blood pleuritic chest pain hypoxia raised RR ``` tachycardia low grade fever haemodynamic instability

Question 414

1st line ix for DVT?

Answer 414

doppler US

Question 415

What are the 1st line and definitive diagnosis ix for PE?

Answer 415

1st line: cxr ECG definitive: CTPA = best ventilation-perfusion scan

Question 416

Is d-dimer helpful in pregnancy?

Answer 416

no - pregnancy is a cause of raised d-dimer | wells score not validated

Question 417

How is a VTE in pregnancy managed?

Answer 417

LMWH - start immediately, before dx if delay in scan continue for pregnancy + 6weeks after is confirmed massive PE/haemodynamic compromise > life-threatening > consider unfractioned heparin, thrombolysis, surgical embolectomy

Question 418

What is the spectrum and timeline of postnatal mental health illness?

Answer 418

baby blue - majority of women in 1st wk after birth postnatal depression - 1 in 10, peaks 3mo after birth puerperal psychosis - starts a few weeks after birth

Question 419

How long must sx last for a dx of postnatal depression?

Answer 419

2 wks | same triad as depression

Question 420

How is mild, moderate and severe postnatal depression managed?

Answer 420

mild: additional support, self-help, follow-up with GP mod: SSRI, CBT severe: specialist services, possibly inpatient care in mother + baby unit

Question 421

What is the screening tol for postnatal depression?

Answer 421

edinburgh scale out of 30, >10 suggests PND

Question 422

What is the risk to neonates if the mother has taken SSRIs during pregnancy?

Answer 422

neonatal abstinence syndrome presents in 1st few days > irritability + poor feeding supportive mx

Question 423

Irregular menstruation indicates what about ovulation?

Answer 423

anovulation or irregular ovulation

Question 424

What are the DDx of irregular menstruation?

Answer 424

early menarche/perimenopause physiological stress - excess exercise, low body weight, chronic disease, pyschosocial medication - prog only contraception, ADs, antipsychotics hormonal imbalances eg thyroid, cushing's, high prolactin PCOS

Question 425

What are the DDx of IMB?

Answer 425

cervical ectropion cervical/endometrial/vaginal polyps or cancer = possible RF STI hormonal contraception pregnancy ovulation - can cause spotting, in some women medications eg SSRIs, anticoags

Question 426

What are the DDx of dysmenorrhoea?

Answer 426

primary dysmenorrhoea - no pathology endometriosis/adenomyosis fibroids PID cervical/ovarian cancer copper coil

Question 427

Define menorrhagia

Answer 427

excessive menstrual blood loss that occurs regularly which interferes with a woman's physical, emotional, social and material quality of life usually >80ml blood loss (usually 40ml)

Question 428

What is normal versus excessive menstrual blood loss?

Answer 428

excessive = 80ml+ +/- duration of 7+ days +/- need to change menstrual products every 1-2hrs +/- passage of clots greater than 2.54cm +/- reported as 'very heavy' by woman average = 30-40ml

Question 429

What is abnormal versus dysfunctional uterine bleeding?

Answer 429

any variance of normal menstrual cycle on basis of frequency, regularity, duration or volume + dysfunctional = AUB dx after excluding pregnancy and pathology

Question 430

What are the DDx of menorrhagia?

Answer 430

dysfunctional uterine bleeding extremes of reproductive age contraceptives esp copper coil ``` fibroids endometriosis/adenomyosis PID endometrial hyperplasia/cancer PCOS ``` anticoag meds bleeding disorders endocrine disorders eg diabetes, hypothyroid connective tissue disorders

Question 431

How to distinguish between placental abruption and praevia?

Answer 431

abruption: shock sx inconsistent with vaginal loss, pain common and severe, bleeding often absent/may be dark, lie normal/often engaged/may be distressed praevia: shock sx consistent with vaginal loss, PAINLESS, red profuse bleeding/often hx of small APHs, lie abnormal/head high/not in distress

Question 432

What is the pathway of tests for a male in an infertile couple?

Answer 432

semen analysis if azoospermic > LH, FSH, serum karyotype MRI brain to rule out pit/hypothalamic tumour ?arrested spermatogenesis > testicular biopsy

Question 433

What is the most common type of vaginal cancer?

Answer 433

mets | primarily from cerix or endometrium

Question 434

What is the most common type of primary vaginal cancer?

Answer 434

squamous cell carcinoma | less common = adenocarcinoma

Question 435

Where is a vaginal cancer most likely to metastasise to?

Answer 435

lungs | liver

Question 436

Positive routine asymptomatic bacteriuria screen in a pregnant woman. Next steps?

Answer 436

asymptomatic bacteriuria requires tx | contamination of 1st culture possible > confirm with 2nd test

Question 437

Define oligo and polyhydramnios in terms of AFI?

Answer 437

poly: AFI >24cm or 2000ml+ oligo: AFI <5cm or <200ml

Question 438

What are the causes of polyhydramnios?

Answer 438

most idiopathic macrosomia maternal diabetes structural deformities of fetus viral infectins

Question 439

What is the most common treatable cause of recurrent miscarriage?

Answer 439

Anti-phospholipid syndrome (a/w SLE)

Question 440

How does endometritis vs RPOC present as causes of 2ndary PPH?

Answer 440

both vaginal bleeding thats getting worse, lower abdo pain ``` endometritis = foul smelling discharge + fever (risk of sepsis) RPOC = odourless discharge, no fever unless infected ```

Question 441

How does lochia present?

Answer 441

normal bleeding after pregnancy due to endometrium breaking down bright red then darkens, gets less

Question 442

For how many weeks are women considered infertile after pregnancy?

Answer 442

3wks

Question 443

Exclusive breastfeeding after birth + amenorrhoea, does she need contraception?

Answer 443

lactational amenorrhoea covers for 6mo

Question 444

Differential of itching in pregnancy?

Answer 444

obstetric cholestasis acute fatty liver > can cause hepatitis both in 3rd trimester

Question 445

How to treat acute fatty liver?

Answer 445

admit | emergency c-section

Question 446

What are the SEs of ERPOC?

Answer 446

``` endometritis ashermans (adhesions in the uterus due to trauma) ```

Question 447

What contraception can be used straight after birth?

Answer 447

lactational amenorrhoea | POP/implant

Question 448

When can a coil be inserted after birth?

Answer 448

within 48hrs | or after 4wks

Question 449

What contraception should be avoided in breastfeeding?

Answer 449

COCP

Question 450

How long after birth if not breastfeeding should the COCP be avoided?

Answer 450

6wks

Question 451

How may Sheehan's present?

Answer 451

woman struggling to breastfeed | necrosed pituitary > no prolactin

Question 452

2nd repeat smear is HPV+ve with normal cytology, next step?

Answer 452

colposcopy

Question 453

What is the diagnostic traid for HG?

Answer 453

>5% weight loss dehydration electrolyte imbalance

Question 454

What scoring system is used to determine the severity of HG?

Answer 454

PUQE - pregnancy unique classification of emesis

Question 455

When in pregnancy is HG most likely?

Answer 455

8-12wks | can be up to 20wks

Question 456

What conditions are a/w HG?

Answer 456

``` multiple pregnancy trophoblastic disease hyperthyroid nulliparity obesity ```

Question 457

What is a protective factor for hyperemesis?

Answer 457

smoking

Question 458

When should a pt with HG be admitted?

Answer 458

unable to keep down fluids/oral antiemetics ketonuria +/- >5% weight loss despite oral antiemetics confirmed/suspected comorbidity

Question 459

How is HG treated?

Answer 459

1st line: antiemetic - oral cyclizine/promethazine or alternative - prochlorperazine 2nd line: ondansetron (increased risk of cleft lip in 1st tri) or metoclopramide (extrapyramidal SE, use for no longer than 5 days) admission for IV hydration may be required

Question 460

Tx for urge incontinence

Answer 460

1. bladder retraining | 2. muscarinic antagonist: oxybutynin, tolterodine, solifenacin

Question 461

When must methotrexate be stopped before pregnancy?

Answer 461

stopped in both partners 6mo before conceiving inhibition of dihydrofolate reductase affects DNA synthesis

Question 462

What medication can be used to reduce fibroid size before surgery?

Answer 462

GnRH agonist eg triptorelin

Question 463

What usually happens to BP in pregnancy?

Answer 463

falls in 1st tri, continues to fall until 20-24wks | then increases to pre-pregnancy levels by term

Question 464

Women at high risk of pre-eclampsia should take what medication?

Answer 464

aspirin 75mg from 12wks - birth

Question 465

Which women are high risk for pre-eclampsia?

Answer 465

hypertensive disease in previous pregnancies CKD AI disease DM

Question 466

How should gestational HTN be treated?

Answer 466

1. oral labetalol | 2. nifedipine

Question 467

What is the most common cause of cord prolapse?

Answer 467

AROM

Question 468

Which abx is used for GBS prophylaxis? When is it given?

Answer 468

IV benzylpenicillin | women with a previous pregnancy with neonatal sepsis remember strep agalactiae is a GBS

Question 469

What are the differentials of postcoital bleeding?

Answer 469

``` cervical cancer/ectropion/infection trauma atrophic vaginitis polyps endometrial/vaginal cancer ```

Question 470

What are fibroids?

Answer 470

benign oestrogen-sensitive smooth muscle tumours in the uterus

Question 471

How do fibroids present?

Answer 471

mostly asymptomatic ``` HMB!! + prolonged bleeding cyclical pelvic pain, deep dyspareunia bloating, feeling full urinary + bowel sx O/E: pelvic masses, enlarged firm uterus infertility ```

Question 472

How are fibroids investigated?

Answer 472

submucosal fibroid presenting with HMB > hysteroscopy larger fibroids > pelvic US before surgery > MRI

Question 473

How are fibroids <3cm managed?

Answer 473

1st line = mirena + sx mx with NSAIDs/tranexamic acid alternatives = COCP/cyclical prog surgical options: endometrial ablation, resection during hysteroscopy, hysterectomy

Question 474

How are fibroids >3cm managed?

Answer 474

Refer to gynae medical mx options = NSAIDS/tranexamic acid, mirena depending on shape/size of fibroids (or COCP, cyclical prog) surgical options = uterine artery embolisation, myomectomy, hysterectomy

Question 475

Which is the only treatment of fibroids known to potentially increase fertility?

Answer 475

myomectomy

Question 476

Which medication can be given short-term before surgery to reduce the size of fibroids?

Answer 476

GnRH agonist eg goserelin, leuprorelin > menopausal state > oestrogen > reduce size

Question 477

What are the possible complications of fibroids?

Answer 477

``` infertility HMB red degeneration torsion malignant change (rare) miscarriage/preterm birth if pregnant ``` constipation urinary obstruction, UTIs

Question 478

What is red degeneration of a fibroid?

Answer 478

necrosis, infarction and ischaemia of a fibroid during pregnancy

Question 479

When in pregnancy is red degeneration of a fibroid likely to happen? Why?

Answer 479

2nd/3rd trimester in larger fibroids rapidly enlarges during pregnancy > outgrows blood supply

Question 480

How does red degeneration of a fibroid present?

Answer 480

severe abdo pain low grade fever vomiting tachycardia

Question 481

How is red degeneration of a fibroid managed?

Answer 481

supportive: rest, fluids, analgesia

Question 482

What are functional ovarian cysts?

Answer 482

related to fluctuating hormones majority benign very common in premenopausal women

Question 483

What is the traid a/w Meigs syndrome?

Answer 483

1. benign ovarian fibroma 2. pleural effusion 3. ascites resolves on tumour resection

Question 484

How do ovarian cysts present?

Answer 484

usually asymptomatic pelvic bloating/pain/fullness mass felt disrupted menstruation acute pain > torsion, rupture, haemorrhage

Question 485

Name the 6 types of ovarian cysts

Answer 485

follicular: most common, developing follicle persists, resolves in a few cycles, benign, thin walled + empty corpus luteum cyst: benign, often in early pregnancy, pelvic discomfort/pain + delayed menstruation mucinous/serous cystoadenoma: benign tumours of epithelial cells, mucinous can get extremely big dermoid: contain hair/teeth/bone stromal/sex-cord tumour: can be benign or malignant endometrioma: pain + disrupted ovulation

Question 486

What is there an increased risk of with dermoid cysts?

Answer 486

torsion

Question 487

How are ovarian cysts investigated?

Answer 487

1st line = USS pre-men + simple cyst + <5cm: no further ix CA-125 if <40 + complex cyst > dermoid cyst markers = lactase dehydrogenase, AFP, hcg

Question 488

Which 3 factors make up the risk of malignancy index for ovarian cysts?

Answer 488

menopause status USS findings CA-125

Question 489

How are ovarian cysts managed?

Answer 489

dermoid cyst likely > refer complex cyst/increased CA-125 > 2ww Pre-men + simple + normal CA-125: <5cm = nothing 5-7cm = routine referral, USS monitoring yrly >7cm = MRI/surgical evaluation Post-men + simple + normal CA-125: USS monitoring 4-6monthly increasing in size/persisting: consider ovarian cystectomy +/- oopherectomy

Question 490

What are the complications of ovarian cysts?

Answer 490

haemorrhage rupture > bleed into abdomen torsion

Question 491

How should HMB be investigated?

Answer 491

none is simple hx w/o other RFs/sx speculum + bimanual FBC - IDA hysteroscopy if suspected fibroids/endometrial pathology/persistent IMB pelvic + TVUS if possible fibroids/adenomyosis/exam difficult swabs, coagulation, ferritin, TFTs if indicated

Question 492

How is non-pathological HMB managed?

Answer 492

no contraception: - tranexamic acid (antifibrinolytic) if no pain - mefenamic acid (NSAID) is a/w pain contraception wanted: 1. mirena 2. COCP 3. cyclical oral prog eg norethisterone 4. prog only contraception tx unsuccessful > referral > consider endometrial ablation, hysterectomy

Question 493

Define the 3 criteria used to make a dx of PCOS?

Answer 493

Rotterdam crtieria: 2/3 needed 1. oligo/anovulation 2. hyperandrogenism - biochemical or sx eg hirsutism 3. polycystic ovaries on US

Question 494

How is a woman with PCOS likely to present?

Answer 494

oligo/amenorrhoea infertility obesity hirsutism acne hair loss in a male pattern insulin resistance

Question 495

What are the DDx of hirsutism?

Answer 495

PCOS meds eg phenytoin, ciclosporin, steroids, testosterone ovarian/adrenal tumours that secrete androgens cushing's CAH

Question 496

How does insulin resistance in COS drive hyperandrogenism and anovulation?

Answer 496

insulin promotes androgen release from ovaries + adrenals + suppresses SHBG production by liver which binds to androgens and suppresses their function resistance > produce more insulin to get response from cells > increased androgens + reduced SHBG > promotes hyperandrogenism high insulin halts follicle development > anvoluation > multiple partially developed follicles in ovaries = polycystic

Question 497

What are the key blood test changes in PCOS?

Answer 497

high LH high LH:FSH high testosterone + insulin normal/high oestrogen

Question 498

What is the diagnostic US criteria for PCOS?

Answer 498

TVUS follicles around periphery of ovary = string of pearls 12+ developing follicles in 1 ovary ovarian volume >10cm3

Question 499

How is the increased risk of obesity/T2DM/high cholsterol/CVD in PCOS managed?

Answer 499

weight loss, diet, exercise, smoking cessation, BP control, statins - orlistat = lipase inhibitor to aid weight loss in women with BMI >30

Question 500

Which gynae cancer are women with PCOS at high risk of?

Answer 500

endometrial anovulation = don't produce sufficient prog = unopposed oestrogen + endometrial proliferation

Question 501

How is the increased risk of endometrial cancer managed in PCOS? When should it be monitored?

Answer 501

reduce risk of endometrial cancer: mirena/induce withdrawal bleed at least every 3-4mo with cyclical prog or COCP >3mo between periods/abnormal bleeding > pelvic US - use cyclical prog to induce period prior to US endometrial thickness>10mm > biopsy

Question 502

How is infertility managed in PCOS?

Answer 502

1. weight loss 2. clomifene 3. laparoscopic ovarian drilling 4. IVF (some evidence metformin + letrozole restore ovulation)

Question 503

What blood tests are done at booking and 28wks?

Answer 503

FBC (anaemia) blood group, rhesus, red cell alloantibodies, haemoglobinopathies hep B, HIV, syphillis

Question 504

How is GD managed depending on fasting glucose level?

Answer 504

<7: trial of diet + exercise target not met within 1-2wks > start metformin still not met > + insulin (short-acting) 7+: insulin 6-6.9 + complications eg hydramnios, macrosomia = insulin glibenclamide if cannot tolerate metformin/fail on metformin and decline insulin

Question 505

For how long after delivery/last seizure should MgSO4 be continued in a woman with eclampsia?

Answer 505

24hrs

Question 506

How is endometrial hyperplasia managed?

Answer 506

simple > high dose prog eg LNG-IUS + repeat sampling in 3/4m atypia > hysterectomy advised, in postmenopausal women > total hysterectomy with bilateral salpingo-oopherectomy

Question 507

What can be given when a cord prolapse is identified whilst waiting for an LSCS?

Answer 507

terbutaline

Question 508

Define menopause

Answer 508

amenorrhoea >1yr

Question 509

What are the 4 CI to menopause?

Answer 509

undiagnosed vaginal bleeding oestrogen sensitive cancer current/past breast ca untreated endometrial hyperplasia

Question 510

What must be avoided in HRT to women with a uterus?

Answer 510

unopposed oestrogen > risk of endometrial ca

Question 511

What HRT can be given if a woman does not have a uterus?

Answer 511

oestrogen only, as a patch or orally

Question 512

What can HRT increase the risks of?

Answer 512

VTE/stroke (all oral forms, not transdermal) CHD (combined forms) breast ca (combined forms) ovarian ca

Question 513

What HRT is preferred in women with increased risk of VTE?

Answer 513

transdermal

Question 514

What HRT is preferred in women with migraine and aura?

Answer 514

transdermal

Question 515

What regime of HRT should be given to women with definite menopause versus before?

Answer 515

amenorrhoea >1yr = continuous regime before = cyclical (oestrogen daily, prog for a few weeks of the cycle)

Question 516

Which contraception is licensed as the prog part of HRT?

Answer 516

mirena - only need oestrogen on top licensed for 4yrs