Women's Health Flashcards
What is the menstrual cycle?
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
Is bleeding between taking the OCP a period?
Occurs due to the drop in oestrogen + progesterone
= withdrawal bleed
It is not induced by cyclical hormonal changes so is not a period
When is the last menstrual period (LMP) defined as?
1st day of last period
What is menarche? When does it occur?
onset of menstruation
occurs 12-13yrs but age is decreasing (95% between 11-14.5yrs)
What are the 4 stages of the menstrual cycle? Which days do they occur?
Menstruation (day 1-5) > proliferation (day 6-15) > ovulation (day 14) > secretion (day 16-28)
What hormones cause the onset of menses and secondary sexual characteristics?
from 8yrs:
GnRH pulses increase in amplitude and frequency > FSH and LH release increases > stimulate oestrogen release from ovaries > development of secondary sexual characteristics
What is thelarche? When does it occur?
breast development
9-11yrs
What is adrenarche? When does it occur?
growth of pubic hair
11-12yrs
How regular is the menstrual cycle shortly after menarche? How does it change?
initial cycles often irregular > as oestrogen secretion rises > become more regular + pregnancy is then possible
When does growth in a female usually finish by?
By 16yrs most growth has finished and epiphyses fuse
What is primary amenorrhea?
Failure to menstruate by the age of 16
OR failure to menstruate by the age of 14 in someone with no secondary sexual characteristics
What happens to hormone levels in the follicular phase of the ovarian cycle? What do these changes result in?
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
What cells produce oestrogen?
granulosa cells
What happens to hormone levels on day 14 of the ovarian cycle?
- 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
What happens in the luteal phase of the ovarian cycle IF the egg is fertilised?
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
What happens in the luteal phase of the ovarian cycle if the egg ISN’T fertilised?
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
How can contraception prevent menstruation?
continuous administration of exogenous progesterones maintains a secondary endometrium
it’s the FALL in progesterone that triggers menstruation
How does contraception prevent ovulation?
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
What medication can be taken when needing to delay a period e.g. a holiday?
noresthisterone - stop taking when acceptable to have a period again
What is the first phase of the uterine cycle?
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
What is the second phase of the uterine cycle?
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
What is the 3rd phase of the uterine cycle?
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)
How do oestrogen levels change throughout the menstrual cycle?
increase up to day 14 (peak) and then decrease until menses with a small rise at the beginning of the secretory phase
How do progesterone levels change throughout the menstrual cycle?
increase more slowly than oestrogen, peak at secretory phase (day 21ish) and then decrease until menses
When is labour diagnosed?
painful uterine contractions accompany dilatation and effacement of the cervix
Define a normal birth
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
What are the 3 mechanical factors that affect labour?
- power - degree of force expelling the foetus
- passage - dimensions of the pelvis and resistance of soft tissues
- passenger - diameters of the foetal head
Where do contractions originate from?
arise in one of the pacemakers at each cornua of the fundus of the uterus
What happens to the uterus in a contraction?
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)
What is the expected frequency of contractions once labour is established?
build in amplitude as labour progresses
contracts for 45-60 seconds every 2-4 minutes
What is the cervix like before labour?
hard close tube, around 4cm long
tightly closed throughout pregnancy, protected by a plug of mucus
What is cervical effacement? When does it occur during labour?
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
What factors allow cervical dilatation?
caused by contracting muscle + pressure on the cervical opening + ability of cervix to soften and allow distension
measured in cm by vaginal examination
What are the features of the latent phase of labour?
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
How long does the latent phase of labour usually last?
can be the longest stage
especially in primiparous women - can last 2-3 days
What is SROM?
spontaneous rupture of membranes - can happen any point prior to/during labour
What is ARM?
artificial rupture of membranes > can speed up/augment process/induce labour
Where is the amniotic fluid? What does it do?
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
How much amniotic fluid should there be at term?
500-800mls
What is the term for when a foetus is born within the amniotic sac?
en caul = very rare
When is the 1st stage of labour defined as?
from 4cm to full dilatation (10cm)
= active/established labour
What happens in the 1st stage of labour?
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
What rate of dilatation is normal in the first stage of labour?
Nulliparous = 0.5cm/hr Multiparous = 1cm/hr (normal progression)
How long does the 1st stage of labour usually last?
no longer than 16hrs
average = 8hrs in nulliparous, 5h in multiparous
When is the 2nd stage of labour defined as?
from full dilatation to the birth of the foetus
How long does the 2nd stage of labour last?
from 5 mins (multiparous) to 2-3hrs
What is a passive stage in the 2nd stage of labour?
woman is fully dilated but does not have urge to push yet
can slow down contractions before pushing starts
What happens in the active stage in the 2nd stage of labour? How long does it last?
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
After how long pushing does spontaneous delivery become increasingly unlikely?
> 1hr
What are the steps of the delivery of the foetal head?
- descent
- flexion
- internal rotation
- extension
- restitution/external rotation
- delivery of the body
What happens in descent of the foetal head?
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)
What happens in flexion of the foetal head?
foetal neck flexes, foetal skull has a smaller diameter in this position = aids passage through pelvis
flexion increases throughout labour > reaches vertex position
What happens in internal rotation of the foetal head?
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
What happens in extension of the foetal head?
Occiput slips beneath the suprapubic arch, allowing the head to extend
Foetal head is now born, usually facing mum’s back depending on position
What happens in restitution/external rotation of the foetal head?
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
What happens in delivery of the body? How can delivery of the shoulders be assisted?
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
What injury can occur if force applied during delivery of the shoulders is too excessive?
brachial plexus damage
What is delayed cord clamping?
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)
What are the potential advantages of delayed cord clamping?
- 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
When is the 3rd stage of labour defined as?
from the birth of the foetus to the expulsion of the placenta
usually lasts about 15 mins
How is the placenta expelled by the uterus?
Uterine muscle fibres contract to compress the vessels formerly supplying the placenta which shears away from the uterine wall
What are the two ways the placenta can be delivered?
- physiological - body expels it without intervention
- active - mum given an IM oxytocin drug > uterus contracts and expels the placenta > delivered using controlled cord traction
What are the risks when a placenta is delivered using cord traction?
excessive force > snapped cord, inverted uterus
Why is it important to check the placenta and membranes once they are delivered?
must check if any is left in the uterus
= risk of serious PPH
What membranes should be delivered with the placenta?
amnion (bag around baby)
chorion (membranes around placenta)
What is the role of the placenta?
- 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
Some midwives describe a 4th stage of labour, what is this?
early postnatal phase
skin to skin contact increases oxytocin for mum and baby
= bonding, uterus contracts, regulates baby’s HR and breathing
What role does oxytocin have in labour?
a surge in oxytocin at the onset of labour contracts the uterus
What role does prolactin have in labour?
begins the process of milk PRODUCTION in the mammary glands
What role does oestrogen have in labour?
surge at onset of labour to inhibit progesterone to prepare the smooth muscles for labour
What role do prostaglandins have in labour?
aid with cervical ripening
What role do beta-endorphins have in labour?
natural pain relief
What role does adrenaline have in labour?
released as birth is imminent to give woman the energy to give birth
What damage occurs in a 1st degree perineal tear?
minor damage to the fourchette
What damage occurs in a 2nd degree perineal tear or an episiotomy?
involves the perineal muscle
What damage occurs in a 3rd degree perineal tear?
involves the anal sphincter (1% of deliveries)
What damage occurs in a 4th degree perineal tear?
also involves the anal mucosa
Define malpresentation
when the foetus is not presenting by the vertex
What term describes a normal lie of the foetus?
cephalic (94% of deliveries)
Define breech presentation
presenting part of the foetus is not the head - foetus is in a longitudinal lie with buttocks or feet closest to the cervix
What is the most common type of breech presentation?
extended breech - presenting part is the bottom
What are some causes of breech presentation?
Idiopathic
Uterine abnormalities (bicornuate uterus, fibroids)
Prematurity (baby hasn’t turned around yet)
Placenta praevia
Oligohydramnios
Foetal abnormalities eg hydrocephalus
How are breech babies identified?
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
How are breech babies managed?
- External cephalic version (ECV) - manoeuvring baby to correct the breech, can be done at 37 wks
- If unsuccessful/CI > LSCS
When might external cephalic version be contraindicated for a breech baby?
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
What is the most ideal lie of a foetus?
LOA - left occiput anterior
back of foetus is on mother’s left side and towards the front so the occiput leads in delivery
What is the most common pelvis type in females?
gynecoid > lots of adaptation for childbirth e.g. wide subpubic arch, transverse oval inlet
What bones and fontanelles is the foetal skull made up of? How does the foetal skull aid passage through the pelvis?
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
What general care should be provided to support a women’s physical health during labour?
- 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)
What positions are most ideal for giving birth in?
all fours > increases diameter of pelvic inlet, less compression on aorta, gravity
squatting, kneeling, left-lateral position also
Why is the supine position avoided during birth?
- has to push the baby around a u-bend
- uterus compresses vessels > reduced CO > hypotension (aortocaval compression)
combine with left-lateral tilt to improve position
How and why should pyrexia in labour be managed?
increased risk of neonatal illness
more common with epidurals, prolonged labour
vaginal, blood + urine cultures
give paracetamol
if 38: IV abx + CTG monitoring
Why is bladder care important during labour?
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
What general care should be provided to support a women’s psychological health during labour?
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
What non-invasive, holistic methods can be used for pain management during labour?
water immersion comfortable positions/environment aromatherapy massage hypnobirthing TENS machine
What pharmacological methods can be used for pain management during labour?
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
What are the advantages of entonox?
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
What are the disadvantages of entonox?
nausea, light-headedness
wears off quickly
What are the advantages of opioids as pain management in labour?
can be given by a midwife
still able to mobilise
does not slow labour
drowsiness - can sleep between contractions
What are the disadvantages of opioids as pain management in labour?
maternal SE: N&V, eu/dysphoria, can prolong 1st/2nd stages, resp depression, pruritus
foetal SE: resp depression, diminishes breast seeking and feeding behaviour
What medication does an epidural contain?
mixture of bupivacaine and fentanyl (i.e. a local anaesthetic and an opioid)
Where is an epidural inserted? How does it work?
epidural catheter inserted into the epidural space at L3/4 by an anaesthetist
drugs administered through this via a pump
When is an epidural indicated?
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
CI to an epidural?
local infection
allergy to local anaesthetics
What are the advantages of an epidural?
total pain relief in 90% of ptients
effect lasts until baby is born
What are the disadvantages of an epidural?
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
What are the potential complications of an epidural?
damage to spinal cord, hypotension + bradycardia, haematoma/abscess at injection site, anaphylaxis, post dural puncture headache
How is progress in labour recorded and monitored?
partogram
What is the NICE definition of slow progress labour?
<2cm dilatation in 4hrs
What on the partogram indicates slow progress?
alert and action lines
an action line = ACTION must be taken
point at which progression stops may indicate a cause
What factors does the partogram assess?
FHR cervical dilatation contractions per 10mins drugs + fluids given maternal pulse + BP urine
When is progression of labour abnormal?
slow from beginning = dysfunctional labour
sudden slowing of labour = secondary arrest
What are the RFs for failure to progress in labour?
large baby breech baby 1st time mother previous delayed labour premature ROM
How is failure to progress in labour assessed?
Palpate abdomen for lie, head and contractions
CTG
Colour of amniotic fluid
Vaginal examination
What are the 3 main causes of slow progress in labour?
power
passenger
passage
or a combination
What is the most common cause of slow progress in labour? Who is it most common in?
inefficient uterine action
common in nulliparous women (+ induced labour)
What are the power causes of slow progress of labour?
inefficient uterine action
hyperactive uterine action
maternal exhaustion
How can hyperactive uterine action be managed?
excessively strong/frequent/prolonged contractions
depends on cause
if no abruption > tocolytic e.g. salbutamol IV/SC
LSCS often indicated due to foetal distress
What are the passenger causes of slow progress of labour?
malpresentation
malposition of large baby (presenting part is in the right place but wrong position e.g. occipital-transverse/posterior, brow)
What are the passage causes of slow progress of labour?
inadequate pelvis cephalopelvic disproportion (big baby, small pelvis)
What is augmentation vs induction of labour?
augmentation: artificial strengthening of contractions in established labour
induction: artificial initiation of labour
How is failure to progress in the 1st stage of labour managed?
augmentation by ARM/amniotomy
CTG monitoring, FBS if concerns
if membranes already ruptured/fails to dilate further > oxytocin infusion
then consider LSCS
How is failure to progress in the 2nd stage of labour managed?
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
What factors is the mode of delivery influenced by?
size + presentation of baby
well-being of both, length of labour, maternal exhaustion
adequacy of pelvis
What are the foetal consequences of slow progress in labour?
foetal distress
foetal hypoxia > hypoxic-ischaemic encephalopathy
increased morbidity/mortality
What are the maternal consequences of slow progress in labour?
bleeding
tears
Which drug can stop the effect of oxytocin by blocking its receptor?
atosiban
can inhibit myometrial contractions by blocking oxytocin > used to prevent premature birth
What are some causes of meconium stained liqour?
foetal distress
foetal maturity - late baby ready to be born
What can meconium aspiration result in?
severe pneumonitis
Define APH
any bleeding from the genital tract after 24 weeks
What are the possible causes of an APH?
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
How is an APH investigated and diagnosed?
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
What must you avoid before confirming the position of the placenta?
NO INTERNAL EXAM ESP VAGINAL IF YOU HAVEN’T CONFIRMED POSITION OF PLACENTA
= risk you may put your fingers through it
How is an APH managed?
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)
Define a primary PPH
Primary = within 24hrs of delivery
AND >500ml blood loss (or >1000ml after caesarean)
How is major bleeding in a PPH defined?
> 1500ml/signs of clinical shock
What are the causes of PPH?
Tone - uterine atony (most common)
Thrombin - bleeding disorders
Trauma - eg perineal tear
Tissue - retained products
What are the 4T’s of causes of PPH?
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
What makes uterine atony more likely?
prolonged labour
grand multiparity
over distension of the uterus e.g. polyhydramnios, multiple pregnancy
fibroids
When should antenatal thromboprophylaxis be stopped?
at least 12hrs before labour/delivery to reduce chances of a PPH
What are the RFs for a PPH?
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
How should a primary PPH be investigated?
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?
What will an atonic uterus feel like on palpation?
uterus impalpable (would normally be palpable after delivery)
What medication in the 3rd stage of labour can reduce incidence of a PPH?
oxytocin
How should a primary PPH be immediately managed?
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
What interventions can be taken in a PPH if the uterus is atonic?
Empty bladder
Massage uterus/rub abdomen
Bimanual compression of uterus
Then pharmacological > IV syntocinon > IM carboprost > surgery
After immediate management, how should a PPH be treated?
- Uterine massage + catheter
- oxytocin/syntocinon IV infusion
- ergometrin (CI = HTN)
- carboprost (must be IM/inject directly into uterus) = prostaglandin (PGF2a)
- misoprostol PR > long lasting uterine contraction
- surgery
What surgical options are there for the tx of a PPH?
- 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
Define a secondary PPH
excessive blood loss >24hrs and <12wks after delivery
What are the possible causes of a secondary PPH?
Most common = endometritis or retained placental tissue
Investigations for a secondary PPH?
high vaginal swabs (endometritis) - look for CT/GC
USS - retained products
How to manage a secondary PPH?
Depending on cause:
endometritis: abx
RPC: evacuation of retained products of conception (ERPC)
What is synctocinon?
combination of ergometrine and oxytocin to help uterus contract
What are the 4 types of HTN that can occur in pregnancy?
- Gestational HTN = only during pregnancy and occurs for the 1st time during pregnancy
- Preeclampsia-eclampsia
- Chronic HTN = occurs prior to pregnancy
- Preeclampsia superimposed upon chronic HTN/renal disease
How are spiral arteries different in a pregnant woman with preeclampsia?
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
RFs for developing preeclampsia?
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
Define gestational HTN
After 20wks
Systolic >140 or Diastolic >90
or increase above booking levels of >30 systolic or >15 diastolic
no proteinuria
resolves following birth
When is HTN chronic rather than gestational in a pregnant female?
HTN diagnosed before pregnancy/before 20th wk of gestation if not checked before pregnancy/during pregnancy and not resolved postpartum
Define preeclampsia
New HTN after 20th wk (earlier with trophoblastic disease)
with proteinuria
+/- oedema
What is eclampsia?
features of pre-eclampsia + generalised tonic-clonic seizures
What are the 2 criteria for preeclampsia superimposed upon chronic HTN?
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
What are the sx of preeclampsia?
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)
What signs does preeclampsia present with?
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
How should preeclampsia be investigated?
- 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
Define the criteria for diagnosis of preeclampsia
- Gestational HTN = systolic >140, diastolic >90 (repeat measurement 6hrs after 1st to see if still exceeded)
- 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
What indicates a patient’s preeclampsia is severe?
BP: >160 systolic, >100 diastolic +/- sx
+/- biochemical/haematological impairment
What is the cure for preeclampsia?
delivery = always beneficial for mum, sometimes not for foetus
How is mild/moderate preeclampsia managed?
oral labetalol
(nifedipine if asthmatic, methyldopa)
bp monitoring every 48hrs
FBC, LFT, renal function 2x wk
Which patients should be given MgSO4 with caution?
renal failure
Mg toxicity > cardiac arrest
Which antihypertensives are teratogenic? How is pre-existing HTN managed in pregnancy?
ACEi are teratogenic
1st line = labetalol
2nd = nifedipine
How is acute severe preeclampsia treated? When is it severe?
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
When should baby be delivered if the mother has preeclampsia?
<34wks: continue surveillance, offer MgSO4 + corticosteroids
36-37: continue surveillance, corticosteroids, decision based on risk if needed early
37: initiate birth within 24-48hrs
What mode of delivery is preferable in women with preeclampsia? What can be given during delivery to reduce HTN
vaginal
hydrazine/labetalol (only in severe HTN as can also reduce supply to placenta)
What postpartum care will the mother need after having preeclampsia?
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
What are the maternal complications that can occur due to preeclampsia?
CVA eclampsia pulmonary oedema liver complications renal failure
What are the foetal complications that can occur due to preeclampsia?
IUGR
preterm birth
placental abruption
hypoxia
For how long after delivery/last seizure should MgSO4 be continued in a woman with eclampsia?
24hrs
What is HELPP syndrome?
H = haemolysis EL = elevated liver enzymes LP = low platelets
What S&S does HELPP syndrome cause?
haemolysis > dark urine, raised lactic dehydrogenase
elevated liver enzymes > epigastric pain, liver failure, abnormal clotting
low platelets
How is HELPP syndrome managed?
supportive tx
magnesium sulphate prophylaxis against eclampsia
immediate delivery depending on gestation
Why is anaemia more common in pregnant women?
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
High Hb is a/w with that risks in pregnancy?
preterm delivery
IUGR
What are the causes of anaemia in pregnancy?
inadequate intake poor absorption haemolytic e.g. sickle cell excessive demands e.g. twins vaginal loss/preexisting haemorrhage
When does IDA become symptomatic in a pregnant woman?
hb <9g/dL
How does IDA present on blood tests?
MCV reduced, ferritin reduced
How is IDA treated in pregnant women?
oral iron (can cause GI upset) if severe > IV iron is quicker, may prevent need for blood transfusion
If a pregnant woman present with anaemia without microcytosis what should the cause be assumed to be?
folic acid deficiency - more common than vit b12
How does folic acid and vit B12 deficiency present on blood tests?
MCV usually increased
red cell folic acid/vit B12 levels low
How can anaemia be prevented in pregnancy?
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)
What is the difference between adult and foetal Hb?
Adult Hb: 2 alpha and 2 beta
Foetal Hb: 2 alpha and 2 gamma
What happens to Hb in sickle cell disease?
abnormal beta-chain formation (S chain) in Hb > made up of 2 alpha an 2 S chains (or C chains)
How is sickle cell disease inherited?
autosomal recessive
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?
Hb electrophoresis
If a heterozygote > partner is tested > if +ve > prenatal dx for homozygosity is offered
What are the sx of sickle cell disease?
Crises of bone pain and pulmonary sx
Lifetime chronic haemolytic anaemia
Pulmonary HTN, proliferative retinopathy possible
What are the possible maternal and foetal complications of sickle cell disease?
Maternal complications: acute painful crises, pre-eclampsia, thrombosis
Foetal complications: miscarriage, IUGR, preterm labour, death
Which medication used to tx sickle cell disease is teratogenic?
hydroxycarbamide = should be stopped
How is sickle cell disease managed during pregnancy? And during crises?
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
Define endometriosis
The presence of endometrial tissue outside the endometrial cavity
Where can endometriosis occur? What are the most common locations?
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
When in a women’s lifetime might endometrial sx regress?
oestrogen dependant =
starts after puberty
regresses during pregnancy, after menopause, if on androgens
What does changes can the bleeding in endometriosis cause in the uterus ?
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
What can happen in severe grade 4 endometriosis?
frozen pelvis > uterus adhered to bowel so can’t have a hysterectomy in case of perforation
What are the 3 theories behind the pathophysiology of endometriosis?
- Sampson’s theory - retrograde menstruation > shedded endometrial tissue in a period goes back through the fallopian tubes and implants elsewhere
- Halban’s theory - more distant tissue > mechanical, lymphatic, blood-borne spread
- Meyers theory > metaplasia of mesothelial cells
Retrograde menstruation is very common. Why doesn’t everyone with it have endometriosis?
individual factors determine whether the endometrial tissue implants and grows (eg impaired immunity, genetics)
Why do endometrial sx increase towards a women’s period?
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)
Who is more likely to be affected by endometriosis?
low parity women (the more someone is pregnant > more exposed to progesterone > endometrium shrinks)
usually dx in younger women (30-45yrs)
Differential diagnoses of endometriosis?
1 = adenomyosis
Chronic PID
Chronic pelvic pain
Pelvis masses
IBS
What are the key sx of endometriosis?
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
What is the pattern of pain in endometriosis? What other painful sx is it a/w?
- 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
Why can endometriosis affect fertility?
Due to immune factors (cytokines released by areas of endometriosis), oocyte toxicity, adhesions, tubal/ovarian dysfunction
How might endometriosis present O/E?
tenderness/thickening behind uterus/in adnexa
in mild disease = often normal
What is the gold standard investigation for endometriosis?
laparoscopy
What would be seen on laparoscopy in a women with endometriosis?
Red vesicles/punctate marks = acute lesions
white scars/brown spots = less active
Ovarian endometriomas/extensive adhesions = severe
can be graded from 1-4
Investigations for endometriosis?
laparoscopy +/- biopsy
transvaginal USS can exclude an endometrioma (mottled white)
very extensive disease > MRI
How can endometriosis be managed?
Sometimes it regresses/doesn’t progress > asymptomatic endometriosis doesn’t need tx
- analgesia (may be enough if pt doesn’t wan’t hormonal therapy)
- hormonal therapy to either abolish cyclicity or do glandular atrophy
- surgery
What is the aim behind medical management of endometriosis?
oestrogen dependant
tx either mimics pregnancy or menopause
What are the hormonal therapy options for endometriosis?
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)
How does the COCP treat endometriosis? How is it given?
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
How do GnRH agonists work in the treatment of endometriosis?
Overstimulation of the pituitary > down regulation of its GnRH receptors > FSH/LH inhibited > ovarian hormone production inhibited
= induces temporary menopause without affecting the ovaries
What are the downsides to GnRH agonists?
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
What are the downsides of oral prostagens/depot provera as a tx for endometriosis? How do they work?
= mimics pregnancy
SEs: poor cycle control, erratic bleeding, PMS like sx, fluid retention, weight gain
Why is the mirena coil an effective tx for endometriosis?
effective progesterone delivery, contraception + lightens periods
especially good if pt gets SEs from COCP/POP as progesterone directly to the uterus reduces SEs
What are the surgical options for treating endometriosis?
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)
What can unopposed oestrogen put a women at risk of?
endometrial carcinoma
Define stillbirth
a baby delivered with no signs of life known to have died after 24 completed weeks of pregnancy
Define intra-uterine foetal death
the death is diagnosed when the baby is still inside eg on scan
Epidemiology of stillbirth?
1/3rd are SGA
50% unexplained
Suboptimal care identified in half of cases
Why have the rates of stillbirth remained constant?
rising obesity rates
average maternal age
What factors make a women’s pregnancy high risk?
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
How are high and low risk pregnancies managed differently?
low risk can just be managed in the community
high risk managed by hospital and community
How is the foetus monitored in the antenatal period?
USS + umbilical artery doppler
Intermittent auscultation with hand-help doppler/pinard stethoscope
CTG
What does an USS assess during the antenatal period?
- growth - HC, AC, FL + these 3 give estimated foetal weight > plot on customised growth chart
- liquor volume
What does an umbilical artery doppler measure? How is it read? What should it show?
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)
What are the red flag signs on umbilical artery doppler?
no flow (absent EDF/ADEF) or reversed flow (REDF) compared to systole
= evidence of high (rather than low) resistance circulation
Define IUGR?
EFW <10th centile
What are the causes of asymmetrical IUGR? When does it usually happen? What happens to the measurements?
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
When is US used for foetal monitoring in pregnancy?
after the 1st trimester
What can low pregnancy-associated plasma protein A indicate?
chromosomal abnormalities (screening for Down’s), high risk of IUGR, placental abruption, stillbirth
What are the causes of symmetrical IUGR? What happens to the measurements?
Intrinsic factors eg early infections (TORCH), aneuploidy (chromosomal)
Shows global growth restriction
Increased risk neurological sequelae
What are the TORCH infections?
toxoplasmosis, other agents, rubella, CMV, HSV
What signs of IUGR may show on US?
- EFW <10th centile
- Oligohydramnios - too little amniotic fluid
- Reduced FM possible due to reduced O2
How is the amount of amniotic fluid measured?
Either look at single deepest pocket they can see
Or measure amniotic fluid index (AFI) by scanning the 4 quadrants of the stomach
What are the possible causes of oligohydramnios?
reduced excretion - urinary tract problem?
leakage
ruptured membrane
reduced production e.g. reduced renal perfusion
How is the foetus monitored intrapartum? Which is used for low vs high risk pregnancy?
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
What are the NICE guidelines for intermittent auscultation of low risk pregnancies during labour?
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
What does the foetal HR vs placenta sound like on intermittent ausculation?
foetal HR = clip clop sound, much faster than mum’s
placenta = whoosh sound
What are the drawbacks of intermittent auscultation?
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
What is the most common method to continuous monitoring? When is it used?
CTG
2 straps over the abdomen - one over foetus, one to pick up contractions
not useful it patient it low risk
from 26wks gestation
What are the advantages of CTG?
shows FHR and uterine contractions
long-term monitoring
average variability can be determined
What are the disadvantages of CTG?
can only be done in hospital number of contractions not strength
some foetal exposure to US insonation
not true beat to beat info
What is an acronym to help interpret a CTG?
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
What is the ideal number of contractions during labour? How many is too many?
ideally 4 in 10, regular and strong
with each squeeze, potentially reduce blood supply so baby needs time to recover
tachysystole = >5 in 10
What is a reassuring CTG?
Baseline: 110-160
Variability: >5bpm
Accelerations present
No or early decelerations
What is a normal amount of variability on CTG? How long can it be abnormal for?
5-25bpm
reduced level of variability acceptable for 40 mins (baby may be sleeping)
What are the 3 types of deceleration? What do they indicate?
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)
What are the concerning features of variable decelerations?
last >60 secs, reduced variability within the deceleration, biphasic W (taking longer to recover), loss of shouldering, failure to return to baseline
What is the gold standard for FHR monitoring? Why is it the gold standard?
direct foetal ECG by scalp ECG
= gives true beat to beat information
What are the downsides to a scalp ECG?
Invasive, only in labour, must be >2cm dilated/membranes absent, a/w scalp injury and perinatal infection
What is a method of obtaining an indirect foetal ECG? What are the advantages of this method?
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
What is foetal blood sampling used? When is it used?
analyses like an ABG
cervix must be 4cm dilated
What is a normal and abnormal foetal blood sampling result?
- 25+ pH = normal, repeat after 1hr if CTG remains the same
7. 20 or less = abnormal, consider delivery
Other than umbilical artery, what other methods of doppler are sometimes used?
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
Define placenta praevia/LLP
Any part of the placenta that has implanted into the lower segment
What is the difference between a major and minor placenta praevia?
Major = covering/partially covering os = obstructs head Minor = in lower segment, not cover os
Why do LLPs found at the 20wk scan usually resolve by term?
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
What examinations should be avoided if the patient has a LLP?
Vaginal exams and penetrative intercourse should be avoided = can go through placenta > risk of massive bleeding
Speculum exam safe
What are the RFs for placenta praevia?
Previous c-section Previous termination of pregnancy (uterine evacuation) Multiparity Multiple pregnancy Mother >40yrs Assisted conception Manual removal of previous placenta Fibroids Endometriosis
How does placenta praevia present?
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
How does the bleeding differ in placenta praevia vs abruption?
abruption = painful and smaller amount of blood praevia = painless, lots of blood
How is placenta praevia diagnosed? When are scans repeated to confirm?
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
How is a placenta praevia managed?
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
How is a bleeding placenta praevia managed?
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)
What is a key complication of placenta praevia?
severe APH
bleeding commonly continues during and after delivery (PPH) as lower segment is less able to contract and constrict the maternal blood supply
What can happen if a LLP implants into a previous c-section scar?
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
Define placental abruption
Premature separation of part of all of the placenta from the uterine wall
What are the 2 types of placental abruption?
- concealed (blood fluids up behind placenta and can’t drain)
- revealed (blood can drain > vaginal bleeding)
What are the RFs for a placental abruption?
IUGR Pre-eclampsia Pre-existing HTN Maternal smoking, cocaine use Previous abruption
AI disease, multiple pregnancy, high parity, trauma
What sx does a placental abruption present with?
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
How can you tell if a placental abruption is concealed or revealed by the patient’s sx?
If pain occurs alone = concealed, if there is bleeding = revealed
What are the signs of a placental abruption?
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
What are the signs of a major placental abruption?
maternal collapse, coagulopathy, foetal distress, woody hard uterus, poor urine output/renal failure
How is a placental abruption diagnosed?
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
How are small abruptions managed? Do they need admission?
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
How are large placental abruptions managed?
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
When is a foetus delivered if the mother has a placental abruption?
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
What are the possible complications of a placental abruption?
foetal death common (30%)
APH/PPH (> sheehan’s syndrome)
uterine hyper-contractibility
DIC, renal failure
What is Sheehan’s syndrome?
pituitary necrosis following PPH
Describe the key differences between placental abruption and placental praevia?
In terms of pain, bleeding, tenderness, foetus, on USS?
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
Define rhesus disease
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
How is blood classified?
ABO and rhesus genotype
How many gene pairs are there in the Rhesus system? How are they inherited?
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
What genetics of the parents make a baby most at risk of developing rhesus disease?
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
Why doesn’t rhesus disease occur in the first pregnancy? As opposed to subsequent pregnancies?
- 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
What are some example of sensitising events?
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
What method of prophylaxis can be used to prevent rhesus disease?
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
Can you give anti-D if sensitisation has already occurred?
Anti-D is pointless if maternal anti-D is already present > sensitization has already occurred
What is the only antibody that can cross the placenta?
IgG
How does rhesus disease present in mild and severe disease?
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)
How is the risk of rhesus disease identified?
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
How is the severity of foetal anaemia investigated in a foetus with rhesus disease?
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
How is foetal anaemia due to rhesus disease treated?
transfuse blood
deliver if >36wks
How is rhesus disease managed postnatally?
- 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?
What are the RFs for GD?
previous GD previous macrosomic baby BMI >30 ethnic origin FHx diabetes
How is pre-existing diabetes managed during pregnancy?
weight loss
stop hypoglycaemic agents except metformin + commence insulin
5mg folic acid/day until 12 wks
How is GD managed depending on fasting glucose level?
<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
What is the screening test for GD? Who has it? Whata re the cut-off scores?
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)
How is antenatal care different for women with GD?
- 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
How much folic acid should diabetic women take until 12wks?
5mg
Do pregnant women with pre-existing diabetes need extra antenatal care?
retinopathy screening at booking + 28wks
planned delivery between 37-39wks
continue managing diabetes as before pregnancy
When can women with GD stop their diabetic medication?
should improve immediately after birth = stop meds
test fasting glucose for 6wks after
existing diabetes - lower insulin = higher risk of hypoglycaemia
What events decrease and increase insulin sensitivity?
decrease = pregnancy
increase = after birth, breastfeeding
What are the 2 key complications of GD?
macrosomia > shoulder dystocia
neonatal hypoglycaemia - accustomed to large supply of glucose in pregnancy > cannot maintain usual supply with oral feeding
How is neonatal hypoglycaemia managed? What is the target blood sugar?
> 2mmol/L
IV dextrose + NG feeding
What is obstetric cholestasis?
reduced outflow of bile acids from liver which resolves after delivery
When is obstetric cholestasis likely to occur during pregnancy?
usually after 28wks
How does obstetric cholestasis present?
ITCHING (build up of bile in blood) - esp palms of hands/soles of feet
fatigue, dark urine, pale/greasy stools, jaundice
NO rash
What are causes of pruritus and deranged LFTs during pregnancy?
obstetric cholestasis
gallstones
acute fatty liver
AI or viral hepatitis
How will obstetric cholestasis present in bloods?
abnormal LFTs - esp ALT, AST, GGT
raised bile acids
A rise of which LFT with otherwise normal LFTs is normal during pregnancy?
ALP - produced by placenta
How is obstetric cholestasis treated?
ursodeoxycholic acid
itching mx with emollients + antihistamines
water-sol vit K if clotting deranged
Obstetric cholestasis is a/w with what risk to fetus?
still birth
monitor LFTs
consider planned delivery after 37wks depending on severity
Define monozygotic versus dizygotic twins
mono = identical twins from single zygote di = non-identical from two zygotes
Define mono versus dichorionic twins?
mono = share single placenta di = two separate placentas
What type of twin pregnancy have the best outcome?
diamniotic dichorionic
How can each type of twin pregnancy be determined on US?
dichorionic diamniotic = lambda sign (triangular)
monochorionic diamnoitic = T sign
monochorionic monoamniotic = no membrane between twins
What are the risks of multiple pregnancy to the mother?
anaemia polyhydramnios HTN malpresentation preterm birth/instrumental delivery/c-section PPH
What are the risks of multiple pregnancy to the fetus?
miscarriage/stillbirth growth restriction prematurity twin-twin transfusion syndrome twin anaemia polycythaemia sequence congenital abnormalities
What is twin-twin transfusion syndrome? Which type of twin pregnancy can it occur in?
monochorionic pregnancies
one fetus receives the majority of the blood from the placenta
What are the different risks to the recipient and donor fetus in twin-twin transfusion syndrome?
recipient: fluid overload > HF, polyhydramnios
donor: growth restriction, anaemia, oligohydramnios
What is twin anaemia polycythaemia sequence?
less acute than twin-twin transfusion syndrome
one twin becomes anaemic + one becomes polycythaemic
How are women with multiple pregnancy managed differently?
extra anaemia monitoring - FBC @ booking, 20 + 28wks
additional USs for growth monitoring
early planned birth depending on type of twin pregnancy
When/what type of delivery is aimed for in mono versus diamniotic twins?
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
How is prematurity classified?
<23: non-viable
<28: extreme preterm
28-32: very preterm
32-37: mod-late preterm
What are 2 methods of preventing preterm labour?
- vaginal progesterone - maintains pregnancy, decreases activity of myometrium + prevents cervix remodelling
- 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
What needs to be given after preterm prelabour ROM?
prophylatic abx for chorioamnionitis - erythromycin
induction from 34wks
What tests can check the likelihood of preterm labour if unsure/intact membranes?
TVUS - cervical length >15mm = unlikely fetal fibronectin (glue between chorion + uterus = in vagina during labour) <50ng/ml = unlikely
What measures are used to improve outcomes in preterm labour?
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)
What is tocolysis? What is the medication of choice?
stop uterine contractions to delay delivery
can be given between 24 + 34 wks
nidefipine
Why are antenatal steroids given in suspected preterm labour? What is an example regime?
develop fetal lungs > reduce RDS postnatally
can be given <36wks
2x dose IM betamethasone 24hrs apart
Why is MgSO4 given in suspected preterm labour? When must it be given?
help protect fetal brain > reduces risk of cerebral palsy
given within 24hrs of delivery in babies <34weeks
require monitoring for Mg toxicity
What causes a neural tube defect?
incomplete closure of the neural tube within 28 days of conception > birth defect of brain/spinal cord
What are the 3 most common NTDs?
anencephaly
spina bifida
encephalocele
What are the RFs for NTDs?
maternal folate/vit B12 deficiency previous hx of infant with NTD smoking diabetes obesity antiepileptic drugs
What is an important preventative method for NTDs?
400mcg daily folic acid before conception + until week 12
5mg daily for women at higher risk
When is the first prenatal US? What does it check for?
11-13 weeks
number of fetuses, heartbreat, crown rump length, nucha translucency, ovaries
What is the miscarriage risk in amniocentesis and CVS?
amnio: 1%
CVS: 1-2%
What can amniocentesis detect?
chromosomal abnormalities, infections eg CF, CMV, SCD, toxoplasmosis
How long does amniocentesis take compared to CVS?
3 weeks versus 2 days
What is CVS?
biopsy of trophoblast
What is hydrops fetalis?
abnormal fluid accumuldation in 2+ fetal compartments eg ascites, pleural effusion, pericardial effusion, skin oedema
What are the 2 types of hydrops fetalis and the main causes of each?
- immune - complication of severe Rh incompatability
- 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
How can hydrops fetalis be detected antenatally?
high AFV
abnormally large placenta
fluid causing swelling in/around organs - liver, spleen, heart, lungs
amniocentesis/frequent US to monitor severity
How is hydrops fetalis managed? What is the prognosis?
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
What is the difference between SGA and IUGR?
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
What are the causes of placenta mediated growth restriction?
idiopathic pre-eclampsia maternal smoking/alcohol anaemia malnutrition infection maternal health conditions
What are the causes of placenta mediated growth restriction?
ie pathology of fetus
genetic or structural abnormalities
fetal infection
errors of metabolism
What signs would indicate IUGR as the cause for a baby SGA?
reduced AFV
abnormal doppled
reduced movement
abnormal CTG
What are the short term complications of IUGR?
fetal death/stillbirth
birth asphyxia
neonatal hypothermia or hypoglycaemia
What are the long term complications of IUGR?
CVD, esp HTN
T2DM
obesity
mood/behavioural problems
Define SGA + severe SGA
<10th centile for their GA
severe = <3rd centile
based on estimated fetal weight + fetal abdo circumference
What factors are considered in a customised growth chart?
with women’s weight, height, ethnicity, parity
Define low birth weight
<2500g
What are the 2 causes of SGA?
- constitutionally small - match mothers/family, growing appropriately
- IUGR
What are the RFs for having a baby SGA?
previous SGA baby
obesity smoking diabetes existing HTN >35yrs antiphospholipid syndrome
pre-eclampsia
multiple pregnancy
low PAPPA
APH
Which women require serial growth scans for SGA monitoring?
symphisis fundal height fallen <10th centile from 24wks
3+ minor or 1+ major RFs
issues measuring SFH eg fibroids, high BMI
What is measured in serial growth scans of women with/at risk of a SGA baby?
serial US scans with umbilical artery doppler measuring:
EFW + AC
umbilical arterial pulsatility index
AFV
How is an SGA baby managed antenatally?
identify underlying cause
tx modifiable RFs
aspirin if risk of pre-eclampsia
serial growth scans
early delivery if growth static/other concerns + corticosteroids before
What ix are done to explore an underlying cause of SGA babies?
BP + urine dipstick (pre-eclampsia) uterine artery doppler scanning fetal anatomy scan karyotyping (chromosomal abnormalities) test for infections
Can pregnant women have the MMR vaccine?
NO - live vaccine
given before if planned/offer after giving birth
What window of pregnancy can congenital rubella syndrome occur?
maternal infection in 1st 20wks
risk highest <10wks
Why is chickenpox dangerous during pregnancy?
more severe case in mother eg varicella pneumonitis/heptitis/encephalitis
fetal varicella syndrome
severe neonatal varicella syndrome
If a pregnant woman is exposed to chickenpox during pregnancy and are not immune, what can they be treated with?
IV varicella IGs as prophylaxis within 10 days of exposure
How is chickenpox during pregnancy treated? When can it be?
oral aciclovir if present within 24hrs + >20wks
How does congenital varicella syndrome present? When does the infection have to occur?
<28wks
IUGR
microcephaly, hydrocephalus, LDs
scars/sig skin changes in specific dermatomes
limb hypoplasia
cataracts + inflammation in eye (chorioretinitis)
What type of bacteria is listeria? How is it transmitted?
gram +ve bact
transmitted by unpasteurised dairy products, processed meat, contaminated food = AVOID in pregnancy eg blue cheese + good food hygiene
How does listeriosis present in a pregnant woman?
much more likely in pregnant women
may be asymptomatic
flu-like illness
possibly pneumonia/meningoencephalitis
Why is listeriosis dangerous in pregnant women?
high rate of miscarriage/fetal death
severe neonatal infection
How is CMV transmitted?
via infected saliva/urine of asymptomatic children
How does congenital CMV present? How common is it?
most CMV in pregnancy don’t cause congenital CMV
IUGR
microcephaly, hearing/vision loss, LDs, seizures
How is toxoplasmosis transmitted?
usually contamination with faeces from a cat that is host of the parasite
How does toxoplasmosis present in a pregnant woman?
usually asymptomatic
What is the classic triad of congenital toxoplasmosis? When is the risk highest?
risk higher later in pregnancy
intracranial calcification
hydrocephalus
chorioretinitis
How does congenital parvovirus B19 present? When does parvovirus in pregnancy cause the most complications?
1st + 2nd trimesters
miscarriage/fetal death
severe fetal anaemia
hydrops fetalis
maternal pre-eclampsia-like syndrome (hydrops + placental oedema + maternal oedema)
Define cord prolapse
umbilical cord descends below presenting part of fetus into vagina, after ROM
What is the main danger in cord prolapse?
presenting part of fetus compresses cord = feta hypoxia
What is the most significant RF for cord prolapse?
abnormal lie after 37 wks - provides space for cord to prolapse below presenting part
When should cord prolapse be suspected?
fetal distress on CTG
confirm by vaginal exam
How is cord prolapse managed?
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
What is recommended after instrumental delivery to reduce risk of infection?
co-amoxiclav single dose
When is an instrumental delivery indicated?
failure to progress
fetal distress
maternal exhaustion
control of head in various fetal positions
What type of pain management during labor increases the risk of needing an instrumental delivery?
epidural
What are the increased risks to mother during an instrumental delivery?
PPH
episiotomy, perineal tears, injury to anal sphincter
incontinence
temporary nerve injury (obturator/femoral nerve)
What is the key risk to baby during a ventous delivery?
cephalohaematoma
What are the risks to baby during a forceps delivery?
key risk = facial nerve palsy
bruising on face fat necrosis (hardened lumps on cheeks)
What are the indications for an elective caesarean?
previous caesarean symptomatic after previous sig perineal tear placenta/vasa praevia breech multiple pregnancy uncontrolled HIV cervical Ca
What is a category 1 emergency caesarean? How long must the time to delivery be?
immediate threat to life of mother/baby
30 mins
What is a category 2 emergency caesarean? How long must the time to delivery be?
not an imminent threat to life but ceasarean required urgently due to compromise
75 mins
What is a category 3 emergency caesarean?
delivery required by mum/baby are stable
What is a category 4 emergency caesarean?
elective
What medications can be given before/during to reduce risks during a c-section?
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
What are the increased risks for future pregnancies caesarean?
repeat caeserean
uterine rupture
placenta praevia
stillbirth
What are the possible complications in the postpartum period after a caeserean?
PPH
wound infection/dehiscence
endometritis
What VTE prophylaxis methods should be considered for women post-caeserean?
early mobilisation
anti-embolism stockings
LMWH eg enoxaparin
What is the most common cause of shoulder dystocia?
macrosomia 2ndary to gestational diabetes
What are 2 key signs that failure to deliver the body is due to shoulder dystocia?
failure of restitution - head remains face down and doesn’t turn sideways
turtle neck sign - head delivered but retracts back into vagina
What techniques can be used to manage shoulder dystocia?
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
What are the 4 key complications of shoulder dystocia?
fetal hypoxia
brachial plexus injury + Erb’s palsy
perineal tears
PPH
What are the RFs for VTE in pregnancy?
smoking parity 3+ age >35 BMI >30 reduced mobility multiple pregnancy pre-eclampsia gross varicose veins family hx thrombophilia IVF
When should VTE prophylaxis be started from, in which women?
4+ RFs > 1st trimester
3 RFs > 28 wks
risk assessed at booking + after birth + extra if admission/surgery etc
What VTE prophylaxis is given to women at higher risk?
LMWH eg enoxaparin, dalteparin (continued until 6wks postnatally, temporarily stopped during labour)
if CI:
intermittent pneumatic compression
anti-embolic compression stockings
What are the key sx to look out for in a DVT?
UNILATERAL calf/leg swelling + tenderness + oedema + colour change
dilated superficial veins
How is leg swelling defined in a suspected DVT?
measure calf 10cm below tibial tuberosity
> 3cm difference between legs = significant
What are the key sx to look out for in a PE?
SoB cough +/- blood pleuritic chest pain hypoxia raised RR
tachycardia
low grade fever
haemodynamic instability
1st line ix for DVT?
doppler US
What are the 1st line and definitive diagnosis ix for PE?
1st line:
cxr
ECG
definitive:
CTPA = best
ventilation-perfusion scan
Is d-dimer helpful in pregnancy?
no - pregnancy is a cause of raised d-dimer
wells score not validated
How is a VTE in pregnancy managed?
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
What is the spectrum and timeline of postnatal mental health illness?
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
How long must sx last for a dx of postnatal depression?
2 wks
same triad as depression
How is mild, moderate and severe postnatal depression managed?
mild: additional support, self-help, follow-up with GP
mod: SSRI, CBT
severe: specialist services, possibly inpatient care in mother + baby unit
What is the screening tol for postnatal depression?
edinburgh scale
out of 30, >10 suggests PND
What is the risk to neonates if the mother has taken SSRIs during pregnancy?
neonatal abstinence syndrome
presents in 1st few days > irritability + poor feeding
supportive mx
Irregular menstruation indicates what about ovulation?
anovulation or irregular ovulation
What are the DDx of irregular menstruation?
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
What are the DDx of IMB?
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
What are the DDx of dysmenorrhoea?
primary dysmenorrhoea - no pathology
endometriosis/adenomyosis
fibroids
PID
cervical/ovarian cancer
copper coil
Define menorrhagia
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)
What is normal versus excessive menstrual blood loss?
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
What is abnormal versus dysfunctional uterine bleeding?
any variance of normal menstrual cycle on basis of frequency, regularity, duration or volume
+ dysfunctional = AUB dx after excluding pregnancy and pathology
What are the DDx of menorrhagia?
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
How to distinguish between placental abruption and praevia?
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
What is the pathway of tests for a male in an infertile couple?
semen analysis
if azoospermic > LH, FSH, serum karyotype
MRI brain to rule out pit/hypothalamic tumour
?arrested spermatogenesis > testicular biopsy
What is the most common type of vaginal cancer?
mets
primarily from cerix or endometrium
What is the most common type of primary vaginal cancer?
squamous cell carcinoma
less common = adenocarcinoma
Where is a vaginal cancer most likely to metastasise to?
lungs
liver
Positive routine asymptomatic bacteriuria screen in a pregnant woman. Next steps?
asymptomatic bacteriuria requires tx
contamination of 1st culture possible > confirm with 2nd test
Define oligo and polyhydramnios in terms of AFI?
poly: AFI >24cm or 2000ml+
oligo: AFI <5cm or <200ml
What are the causes of polyhydramnios?
most idiopathic
macrosomia
maternal diabetes
structural deformities of fetus
viral infectins
What is the most common treatable cause of recurrent miscarriage?
Anti-phospholipid syndrome (a/w SLE)
How does endometritis vs RPOC present as causes of 2ndary PPH?
both vaginal bleeding thats getting worse, lower abdo pain
endometritis = foul smelling discharge + fever (risk of sepsis) RPOC = odourless discharge, no fever unless infected
How does lochia present?
normal bleeding after pregnancy due to endometrium breaking down
bright red then darkens, gets less
For how many weeks are women considered infertile after pregnancy?
3wks
Exclusive breastfeeding after birth + amenorrhoea, does she need contraception?
lactational amenorrhoea covers for 6mo
Differential of itching in pregnancy?
obstetric cholestasis
acute fatty liver > can cause hepatitis
both in 3rd trimester
How to treat acute fatty liver?
admit
emergency c-section
What are the SEs of ERPOC?
endometritis ashermans (adhesions in the uterus due to trauma)
What contraception can be used straight after birth?
lactational amenorrhoea
POP/implant
When can a coil be inserted after birth?
within 48hrs
or after 4wks
What contraception should be avoided in breastfeeding?
COCP
How long after birth if not breastfeeding should the COCP be avoided?
6wks
How may Sheehan’s present?
woman struggling to breastfeed
necrosed pituitary > no prolactin
2nd repeat smear is HPV+ve with normal cytology, next step?
colposcopy
What is the diagnostic traid for HG?
> 5% weight loss
dehydration
electrolyte imbalance
What scoring system is used to determine the severity of HG?
PUQE - pregnancy unique classification of emesis
When in pregnancy is HG most likely?
8-12wks
can be up to 20wks
What conditions are a/w HG?
multiple pregnancy trophoblastic disease hyperthyroid nulliparity obesity
What is a protective factor for hyperemesis?
smoking
When should a pt with HG be admitted?
unable to keep down fluids/oral antiemetics
ketonuria +/- >5% weight loss despite oral antiemetics
confirmed/suspected comorbidity
How is HG treated?
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
Tx for urge incontinence
- bladder retraining
2. muscarinic antagonist: oxybutynin, tolterodine, solifenacin
When must methotrexate be stopped before pregnancy?
stopped in both partners 6mo before conceiving
inhibition of dihydrofolate reductase affects DNA synthesis
What medication can be used to reduce fibroid size before surgery?
GnRH agonist eg triptorelin
What usually happens to BP in pregnancy?
falls in 1st tri, continues to fall until 20-24wks
then increases to pre-pregnancy levels by term
Women at high risk of pre-eclampsia should take what medication?
aspirin 75mg from 12wks - birth
Which women are high risk for pre-eclampsia?
hypertensive disease in previous pregnancies
CKD
AI disease
DM
How should gestational HTN be treated?
- oral labetalol
2. nifedipine
What is the most common cause of cord prolapse?
AROM
Which abx is used for GBS prophylaxis? When is it given?
IV benzylpenicillin
women with a previous pregnancy with neonatal sepsis
remember strep agalactiae is a GBS
What are the differentials of postcoital bleeding?
cervical cancer/ectropion/infection trauma atrophic vaginitis polyps endometrial/vaginal cancer
What are fibroids?
benign oestrogen-sensitive smooth muscle tumours in the uterus
How do fibroids present?
mostly asymptomatic
HMB!! + prolonged bleeding cyclical pelvic pain, deep dyspareunia bloating, feeling full urinary + bowel sx O/E: pelvic masses, enlarged firm uterus infertility
How are fibroids investigated?
submucosal fibroid presenting with HMB > hysteroscopy
larger fibroids > pelvic US
before surgery > MRI
How are fibroids <3cm managed?
1st line = mirena
+ sx mx with NSAIDs/tranexamic acid
alternatives = COCP/cyclical prog
surgical options: endometrial ablation, resection during hysteroscopy, hysterectomy
How are fibroids >3cm managed?
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
Which is the only treatment of fibroids known to potentially increase fertility?
myomectomy
Which medication can be given short-term before surgery to reduce the size of fibroids?
GnRH agonist eg goserelin, leuprorelin > menopausal state > oestrogen > reduce size
What are the possible complications of fibroids?
infertility HMB red degeneration torsion malignant change (rare) miscarriage/preterm birth if pregnant
constipation
urinary obstruction, UTIs
What is red degeneration of a fibroid?
necrosis, infarction and ischaemia of a fibroid during pregnancy
When in pregnancy is red degeneration of a fibroid likely to happen? Why?
2nd/3rd trimester
in larger fibroids
rapidly enlarges during pregnancy > outgrows blood supply
How does red degeneration of a fibroid present?
severe abdo pain
low grade fever
vomiting
tachycardia
How is red degeneration of a fibroid managed?
supportive: rest, fluids, analgesia
What are functional ovarian cysts?
related to fluctuating hormones
majority benign
very common in premenopausal women
What is the traid a/w Meigs syndrome?
- benign ovarian fibroma
- pleural effusion
- ascites
resolves on tumour resection
How do ovarian cysts present?
usually asymptomatic
pelvic bloating/pain/fullness
mass felt
disrupted menstruation
acute pain > torsion, rupture, haemorrhage
Name the 6 types of ovarian cysts
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
What is there an increased risk of with dermoid cysts?
torsion
How are ovarian cysts investigated?
1st line = USS
pre-men + simple cyst + <5cm: no further ix
CA-125
if <40 + complex cyst > dermoid cyst markers = lactase dehydrogenase, AFP, hcg
Which 3 factors make up the risk of malignancy index for ovarian cysts?
menopause status
USS findings
CA-125
How are ovarian cysts managed?
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
What are the complications of ovarian cysts?
haemorrhage
rupture > bleed into abdomen
torsion
How should HMB be investigated?
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
How is non-pathological HMB managed?
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
Define the 3 criteria used to make a dx of PCOS?
Rotterdam crtieria: 2/3 needed
1. oligo/anovulation
2. hyperandrogenism - biochemical or sx eg hirsutism
3. polycystic ovaries on US
How is a woman with PCOS likely to present?
oligo/amenorrhoea
infertility
obesity
hirsutism
acne
hair loss in a male pattern
insulin resistance
What are the DDx of hirsutism?
PCOS
meds eg phenytoin, ciclosporin, steroids, testosterone
ovarian/adrenal tumours that secrete androgens
cushing’s
CAH
How does insulin resistance in COS drive hyperandrogenism and anovulation?
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
What are the key blood test changes in PCOS?
high LH
high LH:FSH
high testosterone + insulin
normal/high oestrogen
What is the diagnostic US criteria for PCOS?
TVUS
follicles around periphery of ovary = string of pearls
12+ developing follicles in 1 ovary
ovarian volume >10cm3
How is the increased risk of obesity/T2DM/high cholsterol/CVD in PCOS managed?
weight loss, diet, exercise, smoking cessation, BP control, statins
- orlistat = lipase inhibitor to aid weight loss in women with BMI >30
Which gynae cancer are women with PCOS at high risk of?
endometrial
anovulation = don’t produce sufficient prog = unopposed oestrogen + endometrial proliferation
How is the increased risk of endometrial cancer managed in PCOS? When should it be monitored?
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
How is infertility managed in PCOS?
- weight loss
- clomifene
- laparoscopic ovarian drilling
- IVF
(some evidence metformin + letrozole restore ovulation)
What blood tests are done at booking and 28wks?
FBC (anaemia)
blood group, rhesus, red cell alloantibodies, haemoglobinopathies
hep B, HIV, syphillis
How is GD managed depending on fasting glucose level?
<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
For how long after delivery/last seizure should MgSO4 be continued in a woman with eclampsia?
24hrs
How is endometrial hyperplasia managed?
simple > high dose prog eg LNG-IUS + repeat sampling in 3/4m
atypia > hysterectomy advised, in postmenopausal women > total hysterectomy with bilateral salpingo-oopherectomy
What can be given when a cord prolapse is identified whilst waiting for an LSCS?
terbutaline
Define menopause
amenorrhoea >1yr
What are the 4 CI to menopause?
undiagnosed vaginal bleeding
oestrogen sensitive cancer
current/past breast ca
untreated endometrial hyperplasia
What must be avoided in HRT to women with a uterus?
unopposed oestrogen > risk of endometrial ca
What HRT can be given if a woman does not have a uterus?
oestrogen only, as a patch or orally
What can HRT increase the risks of?
VTE/stroke (all oral forms, not transdermal)
CHD (combined forms)
breast ca (combined forms)
ovarian ca
What HRT is preferred in women with increased risk of VTE?
transdermal
What HRT is preferred in women with migraine and aura?
transdermal
What regime of HRT should be given to women with definite menopause versus before?
amenorrhoea >1yr = continuous regime
before = cyclical (oestrogen daily, prog for a few weeks of the cycle)
Which contraception is licensed as the prog part of HRT?
mirena - only need oestrogen on top
licensed for 4yrs
