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)
