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1a - Finals pt 2. > Obstetrics + Breast > Flashcards

Obstetrics + Breast Flashcards

1
Q

briefly describe the implantation stage of the development of the placenta

A
  • develops from the trophoblast that surrounds the fetus
  • 6 days after fertilisation, the blastocyst binds to endometrial lining, trophoblast grows and differentiates to form 2 layers (cytotrophoblast and syncytiotrophoblast)
  • syncytiotrophoblast develops finger-like projections (chorionic villi) that invade endometrium to hold the blastocyst in place
  • this syncytiotrophoblast produces bHCG by second week - used for pregnancy testing, needed to enable corpus luteum to produce progesterone until placenta is fully developed at week 12
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2
Q

briefly describe the post-implantation lacunar phase of placental development

A
  • on day 9, the syncytiotrophoblast forms lacunae (spaces) within it
  • also, it erodes maternal tissues so that blood from uterine spiral arteries flows in and fills these lacunae
  • this supplies oxygen and nutrition to blastocyst via diffusion - this is the early maternal circulation in the developing placenta
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3
Q

briefly describe the post-implantation development of the chorionic villae in the placenta

A
  • syncytiotrophoblast invades into endometrium, forming chorionic villi, with the cytotropholast invading into the villi behind that to form an inner layer
  • mesenchyme from embryo then invades into the villi, forming core of connective tissue (now got 3 layers)
  • mesenchyme then forms blood vessels that link up with newly formed fetal circulation

placenta now has blood supply from mum and fetus for more efficient exchange of nutrients, gases and waste products

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4
Q

briefly describe the further development of the villi/placental circulation, after the formation of tertiary villi

A
  • as villi are forming, cytotrophoblast extends through the syncytiotrophoblast at tip of each villus - these are now in direct contact with endrometrial cells, forming a cytotrophoblast shell that holds embryo in place
  • this shell stays connected at the top of chorionic villi, which are surrounded by maternal blood in the lacunae - this is the site of exchange between fetal and maternal blood
  • as placenta grows, lacunae become supplied by spiral arteries and endometrial veins (burrow into spaces and become larger with more flow)
  • remodelling of spiral arteries creates high flow, low resistance system - if this goes wrong, you might see pre-eclampsia, IUGR, late sporadic miscarriage
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5
Q

which part of the development of placental circulation goes wrong in pre-eclampsia?

A

the remodeling of spiral arteries to create a high flow, low resistance system

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6
Q

describe the vasculature transporting blood between fetus and placenta

A

two umbilical arteries, one umbilical vein

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7
Q

describe the structure of the placenta

A
  • maternal blood enters large lacunae from spiral arteries and is drained by endometrial veins
  • there’s NO mixing of maternal and fetal blood in placenta
  • 2 layers separate fetal and maternal blood in villi, a thin syncytiotrophoblast layer, and a single layer of endometrium in the fetal capillary
  • this allows for rapid diffusion between the two circulations
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8
Q

what is the key function of the placenta?

A

supplies the requirements of the developing fetus, while maintaining an environment in which fetus can grow.

has a high metabolic rate which is useful for protein synthesis, active transport and growth

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9
Q

describe how gas transport occurs between fetus and placenta

A

O2 and CO2 transported to fetus by passive diffusion.
rapid metabolism of fetus uses up lots of O2 so maintains the concentration gradient compared to maternal blood.
fetal Hb also has high O2 affinity than HbA

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10
Q

when is the implantation window?

A

days 6-10

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11
Q

describe how nutrient transport occurs between fetus and placenta

A

combo of passive facilitated diffusion and active transport.
towards the end of pregnancy, excess of nutrients is transported so the fetus can develop gylcogen/fat stores (incl. brown adipose, which then gets broken down early in neonatal life to generate heat)

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12
Q

describe the role of the placenta in immune protection

A

fetus inherits mostly paternal MHC gene products, so mum’s immune system sees fetus as ‘non-self’
placenta acts as a barrier to prevent immune rejection - syncytiotrophoblast cells as the fetal-maternal interface don’t have MHC antigens so don’t reject baby

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13
Q

what is capacitation?

A

occurs in the process of fertilisation. changes in sperm cell membranes, results in change of tail movement and allows the acrosome reaction to occur.

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14
Q

what is the acrosome reaction?

A

exposed acrosome enzymes in sperm erode the zona pellucida to allow fertilisation.
once sperm and egg have fused, changes in zona pellucida occur to block polyspermy

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15
Q

where does fertilization occur? what mechanisms aid sperm transport to this place?

A

ampulla of the fallopian tube

transported by sperm motility + oxytocin make uterus contract

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16
Q

describe the development from zygote –> blastocyst

A

zygote = the newly combined sperm and egg.
rapidly divides to form morula (16-32 cells) = ball of cells surrounding a yolk sac
morula develops into blastocyst - cells rearrange themselves into two layers, the inner cell mass (embryoblast, goes on to form the embryo) and the trophoblast.(forms placenta) - blastocyst implants on day 6-7

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17
Q

describe the physiological adaptations to pregnancy seen in the respiratory system

A
  • needs to improve oxygenation and CO2 clearance to support fetus
  • lots of women get SOB in pregnancy - because uterus elevates diaphragm by c.4cm, get a decreased reserve vol. and feel out of breath
  • but - rib cage circumference expands (relaxin), and minute volume increases so they are fine
  • pregnant women live in state of compensated respiratory alkalosis - to do with lowering Co2 in blood to maintain conc gradient so that it’s removed from fetus
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18
Q

describe the physiological adaptations to pregnancy seen in the cardiovascular system

A

increase in progesterone decreases vascular resistance. results in increased cardiac output.
there’s also activation of the RAAS, resulting in retention of sodium, meaning blood volume increases (physiological anaemia).
constriction of peripheral blood vessels - some women get Raynaud’s.
palpitations are common and pretty normal.
there’s ECG changes but cba to learn them.

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19
Q

describe the physiological adaptations to pregnancy seen in the urinary system

A
  • kidneys get bigger
  • GFR increases in first trimester, then falls again - this is responsible for increased urination in first trim, but later in pregnancy that’s due to compression of bladder
  • renal blood flow increased - increased clearance of most substances.
  • glycosuria is normal
  • increased risk of stasis (progesterone relaxes smooth muscles of bladder), increases risk of UTI
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20
Q

describe the physiological adaptations to pregnancy seen in the skin

A

increased oestrogens can lead to hyperpigmentation, striae gravidarum etc

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21
Q

describe the physiological adaptations to pregnancy seen in the MSK system

A
  • often see changes in posture and gait

- ligaments are softened (progesterone, relaxin) - pubic symphysis

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22
Q

describe the physiological adaptations to pregnancy seen in the GI tract

A
  • nausea (morning sickness) - resolves by weeks 16-18
  • progesterone relaxes gut muscle, leads to decreased motility, which leads to constipation and reflux
  • less smooth muscle activity in gallbladder raises risk of stones
  • loads of women get heartburn - due to reduced motility and also big uterus pushing stomach up
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23
Q

describe the physiological adaptations to pregnancy seen in the reproductive system

A
  • enlarging of the uterus (occurs via hypertrophy of cells, not hyperplasia)
  • increased uterine blood flow
  • uterus split into upper and lower segments from 3rd trimester
  • cervix has an increase in vascularity, swollen, softer
  • late in gestation, prostaglandins remodel the cervical collagen
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24
Q

describe the physiological adaptations to pregnancy seen in the breasts

A
  • deposition of fat around glandular tissue, and no. glandular ducts increases
  • prolactin prepares alveoli for milk production, and is needed for stimulation of milk secretion
  • oestrogen during pregnancy suppresses milk secretion - rapidly falls within first 48h, so that’s when milk comes in
  • early suckling helps stimulate pituitary to release prolactin and oxytocin, to initiate lactation
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25
Q

describe the physiological adaptations to pregnancy seen in the endocrine system

A
  • prolactin = anterior pituitary
  • oxytocin = produced hypothalamus, stored posterior pituitary
  • thyroid = stimulated by bHCG - can imitate thyrotoxicosis
  • adrenals = produce more renin and cortisol
  • hCG = produced in massive amounts by syncytiotrophoblast, acting to maintain corpus luteum until placenta can take over - peaks days 8-10 then decreases
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26
Q

what are the three stages of labour/delivery?

A

first stage = between onset of regular contractions and the full dilation of the cervix
second stage = between full dilation to delivery of baby
third stage = from delivery of baby to delivery of placent

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27
Q

what 3 mechanical factors determine progress in labour?

A

3 Ps:
Powers - degree of uterine force
Passage - dimensions of pelvis and resistance of soft tissues
Passenger - dimensions of fetal head/fetal position

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28
Q

what are the three principle planes of the pelvic passage?

A

inlet - transverse diameter is 13cm, AP 11cm
mid-cavity - almost round, similar transverse and AP diameters
outlet = AP diameter (12.5cm) > transverse diameter (11cm)

so baby has to turn head as it passes through

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29
Q

what are the ‘stations’ involved in labour?

A 
station = level of head on vaginal examination, measured in relation to ischial spines
station 0 = head level with spines
station -2 = head 2cm above spines
station +2 = head 2cm below
etc
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30
Q

when is labour diagnosed?

A

painful regular contractions in presence of a fully effaced cervix, which is 4cm or more dilated, with or without a show or ruptured membranes

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31
Q

at what rate would you expect cervical dilatation to occur?

A

roughly 1-2 cm/hour but it’s very variable (lots faster if multiparous)
charted on partogram - highlights slow progress/failure of presenting part to descend (stations)

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32
Q

what 4 bones make up the bony pelvis?

A
  • two innominate bones
  • sacrum
  • coccyx
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33
Q

which part of the body is responsible for the propulsive contractions that deliver a fetus?

A

upper segment of the uterus

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34
Q

what causes effacement of the cervix?

A

contractions generated by upper segment of uterus - it retracts (tightens down), causing lower segment to stretch and thin out

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35
Q

how does a fetus ‘normally’ engage/present for deliver?

A

usually occipito-transverse or occipitio-anterior position
as labour progresses, neck flexes so the suboccipitiobregmatic diameter is presenting (top of head, smallest diameter at c.9.5cm).

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36
Q

describe the movement of the fetus through the birth canal in a typical OA presentation

A

suboccipitiobregmatic diameter presenting.
as baby descends, internal rotation brings the occiput into the anterior position when it reaches pelvic floor.
occiput descends below symphysis pubis, then extension of neck around the pubic bone delivers the face (facing floor).
delivery of head brings shoulders into pelvic cavity - baby then restitutes (external rotation) - head turns relative to shoulders, brings shoulders down further and they rotate into pelvic outlet, passing anterior shoulder under pubis (assisted by gentle downward traction on head).
lateral flexion of fetus deliver posterior shoulder, rest of body follows.

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37
Q

describe the components of routine assessment of a woman presenting in first stage of labour

A

Mum - vital signs, urinalysis, analgesia requirements
Baby - fetal HR pattern (intermittent auscultation or CTG if worried)
Abdo palpation - fetal size/lie/presentation/engagement
Contractions - frequency/duration/intensity
vaginal exam - cervical effacement and dilatation, station and position of presenting part, presence of caput or moulding
liquor - clear, blood stained, meconium

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38
Q

give some examples of analgesia used during labour and when it might be indicated

A

oxygen/NOS - first stage, inhaled
pethidine - first stage, IM injection
pudendal block - second stage, for operative delivery
perineal infiltration - second stage, prior to episiotomy
epidural anaesthesia - first/second stage, C section
spinal anaesthesia - operative delivery, manual removal of the placenta

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39
Q

what are the active vs passive phases of the first stage of labour?

A 
passive = first 3cm, can take several hours
active = 3-10cm, should be 1-2cm dilation an hour, shouldn't last >12 hours
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40
Q

what are the passive vs active phases of the second stage of labour?

A

passive is from fully dilated until the head hits pelvic floor and woman feels urge to push (lasts only a few mins)
active stage is when mum is pushing - if this takes >1h, spontaneous delivery is unlikely

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41
Q

describe the third stage of labour

A

delivery of placenta - usually takes 15 mins.
blood loss up to 500ml.
uterine muscle fibres contract to compress blood vessels to placenta which shears away from uterine wall.

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42
Q

describe the typical active management of the third stage of labour

A

usually IM syntocinon (oxytocin) given with delivery of shoulder.
cord is clamped and cut.
controlled cord traction used once placenta has separated from uterus (involves fundal pressure too I think).
placenta and membranes checked to ensure complete, vagina/labia/perineum checked and estimated blood loss recorded.

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43
Q

give some fetal and maternal indications for induction of labour

A

maternal - severe pre-eclampsia, pre-existing disease (e.g. diabetes), social
fetal - prolonged pregnancy, IUGR, rhesus disease

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44
Q

what is the Bishop score?

A

used to assess cervix prior to induction of labour (higher score reflects more favourable cervix)

  • unfavourable cervix = hard, long, closed, not effaced
  • favourable cervix = soft, beginning to dilate and efface
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45
Q

describe different methods used in induction of labour

A

prostaglandins - prostaglandin E2 vaginal gel, helps ripen cervix
amniotomy - artificial rupture of membranes using amnihook, used in induction and also to accelerate slow progress in labour
oxytocin - IV infusion of oxytocin (syntocinon) often used, stimulates contractions after amniotomy/spotaneous rupture of membranes

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46
Q

what factors related to the Passages might cause failure to progress?

A

Pelvis - abnormal shape (loads of causes e.g. osteogenesis imperfecta, cephalopelvic disproportion (suspect if head not engaging, small woman)
Soft tissues - uterine malformation, failure of cervical dilation, past vaginal surgeries, vulva (FGM)

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47
Q

what factors related to the Passenger might cause failure to progress?

A

fetal size - if they’re chunky
fetal abnormality - esp with neck/skull
fetal malposition - if in OT or OP position
fetal malpresentation - non-vertex e.g. face, brow, breech, shoulder

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48
Q

what factors indicate that Power is the issue causing failure to progress?

A

monitored by uterine palpation and CTG (although CTG readings altered by position of monitor)
diagnosed with insufficient uterine poser if labour is prolonged and contractions are uncoordinated, fewer than 3-4 in 10 min, lasting less than 60s, pressure less than 40mmHg.

exclude other problems!!! then careful use of IV syntocinon

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49
Q

define malpresentation

what are the common malpresentations?

A

anything other than vertex presentation
vertex = area between parietal eminences and the anterior and posterior fontanelles.

most common = breech
others = shoulder, brow, face

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50
Q

what is the key risk factor for a breech presentation?

A

prematurity!
risk at term = 3%
at 32 weeks = 15%
at 28 weeks = 25%

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51
Q

what are the three types of breech presentation?

A

extended/frank breech - around 50% - hips flexes and knees extended (feet right up by head)
flexed/complete breech - bent at knees and hips
footling breech - feet presenting

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52
Q

how do you diagnose a breech presentation?

A

head felt as large lump at fundus
auscultation of fetal heart at higher level than usual
vaginal examination (palpation of buttocks as presenting part if in labour)
ULTRASOUND is diagnostic

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53
Q

what are the possible complications of a breech presentation?

A

big risk of entrapment of head, cos body is softer and smaller so will get through a smaller pelvis than a head will - compression and decompression of head in pelvis can injure the brain.
perinatal mortality due to prematurity, cord prolapse, birth trauma, congenital anomaly
perinatal morbidity - nerve palsies, fractures etc

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54
Q

how do you manage a breech presentation?

A

recommendation is trial of ECV at 36-37 weeks, followed by ELCS if unsuccessful.
planned vaginal breech delivery is risky but can be performed by skilled midwife - not current recommendation.

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55
Q

list some contra-indications to external cephalic version

A 
pelvic mass
antepartum haemorrhage
placenta praevia
previous C section
multiple pregnancy
rupture membranes
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56
Q

what is external cephalic version?

A

attempt to turn fetus to a cephalic presentation by manual manipulation - should be done on labour ward (risk of fetal distress needing immediate delivery - give anti-D if indicated). can use tocolytics and ultrasound as well.

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57
Q

describe baby’s position in a transverse lie. what is the most serious complication you’re likely to see?

A

long axis of baby is transverse/oblique - sideways basically - shoulder is most likely to present
risk is of cord prolapse - associated with spontaneous rupture of membranes.

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58
Q

what is an unstable foetal lie?

A

when it’s different every time it’s palpated/assessed

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59
Q

what factors are associated with a transverse lie (alongside those associated with malpresentation in general)?

A

multiparity - poor tone of uterus and abdo wall
premature labour
second twin

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60
Q

what factors are associated with malpresentation?

A

maternal - contraction of the pelvis, pelvic tumour, Mullerian abnormality, multiparity
fetoplacental - placenta praevia, polyhydramnios, multiple pregnancy, fetal anomaly

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61
Q

how do you manage a mother with a baby in transverse lie?

A

try ECV
if not C section probs best bet
if unstable lie - expectant management at term as often converts to cephalic presentation.
if multiple pregnancy and second twin transverse - don’t rupture membranes, try and do ECV to longitudinal lie and then deliver as usual

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62
Q

can you deliver a face presentation baby vaginally?

A

if it’s metoanterior (chin forward) then yes, but metoposterior won’t
delivery occurs by flexion of head - deliver essentially as for vertex - warn parents of bruising to face, try not to poke baby in eye/splash with antiseptic during vaginal exams

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63
Q

can you deliver a baby in brow presentation vaginally?

A

not normally as an average-sized fetus will have a brow diameter that’s wider than normal pelvis - obstructed labour.
if small baby/big pelvis - manage expectantly, might present face or vertex

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64
Q

give some indications for an episiotomy

A

maternal - FGM, previous perineal reconstructive surgery

fetal - instrumental delivery, breech delivery, shoulder dystocia, abnormal CTG

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65
Q

briefly describe how an episiotomy is carried out

A

ensure adequate analgesia - epidural or perineal infiltration with local anaesthetic
start in midline at posterior fourchette, then incision is made mediolaterally (diagonally) - harder to repair than midline incision, but protects anal sphincter

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66
Q

describe the classification of perineal trauma

A

1st degree - skin only
2nd degree - skin and perineal muscle
3rd degree - partial/complete rupture of anal sphincter
4th degree - as for 3rd degree, but + anal mucosa

some 1st degree tears can be left to heal themselves if not actively bleeding. the rest require a repair.

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67
Q

give some indications for a ventouse delivery

A

maternal - delay in 2nd stage due to maternal exhaustion

fetal - delay in 2nd stage due to fetal malposition (OP or OT position), abnormal CTG

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68
Q

list the 5 criteria that must be met before an instrumental delivery is performed

A
  1. adequate analgesia - perineal infiltration/pudendal block/epidural
  2. abdo exam - head either 1/5 or 0/5 palpable
  3. vaginal exam - fully dilated cervix, head at/below ischial spines, known fetal position
  4. adequate maternal effort and regular contractions needed for ventouse
  5. empty bladder needed for forceps

if head is above ischial spines - has to be a c section!

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69
Q

briefly describe the technique used in a ventouse delivery

A

cup applied in midline, avoiding vaginal mucosa. pressure applied. traction used in time with maternal contractions and effort - initially downwards, then changing angle up as head crowns

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70
Q

give some indications for a forceps delivery

A

maternal - medical conditions complicating labour, unconscious mother/motherotherwise unable to assist with delivery
fetal - gestation <34 weeks, face presentation, known or suspected fetal bleeding disorder

non-rotational forceps only suitable for direct OA or OP presentation

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71
Q

give some maternal complications of instrumental delivery

A

genital tract trauma, risk of haemorrhage and/or infection

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72
Q

give some fetal complications of instrumental delivery

A

ventouse - chignon (scalp oedema) or cephalohaematoma (subperiosteal bleed)
forceps - bruising, facial nerve palsy, depression skull fracture

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73
Q

give some maternal indications for a LSCS

A 
two previous LSCS
placenta praevia
maternal disease e.g. fulminating pre-eclampsia
maternal request
active primary genital HSV
HIV - where viral load high
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74
Q

give some fetal indications for a LSCS

A

breech
twin pregnancy if first twin not cephalic presentation
abnormal CTG or FBS
cord prolapse
delay in first stage of labour e.g. due to malpresentation/malposition

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75
Q

briefly describe the procedure of an LSCS

A

ideally 39+ weeks gestation (reduces risk of TTN in baby)
regional analgesia e.g. spinal/epidural
low transverse skin incision, rectus sheath cut and muscles divided, uterovesical peritoneum incised so bladder can be reflected inferiorly, lower uterine segment incised transversely and baby taken out.

IV oxytocin given by anaesthetists, placenta and membranes removed. uterus closed in two layers with absorbable sutures.

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76
Q

give some possible complications of an LSCS

A

haemorrhage - always send a group and save, cross-match if high risk for bleed
gastric aspiration - risk if GA used, or in emergency when hasn’t be NBM
visceral injury - damage to bladder or bowel
infection
thromboembolic disease
future pregnancy - VBAC or repeat operations with increasing risk of complications

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77
Q

when might a trial of a VBAC be considered? what extra measures would be done in labour?

A

if LSCS was done for a non-repeatable cause (e.g. cord prolapse), if counselled appropriately for risk of needing CS.
extra measures basically just preparing in case of scar rupture necessitating immediate C section - cannula, FBC, group and save, continuous CTG etc

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78
Q

define preterm labour

differentiate this from ‘threatened’ preterm labour

A

labour occurring after 24 week and before 37 weeks gestation

if uterine contractions but cervix is closed = threatened

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79
Q

what drug should ideally be given to mum to protect baby’s lungs if preterm labour is suspected

A

corticosteroids - IM betamethasone x2 injections, 12 hours apart - ideally.
reduces neonatal respiratory distress by stimulating fetal surfactant.

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80
Q

give some risk factors for preterm labour

A 
BMI <19
low SE status
unsupported
afro-caribbean ethnic group
extremes of reproductive age (<20 or >35 yrs)
domestic violence
smoking
*prev preterm labour*
BV
chronic medical conditions
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81
Q

give some cause of preterm labour

A
  • infection (20%) e.g. chorioamnionitis, maternal pyelophritis/appendicitis
  • uteroplacental ischaemia e.g. abruption
  • uterine overdistension e.g. polyhydramnios, multiple pregnancy
  • cervical incompetence
  • fetal abnormality
  • iatrogenic (1/3rd) - when obs think delivery is necessary for fetal or maternal health
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82
Q

list some pathogens implicated in infective causes of preterm labour

A
  • sexually transmitted - Chlamydia, Trichomonas, Syphilis, Gonorrhoea
  • Enteric organisms - E coli, Strep faecalis
  • BV - Gardnerella, Mycoplasma and anaerobes
  • Group B Strep (if very growth)
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83
Q

what is tocolysis? what drugs might be used?

A

attempting to use drugs to stop contractions and delay delivery (by up to 24-48h) - gives time for steroids to work and for transfer to another hospital if needed.

drugs - atosiban, nifedipine, ritodrine, salbutamol, indomethacin, GTN patches

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84
Q

give some situations which would suggest tocolysis to delay preterm labour is inadvisable

A
  • maternal illness that would be helped by delivery e.g. pre-eclampsia
  • evidence of fetal distress
  • chorioamnionitis
  • if there’s significant vaginal bleeding
  • if membrane’s have ruptured
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85
Q

what is cervical cerclage?

A

used in cases of preterm labour where cervical incompetence means there’s cervical dilation but patient isn’t actively labouring
suture placed in cervix to minimise prolapse of membranes

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86
Q

what is the role of antibiotics in preterm labour?

A

prophylactic erythromycin given if membranes have ruptured before term
if membranes intact, woman should be swabbed and given abx if needed

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87
Q

does preterm labour affect mode of delivery used?

A

C section rate might be higher - more due to higher incidence of low-lying placenta, fetal distress and abnormal lie in prematurity.

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88
Q

how does a preterm labour/delivery affect management of future pregnancies?

A

doesn’t really - high risk for another preterm labour so be aware of that.

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89
Q

describe basic management of a mother presenting with preterm rupture of membranes (PROM)

A

admit her for 48h as massive risk of preterm labour - rule out chorioamnionitis/sepsis.
give steroids to protect baby’s lungs
erythromycin prophylaxis to prevent ascending infection

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90
Q

what is preterm rupture of membranes (PROM)?

A

when the membranes rupture, causing flooding/leaking of amniotic fluid, before the baby is term - may or may not be accompanied by preterm labour.

risk is of infection and preterm delivery

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91
Q

what are the two different categories you might put a foetus that is small-for-dates into?

A

small for gestational age - small for their age, but continuing to grow at a normal rate

IUGR - foetus is small or normal sized but growth rates slowing as pregnancy advances

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92
Q

what placental factors could cause a foetus to be small for gestational age?

A

abnormal trophoblast invasion - pre-eclampsia, infarction, abruption
causes asymmetrical growth restriction with head sparing and reduced abdo circumference

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93
Q

what foetal factors could cause a foetus to be small for gestational age?

A

genetic abnormalities, esp. trisomies 13, 18 and 21, Turner syndrome
congenital anomalies
infection e.g. CMV, rubella
multiple pregnancy

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94
Q

list the major risk factors for having a small-for-gestational age baby.
how would the antenatal care of these women be managed?

A 
maternal age >40
smoker
cocaine use
previous SGA baby
prev still birth
maternal/paternal SGA
chronic hypertension
diabetes
renal impairment
antiphospholipid syndrome
heavy antepartum bleeding
pre-eclampsia

refer for consultant-led care and have serial US measurements of fetal size, incl umbilical artery Doppler from 26-28 weeks

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95
Q

in considering risk of small for gestational age babies - who should be referred for serial growth scans?

A

women with a single “major” risk factor - serial US, umbilical artery Doppler at 26-28 weeks.
women with 3+ “minor” risk factors - Doppler at 20-24 weeks, then serial scans if abnormal

any single fundal height measurement <10th centile or incident of static growth should prompt refer for USS - use funal height charts generated for the mum based on her height, age etc etc

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96
Q

list some minor risk factors for having a small-for-gestational age baby

A 
maternal age >35
nulliparity
BMI <20
IVF
pregnancy-induced hypertension
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97
Q

what is the definition of large vs small for gestational age

A 
small = estimated fetal weight OR abdo circumference <10th centile for their gestational age
large = above 95th centile in estimated fetal weight
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98
Q

define gestational diabetes

A

‘carbohydrate intolerance which is diagnosed in pregnancy and may/may not resolve after pregnancy’
fasting glucose >7mmol/L
>7.8mmol/L 2 hours after a 75g glucose load at glucose tolerance test (NICE)

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99
Q

who is screened for gestational diabetes / how is it diagnosed in pregnancy?

A

oral glucose tolerance test at 24-28 weeks (or ASAP after booking if prev gestational diabetes or glycosuria).

screen women with RFs:
BMI >30
prev macrosomic baby >4.5kg
FHx diabetes
minority ethnic family origin with a high prevalence of diabetes
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100
Q

what are the possible foetal complications of mum having diabetes?

A

increased risk of - congenital abnormalities, risk of preterm labour
foetal lung maturity reduced at any age
MACROSOMIA - fetal pancreatic islet cell hyperplasia leads to hyperinsulinaemia and fat deposition - also increased urine output and polyhydramnia
risk of dystocia/birth trauma due to giant baby
more likely to have fetal compromise/distress/death

NB - these typically affect mothers with T1/T2DM rather than gestational diabetes

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101
Q

what are the possible maternal complications of pregnancy with diabetes?

A 
raised insulin requirements
ketoacidosis - rare, but hypos common
UTI and other infections more common
pre-eclampsia more common
C section/instrumental more likely
diabetic retinopathy can deteriorate in pregnancy
102
Q

describe how pre-existing diabetes changes antenatal management for a pregnancy mother?

A

needs precise glucose control and more fetal monitoring - check levels multiple times a day, aim for <6mmol/L.
baby has usual scans and fetal echo - might need serial growth scans
low dose aspirin daily from 12 weeks to reduce risk of pre-eclampsia
deliver by 39 weeks - elective LSCS is estimate fetal weight >4kg

neonate often hypoglycaemic - breastfeeding strongly encouraged

103
Q

how would you manage a mother with gestational diabetes?

A

encourage diet and exercise
regular glucose monitoring
metformin
minority will need insulin

104
Q

what is pregnancy-induced hypertension (aka gestational hypertension)? how do you differentiate this from pre-eclampsia?

A

BP >140/90 after 20 weeks gestation.
(normally, you’d expect BP to drop)
in pre-eclampsia, you’d see hypertension and proteinuria

105
Q

what is pre-eclampsia?

A

condition in which placental development has gone wrong, leading to increased vascular resistance and permeability - leads to the characteristic hypertension and proteinuria.
may have reduced placental blood flow leading to IUGR.

106
Q

what is eclampsia?

A

woman with pre-eclampsia goes into grand mal seizures due to cerebrovascular vasospasm - emergency.
Rx - magnesium sulphate and deliver

107
Q

briefly explain the pathophysiology of pre-eclamspia

A

incomplete trophoblastic invasion of spiral arteries, possibly due to altered immune responses. spiral arteries might also have atheromatous lesions.
results in reduced uteroplacental blood flow, and widespread endothelial cell damage - leading to increased vascular resistance and permeability

108
Q

list some risk factors/possible causative factors of pre-eclampsia

A 
high risk - 
prev pre-eclampsia
chronic hypertension/hypertension in prev pregnancy
CKD
diabetes
autoimmune disease
medium risk - 
nulliparity
obesity
extremes of maternal age
pregnancy interval >10y
multiple pregnancy
FH pre-eclampsia
109
Q

what clinical features might you see in a woman with pre-eclampsia?

A

often asymptomatic

headache, N&V, drowsiness, visual disturbance, epigastric pain, massive oedema

110
Q

if a woman is at high risk of pre-eclampsia, what might be done to prevent it?

A

low dose aspirin started at 13-14 weeks

111
Q

how would you manage a woman with pre-eclampsia?

A

if mild - consultant care, more scans.
if >150/100, labetalol used (nifedipine may be used)
aiming for 140/90
if eclampsia - magnesium sulphate

delivery only cure - don’t forget steroids if think a pre-term delivery needs to happen!
mild = deliver at 37 weeks
moderate/severe = deliver by 34-36 weeks

112
Q

what is HELLP syndrome?

A

severe variant of pre-eclampsia:
Haemolysis
Elevated Liver enzymes
Low Platelets

usually liver enzymes rise first, then platelets drop, then haemolysis - only cure is delivery.

113
Q

what symptoms might you see in a woman who has developed HELLP syndrome? how is HELLP syndrome treated?

A

symps - epigastric/RUQ pain, N&V, dark urine due to haemolysis
Rx - deliver, manage as for eclampsia

114
Q

if a woman has essential hypertension, and is planning on becoming pregnant/becomes pregnant, should you change her antihypertensive?

A

probably - labetalol is the best one to be using.

ACEi’s and thiazides can cause congenital abnormality.

115
Q

what is placenta accreta? who is more at risk of having one? why do we worry about it?

A

abnormal adherence of all/part of placenta to the uterus - more likely if previous C sections as placenta adheres to scar.
increases risk of PPH, more likely to end up needing a caesarean hysterectomy

116
Q

what is placenta increta?

A

subset of placenta accreta, where the myometrium is infiltrated

117
Q

what is placenta praevia?

A

placenta lies in lower uterine segment - big risk of bleeding - avoid digital PV examinations and sex.

118
Q

how is placenta praevia diagnosed? how is it classified?

A 
may be picked up on USS - rescan at 32 weeks (if major) or 36 weeks (if minor).
may also present with APH.
major = covering os
minor = not covering os
some places split that into Grades I-IV
119
Q

how would you manage a woman with major placenta praevia on scans?

A

requires C section for delivery as os is covered by the placenta
keep scanning regularly to monitor

120
Q

how would you manage a woman with minor placenta praevia on scans?

A

aim for a NVD unless placenta within 2cm of internal os.

121
Q

list the dangerous vs less concerning causes of APH

A

dangerous - abruption, placenta praevia, vasa praevia
less concerning - circumvallate placenta, placental sinuses, cervical polyps/erosions/carcinoma/ectropions, cervicitis, vaginitis, vulval varicosities

122
Q

what is vasa praevia?

A

fetal vessels cross/run near internal os - risk of them being damaged at membrane rupture, causing foetal haemorrhage - needs C section, either emergency if didn’t know about it or elective if detected on scans

123
Q

what is placental abruption? how might it present?

A

part of placenta detaches from uterus - varying degrees of severity.
presents with painful APH - but beware concealed bleeding (mum may not be bleeding PV as much as she is internally).
will have tender, tense uterus, foetal HR absent/distressed, shock out of keeping with the visible blood loss

124
Q

list some risk factors associated with placental abruption

A

pre-eclampsia, smoking, IUGR, PROM, multiple pregnancy, polyhydramnios, older maternal age, thrombophilia, abdominal trauma, cocaine use, infection

125
Q

what are the possible consequences of placental abruption?

A

placental insufficiency may cause foetal anoxia or death.
uterine muscles might be compressed by all the blood - may prevent good contractions in labour (risk of PPH).
concealed bleeding can cause maternal shock - beware renal failure and Sheehan’s syndrome.

126
Q

describe basic management of APH

A

admit - ABCDE approach if severe, consider delivery (C section for placenta praevia).
active management of 3rd stage with Syntometrine to help prevent PPH.
milder bleeding - US scan of placenta, speculum examination - if praevia, consider admitting till delivery. if pain and bleeding from small abruption settles, mum might be able to go home.
if APH at term - induce labour.

127
Q

what is the main cause of uterine rupture in the UK? give some other risk factors

A

due to dehiscence of c section scars - LSCS scars way less likely to rupture than ‘classical’ scars.
other RFs - obstructed labour in multiparous woman, prev uterine surgery, high forceps delivery, internal version, breech extraction
rupture happens in 3rd trim or during labour (most commonly)

128
Q

what are the signs/symptoms of uterine rupture in labour? how would you manage?

A

pain (might be slight or severe), same goes for vaginal bleeding (mostly intraperitoneal bleeding).
basically - sudden and unexplained maternal shock, disappearance of placental part from pelvis, metal distress, contractions stopped.

management - Cat 1 C section, manage shock, might be able to repair but often hysterectomy needed.

129
Q

define primary vs secondary PPH

A 
primary = loss of >500ml blood in first 24h after delivery
secondary = excessive loss after the first 24h post-delivery
130
Q

define major PPH / massive obstetric haemorrhage

A

major PPH = loss of >1 litre

massive obs haemorrhage = loss >1500mls - call crash team!!

131
Q

what are the causes of primary PPH?

A 
4 Ts:
Tone - uterine atony
Tissue - retained products of conception
Trauma - genital tract trauma
Thrombin - clotting disorder

uterine atony by far most common - failure of uterus to contract down after delivery

132
Q

what usually causes secondary PPH and how would you manage this?

A

retained placental tissue or clot, often with infection.
usually occurs on days 5-12
Rx = abx, check for retained products on US

133
Q

list the antenatal RFs for PPH

A

prev PPH or retained placenta
BMI >35
low Hb at onset of labour
APH
multiparity >4
age >35
uterine malformation/fibroids
large placental site e.g. twins, large baby, severe rhesus disease
low placenta
overdistended uterus (polyhydramnios, trwins)
extravasated blood in myometrium (abruption)

134
Q

list RFs for PPH that occur in labour

A

prolonged labour (any stage)
induction or oxytocin use
precipitate (fast) labour
instrumental/C section

135
Q

describe the steps involved in managing a PPH

A

high flor O2 / ABCDE approach - take bloods, start fluids etc
deliver placenta, empty uterus of clots/retained tissue
massage uterus/bimanual compression
drugs - Syntometrine IM, oxytocin infusion, ergometrine, misoprostol, carboprost
repair vaginal/cervical tears
if bleeding continues after all of the above - take to theatre, exam under anaesthetic.
Rusch balloon - sits in uterus and compresses placental site.
if STILL not working - B-Lynch suture - like belt and braces on uterus.
then - ligation
then subtotal/total hysterectomy

136
Q

what are the “baby blues”?

A

transient, self-limiting dip in mood typically 3-5 days after delivery, lasting 1-2 days (up to 2 weeks for some).
mum is tearful, anxious and irritable.

Rx - reassurance and support from family and midwife. Review if symptoms persist.

137
Q

what is popstpartum depression?

A

major depressive disorder occurring in postpartum period.

usualkly resolves within 6 months - but that’s quite a long time to live with it. has adverse affects on baby.

138
Q

what screening tool is used to detect postpartum depression?

A

Edinburgh postnatal depression scale

139
Q

how is postpartum depression managed?

A

depebds on severity - increased support, counselling.
antidepressants are as good as CBT - tricyclics or SSRIs (not fluoxetine) are sage in breastfeeding.
might need admission - mother-baby units.

beware - PND kills!

140
Q

give some RFs for postpartum depression

A

prev postpartum depression or depression/other psych hx.

also - unplanned pregnancy, perceived lack of support, marital problems, sleep deprivation. low SE status,

141
Q

what is puerperal psychosis and when does it occur?

A

peak onset at 2 weeks.
psychotic episode with prominent affective symptoms (depression or mania).
symptoms fluctuate massively.
often needs hospitalisation

142
Q

what are the effects on the foetus of antenatal cytomegalovirus infection?

A

IUGR, pneumonia and thrombocytopenia seen in 10% (vertical transmission rate = 40%)
if symptomatic at birth - will go on to have hearing loss and/or disability

143
Q

how is maternal cytomegalovirus infection diagnosed and managed?

A

might see anomalies on US scan that prompt testing.
if maternal infection confirmed, do amniocentesis 6 weeks later to determine whether vertical transmission has occurred - may offer TOP

144
Q

what are the risks to baby of active genital herpes infection in the mother?

A

vertical transmission occur at vaginal delivery, especially if vesicles present - neonatal infection rare but high mortality.
might consider C section to avoid transmission.
neonates can be given acyclovir.
refer to GUM!

145
Q

how would you manage a pregnant woman who becomes infected with rubella?

A

if <16/40, offer termination.
after that, baby unlikely to be affected.

to confirm infection - antibody levels taken.

affected babies suffer deafness, cardiac and eye problems etc

146
Q

how would you manage a pregnant woman who becomes infected with toxoplasmosis? what are the effects of this infection on baby?

A

give spiramycin as soon as mum is diagnosed.

risk to baby of severe neurological sequelae.

147
Q

how would you manage a mother presenting with chicken pox at 37+5/40 gestation?

A

aim for delivery after 7 days if possible, give baby varicella immune immunoglobulin at birth and monitor - if neonate develops chickenpox, give aciclovir

148
Q

how would you manage a pregnant mother who tells you she’s been exposed to someone with chickenpox?

A

establish whether any prior infection - history, check blood fo varicella abs - if none, give VZIG.
if they develop chicken pox - acyclovir.

149
Q

how would you manage a pregnant mother who becomes infected with parvovirus B19? what are the risks for baby?

A

virus suppresses foetal erythropoiesis - anaemia. can cause foetal death.
if mum tests positive for the virus - close monitoring of foetus, might need in utero blood transfusion if severe hydrops fetalis

150
Q

list some risk factors for cord prolapse

A 
preterm labour
breech presentation (esp. footling)
polyhydramnios
abnormal lie (esp unstable transverse)
twin pregnancy (2nd twin)

artificial rupture of membranes is a major RF/cause!!

151
Q

how does cord prolapse present / how is it diagnosed?

A

might literally see cord.

or might be foetal bradycardia/foetal heart decels - do PV exam to palpate for cord

152
Q

how would you manage a woman in labour with cord prolapse?

A

get her on all fours, with member of team holding presenting part off the cord with the examining finger
DELIVER ASAP - by LSCS or instrumental if fully dilated - whichever is going to be faster.
tocolytics (terbutaline) given to reduce contractions and help bradycardia

153
Q

what is shoulder dystocia? how is it managed?

A

where baby’s anterior shoulder gets stuck during delivery - big risk of harm to baby - risk of death from asphyxia.

Rx - be quick cos cord is probably stuck in pelvic inlet.
assess for episiotomy
McRoberts - hyper flexed lithotomy position - abduct, rotate outwards, and flex mums legs so each thigh touches tummy (two assistants needed to hold each leg)
apply suprapubic pressure
episiotomy and enter pelvis for internal manouvres that try to rotate foetal shoulders

other options - symphysiotomy, Zavanelli (push baby back in and do C section - Cat 1 for sure)

154
Q

what are the different categories of caesarean section?

A

Category 1 - crash - immediate threat to life of woman/baby - delivery should be achieved within 30 mins of decision
Category 2 - 30-60 mins e.g. failure to progress
Category 3 - semi-elective e.g. failed IOL, pre-eclampsia
Category 4 - elective e.g. breech

155
Q

what is an amniotic fluid embolism?

A

when liquor enters maternal circulation, usually occurs when membranes rupture but also can occur during labour/C sect.

156
Q

give some risk factors for amniotic fluid embolism

A 
multiple pregnancy
mum >35 yrs
instrumental del
C sect
eclampsia
polyhydramnios
placental abruption
uterine rupture
induction of labour
157
Q

what are the clinical features of amniotic fluid embolism?

A 
first sign may be maternal collapse!
dyspnoea, chest pain, hypoxia, respiratory arrest leading to ARDS
hypotension
fetal distress
seizures (20%)
reduced consciousness
cardiac arrest
will develop DIC within 48h
158
Q

how do you manage a mother with a suspected amniotic fluid embolism?

A

ABCDE - will need anaesthetist to come and intubate.
get IV access.
essentially supportive treatment focussing on ABCDE.
most mortality occurs in <1h.

159
Q

give some risk factors for VTE in pregnancy

A 
high risk (give antenatal LMWH prophylaxis) - hx of >1 prev VTE, unprovoked or oestrogen-related VTE, single provoked VTE, thrombophilia
intermediate risk - thrombophilia but no VTE, single provoked VTE, medical comorbidities e.g. cancer, SLE, sickle cell, IVDU, antenatal surgery
160
Q

how does pregnancy change definitions of anaemia?

A

Hb drops anyway - physiological anaemia of pregnancy.
defined after 20 weeks as Hb <105g/L.

beware - even a small PPH can become life threatening in an anaemic mother.

161
Q

what causes anaemia in pregnancy? how is it detected?

A

usually physiological! if actual anaemia - usually iron deficiency, then folate deficiency.
screened at booking and at 28 weeks.

162
Q

what is the definition of hyperemesis gravid arum?

A

persisting vomiting in pregnancy which causes weight loss >5% of pre-pregnancy weight and ketosis.

163
Q

how do you manage a woman suffering hyperemesis gravidarum?

A

admit if unable to keep anything down DESPITE oral antiemetics.
rehydrate and correct metabolic disturbance - give them a shit load of fluids.
anti-emetics - promethazine, cyclising or metoclopramide.

164
Q

what are the effects of gonorrhoeal infection during pregnancy on the baby? how is this managed?

A

gonococcal conjunctivitis - baby develops purulent discharge, lid swelling, corneal hazing ± rupture etc within 4 days of birth.

give IM cefotaxime at birth to babies born to mum with known gonorrhoea, + chloramphenicol eye drops within an hour.

if unknown until conjunctivitis occurs - ben pen IM and chloramphenicol drops

165
Q

when would you administer IV abx for GBS infection?

A

during labour if:
+ve GBS high vaginal swab at any time in pregnancy
any baby prev infected with GBS
any documented GBS bacteriuria this pregnancy
gestation <37 weeks
intrapartum fevere

if a woman in GBS +ve with prelabour rupture of membranes at erm - give abx and induce

166
Q

following booking visit, a woman is noted to have asymptomatic bacteriuria - how is she managed?

A

second sample sent for culture - if bacteriuria persists then treat with abx per local guidelines e.g. nitrofurantoin

if a suspected actual UTI in pregnancy, always prescribe abx

167
Q

briefly explain how rhesus D isoimmunisation comes about

A

RhD- woman has baby with RhD+ man, and baby is also RhD+. mum’s blood comes into contact with baby’s, and mum develops antibodies against RhD+ blood cells (anti-D abs).

Mum then has another child that’s also RhD+

Mum’s anti-D antibodies cross placenta and attack foetal blood - haemolytic disease of the newborn

168
Q

In the UK, what is done antenatally to prevent haemolytic disease of the newborn ?

A

pregnant women have a maternal blood group (ABO and RhD typing), and an antibody screen performed at the booking visit (8-12 weeks gestation) and again at 28 weeks.

any RhD- woman is given antenatal anti-D immunoglobulin prophylactically at 28 and 34 weeks gestation.

169
Q

what are the different types of twin/multiple pregnancy?

A

dizygotic twin - fertilisation of two oocytes by two different sperm
monozygotic twins - result from mitotic division of a single zygote.
they may share the same amnion/placenta - can have dichorionic diamniotic twins (separate amnions and placentas) or monochorionic diamniotic twins.

170
Q

list some possible antenatal complications as a result of multiple pregnancy

A

maternal - gestational diabetes, pre-eclampsia, anaemia
foetal - increased mortality and morbidity (and increases with number of multiples, i.e. worse for triplets than twins etc), often premieres, risk of IUGR

171
Q

what is TTTS?

A

due to shared blood supply - can get twin-twin-transfusion syndrome (only in MCDA twins!).
unequal blood distribution through shared placenta - ‘donor’ twin is volume depleted, anaemic, IUGR, oligohydramnios
‘recipient’ twin has volume overload, polycythaemia, cardiac failure, massive polyhydramnios.

high risk of in utero death/severe prem

172
Q

define oligohydramnios - list some causes

A 
amniotic fluid index <5th centile
causes:
Preterm prelabour rupture of membranes
Placental insufficiency – blood flow being redistributed to the fetal brain rather than kidneys, causes poor urine output.
Renal agenesis / non-functioning fetal kidneys
Obstructive uropathy
Genetic/chromosomal anomalies
Viral infections
173
Q

define polyhydramnios - list some causes

A

amniotic fluid index >95th centile
causes:
Any condition that prevents the fetus from swallowing – e.g. oesophageal atresia, CNS abnormalities, muscular dystrophies, congenital diaphragmatic hernia obstructing the oesophagus
Duodenal atresia – ‘double bubble’ sign on ultrasound scan
Anaemia – alloimmune disorders, viral infections
Fetal hydrops
Twin-to-twin transfusion syndrome
Increased lung secretions – cystic adenomatoid malformation of lung
Genetic or chromosomal abnormalities
Maternal diabetes
Maternal ingestion of lithium – leads to fetal diabetes insipidus
Macrosomia – larger babies produce more urine.

174
Q

what does the routine 12(ish) week USS look for?

A

used for dating and finding out the EDD (estimated delivery date)
also nuchal translucency - excludes miscarriages, dates pregnancy, diagnoses multiple pregnancy.
abnormalities detected include anencephaly, chromosomal abnormalities (combined with blood test), cardiac anomalies (referred for further scans)

175
Q

when would invasive testing be offered after the nuchal translucency scan?

A

if deemed high risk i.e. <1:150 after results of NT scan and blood test
NB - risk if pregnant at 40yrs is 1:110 !

176
Q

what is the combined test for aneuploidy?

A

nuchal translucency + free hCG + pregnancy-associated plasma protein (PAPP-A) + woman’s age to determine risk of aneuploidy
performed between 11+0 and 13+6 weeks

177
Q

what is the integrated test for aneuploidy? what about the quadruple test?

A

integrated = expensive so rarely used - uses NT + PAPP-A in first trimester plus quadruple test in 2nd trimester
quadruple test = blood test at 16 weeks - uses dating scan + maternal alpha-fetoprotein (AFP) + unconjugated estriol + free beta hCG or total beta hCG + inhibin A + woman’s age

178
Q

what is the anomaly scan and when is it performed?

A 
USS at 18-22 weeks looking for structural anomalies.
looks at:
skull shape and internal structures
spine
abdomen for shape and content
arms and legs
heart - 4 chamber view
face and lips
179
Q

what is preimplantation genetic diagnosis?

A

early form of prenatal diagnosis - embryos made in vitro analysed for well-defined genetic disease or chromosomal abnormalities
FISH used for chromosomes, PCR for genetic diseases

180
Q

explain a bit about chorionic villus biopsy

A

10-13 weeks

placenta sampled by transabdominal approach and karyotyping/gene analysis done

181
Q

what are the risks of chorionic villus biopsy?

A

miscarriage (excess risk 1-2%)
increased transmission of blood borne viruses
anti-D might be required

182
Q

explain a bit about amniocentesis

A

> 16 weeks
aspiration of fluid containing fetal cells from skin and gut
needle passed transabdominally under continous US

183
Q

what are the risks of amniocentesis?

A

fetal loss rate of around 1%

anti-D needed in all Rh-ve women

184
Q

give some complications of amniocentesis

A
  • leakage of amniotic fluid
  • injury to fetus causes e.g. clubfoot
  • infection e.g. blood borne viruses
  • miscarriage
185
Q

give some complications of chorionic villus sampling

A
  • inadequate sample
  • miscarriage
  • rhesus sensitisation
  • infection
186
Q

what are mammograms? how do they work?

A

low dose X rays of breasts - breast squished between two plates.
HRT or age <40yrs make breasts look denser and glandular so not that useful here as can’t really see cancers (so don’t do them! as XR does contribute to cancer risk)

187
Q

list some indications for a mammogram

A
  • clinically suspicious lump in pt >40
  • breast Ca where mammogram not performed before
  • residual lump after cyst aspiration
  • single duct blood stained nipple discharge
  • nipple skin change
  • every 3 yrs if age 47-73 (breast screening)
  • also every yr if age 40-50 with increase familial risk
188
Q

what are some contra-indications to mammography?

A
  • breast pain without a lump
  • symmetrical thickening
  • if on HRT
  • if under 40yrs unless diagnosed with breast Ca already
189
Q

what other imaging modalities (apart from mammograms) are used in assessing breast lumps/abnormalities?

A

US - useful if woman <40 or mammogram otherwise CI - also as adjunct to mammogram
MRI - used if age 30-50y and high risk family history, as annual screening. also used in addition to mammogram/USS.

190
Q

what investigations should a woman presenting with a palpable breast lump have if aged <25 yrs?

A

histology/cytology only, no imaging if feels benign, or USS if suspicious.

191
Q

what investigations should a woman presenting with a palpable breast lump have if aged 25-40yrs?

A

breast USS + histology or cytology (triple assessment)

192
Q

what investigations should a woman presenting with a palpable breast lump have if aged >40 yrs?

A

mammography and USS and histology or cytology (triple assessment)

193
Q

what are the different methods used to take a tissue biopsy for histology/cytology of suspected breast Ca?

A

fine needle aspiration cytology (FNAC) - not used much now due to low sensitivity/specificity
core biopsy - gives histological diagnosis, can differentiate between invasive cancer and DCIS, performed under local.
Vacuum Assisted Biopsy (VAB) - used if uncertain diagnosis after core biopsy
Open biopsy - only really used in skin lesions e.g. Paget’s disease of nipple

194
Q

what is triple assessment, as used in diagnosis of breast Ca?

A

1) clinical assessment
2) radiology e.g. US/mammogram
3) pathology - FNAC, core biopsy

aim of MDT is to check for concordant results across all 3 before either a) reassuring and discharge as benign or b) removing breast/treating

195
Q

describe the current UK breast cancer screening programme

A

women aged 50-70 receive invitations to attend breast cancer screening appts every 3 years (in some parts of the country this can include women age 47-49 and 71-73).
if over 70, women can request screening.

196
Q

what are the two common histological types of invasive breast cancer?

A

ductal and lobular
lobular - harder to feel/see on mammography, generally more diffuse so harder to excise etc.

also - tubular, mucinous, medullary - rarer types, treatment is the same

197
Q

what are the three tumour receptors relevant to breast cancer?

A

oestrogen receptor (ER+ve)
Her-2 receptor
Ki 67

198
Q

briefly explain what is meant by an ER positive breast cancer

A 
oestrogen receptors are expressed on over half of all breast Cas - tumour growth is stimulated by oestrogen - marker of good prognosis cos will respond to anti-oestrogen therapy.
progesterone receptors (PgR) also exist, the two are linked.
199
Q

briefly explain what is meant by a Her-2 receptor positive breast cancer

A

poor prognostic marker.
Her-2 receptor over expressed (occurs in 15%). her-2 up-regulates growth, so having excess her-2 receptors = more aggressive cancers.
BUT - we have Herceptin (trastuzumab) which really improves prognosis - there’s a few other new drugs that work on this receptor too.

200
Q

briefly explain what is meant by Ki 67 positive breast cancer

A

this is a new thing - proliferation marker Ki 67 - it’s a stain that shows up percentage of cells in active cell cycle - so high score is poor prognostic marker as indicates loads of cell division going on.

201
Q

briefly explain what is meant by a triple negative breast cancer

A

cancers that don’t express any hormone receptors - ER, PgR, Her-2 - v aggressive and bad news as can’t use anti-oestrogens/Herceptin.

linked to BRCA-1.

202
Q

list some risk factors for breast cancer

A 
BRCA genes
first degree relative with breast cancer
nulliparity, first pregnancy >30yrs
early menarche, late menopause
HRT, COCP
past breast Ca
not breastfeeding
ionising radiation
p53 gene mutations
obesity
203
Q

what surgical options are there for breast cancer?

A

surgery aims to achieve local control (half will already have systematic disease e.g. micrometastases)
mastectomy - transverse incision, leaves pec major/minor behind - or may be done in combination with reconstruction.
breast conservation surgery
- wide local excision, with adjuvant radiotherapy

204
Q

give some indications for a mastectomy

A
  • patient choice
  • large tumour relative to breast volume
  • multi-focal/multicentric disease
  • sub-areolar tumour (or may use nipple removing WLE)
  • CI to radiotherapy
  • failed conservative surgery
  • very strong FHx in young patient
  • bilateral prophylactic mastectomy in BRCA gene carriers
  • local recurrence after WLE
  • inflammatory breast cancer
205
Q

give some indications for breast conservative surgical management of breast Ca

A
  • patient choice
  • operable unifocal primary tumour (<20% breast volume)
  • tumour at favourable site for conservation
  • suitable for radiotherapy
206
Q

what different types of axilla surgery may be used in management of breast ca and why do them?

A

aims to remove Ca deposits in lymph glands (local disease control) + to provide prognostic info

1) axillary node clearance (ANC) - standard in woman with known axillary node disease - removes all lymph nodes in axilla, won’t need further radiotherapy
2) sentinel node biopsy - biopsy of first node in ‘chain’ of lymph nodes to decide if spread to axilla - node is identified before surgery using radioisotope/dye. if node is positive, ANC usually performed.

207
Q

give some possible complications of axillary node clearance

A
  • seroma formation
  • need for drain for 1 week post-op
  • shoulder stiffness
  • permanent paraesthesia under arm
  • lymphoedema of arm
  • damage to long thoracic nerve of Bell
  • damage t nerve/blood supply of lat dorsi (might need for reconstruction later on!)
  • damage to axillary vein
208
Q

briefly explain TNM staging of breast cancer

A

stage 1 - T1, N0, M0 - tumour <2cm, no nodes/mets
stage 2 - T2 or T3 or N1 - so tumour 2-5cm, no chest wall/skin involvement, ipsilateral axillary node(s)
stage 3 - anything more, but no distant mets (i.e. not M1)stage 4 - M1, distant mets

NB - Tis = in situ carcinoma.
Tis-T3 considered operable tumours, T4 may be operable with neo-adjuvant therapies pre/post op

209
Q

what is the Nottingham prognostic index?

A

staging system used in UK to predict 5-10yr survival rates.

uses tumour grade, lymph node status and tumour size - doesn’t take into account receptor status (bit of a limitation)

210
Q

list three tools used in the UK to assess breast cancer prognosis

A

Nottingham prognostic index
adjuvant online
PREDICT

211
Q

define adjuvant vs neo-adjuvant therapy

A

adjuvant = any treatment given following the primary treatment (typically surgery). pt doesn’t have active disease but chemo/radio/endocrine therapies given to attempt to eliminate micro-metastases

neo-adjuvant = treatment given before surgery to make a cancer operable/to allow easier surgery

212
Q

describe the role of radiotherapy in the management of breast cancer

A
  • always given to remaining tissue after WLE
  • given after some mastectomies
  • for palliation of large/inoperable cancers
  • to treat axilla if axillary clearance impossible

reduces local recurrence rate by 2/3rds ish

213
Q

briefly describe the role of chemotherapy in management of breast cancer

A

tumour and patient factors determine whether indicated - more aggressive tumour + younger patient means it’s more likely to be useful.
regimes vary but e.g. is epirubicin, 5 fluourouracil and cyclophosphamide, 6-8 courses for 12 weeks.

214
Q

describe the role of hormone therapy in the management of a pre-menopausal woman with oestrogen sensitive breast cancer

A

1st line = tamoxifen, offered for 5+ years.

SEs incl - GI disturbance, hormonal disturbance (hot flushes), headache, rash, visual disturbance, VTE.

215
Q

describe the role of hormone therapy in the management of a post-menopausal woman with oestrogen sensitive breast cancer

A

all women with oestrogen sensitive breast Ca given 5+ yrs of hormone therapies.

aromatase inhibitors e.g. exemestane, letrozole, anastrozole -prevent peripheral conversion of adrenal androgens to oestrogens by inhibiting aromatase enzyme (only source of oestrogen in post-menopausal women, but if pre-menopause there are other sources so this doesn’t work).
superior to tamoxifen in all settings, and with fewer SEs etc so always choose these if post-menopause.

216
Q

describe the role of trastuzumab in management of breast cancer

A

aka Herceptin - binds to Her-2 receptors (over-expressed in 1/3rd of breast cancers).
all women <70yrs with Her-2 positive tumours should have trastuzumab as adjuvant therapy for a year

217
Q

list some features suggesting locally advance breast cancer - how does this alter management plan?

A

ulceration, peau d’orange, inflammatory breast Ca, fixed to chest wall, fixed axillary lymph nodes.

non-surgical treatment used first, then subsequent mastectomy depending on response. screen for mets.

218
Q

what is Paget’s disease of the nipple?

A

eczematous change of nipple due to underlying malignancy (invasive or in-situ).
suspect in nipple eczema if doesn’t resolve with 2 weeks of steroids/anti-fungal cream.
Rx - nipple excising WLE / mastectomy

219
Q

what are the most common sites of metastases from breast cancer?

A

bone - rx is endocrine therapy/radiotherapy
lung
liver
brain

220
Q

what is ductal carcinoma in situ?

A

DCIS - pre-malignant condition
usually asymptomatic - picked up be screening. lining epithelium of ducts becomes thickened as cells proliferate.
micro-calcifications on mammography.

221
Q

how do you treat DCIS picked up following breast screening?

A

wide excision and radiotherapy, maybe mastectomy if extensive disease.
explain treating to prevent breast cancer - they don’t actually have breast cancer.

222
Q

list some of the cosmetic options available following mastectomy

A

1) external prosthesis - most women in UK don’t have reconstructions, just fake boobs!
2) primary reconstruction - done at time of mastectomy, might do a skin-sparing mastectomy to keep most natural look.
3) implant/expander reconstructions - insertion of expandable silicone and saline implants under muscle layer of chest wall.
4) acellular dermal matrix and dermal sling - pig or cow dermis used to add space for larger implant
5) latissimus dorsi flap - latissimus dorsi muscle detached from back and slipped through to front, either on its own or over an implant, good for a more natural shape
6) TRAM/DIEP flaps - get a tummy tuck and that’s used to reconstruct breast - performed by plastic surgery.
7) nipple reconstruction - to top it all off

223
Q

what are the features of a surgically significant nipple discharge?

A

persistent
unilateral and unifocal
spontaneous
bloody or clear

224
Q

what usually cause bloody nipple discharge?

A

duct papilloma
duct ectasia
occasionally - due to invasive/in-situ carcinoma, so most of the time offending duct is removed

225
Q

list some non-neoplastic causes of nipple discharge, describing the type of discharge seen for each

A

duct ectasia - yellow, green, thick, sometimes bloody
papilloma - benign warty growth, usually bloody/clear
galactorrhoea - milky - physiological or due to drugs
purulent discharge = infective causes, usually S aureus

226
Q

how would you manage a breast abscess?

A

don’t usually use incision and drainage.

aspirations plus oral abx.

227
Q

what are the management options for cyclical breast pain?

A

1) explain and reassure.
2) danazol - weak androgen, mild inhibitor of LH/FSH, bit nasty with SEs so only used when severe
3) tamoxifen - don’t use long term due to risk of endometrial Ca. unlicensed, consultant only prescription.
4) goserelin - rarely used, again unlicensed consultant only.

228
Q

what are the management options of non-cyclical breast pain?

A

NSAIDs usually most successful.
don’t forget non-breast causes of chest pain though - cardiac, MSK etc.
evening primrose oil doesn’t do anything.

229
Q

list some causes of benign breast lumps

A

1) nodularity - cyclical lumpy changes (re-examine after period)
2) fibroadenoma - common if <35yrs
3) cysts - common age 40-60y

230
Q

what is the usual natural history of a fibroadenoma?

A

1/3rd shrink, 1/3rd stay same size, 1/3rd enlarge over time.

NB - can be really mobile pm examination

231
Q

what criteria must a breast cyst fulfil to be considered benign?

A
  • fluid not blood stained
  • no residual lump
  • same cyst does not continuously refill
232
Q

what is gynaecomastia?

A

lump >2cm behind the male nipple.
occurs at all ages, can be uni- or bi-lateral.
if man >50y, exclude breast Ca via biopsy.

233
Q

list some causes of gynaecomastia

A

physiological - due to slight imbalance of oestrogen + testosterone.
pathological:
- drugs (spironolactone, digoxin, oestrogen, anabolic steroids etc)
- cannabis
- liver failure, renal failure, malnutrition
- testicular failure
- testicular tumours

234
Q

briefly describe the principles of treating gynaecomastia

A
  • treat underlying cause/stop causative drug
  • exclude cancer if >50y
  • reassure - should resolve itself really, results of surgery to correct not very good anyway!
235
Q

what are the genetics of the BRCA1 gene?

A

chromosome 17, it’s normally involved in DNA repair and cell cycle regulation (tumour suppressor)
high penetrance / autosomal dominant

236
Q

how do you manage the female family members of someone with identified BRCA1 gene?

A

can do gene tests but there’s loads of mutations out there so it can be tricky.
bilateral prophylactic mastectomy, bilateral oophorectomy as well if completed family - both of these are huge, very personal decisions.
some women even used IVF with PGD when starting family to avoid passing gene to the kids (available on NHS)

237
Q

what are the genetics of BRCA2?

A

chromosome 13
autosomal dominant, high penetrance.
not as strong a risk factor, but still definitely one!
less associated with ovarian cancer, but more risk for male breast cancer

238
Q

what is Li-Fraumeni syndrome?

A

rare, but nasty genetic predisposition to breast cancer.
germ line mutation of TP53 gene (a tumour suppressor).
strong risk of lots of cancers.

239
Q

what are the characteristic features of a fibroadenoma?

A

woman under 30yrs - ‘breast mice’ - discrete, non-tender highly mobile lumps

240
Q

what are the characteristic features of fibroadensosis aka fibrocystic disease?

A

middle-aged women - lumpy breasts, may be painful. symptoms can worsen prior to menstruation.

241
Q

what clinical features might make you worry about breast cancer?

A

hear, irregular lump. nipple inversion or skin tethering is worrying.

242
Q

what is Paget’s disease of the breast?

A

intraductal carcinoma associated with reddening and thickening (eczematous appearance) of nipple/areola

243
Q

what are the characteristic features of mammary duct ectasia?

A

presents around menopause with tender lump near areola, with green nipple discharge.
due to dilatation of large breast ducts.
can rupture causing local inflammation.

244
Q

what are the characteristic features of duct papilloma? management?

A

bloody discharge.
there’s local areas of epithelial proliferation in large mammary ducts - hyperplastic lesions rather than malignant/premalignant.
rx - microdochectomy (remove the duct)

245
Q

what are the characteristic features of fat necrosis in breasts? management?

A

more common in obese women with big breasts.
can follow trivial/unnoticed trauma.
initial inflammatory response - firm and round lesion - but can change into hard, irregular lump.
rare and mimics breast ca so always investigate.
rx - imaging and core biopsy!

246
Q

what are the characteristic features of a breast abscess? management?

A

red, hot tender swelling in a lactating/breast feeding woman.
can require incision and drainage.

247
Q

what are the characteristic features of a breast cyst? management?

A

smooth, discrete, maybe fluctuating lump.

rx - aspirate, then any which are blood stained or persistently refill should be biopsied and excised.

248
Q

what are the characteristic features of a fibroadenoma? management?

A

mobile, firm breast lump.

rx - excise if >3cm.

249
Q

what is mastitis? how does it present and how do you treat?

A

pain and inflammation in breastfeeding women.
treat if systemically unwell, nipple fissure, or symptoms persist for 12-24h after advise re keep removing milk (i.e. pump breast dry after feeding) and use of warm compresses.
treat - fluclox oral.
continue breastfeeding/pumping!
risk is development of abscess.

250
Q

list some blood tests you might order for gynaecomastia? any other Ix?

A
  • Renal function.
  • LFTs.
  • TFTs.
    Hormone profile: Estradiol, testosterone, prolactin, bhCG level, Alpha-fetoprotein (AFP).
    Luteinising hormone (LH):
    LH high and testosterone low - indicates testicular failure.
    LH and testosterone both low - indicates increase in oestrogens.
    LH and testosterone both high - androgen resistance or neoplasm secreting gonadotrophins.
    Chromosomal karyotyping may need to be considered

USS/biopsy if male breast Ca suspected

251
Q

how is Down syndrome screened for in UK antenatal care?

A

11-13+6 weeks:
Nuchal translucency + PAPP-A + bHCG

if presents late:
triple - AFP + oestriol + HCG
quadruple - AFP + oestriol + HCG + inhibin A

1a - Finals pt 2. (12 decks)

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