Obs n Gynae Flashcards

1
Q

define preterm labour

A

<37 weeks gestation

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2
Q

define prolonged labour

A

no definite time period

cervical dilatation <2 cm in 4 hours during active labour

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3
Q

describe the first stage of labour

A

onset to contractions to full dilatation

early latent phase = cervix becomes effaced, shortens and dilates up to 4 cm

active phase = 4 cm cervical dilatation to full dilatation (10 cm)

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4
Q

describe the 2nd stage of labour

A

full dilatation to delivery of fetus

passive stage = full dilatation prior to or in absence of persistent involuntary expulsive contractions

active stage = when baby is visible OR persistent involuntary expulsive contractions/active maternal effort with a finding of full dilatation

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5
Q

describe the 3rd stage of labour

A

delivery of fetus to delivery of placenta and membranes

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6
Q

how long can the 3rd stage of labour last

A

usually 5-10 minutes after delivery

> 30 minutes = abnormal

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7
Q

how long does labour normally last

A

first labour = average 8 hours

subsequent labours = average 5 hours

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8
Q

when is delay in labour diagnosed

A

nulliparous: active second stage has reached 2 hours
multiparous: active second stage has reached 1 hour

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9
Q

what is the difference between physiological and active management of the 3rd stage of labour

A

physiological: uterotonic drugs (oxytocin) are not used, cord not clamped until pulsations have ceased, placenta is delivered by maternal effort

active management: use of oxytocin before cord stops pulsating, bladder catheterisation, deferred clamping and cutting of the cord, controlled cord traction after signs of separation of the placenta

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10
Q

what are the signs that indicate separation of the placenta and membranes

A

uterus contracts, hardens and rises

umbilical cord lengthens permanently

gush of blood variable in amount

placenta and membranes appear at introitus

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11
Q

when should you change from physiological to active management of 3rd stage of labour

A

excessive bleeding or haemorrhage

failure to deliver placenta within 1 hour

patient’s desire to shorten 3rd stage

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12
Q

what are clinical signs of onset of labour

A

regular, painful contractions which increase in frequency and duration and produce progressive cervical dilatation

passage of blood-stained mucus from the cervix is associated with onset of labour nut not an indicator

rupture of membranes not always at start of labour

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13
Q

what is the definition of prelabour rupture of membranes

A

> 4 hours between rupture of membranes and onset of painful contractions

can be preterm or term

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14
Q

what are Braxton hicks contractions

A

non-labour contractions towards the end of gestation

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15
Q

which hormones are involved the initiation of labour

A

decreased progesterone

increased oestrogen and prostaglandin

oxytocin promotes PG release and initiates/sustains contractions

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16
Q

what are special features of uterine myocytes

A

contract and shorten, and return to precontraction length

contain ion channels that influence the influx of calcium ions into the myocytes and promote contraction of myometrial cells

affected directly by hormones such as relaxin, activin A (cAMP)

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17
Q

describe changes in the cervix leading up to labour

A

contains myocytes and fibroblasts

towards terms, there is a decrease in collagen (becomes softer and stretchy)

increased hyaluronic acid reduces the affinity of fibronectin for collagen and affinity of hyaluronic acid for water causes cervix to soften and stretch

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18
Q

what are the cardinal movements of labour

A
engagement
descent 
flexion 
internal rotation 
extension
external rotation 
expulsion
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19
Q

describe engagement (1st cardinal movement)

A

passage of widest diameter of the presenting part to a level below the plane of the pelvic inlet

engagement is measured in fifths (proportion of fatal head that is unpalpable)

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20
Q

describe descent (2nd cardinal movement)

A

downward movement of the presenting part through the pelvis

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21
Q

describe flexion (3rd cardinal movement)

A

flexion of the fatal head occurs passively as the head descends due to the shape of the bony pelvis and resistance by soft tissues

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22
Q

describe internal rotation (4th cardinal movement)

A

rotation of the presenting part from its original position (usually transverse with regard to the birth canal) to the anterior position as it passes through the pelvis

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23
Q

describe extension (5th cardinal movement)

A

occurs once the fetus has reached the introitus, and the base of occiput is in contact to the inferior margin of the pubic symphysis

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24
Q

describe external rotation/restitution (6th cardinal movement)

A

return of the fetal head to the correct anatomical position in relation to the fatal torso and shoulders

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25
Q

describe expulsion (7th cardinal movement)

A

delivery of rest of fetal body

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26
Q

what are causes of abnormal labour

A
malpresentation
malposition 
too early (preterm <37 weeks)
too late (post-term >42 weeks)
too painful
too quick (<2 hours)
too long (failure to progress, obstruction)
fetal distress
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27
Q

what is malpresentation

A

non-vertex presentation

vertex is bounded by the anterior and posterior fontanelles and the parietal eminences

involves breech presentation, transverse, shoulder/arm, face or brow presentation

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28
Q

what is malposition (labour)

A

occipitoposterior or occipitotransverse

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29
Q

what are the main causes of failure to progress

A

powers: inadequate contractions either in strength or frequency
passages: trauma, shape, cephalopelvic disproportion
passenger: big baby, malposition causing a relative cephalopelvic disproportion

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30
Q

what are potential complications of obstructed labour

A
sepsis: ascending genitourinary tract infection 
postpartum haemorrhage 
fistula formation 
fetal asphyxiation 
neonatal sepsis 
uterine rupture
obstructed acute kidney injury
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31
Q

how is progress in labour assessed

how often should it be performed

A

vaginal examination every 4 hours

cervical dilatation
descent of presenting part
signs of obstruction (moulding, caput, anuria, haematuria, vulval oedema

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32
Q

what are the three main types of forceps

A

outlet forceps
mid-cavity/low-cavity forceps
rotational forceps

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33
Q

indications for outlet forceps

A

fetal scalp is visible without separating the labia
the fatal skull has reached the pelvic floor
sagittal suture is in the AP diameter or right or left occiput anterior or posterior position (not >45 degrees)
fatal head is at or on perineum
can be used for lift-out deliveries at c-section

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34
Q

indications of mid/low-cavity. forceps

A

when fatal head is 1/5 palpable abdominally

leading point of the skull is above station +2 but not above the ischial spines

rotation of <45 degrees

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35
Q

indications for rotational forceps

A

should be performed in theatre with effective regional anaesthesia

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36
Q

what are the indications for FORCEPS

A

fully dilated (10 cm)
occipitoposterior position
ruptured membranes
cephalic presentation
engaged presenting part (fetal head must not be palpable abdominally and must be below the ischial spines)
pain relief
sphincter (bladder) empty (catheterisation)

standard indications: failure to progress in 2nd stage, fatal distress, maternal exhaustion

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37
Q

what are the advantages of operative vaginal delivery over C-section

A

80% will have a spontaneous vertex delivery subsequently

reduced analgesic requirements

shorter hospital stay and quicker recovery

less physical restrictions on bonding with the baby

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38
Q

what are the advantages of c-section compared to operative vaginal delivery

A

avoids tears to perineum and therefore problems with long term urinary and faecal incontinence

no injury to cervix or high vaginal areas

less change of neonatal trauma

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39
Q

what are disadvantages of operative vaginal delivery compared to c-section

A

neonatal trauma

urinary symptoms if retention occurred around the time of delivery

high risk of postpartum haemorrhage

shoulder dystocia as the traction applied cases head to deflex and shoulders to abduct, widening their diameter

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40
Q

what types of neonatal trauma can occur as a result of operative vaginal delivery

A

intracranial haemorrhage

skull fracture

jaundice due to cephalohaematoma and caput succedaneum (ventouse)

facial nerve palsy

forceps leave mark on face

brachial plexus injury

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41
Q

disadvantages of c-section compared to operative vaginal delivery

A
haemorrhage/infection 
visceral injury 
VTE 
longer hospital stay 
risk of uterine rupture in future labours and placenta accreta in future pregnancy 
greater maternal mortality 
transient tachypnoea of newborn
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42
Q

advantages and disadvantages of ventouse delivery

A

less perineal trauma but more likely to fail than forceps

more likely to cause cephalohaematoma, chignon (swelling on baby’s heads) and retinal haemorrhage

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43
Q

contraindications to ventouse delivery

A
prematurity <34 weeks 
face presentation 
suspected fatal bleeding disorder eg haemophilia 
fetal predisposition to fracture
maternal HIV or HepC
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44
Q

describe caput succedaneum in terms of onset, pathology, site, associated features and management

A

onset: present at birth
pathology: due to pressure of the presenting part against the cervix
site: tissue swelling that forms over the vertex and crosses suture lines
features: prolonged labour; soft puffy swelling; skin over swelling may look bruised; often with moulding
management: conservative, resolves in days

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45
Q

describe cephalohaematoma in terms of onset, pathology, site, associated features and management

A

onset: several hours after birth
pathology: subperiosteal haemorrhage due to prolonged second stage or instrumental delivery
site: forms below the first layer of periosteum, limited by suture lines
features: jaundice in newborn; often following operative delivery; swelling is firm with distinct margins; no skin discolouration; increases in size 12-24 hours after birth
management: conservative unless hyperbilirubinaemia in neonate, resolves over months

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46
Q

what is a chignon

A

temporary swelling after a ventouse suction cap has been used

2 hours - 2 weeks

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47
Q

describe subgleal haemorrhage in terms of onset, pathology, site, associated features and management

A

onset: at delivery and may progress rapidly
pathology: severing of the emissary veins that are located between the dural sinuses that cover the skull and scalp
site: forms above the periosteum, between the skull and the scalp aponeurosis; crosses the suture lines and covers a greater area than cephalohaematoma
features: delay in recognition may lead to neonatal encephalopathy, seizures, death; diffuse ill-defined swelling may shift when palpated and shift with reposition of the head; forceps/ventouse deliveries
management: resus and blood transfusions, assess for coagulopathies

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48
Q

what are the main diagnostic features of amniotic fluid embolism

A

occurs during or within 30 minutes of labour

respiratory distress, hypoxia, hypotension

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49
Q

after 30 minutes of physiological management of 3rd stage of labour and placenta still hasn’t been delivered

abs are stable and blood loss is minimal - what is the next best step

A

observe for 30 mins with IM syntocinon and breastfeeding

can wait up to 30 minutes total for physiological management of 3rd stage of labour
give syntocinon IM rather than In infusion
breastfeeding will stimulate spontaneous expulsion

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50
Q

29 yo primiparous women in prolonged labour following induction at 41 wks
6 cm dilated, fatal head is 1 cm above ischial spines
fetal heart rate is progressively dropping, <100 bpm, not recovered for more than 3 minutes

management?

A

category 1 C-section

fetal HR <100 bpm is a worrying sign
not fully dilated to instrumental delivery in theatre may not be advised

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51
Q

when is terbutaline given?

A

given in premature labour to reduce contractions

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52
Q

which of the following is not an indication for induction of labour?

prolonged pregnancy
diabetes in pregnancy 
macrosomia 
pre-eclampsia at term 
IUGR
A

macrosomia

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53
Q

a baby born 4 hrs ago by forceps has a swelling in the parietal region which does not cross suture lines

what is it

A

cephalohaematoma

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54
Q

31 yo due to have induction of labour at 38 wks due to cholestasis of pregnancy
bishop’s score of 1 calculated with the station at -1 but her cervix is closed and firm

treatment?

A

vaginal prostaglandins (PGE2)

PGs will ripen the cervix and cause a dilation allowing ARM to occur later

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55
Q

what is syntometrine used for?

A

management of postpartum haemorrhage

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56
Q

38 yo prim at 39+3 presents in spontaneous labour

she has only dilated 3 cm in last 6 hrs

she is now 6 cm dilated, CTG shows no fatal distress, uterine contractions are palpable but irregular and not very strong

management?

A

vaginal examination followed by amniotomy and reassess after

PV exam to assess dilatation, position and presentation of fetus

membranes are intact, so amniotomy is performed to accelerate progress of labour

CTG monitoring continued

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57
Q

what is the average rate of dilation in a primiparous woman

A

1 cm per hour

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58
Q

indications for induction of labour

A
prolonged pregnancy (>42 weeks)
pre-eclampsia 
placental insufficiency and IUGR
antepartum haemorrhage (includes abruption)
Rh immunisation 
diabetes mellitus 
chronic renal disease
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59
Q

what does the bishop score measure

A

assessment of the cervix to predict outcome following induction

dilatation 
effacement 
station 
cervical consistency 
cervix position
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60
Q

a bishop score of ____ is strongly predictive of labour following induction

A
>6 = labour follows induction 
<5 = needs cervical ripening
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61
Q

what are the criteria of the Bishop’s score

A

dilatation: 0, 1-2, 3-4, 5+

effacement (?%): 0-30, 40-50, 60-70, 80-100

station: -3, -2, -1, >0

cervical consistency: firm, medium or soft

cervix position: posterior, middle, anterior

all criteria start at a score of 0 and up to a max of 3

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62
Q

what are mechanisms of induction of labour

A
stripping of membranes 
artificial rupture of membranes 
medical induction following amniotomy
medical induction and cervical ripening
mechanical cervical ripening
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63
Q

stripping of the membranes

requirements and hazards/precautions

A

requirements
aseptic conditions: finger is inserted into cervix and the fetal membranes are separated from the lower segment
hazards/precautions:
if 7 people have sweeps, only 1 will labour in 48 hours

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64
Q

artificial rupture of membranes (amniotomy)

requirements and hazards/precautions

A

requirements:
aseptic conditions to prevent infection
cervix should be soft, effaced and at least 2 cm dilated
head should be engaged in pelvis and should be presenting by the vertex

hazards/precautions:
cord prolapse, vasa praevia )make sure to assess the fetal membranes and make sure there are no pulsating vessels present before amniotomy)
need to monitor fetal heart rate on CTG

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65
Q

medical induction following amniotomy using synthetic oxytocin infusion (syntocinon)
requirements and hazards/precautions

A

requirements:
aseptic conditions to prevent infection
cervix should be soft, effaced and at least 2 cm dilated
head should be engaged in pelvis and should be presenting by the vertex
hazards/precautions:
uterine hyperstimulation (>5 contractions in 10 minutes); reduces uterine blood flow and results in fetal asphyxia
discontinue infusion if excessive uterine activity or signs of pathological fetal heart rate of concern
can cause uterine rupture, particularly if there is a uterine scar

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66
Q

medical induction of labour and cervical ripening by administration of PGE2
requirements and hazards/precautions

A

requirements:
method of choice when the membranes are intact or where the cervix is unsuitable for surgical induction
oral route: causes nausea and vomiting and not commonly used
pessaries: most commonly used; 3 mg doses if no response repeat after 6 hours
hazards/precautions:
PG contraindicated if previous uterine scar (risk of hyper stimulation and uterine rupture)
if hyperstimulation, remove pessary and use a bolus of short acting tocolytic eg terbutaline

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67
Q

what is mechanical cervical ripening

A

insertion of balloon catheter through the cervix which is used to distend the cervical canal over a 12 hour period and then removed to allow amniotomy

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68
Q

what is measure on a cartogram

A
fetal heart rate 
cervical dilatation 
duration of labour 
colour of liquor 
frequency and duration of contraction 
caput and moulding 
station/descent of the head 
maternal heart rate, BP and temperature
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69
Q

how is descent of fetal head/station measured

A

assessing the level of the presenting part in cm above or below the ischial spine and marked as +1/2/3 if below the spines and _1/2/3 if above the spines

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70
Q

pros and cons of narcotic analgesia in labour

A

pros:
suitable for women who can’t have regional analgesia eg women on anticonvulsants
remifentanil is ultra-short acting and is superior to pethidine

cons:

maternal: nausea and vomting (give anti-emetic too)
fetal: respiratory depression

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71
Q

pros and cons of inhalation analgesia (gas and air)

A

pros:
easy to administer
short-acting

cons:
may cause nausea
sometimes inadequate as labour progresses

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72
Q

contraindication to regional anaesthesia

A
maternal refusal
coagpulopathy 
local or systemic infection 
uncorrected hypovolaemia 
inadequate or inexperiences staff/facilities
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73
Q

pros and cons of epidural anaesthesia

A

pros:
complete pain relief in majority
can be commenced at any time and does not increase risk of C-section
can be controlled by patient
can be topped up to allow operative deliveries

cons:
may reduce desire to bear down in second stage of labour due to lack of sensation at the perineum and reduced uterine activity 
increased risk of a assisted delivery 
causes abnormal fetal HR 
hypotension
accidental dural puncture 
postural headache 
high block which may cause resp depression in mother 
atonic bladder
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74
Q

describe how an epidural anaesthetic works

A

fine catheter placed into lumbar epidural space (L3-4) and a local anaesthetic agent such as bupivacaine is injected
adding an opioid to the local anaesthetic reduces dose requirements to spare motor function of the lower limbs and reduced complications eg hypotension and abnormal fetal HR

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75
Q

describe a pudendal nerve block

A

injection of local anaesthetic around the pudendal nerve at the level of the ischial spine

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76
Q

pros and cons of pudendal nerve block

A

pros:
used in operative vaginal delivery

cons:
risk of haemorrhage from pudendal artery
risk of lignocaine toxicity if inadvertent intravascular injection
can be ineffective

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77
Q

describe a spinal anaesthetic

A

catheter is placed at L3-4 and inserted into the subarachnoid space where anaesthetic agent is injected

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78
Q

pros and cons of spinal anaesthesia

A

pros:
commonly used for operative delivery

cons:
not used in pain control because of superior safety of epidural and its ability to top up with doses or as continuous infusion to get pain relief over a long period of time

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79
Q

maternal indication for continuous electronic fetal monitoring

A

gestation <37 weeks or >42 weeks
induced labour
administration of oxytocin
ante/intrapartum haemorrhage
maternal illness
pre-eclampsia
previous uterine scar (C-section or myomectomy)
contractions >5 in 10 mins or lasting >90 seconds
during/following insertion of epidural block
maternal request

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80
Q

fetal indication for continuous electronic fetal monitoring

A

abnormal doppler artery velocimetry
known or suspected IUGR
oligohydramnios or polyhydramnios
malpresentation
meconium stained liquor
multiple pregnancy
suspected small for gestational age or macrosomia
reduced fetal movements in the last 24 hours reported by mother
two vessel cord
prolonged ROM >24 hours unless delivery imminent
rise in baseline, repeated decelerations or slow to recover decelerations or overshoots
fetal structural abnormalities

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81
Q

which mnemonic is useful while interpreting CTGs and what does it stand for

A

DR BRAVADO

Define Risk: why are they on CTG (pre-eclampsia, antepartum haemorrhage, maternal obesity, DM, HTN etc)

Contractions: normal = 3-5 contractions/10 minutes

Baseline RAte: fetal HR 110-160 bpm

Variability: good 5-25 bpm, reduced <5 bpm,

Accelerations: rise in fetal HR of at least 15 bpm for 15 seconds (fetal movement), occur with contractions, at least 2 every 15 mins

Decelerations: reductions of 15 bpm for 15 secs, generally abnormal, early or late in relation to contractions (late decelerations are worse)

Overall impression: reassuring or not, BE AWARE of terminal bradycardia (<100 bpm for 10 mins) and terminal decelerations (HR drops and doesn’t recover for 3 mins)

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82
Q

describe a normal CTG in terms of baseline, variability and decelerations

A

baseline: 100-160
variability: 5 or more accelerations
decelerations: none of early

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83
Q

describe a non-reassuring/suspicious CTG in terms of baseline, variability and decelerations

A

baseline: 161-180
variability: <5 accelerations for 30-90 minutes

decelerations: variable decelerations dropping <60 bpm, recovering in <60 secs, present for over 90 minutes, occurring with >50% of contractions
OR
variable decelerations dropping >60 bpm, recovers in >60 secs, present for up to 30 minutes, occurring with >50% of contractions
OR
late decelerations present up to 30 minutes, occurring with 50% of contractions

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84
Q

describe an abnormal/pathological CTG in terms of baseline, variability and decelerations

A

baseline: >180 or <100 bpm, sinusoidal pattern
variability: <5 for >90 minutes

decelerations: non-reassuring variable decelerations still observed 30 mins after conservative management
OR
late decelerations present over 30 mins, do not improve with conservative measures, with >50% of contractions
OR
bradycardia or single prolonged deceleration lasting >3 mins

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85
Q

definition and management of normal CTG

A

baseline, variability and decelerations all normal

Continue CTG and normal care

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86
Q

definition and management of non-reassuring CTG

A

1 non-reassuring features and 2 normal features

inform senior, move to left lateral position, encourage fluids (IV or oral), stop oxytocin, consider tocolysis

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87
Q

definition and management of abnormal CTG

A

1 abnormal feature or 2 non-reassuring features

inform senior, start conservative measures, offer fetal blood sampling
exclude factors indicating need for immediate delivery (cord prolapse, uterine rupture, hyperstimulation, abruption)
treat dehydration, hyperstimulation, hypotension and change position

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88
Q

definition and management of pathological CTG

A

bradycardia or a single prolonged deceleration with baseline <100 bpm for >3 minutes

inform senior, start conservative measures, make preparations for urgent birth (c-section)

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89
Q

early decelerations

definition, cause and management

A

drop in fetal HR of >15 bpm for >15 min that occurs at the beginning of the contraction with the lowest point occurring at the peak of the contraction and recovery when contraction stops

often due to head compression during a contraction and increased vagal tone, occurs in late first and second stage of labour

physiological management

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90
Q

late decelerations

definition, cause and management

A

occurs well after contraction is established and does not return to normal baseline rate until at least 20 seconds after contraction is completed

due to placental insufficiency and may indicate fetal hypoxia (maternal hypotension, pre-eclampsia, uterine hyperstimulation)

call senior help, get fetal blood sample to check for hypoxia, may need to expedite delivery

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91
Q

reduced variability

definition and cause

A

variability of <5 bpm for >40 minutes OR more than 25 bpm 15-25 minutes

fetal sleeping (<40 mins), fetal acidosis and hypoxia, fetal tachycardia, drugs, prematurity, congenital heart problems

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92
Q

variable decelerations

definition, cause and management

A

vary in timing and amplitude and may not have a relationship to uterine contractions

cord compression

change position of mother, increase monitoring

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93
Q

what makes a variably deceleration more concerning

A

shoulders of deceleration are accelerations before and after a deceleration: indicate the fetus is not yet hypoxic and is adapting to the reduced blood flow

variable decelerations without shoulders suggest that the fetus is hypoxic

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94
Q
sinusoidal pattern (CTG)
definition, cause and management
A

smooth irregular wave-like pattern, no beat-to-beat variability, stable baseline of 120-160 bpm

severe fetal hypoxia, fetal anaemia, fetal/maternal haemoarhage

urgent C-section

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95
Q

how often is fetal heart rate monitored in the first and second stage of labour

A

1st stage: every 15 mins for a period of 1 minute soon after a contraction

2nd stage: every 5 mins or after every other contraction for 1 minute

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96
Q

how is a fetal blood sample taken

A

amnioscope used to obtain blood from fetal scalp

cervix must be at least 3 cm dilated to allow insertion

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97
Q

what is the normal fetal pH

A

7.25-7.35

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98
Q

what does management of fatal distress involve

A

changing maternal position
maternal assessment (pulse, BP, abdomen palpation, PV)
IV fluids
stopping contraction (stop/reduce syntocinon or start terbutaline)
scalp stimulation during PV (should have an acceleration)
fetal blood sampling
operative delivery

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99
Q

what is maternal collapse

A

acute event involving the cardiorespiratory systems and/or brain resulting in reduced or absent conscious level

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100
Q

what are the 4H’s of maternal collapse

A

hypovolaemia: bleeding, relative hypovolaemia of dense spinal block, septic or neurogenic shock
hypoxia: peripartum cardiomyopathy, MI, aortic dissection, large vessel aneurysms

hypo/hypoerkalaemia (and other electrolytes)

hypothermia

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101
Q

what are the 4T’s of maternal collapse

A

thromboembolism: amniotic fluid embolism, PE, air embolus, MI
toxicity: local anaesthetic magnesium

tension pneumothorax

tamponade (cardiac)

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102
Q

how does amniotic fluid embolism cause maternal collapse

A

amniotic fluid enters the maternal circulation and triggers a syndrome similar to anaphylaxis and septic shock

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103
Q

if the woman survives the amniotic fluid embolism what is she at risk of developing

A

disseminated intravascular coagulopathy

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104
Q

which dietary supplements are recommended during gestation

A

folic acid 400 mcg from before conception to 12 weeks (reduce neural tube defects)
up to 5 mg if DM, anti-epileptics, BMI >30, previous neural tube dect

10 mg vitamin D, through pregnancy + breastfeeding

250-300 extra calories

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105
Q

what is the guidance for smoking and drinking during pregnancy

A

drinking: no safe limit (risk of fetal alcohol syndrome)
smoking: avoid, increased risk of miscarriage, low birth weight, prematurity

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106
Q

side effects of cocaine, amphetamines and ecstasy in pregnancy

A

maternal: hypersensitive disorders including pre-eclampsia, placental abrupt, death via stroke and arrhythmias
fetal: prematurity, neonatal abstinence syndrome, teratogenicity, IUGR, preterm labour, miscarriage, developmental delay, sudden infant death syndrome, withdrawal

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107
Q

side effects of opiates in pregnancy

A

risk of neonatal abstinence syndrome, IUGR, SIDS, stillbirth, maternal deaths

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108
Q

side effects of cannabis in pregnancy

A

cognitive defects, miscarriage, fetal growth restrictions

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109
Q

side effects of nicotine in pregnancy

A

increased risk of miscarriage
increased risk of preterm labour and IUGR
increased risk of still birth, SIDS

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110
Q

side effects of alcohol in pregnancy

A

fetal alcohol syndrome (smooth philtre, thin vermillion, small palpebral fissures)
IUGR and postnatal restricted growth
learning difficulties
risk of miscarriage
withdrawal
Wernicke’s encephalopathy and Korsakoff’s syndrome
microcephaly

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111
Q

how is substance abuse managed in pregnancy

A

consider methadone programme (avoid chaotic lifestyle)
child protection and social work referral
smear history (put measures in place to ensure the woman gets involved with a screening programme)
breastfeeding education (HIV+ should bottle feed)
labour plan regarding analgesia and labour ward delivery
early IV access
postnatal contraception plan (ASAP)

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112
Q

when does a booking visit take place and what does it consist of

A

10-12 weeks by community midwife

History: medical, drug, social and family, LMP, planned pregnancy, ethnicity of parents

obstetric history: previous pregnancy, mode of delivery, previous miscarriages/terminations

Ix: mother’s blood group, Hb levels, haemoglobinopathies, blood borne infections (HIV/AIDs, syphilis, hep B/C)

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113
Q

when does the anomaly scan take place and which conditions does it screen for

A

18-20+6 weeks

anencephaly, open Spina Bifida, cleft lip, diaphragmatic hernia, gastroschisis, exomphalos, serious cardiac anomalies, bilateral renal genesis, skeletal dysplasia, trisomy 18/13

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114
Q

when is the first stage of Down’s syndrome testing and what does it consist of

A

11-13+6 weeks

combined test = blood test and US

US: nuchal translucency >3.5 mm

bloods: serum PAPP-A, AFP, beta-hCG (down’s = low PAPP-A and aFP, high beta-hCG)

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115
Q

what is the 2nd stage of Down’s syndrome testing andwhe does it take place

A

15-16 weeks

quadruple test = blood test checking aFP, inhibin, estriol and total hCG

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116
Q

how many routine midwife appointments with nulliparous and multiparous women have during pregnancy

A

nulli: 10
multi: 7

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117
Q

women with pre-existing diabetes or gestational diabetes are offered extra monitoring during pregnancy - why?

A

monitor fetal growth and amniotic fluid volume

increased risk of stillbirth, congenital malformation and polyhydramnios

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118
Q

how does exposure to Rh antigen expose future pregnancies to risk of haemolytic disease on newborn

A

when mothers are first exposed to the RH antigen, they form IgM antibodies that are too big to cross the placenta and harm the current fetus

in futur pregnancies when the mother is exposed to the same antigen from the foetus’s red cells, the body forms IgG antibodies which are smaller and can cross the placenta to harm the fetus

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119
Q

how does anti-D work?

A

removed the rhesus positive blood cells from mother’s circulation before antibodies are formed

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120
Q

who is anti-D given to

A

Rh negative mothers who have been exposed to a sensitising event

should be given within 72 hours of the event

prophylactic anti-D given at 28 weeks to cover silent sensitising events, regardless of other sensitising events

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121
Q

what is a sensitising event (in the context of anti-D)

A
placental abruption 
any abdominal trauma 
amniocentesis or CVS
external cephalic version 
IU surgery/transfusion 
fetal death 
vaginal bleeding from 12 weeks 
surgical management of miscarriage at <12 weeks 
evacuation of retained products of conception and molar pregnancy 
termination of pregnancy 
ectopic pregnancy 
delivery (baby is Rh+)
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122
Q

what should always be undertaken before vaginal examination

A

abdominal examination

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123
Q

what equipment is needed to perform a bimanual examination

A
apron
alcohol hand rub 
sterile gloves 
lubricant eg aqua gel
towel or sheet to cover the woman
inco pad
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124
Q

PV examination: inspection

A

inspect the clitoris (size, trauma, ulcers)
external urethral meatus (discharge, prolapse) and 2 para urethral glands at the 3 and 9 o’clock position
remnants of the hymenal ring
vaginal canal (mucosa for colour, texture and rugosity)
vaginal discharge (colour, texture and odour)
older women: ask to cough to demonstrate urinary incontinence or utero-vaginal prolapse

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125
Q

what do you assess the cervix for in PV examination

A

cervical os: open/closed
length of cervix
directed posteriorly (anteverted) or anteriorly
consistency (usually firm when normal but hard in fibrosis/cancer and soft in pregnancy)
cervical excitation tenderness: gently move the cervix from side to side simultaneously assessing the patient’s face to ascertain if painful (positive in PID or ectopic pregnancy)

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126
Q

how to assess the uterus in bimanual examination

A

vaginal fingers are pushed on or behind the cervix to elevate the uterus upwards and towards the anterior abdominal wall and the left hand is placed suprapubically to palpate the uterus between the two hands

size, shape, consistency, position, tenderness, mobility

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127
Q

how to assess the adnexa in bimanual examination

A

vaginal fingers are moved to one of the lateral fornices with the abdominal hand moving into the corresponding iliac fossa

presence of ovary/Fallopian tube, adnexal masses, size, shape, tenderness

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128
Q

what is shoulder dystocia

A

when the baby’s head has been born but one of the shoulders becomes tuck behind the mother’s pubic bone, delaying the birth of the baby’s body

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129
Q

how to manage shoulder dystocia (emergency situation)

A

stop pushing
reposition into all fours position to increase pelvic diameter

OR

lie the woman on her back with her legs pushed outwards and up towards her chest (McRoberts manoeuvre)
ideally have two helpers to abduct each knee to the woman’s chest

press on the abdomen just above the pubic bone in an attempt to dislodge the fetal shoulder

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130
Q

what is the definition of post part haemorrhage

A

loss of >500 ml of blood from the genital tract within 24 hours of the birth of a baby

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131
Q

indications for examination of pregnant abdomen

A

at each antenatal assessment from 24 wks to assess growth
prior to auscultation fo fetal heart and use of CTG (to work out where to listen)
prior to vaginal examination
during labour

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132
Q

which gestational ages are associate with the following fundal heights:
pubic symphysis
umbilicus
xiphoid process of the sternum

A

pubic symphysis: 12 weeks

umbilicus: 20 weeks

xiphoid process: 36 weeks

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133
Q

what is the relationship between the SFH and gestational age

A

gestational age +/- 2 cm

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134
Q

where should you place the stethoscope to listen to the fetal heart rate

A

between the shoulders

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135
Q
which swabs are used for;
trichomonas vaginalis 
bacterial vaginosis 
chlamydia 
gonorrhoea
A

TV and BV: blue swab, vaginal

chlam and gon: orange swab, vulvovaginal

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136
Q

management of miscarriage

A

expectant: up to 14 days
medical: misoprostol
surgical: evacuation of uterus (manual vacuum or electric vacuum)

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137
Q

when to give anti-D in case of miscarriage

A

Rh negative AND >12 weeks or <12 weeks and surgical management

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138
Q

where is most common site of ectopic pregnancy

A

tubes

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139
Q

risk factors for ectopics

A

smoking, PID, previous ectopic, previous tubal surgery

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140
Q

investigation of suspected ectopic pregnancy

A

check HCG 48 hours apart if stable or cannot see pregnancy (PUL)
if >63% rise, likely IUP and offer USS (if HCG >1500)

if >50% drop, likely a failing pregnancy and check urine pregnancy test in 14 days

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141
Q

when is expectant management of ectopic appropriate

A

HCG <1500 and dropping
no significant pain
empty uterus
mass <35 mm and no FH (unruptured)

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142
Q

medical management of ectopic

when/what

A

best if HCG <3000 but up to 5000

methotrexate

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143
Q

side effects of methotrexate management of ectopic

A

bloating and flatulence
transient elevation of LFTs
stomatitis

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144
Q

presentation of molar pregnancy

A

irregular bleeding
hyperemesis
hyperthyroidism

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145
Q

what is a complete molar pregnancy

A

duplication of haploid sperm following fertilisation of an empty ovum
no fetal tissue
USS snowstorm appearance/IU cystic mass

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146
Q

management of complete molar pregnancy

A

surgical evacuation

15% chance of chemo

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147
Q

what are the risks of molar pregnancy

A

becomes invasive and potentially cancer-y

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148
Q

what is a partial molar pregnancy

A

triploid = 2 sets of paternal genes and 1 set of maternal

might be fetal tissue

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149
Q

management of partial molar pregnancy

A

medical management if large fetal tissue
or surgical
0.5% chance of chemo

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150
Q

what is the guidance for future pregnancies after molar pregnancy

A

no pregnancy for 6 months

or 1 year if chemo

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151
Q

fibroids are most common in pre- or post menopausal women

A

pre menopausal

IU masses in post-menopausal women are cancer until proven otherwise

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152
Q

symptoms of fibroids

A
none (50% incidental finding)
HMB
dysmenorrhoea 
pressure effects (frequency, hydronephrosis if compress ureters)
infertility
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153
Q

what further medical complications can be caused by fibroids

A

anaemia if heavy bleeding
degeneration (pain)
torsion if pedunculated
infection

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154
Q

management of fibroids <3 cm

A
Mirena 1st line 
tranexamic acid and NSAIDs 
other contraception (COCP, POP)
if submucosal can have transcervical resection 
endometrial ablation 
hysterectomy
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155
Q

management of fibroids >3 cm

A
tranexamic acid and NSAIDs 
Mirena coil/COCP/POP
uterine artery embolisation 
myomectomy 
hysterectomy 
GnRH analogues (switch off hormone production from ovaries, 3 months pre-op)
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156
Q

tumour marker of ovarian cancer

A

Ca125

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157
Q

what is a complex ovarian cyst

A

multiloculated
has solid parts in it
in any way suspicious of cancer

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158
Q

what is an RMI (risk of malignancy index) in ovarian cancer

A

USS features x menopausal status x ca123

<200 low risk (repeat in USS 3 months or benign surgery)
>200 refer to gynae onc MDT and CT chest abdo pelvis

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159
Q

who is offered cervical screening

A

25-64 year olds

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160
Q

what is tested in cervical screening

A

HPV
if negative - recall in 5 years
if positive do cytology

cytology
if negative HPV in 12 months
if positive colposcopy

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161
Q

when would you diagnose someone with the menopause

A

cessation of menstruation for >1 year

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162
Q

risks of HRT

A

VTE: increased with oral, no increase with transdermal
stroke: increased with oral, not with transdermal
CVS: if <60 no increase
BrCa: increased, no increase if oestrogen only
osteoporosis: reduced risk

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163
Q

when to give combined or oestrogen only HRT

A

if no uterus = oestrogen only

if uterus = combined (oestrogen and progesterone)

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164
Q

what are the two main diagnostic tests available to high risk pregnancies

A

chorionic villous sampling and amniocentesis

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165
Q

what is NIPT

A

non-invasive prenatal testing

analyses cell-free DNA in the mother’s blood from the fetus

better sensitivity and specificity than 1st trimester DS screening

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166
Q

risk factors for multiple pregnancy

A
assisted conception eg clomid, IVF 
ethnicity (African) 
family history on maternal side 
increased maternal age 
increased parity 
tall women > short women
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167
Q

define zygosity and chorionicity

A

monozygotic: splitting of a single fertilised egg
dizygotic: fertilisation of 2 ova by 2 sperm

dichorionic: 2 placentas, always dichorionic diamniotic
monochorionic: 1 placenta, may be mono- or diamniotic

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168
Q

how is chorionicity determined

A

USS, at booking scan

DCDA: lambda sign

MCDA: T-sign

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169
Q

how does management differ between DC and MC twins

A

MC twins need 2 weekly USS to pick up early signs of Twin-Twin transfusion syndrome

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170
Q

signs and symptoms of multiple pregnancy

A

exaggerated pregnancy symptoms (eg hyperemesis gravid arum)
high AFP
large for dates uterus
multiple fetal poles

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171
Q

fetal complications of multiple pregnancy

A
congenital anomalies 
IU death (single and both)
preterm birth 
growth restriction (equal, discordant)
cerebral palsy 
TTTS (monochorionic pregnancies)
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172
Q

maternal complications of multiple pregnancy

A
hyperemesis gravidarum 
anaemia 
pre-eclampsia 
GDM
antepartum haemorrhage (abruption, praaevia)
preterm labour 
c-section
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173
Q

describe antenatal management of multiple pregnancy

A

consultant led care
antenatal clinic every 2 weeks if MC and 4 weeks if DC
iron and folic acid supplements
low dose aspirin to prevent HTN
USS from 16th week with deep vertical pool, bladder and umbilical artery assessment
anomaly scan 18-20 weeks

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174
Q

what is TTS

A

disproportionate blood supply to foetuses in MC pregnancies
one twin has reduced blood supply leading to decreased urine output, anaemia and oligohydramnios while the other twin has increased urinary output, polyhydramnios, polycythaemia and eventually heart failure

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175
Q

management of TTS

A

fetoscopic laser ablation before 26 weeks

after 26 weeks amnioreduction/septostomy and aim to deliver at 34-36 weeks

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176
Q

timing of delivery in DCDA and MCDA twins

A

DCDA 37-38 weeks

MCDA 36+0 with steroids

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177
Q

mode of delivery of multiple pregnancies

A

triplets c-section
MCMA: c-section
one cephalic twin: aim for vaginal but may need to with to CS

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178
Q

labour management of multiple pregnancy

A

epidural to facilitate operative delivery
continuous use of CTG for both
syntocinon after twin 1 to maintain contractions
USS to confirm presentation
intertwine delivery time <30 mins

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179
Q

what are the different types of breech presentation

A

complete breech: legs folded with the leet level with the bottom

footling breech: on or both feet point down so will emerge first

frank breech: feet are up at the baby’s head so bottom emerges first

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180
Q

what is external cephalic version

A

attempting to manually turn the fetus into a cephalic presentation
50% successful

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181
Q

what is prolonged pregnancy

A

> 42 weeks

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182
Q

risks of prolonged pregnancy

A

stillbrith
meconium aspiration
respiratory distress

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183
Q

when should induction be offered in prolonged pregnancy

A

21-42 weeks

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184
Q

role of USS in early pregnancy

A
assessment of viability 
IU or ectopic 
date pregnancy using CR L
determine chorionicity 
off Down syndrome screening
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185
Q

role of USS in 2nd trim

A

fetal anomaly scans
placental site
screen maternal uterine artery resistance

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186
Q

role of USS in 3rd trim

A

monitor fetal growth (abdominal circumference, head circumference, femur length - calculate EFW)
fetal hypoxia
anaemia

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187
Q

how can USS assess for fetal anaemia/hypoxia

A

umbilical artery increases its resistance in fetal hypoxia and middle cerebral artery decreases resistance

MCA shows increased peak systolic volume in anaemia

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188
Q

how many USS does an uncomplicated pregnancy get

A

2: booking and anomaly scan

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189
Q

risk factors for maternal morbidity and mortality

A
black/asian ethnicity 
age >40
deprivation
VTE 
mental health issues
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190
Q

define still birth

A

baby born with no signs of life at or after 28 weeks gestation

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191
Q

major causes of stillbirth

A
labour complications 
post-term pregnancy 
maternal infections eg malaria, HIV
maternal disorders eg DM, HTN
fetal growth restriction 
congenital abnormalities
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192
Q

what are the features of gestational HTN

A

develops after 20 weeks gestation, no proteinuria or oedema

systolic >140 or diastolic >90
or increase above booking readings of >30 or >15

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193
Q

what ar the features of pre-eclampsia

A

after 20 weeks gestation, HTN with proteinuria (>0.3 g/24 hours)

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194
Q

complications of pre-eclampsia

A
fetal prematurity and IUGR
eclampsia 
haemorrhage due to placental abruption 
cardiac failure 
stroke 
VTE
DIC  and HELLP
pulmonary oedema 
multi-organ failure
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195
Q

investigations for PET

A

BP
urinalysis (protein)
Hb, PLT, U&Es, coag screen, rate

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196
Q

management of pre-existing HTN

A

switch from ACEI (teratogenic) to labetalol, nifedipine, methyldopa

consider patient’s allergies and PMH

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197
Q

management of pregnancy induced HTN (if <20 weeks)

A

labetalol
nifedipine
methyldopa
hydralazine

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198
Q

management of PET >20 weeks

A

labetalol, nifedipine, methyldopa, hydralazine

IV MgSulphate

definitive treatment is delivery of baby

steroids if early delivery

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199
Q

secondary preventions in women with history of PET or risk factors for PET

A

low dose aspirin started at 12 weeks
increased surveillance for signs and symptoms of PET
regular growth scans

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200
Q

risk factors for GDM

A
previous GDM
obesity BMI >30
Fix of a first degree relative with GDM
ethnicity (SE asian, Middle Eastern, black Caribbean)
previous big baby
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201
Q

signs of GDM

A

polyhydramnios

glycosuria

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202
Q

complications of GDM

A

overgrowth of insulin sensitive tissues and macrosomia
shoulder dystocia and vaginal trauma
assisted delivery/c-section
hyperaemic state in utero (risk of stillbirth)
short term metabolic complications (fetal hypoglycaemia post-delivery)
long term risk of obesity, insulin resistance and diabetes in baby

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203
Q

complications of pre-exisiting diabetes in pregnancy

A
congenital anomalies (increased risk of NTD and cardiac anomalies)
miscarriage (<24 weeks)
IU death (>24 weeks)
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204
Q

pre-pregnancy counselling in T1DM or T2DM

A
HbA1c monitoring: aim for 48
avoid pregnancy if >86 
stop embryopathic medication 
determine micro-microvascular complications high dose folic acid 
low dose aspirin from 12 weeks
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205
Q

when to deliver in GDM

A

metformin: 39-40 weeks
diet controlled: 40-41
insulin: 38 weeks

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206
Q

describe screening and diagnosis of GDM

A

assess risk factors at booking
previous gestational diabetes
blood glucose monitoring and OGTT in 1st trim (if normal repeat at 24-28 weeks)

fasting: >5.1
2 hour: >8.5

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207
Q

blood sugar targets in pregnancy

A

fasting: 3.5 - 5.5

1 hours post-meal: <7.8

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208
Q

which medications can be used to control GDM if diet and exercise fail

A

metformin

insulin

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209
Q

postnatal care in GDM

A

increased risk of T2DM
fasting BG measured 6-8 weeks
if results suggest T2DM, OGTT at 6 weeks
annual screening for diabetes by GP

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210
Q

aetiology of PROM

A

infection
cervical incompetence
over-distension of uterus
vascular causes eg placental abruption

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211
Q

risk factors for PROM

A
previous pre-term labour 
multiple pregnancy 
smoking 
uterine anomalies 
parity 
ethnicity 
poor socioeconomic status 
drugs (esp cocaine)
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212
Q

what are the complications of PROM

A

neonatal mortality and morbidity (prematurity, sepsis, pulmonary hypoplasia)
chorioamnionitis

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213
Q

how to diagnose PPROM

A

maternal history followed by sterile speculum examination (pooling of blood in posterior vaginal fornix)

USS: oligohydramnios

avoid digital vaginal examination due to risk of infection, unless suspicion woman may be in labour

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214
Q

management of PROM

A

monitor for signs of chorioamnionitis (maternal pyrexia, tachycardia, leucocytosis, uterine tenderness, discharge, fetal tachycardia)
Abx to prevent ascending infection (erythromycin)
tocolytics (nifedipine if 26-33+6)
maternal steroids
magnesium sulphate

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215
Q

causes of fetal anaemia

A
Rh antibodies 
parvovirus 
CMV 
syphilis
toxoplasmosis 
Hb-opathies 
feto-maternal haemorrhage 
MC tiwn complications
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216
Q

what is hydrops fetalis

A

abnormal accumulation of fluid in 2 r more compartments and manifests as ascites, plural effusion, skin oedema, pericardial effusion

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217
Q

causes of APH

A
placenta praaevia 
placental abruption 
local causes (cervical ectropion, polyps, infection, cervical cancer)
vasa praevia 
uterine rupture
indeterminate 
preterm labour
218
Q

how can blood loss by quantified in APH

A

spotting: staining, streaking or blood spotting noted on underwear or sanitary pad

minor haemorrhage: <500 ml that has settles

major: 500-1000 ml with no signs of shock
massive: >1000 ml and/or signs of shock

219
Q

define placenta praaevia

A

placenta covering or within 2 cm of the cervical os

220
Q

investigation of placenta praaevia

A

if early scan (anomaly scan) shows low-lying placenta, another scan is done at 32 weeks to check if the placenta has moved
if unclear offer transvaginal scan

221
Q

presentation of placenta praaevia

A

bright red painless bleeding

222
Q

risk factors of placenta praaevia

A

age
previous c-section
previous praaevia

223
Q

define placental abruption

A

separation of a normally implanted placenta either partially or totally before the birth of the fetus

224
Q

consequences of placental abruption

A

IU death and fetal hypoxia
primary post part haemorrhage
risks of massive bleeding (DIC, low BP, multi-organ failure, risk of death)

225
Q

risk factors for placental abruption

A
PET/HTN
trauma 
smoking, cocaine, amphetamine
medical thrombophilia, renal disease or diabetes 
polyhydramnios 
abnormal placenta 
previous abruption
multiple pregnancy, PROM
226
Q

symptoms of placental abruption

A
severe, continuous abdominal pain 
backache with posterior placenta 
bleeding (concealed)
preterm labour 
maternal collapse
227
Q

signs of placental abruption

A

unwell distressed patient
signs may be inconsistent with revealed blood
uterus large for dates or normal
uterine tenderness
woody, hard uterus
fetal parts difficult to identify
may be in preterm labour with heavy show
fetal heart rate may be absent or bradycardia
CTG shows irritable uterus

228
Q

management of placental abruption

A

resuscitate mother
urgent c-section and replacing blood products
fetal resuscitation if needed
manage complications: anti-D

229
Q

define vasa praevia

A

fetal blood vessels I the membranes overlying close to the internal cervical os

230
Q

presentation of vasa praaevia

A

membranes are ruptured followed by small amount of dark vaginal bleeding and acute fetal bradycardia and decelerations

231
Q

how to prevent vasa praaevia

A

always feel for pulsations or any cord-like structures before performing amniotomy
check fetal head is presenting and engaged before inducing labour or ARM

232
Q

what are the types of vasa praaevia

A

type 1: vessel connected to velamentous umbilical cord

type 2: when it connect to the placenta with a succenturiate or accessory lobe

233
Q

risk factors for vasa praaevia

A

placental abnormalities (bilobed, succinturiate lobes)
low lying placenta in 2nd trim
multiple pregnancy
IVF

234
Q

management of vasa praaevia

A

antenatal diagnosis:
steroids at 32 weeks
inpatient management if risks of preterm birth (32-34 weeks)
elective c-section before labour (34-36 weeks)

diagnosed during labour:
emergency c-section, might need blood transfusion for baby

235
Q

presentation of uterine rupture

A

acute constant abdominal pain even when the uterus is relaxed which may be referred to the shoulder tip
sudden collapse
fetal parts easily palpable as may be in abdominal cavity

236
Q

maternal chicken pox infection in last 4 weeks of pregnancy

A

avoid planned pregnancy for 7 days to allow transfer of maternal Ig

237
Q

pregnancy woman who has never had chicken pox is in contact with chicken pox

A

blood test to check IgG antibodies to varicella zoster will confirm immunity
if not immune offer varicella zoster Ig as post-exposure prophylaxis (effective within 10 days)

238
Q

effects on fetus of CMV infection in pregnancy

A

hearing loss
visual impairment or blindness
mild to severe LD
epilepsy

239
Q

clinical features of congenital CMV

A
jaundice 
petechial rash
hepatosplenomegaly 
microcephaly 
SGA
240
Q

how long is a person with parvovirus infectious for

A

1 day after rash develops

241
Q

parvovirus B19 in fetus causes

A

severe anaemia, heart failure, hydrops fetalis

242
Q

symptoms of congenital rubella

A

sensorineural learning loss
congenital heart disease (PDA)
ocular abnormalities (congenital glaucoma, cataracts)

243
Q

HIV viral load

A

<50 copies/ml

244
Q

babys born the HIV positive mothers receive what postnatal

A

testing at birth and at regular intervals up to 2 yo

245
Q

should HIV positive women pbreast feed?

A

formula is safest way to feed baby
safe to breast feed if:
undetectable viral load and mother is taking ART
exclusive breastfeeding for first 6 months and not mixing formulas or cow’s milk
avoid breastfeeding at high risk times eg mastitis, cracked nipples, detectable viral load, D+V in mother or baby

246
Q

diagnosis f DVT

A

swelling
oedema
leg pain or discomfort
increased leg temperature

247
Q

testing for DVT in peurperium

A

compression duplex US
if normal but high suspicion repeat in one week to exclude an extending thrombosis and give therapeutic dose of LMWH
consider MRI venography if iliac vein thrombosis suspected

248
Q

symptoms and signs of PE

A
dyspnoea 
chest pain
faintness 
collapse 
haemoptysis 
raised JVP
focal signs in chest 
symptoms and signs of DVT
249
Q

diagnosis of PE

A

CTPA or V/Q scan

250
Q

management of PE

A

heparins

251
Q

risk factors for preterm birth

A
previous preterm labour 
multiple pregnancy 
uterine anomalies 
age 
parity (mulligan's- or grand)
ethnicity 
poor socio-economic status 
smoking 
drugs (cocaine)
Low BMI (<20)
252
Q

what is SGA

A

estimated fetal weight or abdominal circumference below the 10 decile in both population and customised gentiles

253
Q

what is LGA

A

> 90th centile

SFH >2cm for gestational age

254
Q

causes of LGA

A

polyhydramnios
multiple pregnancy
macrosomia due to GDM
wrong dates in late bookers

255
Q

what is polyhydramios

A

excess of amniotic fluid with AFI >25 cm or deepest vertical pool >8 cm

256
Q

risks associated with LGA

A

clinician and maternal concern
shoulder dystocia
PPH

257
Q

symptoms and signs of polyhydramnios

A
abdominal discomfort 
PROM
preterm labour 
cord prolapse 
large for dates 
malpresentation 
shiny, tense abdomen 
inability to feel fatal parts
258
Q

innervation of detrusor muscle

A

parasympathetic nerves derived from the pelvic splanchnic S2-4

259
Q

innervation of urethral smooth muscle

A

sympathetic nerves from spinal cord at T10-L2

descend to bladder and urethra via the hypogastric nerves

260
Q

innervation of the striated urethral sphincter and pelvic floor (levator ani) muscles

A

pudendal nerve S2-4

261
Q

describe the three levels of support the pelvic floor gives the vagina

A

cervix and upper vagina
supported by uterosacral, transverse cervical and pubocervical ligaments

middle vagina
supported by pelvic fascia

lower vagina
supported by levator ani muscles and perineal body

262
Q

contents of deep perineal pouch in females

A
part of urethra 
vagina 
clitoral neuromuscular bundle 
extensions of ischioanal fat pads 
smooth muscle 
external urethral sphincter and compressor urethrae
263
Q

contents of deep perineal pouch in males

A
part of urethra 
bulbourethral glands 
neuromuscular bundle of penis 
extension of sischioanal fat pads 
smooth muscle 
external urethral sphincter and compressor urethrae
264
Q

contents of superficial perineal pouch (female)

A
clitoris and crura 
bulbs of vestibule 
bulbospongiosus 
ischiocavernosus 
vestibular glands 
superficial transverse perineal muscle
internal pudendal vessels 
internal pudendal nerve
265
Q

contents of superficial perineal pouch (male)

A
bulb of penis and crura 
bulbospongiosus 
ischiocavernosus 
internal pudendal vessels 
pudendal nerve 
superficial transverse perineal muscle
266
Q

causes of pelvic floor weakness

A

increased intra-abdominal pressure:
obesity, chronic cough, occupational or recreational exercise, constipation, intra-abdominal mass

pelvic floor muscle trauma and denervation:
obstetric trauma, pelvic fracture or surgery, congenital

connective tissue disorder:
age related, oestrogen deficiency, congenital or acquired connective tissue disorder, drug related (steroids)

267
Q

common features of stress incontinence

A

after childbirth, pelvic surgery and oestrogen deficiency

triggers: coughing, sneezing, exercise

268
Q

investigations for stress incontinence

A

exclude UTI
frequency/volume charts (normal frequency and bladder capacity)
urodynamic studies

269
Q

management of stress incontinence

A

lifestyle: weight loss, smoking cessation, avoid constipation, avoid heavy lifting, caffeine reduction
conservative: pelvic floor exercises for 3 months, use of pads
medical: duloxetine (not first line)
surgical: bulking agents, autologous rectus fascial sling, colposuspension, artificial urinary sphincters

270
Q

side effects of duloxetine for stress incontinence

A
difficulty sleeping 
headache 
dizziness 
blurred vision 
change in bowel habit 
nausea and vomiting 
dry mouth 
sweating 
decreased appetite 
weight loss 
decreased libido
271
Q

features of urge incontinence

A

triggers: hearing running water, cold weather
larger volumes that SUI
“I have to go immediately”

272
Q

investigations of urge incontinence

A

frequency/volume charts (increased frequency)

urodynamic testing shows over-activity of detrusor muscle

273
Q

management of urge incontinence

A

lifestyle: decrease fluid intake, minimus caffeine and alcohol, use of pads

bladder retraining

medical: tolterodine/solifenacin (oxybutynin not recommended due to cognitive impairment), mirabegron, topical oestrogen, desmopressin in nocturia
surgery: botox, percutaneous sacral nerve stimulation, augmentation cystoplasty

274
Q

causes of overflow incontinence

A

inactive detrusor muscle: neurological conditions (eg MS)
involuntary bladder spasms: CV disease, diabetes
cystocele or uterine prolapse

275
Q

investigation of overflow incontinence

A

frequency/volume charts

urodynamic testing shows inactivity of detrusor muscle

276
Q

management of overflow incontinence

A

treat the cause

277
Q

what are the stages of prolapses

A

stage 1: mild protrusion on examination (-1 cm)

stage 2: prolapse present at introitus (-1 to +1 cm)

stage 3: beyond +1 cm from the introitus

stage 4: prodicentia (complete inversion)

278
Q

risk factors for prolapse

A
increasing age (40% post menopausal)
multiparity 
vaginal deliveries 
obesity 
Spina Bifida
279
Q

clinical signs of prolapse

A

sensation of pressure, heaviness, bearing down

urinary incontinence, frequency, urgency

280
Q

management of prolapse

A

if mild and asymptomatic may not need treatment

lifestyle: weight loss, avoid constipation, smoking cessation, avoid heavy lifting, caffeine reduction

pelvic floor training: kegels, pilates, supervised PFE with physio

ring pessary
surgery

281
Q

surgical options for prolapse

A

cystocele/cystourethrocele: anterior colporrhaphy
uterine prolapse: hysterectomy, sacrohysteropexy, Sacrospinous fixation (sutured placed in Sacrospinous ligament medial to ischial spine to fix prolapse in place)
rectocele: posterior colporrhapy

282
Q

symptoms of UTI

A
dysuria 
increased frequency/urgency 
cloudy/offensive urine 
lower abdo pain
fever/malaise
delirium in elderly
283
Q

management of UTI in in non-pregnant women

A

urine culture if >65 yo or haematuria

trimethoprim or nitrofurantoin for 3 days

284
Q

management of symptomatic UTI in pregnancy

A

urine culture
nitrofurantoin in 1st and 2nd trim
trimethoprim in 3rd trim

285
Q

management of symptomatic UTI in pregnancy

A

urine culture should be done at 1st antenatal visit
high risk of preogressing to acute pyelonephritis
immediate course of nitrofurantoin (avoid near term), amoxicillin or cefalexin for 7 days
urine culture after treatment for test of cure

286
Q

briefly describe the processes of fertilisation and implantation

A

at ovulation the egg is released into the fallopian tube where it is normally fertilised
cells divide and progress to a morula, then blastocyst as it travels along tube to uterus
blastocyst implants into uterine lining during days 5-8
the inner cells develop into the embryo and the outer cells invade the endometrium to become the placenta

287
Q

what are the four outcomes of fertilisation

A

normal pregnancy: normal embryo in normal locations

miscarriage: normal/abnormal embryo in normal location
ectopic: normal embryo in abnormal location
molar: abnormal embryo in normal location

288
Q

how do HCG values change during a normal pregnancy

A

should double every 48 hours in a normal pregnancy

289
Q

when does HCG level reach peak

A

12-14 weeks

N+V normally reduce after this time

290
Q

what is the effect of human placental lactogen

when does it start to be released

A

growth-hormone like effects and decreases insulin resistance in the mother
also involved in breast development (tenderness)

week 5

291
Q

what are common non-hormonal changes in pregnancy

A

increased cardiac output due to increased blood volume (raised HR, ECG changes, functional murmurs)
increased plasma volume causes decreased Hb by dilution

292
Q

what is implantation bleeding

how does it present and when

A

occurs when the fertilised egg implants into the uterine wall
normally about 10 days after ovulation
generally light brown and limited (earlier and lighter than a period)

293
Q

what is a subchorionic haematoma

what are its symptoms

A

collection of blood between the chorion and uterine wall
symptoms vary by size but include bleeding, cramping and threatened miscarriage
large haematomas may lead to miscarriage, infection or irritability

294
Q

what type is present in the two parts of the cervix

A

ectocervix: tough, squamous epithelium
endocervix: columnar epithelium

295
Q

how does pregnancy affect the location of the transitional zone of the cervix
what can occur as a result

A

location of transitional zone changes as a physiological response to pregnancy
exposes the endocevical (columnar) epithelium to the external environment of the vagina
can cause erosion (ectropion) which may bleed

296
Q

what are causes of bleeding in early pregnancy

A
implantation bleeding 
polyps 
cervical erosion 
infection (STI, herpes, bacterial infection)
suchorionic haematoma 
malignancy 
miscarriage
297
Q

someone presenting with bleeding in early pregnancy may be experiencing non-PV bleeding
what other sources of bleeding should be considered?

A

haematuria: UTI, kidney stones, malignancy

PR bleeding: haemorrhoids, anal fissures, gastroenteritis, IDB, malignancy

298
Q

miscarriage can occur up to ______ weeks gestation

A

23+6

299
Q

what is a threatened miscarriage

A

risk to the pregnancy
bleeding +/- cramping
cervical os is closed

300
Q

USS signs of threatened miscarriage

A

intrauterine pregnancy

foetal pole is present and if measures >7 mm a foetal heart should be present

301
Q

what is an inevitable miscarriage

A

symptoms consistent with miscarriage and the pregnancy can’t be saved
open os, possibly products of conception at the os

302
Q

USS signs of inevitable miscarriage

A

may show viable pregnancy

products that are in the process of expulsion

303
Q

what is an incomplete miscarriage

A

some products have passed, but there are some products remaining in the uterus

304
Q

what is a septic miscarriage

A

infection alongside incomplete or complete miscarriage

305
Q

symptoms of septic miscarriage

A

fevers, riggers, uterine tenderness, bleeding, offensive discharge and pain

306
Q

recurrent miscarriage is defined as

A

3 or more consecutive pregnancy losses

307
Q

what is a missed miscarriage

A

no symptoms or a history of threatened miscarriage but on USS there is no viable pregnancy

308
Q

what are USS signs of early foetal demise

A

pregnancy in situ that has mean sac diameter of >25 mm and/or a foetal pole >7 mm but no heart beat

309
Q

causes of miscarriage

  • embryo
  • maternal factors
  • uterine factors
  • immunologic
  • infections
  • iatrogenic
A

embryo: chromosomal abnormalities

maternal factors: PCOS, uncontrolled DM, increasing age, heavy smoking, alcohol/drugs (cocaine), severe HTN, obesity

immunologic: APS
infections: CMV, rubella, toxoplasmosis, listeria
iatrogenic: CVS or amnio

310
Q

which antibodies are associated with APS

what effect do they have on pregnancy

A

lupus anticoagulant
anticardiolipin antibodies
anti-B2 glycoprotein-1

inhibiting trophoblastic function and differentiation
create localised inflammatory response at maternal-foetal interface
cause thrombosis of uteroplacental vasculature

311
Q

what is cervical shock and how does it present

A

occurs during incomplete miscarriage where the products are sitting in the cervix
cramps, severe abdo pain, N+V, sweating, fainting, bradycardia, hypotension

312
Q

why might IV fluids not correct hypotension in cervical shock

A

due to vagal stimulation of the products sitting in the cervix

313
Q

management of cervical shock

A

remove products from cervix

can be done with a speculum and sponge forceps

314
Q

presentation of ectopic pregnancy

A
localised pelvic pain
light PV bleeding 
shoulder tip pain 
SOB
dizziness
passage of tissue 
rectal pressure or pain on defecation
315
Q

signs of Coptic pregnancy

A

pallor, haemodynamic instability
peritonism, guarding, general abdominal or pelvic tenderness, adnexal tenderness
cervical motion tenderness, abdominal distension, enlarged uterus

316
Q

presentation of molar pregnancy

A
hyperemesis 
funds large for dates 
varied bleeding 
grape-like tissue 
SOB
317
Q

assessment of woman presenting with suspected miscarriage

A

asses haemodynamic stability
FBC, G&S, Rh status
serum HCG (should halve every 48 hours)

318
Q

investigations for ectopic pregnancy

A

FBC, G&S, HCG and TVUSS

suboptimal HCG (doesn’t double every 48 hours)

empty uterus on TVUSS or presence of pseudo sac

free fluid in pouch of Douglas = suspect ruptured ectopic

319
Q

signs of molar pregnancy

A

raised levels of HCG
typical snowstorm appearance on USS
with or without fetus

320
Q

management of miscarriage

A

threatened: watchful waiting

missed/incomplete and stable : conservative, medical or surgical management

missed/incomplete and unstable: ABCDE, resus, surgical management normally safest option

321
Q

what are the surgical options for miscarriage

A

surgical evacuation under GA

manual vacuum aspiration under local anaesthetic

322
Q

advice for women with recurrent miscarriage/APS

A

low dose aspirin and daily fragmin injection for future pregnancies

323
Q

when is surgical management indicated in ectopic pregnancy

A

significant pain
adnexal mass >35 mm
visible heart beat on USS

324
Q

conservative management of ectopic

A

patients asked to return for serum HCG measurements on days 2, 4 and 7 after original test

if they fall by at least 15% from previous value they can be repeated weekly until a negative (<20 IU/L) is obtained

325
Q

medical management of ectopic

A

single of 2 separate doses of methotrexate and continued HCG monitoring

326
Q

surgical management of ectopic

A

laparoscopic salpingotomy or salpingectomy

327
Q

management of molar pregnancy

A

surgery

send tissue for histological examination

328
Q

what is hyperemsis gravid arum

A

vomiting that is excessive, prolonged and begins to alter the woman’s quality of life

329
Q

consequences of unmanaged hyperemesis gravid arum

A

dehydration, ketosis, electrolyte and nutritional imbalance, weight loss, altered liver function

330
Q

other causes of excessive vomiting in pregnancy

A
UTI
gastritis 
peptic ulcer 
viral hepatitis 
pancreatitis
331
Q

management of hyperemesis gravid arum

A

IV fluids and electrolytes
anti-emetic (PO or IV)
first line is cyclising or prochlorperazine

nutritional supplements: thiamine, pabrinex (Vit B/C)
if severe NG/TPN

ranitidine/omeprazole for reflux

steroids if super bad

consider thromboprophylaxis

332
Q
define the following:
menorrhagia 
metrorrhagia 
polymenorrhoea 
polymenorrhagia 
menometrorrhagia 
amenorrhoea 
oligomenorrhoea
A

menorrhagia: prolonged and increased bleeding (heavy menstrual bleeding)
metrorrhagia: regular Intermenstrual bleeding
polymenorrhoea: menses occurring at <21 day interval
polymenorrhagia: increased and frequent cycle
menometrorrhagia: prolonged menses and Intermenstrual bleeding
amenorrhoea: absence of menstruation >6 months
oligomenorrhoea: menses with interval >35 days OR presence of <5 menstrual cycles in a year

333
Q

assessment of menorrhagia

A

thorough history
general exam for signs of anaemia
abdominal and pelvic examination
smears and swabs if necessary

334
Q

what is dysfunctional uterine bleeding

A

menorrhagia in the absence of other pathology

a diagnosis of exclusion, found in 50% of women with abnormal uterine bleeding

335
Q

what are the two types of DUB and what are their characteristics

A
anovulatory:
85% of DUB
occurs at extremes of reproductive life 
irregular cycle 
more common in obese women 

ovulatory:
more common in 35-45 yo
regular heavy periods
due to inadequate progesterone production by corpus luteum

336
Q

investigations for DUB

A

FBC
TFTs (hypothyroid features)
coagulation screen (very heavy bleeding or signs of bleeding tendency)
TVUSS (endometrial thickness, fibroids, other masses)
endometrial sampling (pipette biopsies, hysteroscopy, D&C)
smear (if due - opportunistic, not a test for DUB)
refer to colposcopy if abnormal cervix

337
Q

what are options for medical management of DUB

A

progestogen releasing IUCD (Mirena): 1st line treatment, may cause breakthrough bleeding for 3-9 months after insertion

COCP: compliance issues, check UKMEC for contraindications

antifibrinolytics (tranexamic acid): during menstruation, if contraception not wanted

NSAIDs (mefenamic acid): during menstruation, CI in duodenal ulcers or severe asthma

oral progestogens (norethisterone, medrocyprogesterone)

GnRH analogues: act on pituitary to stop oestrogen production resulting in amenorrhoea, can cause osteoporosis

danazol: synthetic androgen that acts on HPO axis

338
Q

surgical management of DUB

A

endometrial resection/ablation

hysterectomy

339
Q

disadvantages of surgical management of DUB

A

anaesthetic risks
loss of fertility in hysterectomy
complications in future pregnancy after ablation (placenta accreta)

340
Q

causes of intermenstrual bleeding

A
cervical ectropion 
PID and STI
endometrial or cervical polyps 
cervical cancer 
endometrial cancer 
undiagnosed pregnancy/complications of 
Hyatidiform molar disease
341
Q

psychological and physical manifestations of PMS

A

psych: depression, irritability and emotional lability
phys: fluid retention, weight gain, breast tenderness

342
Q

diagnosis of PMS

A

menstrual diary of symptoms for at least 2 cycles

343
Q

management of PMS

A

severe symptoms: SSRIs daily or during luteal phase of cycle and CBT

mild: lifestyle eg stress reduction, alcohol and caffeine reduction, exercise
medical: COCP, transdermal oestrogen, short-term GnRH

hysterectomy with bilateral salpingo-oophorectomy as last resort (trial of GnRH before surgery)

344
Q

how do GnRH analogues work to reduce PMS, improve endometrisos and shrink fibroids

give some examples

A

if GnRH receptors are constantly simulated, they are desensitised, reducing GnRH release and thus reducing LH and SH release

Buserelin and goserelin

345
Q

causes of postcoital bleeding

A
cervical ectropion 
cervical carcinoma 
trauma 
Atrophic vaginitis 
cervicitis due to STI 
polyps 
idiopathic
346
Q

what do the NICE guidelines say about post menopausal bleeding

A

women over the age of 55 with PMB should be investigated within 2 weeks by USS for endometrial cancer

347
Q

causes of PMB

A
Atrophic vaginitis (most common and benign)
endometrial polyps 
endometrial hyperplasia 
endometrial carcinoma 
cervical carcinoma 
ovarian cancer (esp theca cell tumours)
vaginal cancer (rare)
348
Q

investigations of PMB

A

USS (transvaginal > abdominal): endometrial thickens >4 mm, further investigation needed (5 mm cut off if taking HRT)

if taking tamoxifen, endometrium will be thickened, irregular and cystic so do hysteroscopy and biopsy instead

further imaging: CT/MRI

349
Q

management of PMB

A

Atrophic vaginitis: topical oestrogen and vaginal lubricants, HRT

endometrial hyperplasia: D&C, progestogen treatment, Mirena IUS, oral progestogens

endometrial cancer: refer to oncology

cervical cancer: refer to oncology

350
Q

what are the Rotterdam criteria

A

used to diagnose PCOS, presence of two of the following:

clinical or biochemical evidence of hyperandorgenism (hirsutism, acne, hah free testosterone, low sex hormone binding globulin, high free androgen index)

polycystic ovaries on USS (ovarian volume >10 cm^3, at least 12 follicles in one ovary measuring 2-9 mm diameter)

oligo/amenorrhoea

351
Q

features of PCOS

A

obesity/overweight
hypertension
acanthosis nigricans (thickening and pigmentation of skin of neck, axillae, skin folds)
acne and hirsutism
alopecia
insulin resistance, diabetes, lipid abnormalities
irregular periods

352
Q

why are people with PCOS at higher risk of endometrial hyperplasia/carcinoma

A

oligo/amenorrhoea in presence of pre-menopausal levels of oestrogen

353
Q

hormonal changes in PCOS

A

increase in LH:FSH ratio, LH levels very high and FSH low/nomral

354
Q

management of PCOS

A

dependent on how patient presents and what their main concern is

optimise BMI
endometrial protection with hormonal contraception

355
Q

management of infertility in PCOS

A

weight loss 5-10% indicated before ovulation treatment if BMI >30

first line: clomifene

add metformin (improve glucose tolerance, decreases androgen levels and improves ovulation)

ovarian drilling

gonadotrophin injunctions

IVF as last resort

356
Q

what is clomifene

how does it work

what are its side effects

A

selective oestrgoen receptor modulator

block oestrogen negative feedback on hypothalamus resulting in more pulsatile GnRH secretion and therefore FSH and LH

side effects: hot flushes, sweating, increased risk of multiple pregnancy, ovarian cancer (long term use)

357
Q

what is ovarian drilling

A

use in women who fail to conceive on clomifene

diathermy to destroy ovarian storm which reduces androgen-secreting tissue leading to restoration of normal LH:FSH ratio and a fall in androgens

358
Q

how can acne be managed in PCOS

A

co-cyrprindol (Dianette): effective against acne and hirsutism, contains anti-androgen which block action of androgens on pilosebaceous glands

COCP: improves hyperandrogenism and gives withdrawal bleed (endometrial protection), inferior to co-cyrprindol

359
Q

management of amenorrhoea in COCP

A

COCP: withdrawal bleed

cyclical medrocyprogesterone or Mirena coil can reduce risk of endometrial hyperplasia

360
Q

what is the difference between primary and secondary dysmenorrhea

A

primary: no underlying pelvic pathology
- pain starts just before or within hours of period starting
- suprapubic cramping, may radiate to back or down thigh

secondary: due to underlying pathology
- starts 3-4 days before period

361
Q

causes of secondary dysmenorrhoea

A
endometriosis 
adenomyosis (endometrium between muscle layers of the uterus)
PID
intrauterine devices (copper cold)
fibroids
362
Q

clinical features and examination findings of primary dysmenorrhoea

A

features:
pain precedes and accompanies menstruation
onset with or shortly after menarche

examination:
normal exam ind investigations

363
Q

clinical features and examination findings of endometriosis

A

features:
associated with heavy periods and dyspareunia

examination:
uterosacral modularity and/or tenderness
fixed retroverted uterus

364
Q

clinical features and examination findings of adenomyosis

A

features:
associated with prolonged, heavy periods

examination:
bulky uterus

365
Q

clinical features and examination findings of fibroids

A

features:
menstrual pain
pressure effects on the adjacent organs
fibroid red degeneration during pregnancy

examination:
pelvic mass

366
Q

clinical features and examination findings of chronic PID

A

features:
history of STI
pain not limited to menstruation

examination:
mucopurulent discharge
cervicitis
findings suggesting Fitz-Curtis-Hugh syndrome on laparoscopy

367
Q

what is fitz-curtis-hugh syndrome

A

inflammation of the peritoneum and tissues surrounding liver
complication of PID
leads to formation of adhesions in the abdomen

368
Q

investigations for dysmenorrhea

A
high vaginal and endocervical swabs (PID, clam or gon)
pelvic USS (endometriomas, adenomyosis, fibroids)
diagnostic laparoscopy (endometriosis, other investigations normal)
369
Q

management of dysmenorrhoea

A

NSAIDs: menfanamic acid, ibuprofen
COCP
Mirena
GnRH analogues

370
Q

what are the two types of amenorrhage

A

primary: failure of mestruation by 16 yo
secondary: absence of menstruation for at least 6 months in female with history of regular cyclic bleeding

371
Q

causes of primary amenorrhoea

A

genital tract abnormalities: imperforate hymen, vaginal agenesis, cervical stenosis (amenorrhoea + secondary sexual characteristics)

mullerian agenesis (absent mullerian ducts –> absent uterus)

premature ovarian failure/insufficiency

genetic causes (turner’s, androgen insensitivity)

hypothalamic disorders (kallmans)

iatrogenic

autoimmune

endocrine causes (hypothyroid, constitutional delay, congenital hyperplasia, PCOS)

pituitary disorders

372
Q

what is premature ovarian failure/insufficiency

A

cessation of periods <40 yo

can be due to chemo, radiotherapy, turner’s, autoimmune causes

373
Q

causes f secondary amenorrhoea

A

physiological (excessive exercise, weight loss, stress)

autoimmune

pituitary (Sheehan, hyperprolactinaemia, haemochromatosis)

iatrogenic

endocrine (hypo/hypoerthyroid, PCOS)

uterine problems (endometrial atrophy, cervical stenosis, Ashermann’s)

pregnancy/lactation

374
Q

what is Ashermann’s syndrome

A

acquired condition that occurs when adhesions form inside the uterus often secondary to endometrial surgery or infection

it prevents menstruation, reduces fertility and can cause placental abnormalities

375
Q

management/investigation of amenorrhea

A

thorough history
general exam: BMI, secondary sexual characteristics, signs of endocrine disorders
visual fields if possible pituitary
examination of external genitalia

pregnancy test essential

376
Q

what causes the menopause

A

loss of ovarian follicular activity leading to a fall in oestradiol levels below that needed for endometrial stimulation

377
Q

how to confirm premature menopause

A

<45 yo

2 measurements at least 2 weeks apart

378
Q

physical effects of the menopause

A

vasomotor symptoms eg hot flushes and night sweats
joint aches and pains
dry and itchy skin
hair changes
vaginal dryness and soreness (dyspareunia)
recurrent UTI, urgency
urogenital prolapse
osteoporosis increasing risk of fractures
CVD
dementia

379
Q

psychological effects of menopause

A

labile mood, anxiety, tearfulness
loss of concentration, poor memory
loss of libido

380
Q

what type of HRT is best suited for women with personal or family history of VTE or liver problems

A

oestrogen patches

skip first pas metabolism so less likely to affect liver or production of clotting factors

381
Q

what different cycles of HRT are available

who are they most appropriate for

A

continuous combined: menopausal, taken every day

cyclical combined: perimenopausal, oestradiol everyday and progestogen on last 14 days

382
Q

what can be used to treat reduced libido in menopause

A

testosterone

383
Q

what are non-hormonal treatment options for menopause

A

SSRIs eg fluoxetine

CBT

384
Q

how long should contraception be continued after menopause

A

2 years after LMP of <50

1 year if >50

385
Q

side effects of NRT

A

oestrogen: breast enlargement, leg cramps, dyspepsia, fluid retention, nausea, headaches
progestogen: fluid retention, breast tenderness, headaches, mood swings, acne, depression, irritability, constipation, increased appetite

386
Q

risks of HRT

A

breast cancer
VTE (PE and stroke)
endometrial cancer

387
Q

absolute contraindications for HRT

A
suspected pregnancy 
breast cancer 
endometrial cancer 
active liver disease 
uncontrolled HTN
known VTE
known thrombophilia 
otosclerosis
388
Q

relative contradictions for HRT

A
investigated abnormal bleeding 
large uterine fibroids 
past history of benign breast disease 
unconfirmed personal history or strong FH of VTE
chronic stable liver disease 
migraine with aura
389
Q

presentation of lichen sclerosis

A
pruritus and skin irritation of vulva 
hypo pigmented skin
atrophy (shiny appearance)
hair loss
white polygonal papule that coalesce to form plaques 
figure 8 pattern
390
Q

complications of untreated lichen sclerosis

A
persistent inflammation and healing 
scar formation 
atrophy and fusion of labia 
stenosis of introitus 
difficulties in defecation 
vulvar intraepithelial neoplasia
391
Q

management of lichen sclerosis

A

3 months of high dose steroids eg dermovate

2nd line topical calcineurin inhibitors eg tacrolimus, imiquimod (immunosuppressant to reduce inflammation)

if treatment resistant, biopsy to rule out malignancy

392
Q

what is Paget’s disease of the vulva

A

uncommon intraepithelial adenocarcinoma

itching, pain, irritation, hyperpigmentation or leukoplakia

393
Q

management of Paget’s disease of the vulva

A

often a sign of malignancy elsewhere

full work up

394
Q

describe normal, physiological changes to discharge

A

during more fertile days: thin and clear

non-fertile days: thicker, hostile to sperm

395
Q

which bacteria are important in the maintenance of vaginal pH

A

lactobacilli

396
Q

what are risk factors for pelvic infection

A
age <25 years 
multiple sexual partners 
unprotected sex 
recent insertion of IUD 
recent change in sexual partner
397
Q

symptoms of pelvic infection

A
lower abdominal pain 
fever 
abnormal vaginal bleeding 
offensive vaginal discharge 
dysuria or menstrual irregularities
398
Q

examination signs of pelvic infection

A

cervical motion tenderness

adnexal tenderness

399
Q

management f pelvic infection

A

acutely unwell: sepsis 6

partner notification
oral ofloxacin and oral metronidazole OR IM ceftriaxone and oral doxy and met

400
Q

which populations are functional cysts, germ cell tumour and benign epithelial tumours most common in

A

functional: young women or reproductive age

germ cell: young women

benign intraepithelial: older women

401
Q

what are concerning features of an ovarian cyst

A

thick wall septa

solid and cystic components

402
Q

recommended investigation for complex ovarian cysts

A

Inhibin, b-HCG, CA125

403
Q

features of functional ovarian cysts

A

simple, uniloculated cysts >3 cm

regress after several menstrual cycles

404
Q

what causes functional ovarian cysts

A

non-rupture of dominant follicle or failure of stress of a non-dominant follicle

405
Q

features of benign germ cell tumours

A

often lined with epithelial tissue, may contain hair, teeth

often very big so at risk of torsion

406
Q

types of benign epithelial ovarian tumours

A

serous cystadenomas

mutinous cyst adenomas

407
Q

gynae causes of acute abdo pain

A
ectopic pregnancy 
ovarian torsion 
ovarian cyst rupture or haemorrhage 
PID
tubo-ovarina abscess 
endometriosis 
fibroids 
miscarriage 
mittelschmirz
408
Q

signs/symptoms, diagnosis and management of uterine fibroids

A

S&S:
asymptomatic, menorrhagia and dysmenorrhoea, lower abdo pain during menstruation, sub fertility, pressure symptoms

Dx:
TVUSS

management:
Mirena, myomectomy, hysterectomy, short-term GnRH analogues, uterine artery embolisation

409
Q

signs/symptoms, diagnosis and management of endometriosis

A

S&S:
dysmenorrhoea, deep dyspareunia, sub fertility, non-gynae signs (dysuria, urgency, dyschezia)

Dx:
often via laparoscopy, tender modularity on posterior fornix

management:
NSAIDs/paracetamol (symptomatic relief), COCP or progestogens, surgery (excisions of lesions)

410
Q

signs/symptoms, diagnosis and management of ovarian torsion

A

S&S:
sudden onset deep colicky pain, vomiting, distress, adnexal tenderness/acute abdomen

Dx:
USS will show classical whirlpool sign

management:
laparoscopy to untwist ovary and remove cyst
oophorectomy if necrotic

411
Q

signs/symptoms, diagnosis and management of PID

A

S&S:
vaginal discharge, bilateral lower abdo pain

Dx:
FBC, high vaginal or endocervical swab
may need pelvic imaging if doesn’t respond to Abx or pelvic mass

management:
Abx, drainage of pelvic abscess

412
Q

signs/symptoms, diagnosis and management of mittelschmerz

A

S&S:
mid cycle pain
often

Dx:
exclusion of other things

management:
simple analgesia and reassurance

413
Q

how long does the puerperium normally last

A

6 weeks

414
Q

describe the changes in vaginal discharge in the first 3 weeks postpartum

A

3-4 days after birth

  • fresh red discharge
  • rubra

4-14 days after birth

  • brownish-red, watery
  • serosa

10-20 days after birth

  • yellow
  • alba
415
Q

what changes occur in the uterus postpartum

A

endometrial lining regenerates by day 7
funds of uterus returns to physiological position by 2 weeks
uterine weight decreases to 5% of pregnancy weight

416
Q

what is colostrum

A

thick, yellowish substance produced by mammary tissue
first milk a baby is fed
contains more protein and vitamins that normal milk
essential for immunological protection to the newborn

417
Q

what initiates lactiation

A

expulsion of the placenta
decrease in oestrogen and progesterone levels

high levels of oestrogen and progesterone during pregnancy prevent release of prolactin (it is still produced but not released)
drop in oestrogen and progesterone so prolactin is released

418
Q

how is prolactin production maintained during breastfeeding

A

positive feedback from the infant suckling

419
Q

what is the let-down reflex

A

oxytocin stimulates myoepithelial cells surrounding breast alveoli to contract and squeeze milk out of breast

triggered by suckling

420
Q

what is the WHO guidance related to breastfeeding

A

exclusive breastfeeding for 6 months

then up to 2 years along with introduction of solid foods

421
Q

what to ask if patient presents saying she has ‘insufficient milk’ when trying to breastfeed

A

any pain while breastfeeding or skin changes to nipples
is baby irritable after a feed
ask to assess technique

422
Q

risk factors for lactational nastitis

A

improper breastfeeding technique (trauma to breast, milk stasis and ineffective milk release –> harbours bacteria)

smoking

foreign body (breast implant or piercing)

423
Q

what are the main features of a focussed history of mastitis

A

MAIDS
Milk stasis (decreased milk output)
Abscess (tender lump)
Inflammation (warmth, pain, swelling, firmness, erythema)
Discharge
Systemic symptoms (fever, malaise, myalgia)

424
Q

what is duct ectasia

A

blocked duct

425
Q

management of mastitis

A

fluclox 500 mg orally every 6 hours
or co-amoxiclav 625 mg every 8 hours for 7 days

breastfeeding should continue, use breast pump for infected breast if preferred

426
Q

management of breast abscess

A

USS and aspiration for culture

427
Q

define PPH

primary and secondary?

minor and major?

A

PPH = blood loss =/>500 ml after the birth of the baby

primary = within 24 hours of delivery 
secondary = 24 hours - 6 weeks post delivery 
minor = 500-1000 ml
major = >1000 ml or signs of cardiovascular collapse
428
Q

what are the 4 main causes of PPH

A

4T’s

tone: uterine atony
trauma: vaginal tear, cervical laceration, rupture
tissue: retained products of conception, placenta
throbbing: coagulopathy

429
Q

antenatal risks for PPH

A
placental problems (praaevia, accreta)
Hx of retained placenta, c-section, PPH
multiple pregnancy 
polyhydramnios 
obesity 
fetal macrosomia
430
Q

intrapartum risk factors for PPH

A
operative vaginal delivery 
syntocinon/syntometrine use
retained placenta 
c-section
labour >12 hours 
perineal tear/episiotomy
431
Q

ABCDE management of PPH

A

oxygen via non-rebreather mask at 15 l/min
IV access (grey/orange cannula)
bloods: G&S, FBC, coagulation screen, fibrinogen, U&Es, LFTs, lactate
cross-match 6 units of packed red cells
check vitals every 15 mins
determine cause of bleeding (4Ts)
massive haemorrhage protocol
tranexamic acid 0.5-1 g IV to stop bleeding

432
Q

how to stop the bleeding in PPH (non-surgical)

A

tone/tissue:
uterine massage using bimanual compression
administer IV syntocinon
insert urinary catheter to minimise bladder pressure on uterus
ergometrine, carboprost, misoprostol

thrombin:
expel clots manually

trauma: repair trauma

433
Q

surgical management of PPH

A

examine under anaesthetic (trauma, RPOC, rupture)
balloon insertion to put pressure on bleeding vessels
arterial embolisation
B-lynch sutures
uterine artery/internal iliac ligation
hysterectomy (last resort)

434
Q

fluid replacement in PPH

A

2 large bore IV access
rapid fluid resus: warmed crystalloid (eg hartmann’s), 0.9% saline
blood transfusion early (O- if life-threatening)

in DIC/coagulopathy give FFP, cryoprecipitate, platelets
use blood warmer

435
Q

classifcation of perineal tears

A

1st degree: involving skin only
2nd degree: involving skin and levator ani (usually needs stitches)
3rd/4th degree: extend to anal sphincter muscle (may stretch pudendal nerve –> faecal incontinence)

436
Q

what is an episiotomy

A

surgical cut made by medical professional with patient’s consent

437
Q

psychiatric red flags in postnatal period

A

recent significant chage in mental state or emergence of new symptoms
new thoughts or acts of violent self-harm
new and persistent expression of incompetency as a mother or estrangement from their baby

438
Q

when to consider admission to a mother and baby unit

A
a rapidly changing mental state 
suicidal ideation 
pervasive guilt or hopelessness 
beliefs of inadequacy as a mother 
evidence of psychosis
439
Q

who is most at risk of postnatal mental health problems

A
young, single 
domestic issues 
lack of support 
substance abuse 
unplanned/unwanted pregnancy 
pre-existing mental health problems
440
Q

when to refer a new mother to psychiatry

A
severe anxiety/depression 
Hx of BPSD or schizophrenia
Hx of puerperal psychosis 
current psychosis 
developed mental illness in later stages of pregnancy/peurperium 
FHx of significant mental illness
441
Q

features of baby blues

A

brief period of emotional instability where more become tearful, irritable, anxious and confused

arises day 3 postnatally and continues for about a week

442
Q

features of puerperal psychosis

A

sleep disturbance, confusion, irrational ideas, mania, delusions, hallucination

presents 2 weeks postnatally

emergency admission to mother and baby unit

443
Q

when does postnatal depression present and how long does it last

A

2-6 weeks postnatally

can last weeks/months or even up to a year or more

444
Q

how long do the following fetal circulatory adaptions take to close up

foramen ovale
ductus arteriosus 
umbilical arteries
umbilical vein
ductus venosus
A
foramen ovale: minutes 
ductus arteriosus: hours
umbilical arteries: hours
umbilical vein: days
ductus venosus: days
445
Q

what are the parts of the APGAR score

A

appearance:
blue/pale; blue extremities; no cyanosis

pulse:
absent; <100; >100

grimace:
no response; grimace/feeble cry when stimulated; cry or motor response

activity:
none; some flexion; flexed limbs that resist extension

respiration:
absent; weak/irregular gasping; strong cry

446
Q

how often is the APGAR performed

A

60 seconds after delivery

5 mins after

447
Q

which conditions are tested for on heelprick test

A
PKU
CF
congenital hypothyroidism 
MCADD
sickle cell disorder 
maple syrup urine disease 
isovaleric acidaemia 
glutamic aciduria type 1
homocystinuria
448
Q

what is PKU

A

excess phenylalanine in the blood usually from an inherited deficiency of the enzyme that converts it to tyrosine

449
Q

what is CF

A

inherited mutation of the genes encoding the CFTR protein responsible for producing bodily secretions causing them to become thick and sticky

450
Q

what is congenital hypothyroidism

A

congenital thyroxine deficiency as a result of poorly developed/absent thyroid

451
Q

what is MCADD

A

inherited deficiency of an enzyme responsible for breaking down fats to make energy

452
Q

what is maple syrup urine disease

A

deficiency of an enzyme needed to break down amino acids in food and milk, including breast milk

453
Q

what is isovaleric acidaemia

A

deficiency of an enzyme needed to break down leucine in milk to isovaleric acid causing harmful build up of acid in blood and urine

454
Q

what is glutaric aciduria type 1

A

deficiency of an enzyme needed to break down glutamic acid from food and milk, high levels of glutamic acid exists in the blood as a result and causes illness

455
Q

what is homocystinuria

A

lack of CBS enzyme, resulting in a build up of homocysteine and methionine

456
Q

when is heel prick testing done

what is the latest time?

A

ideally 5 days after birth

can do it up to 1st birthday, apart from CF which must be done before 8 weeks

457
Q

what is the most common uterine malignancy

A

endometrial adenocarcinoma

458
Q

risk factors for endometrial cancer

A

high levels of oestrogen: PCOS, late menopause, nulliparity, obesity, unopposed oestrogen HRT, tamoxifen, carbohydrate intolerance, oestrogen secreting tumours

459
Q

presenting symptoms of endometrial cancer

A

abnormal uterine bleeding
- any PMB or irregular bleeding in premenopausal women >40 should be investigated

vaginal discharge (blood, watery, purulent)

pain (normally related to mets)

460
Q

what are the 4 main investigations of endometrial cancer

A

TVUSS: measures endometrial thickness (>4 mm is concerning)

endometrial biopsy: histological analysis

D&C: scrape away endometrium under GA

hysteroscopy: biopsy/curretage can also be performed

461
Q

histological signs of endometrial hyperplasia

A

increased gland-to-stromal ratio

462
Q

treatment of endometria lhyperplasia

A

progestogens in young women (Mirena)

if atypical –> hysterectomy

463
Q

what is the common pattern of spread of endometrial carcinoma

A

direct spread to myometrium and cervix

haematogenous or lymphatic spread can occur

464
Q

what are the two types of endometrial cancer

A

type I: endometrioid

  • more common, shortly after menopause
  • oestrogen dependent

type II: serous and clear cell

  • older women, poorer prognosis, more aggressive
  • not related to oestrogen
  • spreads along Fallopian tubes and peritoneal surfaces so may present with extrauterine disease
465
Q

precursor lesions of endometrial cancer

A

endometrioid: atypical endometrial hyperplasia

serous/clear cell:
serous endometrial intraepithelial carcinoma

466
Q

how is endometrial cancer staged

A

I A/B: confined to uterus, >50% myometrial invasion

II: cervical stromal invasion, not beyond uterus

III A/B/C: tumour invades serosa or adnexa; vaginal or parametrical involvement; node involvement (pelvic/para-aortic)

IV A/B: bladder or bowel invasion; distance mets

467
Q

grading of endometrial tumours

A

1: 5% or less solid growth
2: 6-50% solid growth
3: >50% solid growth

468
Q

management of endometrial cancer

A

surgery: hysterectomy and bilateral salpino-oophorectomy +/-lymphadenectomy

radiotherapy or high dose progestogens if not suitable for surgery

chemo if widespread disease

469
Q

smooth muscle tumours in the myometrium

A

leiomyoma aka fibroids

leiomyosarcoma: rare, poor prognosis

470
Q

risk factors for ovarian cancer

A

increased number of ovulation
genetic predisposition
Lynch syndrome/BRCA
endometriosis

471
Q

what is the most common ovarian cancer

A

serous epithelial

472
Q

precursors for serous ovarian cancer

A

high grade: serous tubal intraepithelial carcinoma

low grade: serous borderline tumour

473
Q

types of epithelial ovarian cancer

A
serous
mucinous 
endometrioid 
clear cell
Brenner
474
Q

types of stromal tumours

A

granulose cell tumours
thecoma/fibroma
sertoli/leydig cell tumours

475
Q

types of germ cell ovarian tumours

A

teratoma
dysgerminoma
yolk sac tumour
choriocarcinoma

476
Q

which primary cancers often metastasise to the ovaries

A

endometrial cancer
breast cancer
pancreatic
GI

477
Q

presentation of ovarian cancer

A

often present late with non-specific symptoms

abdominal distension, GI symptoms

478
Q

what is the risk of malignancy index

A

used to separate benign and malignancy lesions
RMI = USS score x menopausal score x CA125 level
>200 cancer likely

479
Q

what USS features are suspicious of ovarian cancer

how are they scored on the RMI

A
complex mass with solid + cystic area 
mulitloculated 
thick separations 
associated ascites 
bilateral disease 
high doppler flow in solid areas 

no features = 0
1 feature = 1
2+ features = 3

480
Q

which other markers may be raised in ovarian cancer

A

Carcino-embryonic antigen: particularly mutinous tumours

serum hCG
AFP

481
Q

staging of ovarian cancer

A

I A/B/C: one ovary/both ovaries/on surface of ovary

II A/B: spread to Fallopian tube/bowel or bladder

III A/B/C: microscopic cancer in peritoneum/cancer <2 cm in peritoneum/lymph node involvement

482
Q

what are the precursor lesions of cervical cancer

A

squamous: cervical intraepithelial neoplasia
adenocarcinoma: cervical glandular intraepithelial neoplasia

483
Q

what is the classification of CIN

A

CIN I: abnormal cells in basal third of epithelium

CIN II: abnormal cells in middle third

CIN II: abnormal cells in full thickness

484
Q

which types of CIN need treatment

what is done

A

CIN II/III need treatment

large loop excision of transformational zone (LLETZ)
thermocoagulation

485
Q

presentation of cervical cancer

A
post-coital bleeding 
intermenstrual bleeding 
menorrhagia 
pelvic pain 
offensive vaginal discharge 

advanced: backache, leg pain, haematuria, weight loss, anaemia, bowel habit changes

486
Q

common chemotherapy drugs in cervical cancer

A

cisplatin

carboplatin/paclitaxel

487
Q

inter-pregnancy interval of <12 moths is associated with which outcomes

A

increased risk of preterm labour, fetal growth restriction, stillbirth and perinatal mortality

488
Q

when should sex be avoided if using the fertility awareness-based method of contraception

A

7 days prior to ovulation and 2 days after

sperm can survive in genital tract for up to 7 days
ovum can survive up to 2 days after ovulation

489
Q

when does ovulation normally occur

A

10-16 days before the start of the next cycle

490
Q

what are different methods of fertility-awareness contraception

A

temperature measuring: increase in temp for 3 days in a row indicate fertility has decreased

cervical mucous: moist, sticky, white and creamy mucous indicates start of fertile period, watery/clear indicates peak fertility

mobile apps can be used to track symptoms

491
Q

pros and cons of fertility awareness

A

pros:
no side effects, acceptable to all faiths and cultures, avoids hormones, increased awareness of cycle

cons:
higher rate of failure, user-dependent, restricts timing of intercourse, menstrual cycle can change or become irregular, requires constant monitoring, medication can interrupt cervical mucous, not suitable following pregnancy or if irregular cycle

492
Q

pros and cons of male condom

A

pros:
protection against STI, no hormones

cons:
failure rate high with typical use, user dependent, not suitable with oil-based lubricants

493
Q

how to use contraceptive diaphragm

A

reusable circular dome inserted into vagina before sex
must be used with spermicide
leave in place for 6 hours after sex

494
Q

disadvantages of diaphragm

A

lack of spontaneity
user dependent
no protection against STIs
increased risk of cystitis
need refitted if gain/lose >3 kg, deliver baby/miscarriage/abortion
latex and spermicide can cause irritation

495
Q

does COCP provide contraceptive protection immediately

A

if taken in the first 5 days of cycle then YES

if taken after 5 days then NO, needs to be taken for 1 week

if started by day 21 post partum then immediately effective

496
Q

missed pill rules COCP

A

1 pill missed:
take last pill, even if two pills are taken that day
no additional contraception

2 pills missed:
take last pill missed but omit any other previous pills missed
use condoms for 7 days
- if pill missed in week 1, consider emergency contraception if UPSI in pill-free interval or in week 2
- if pill missed in week 2 no EC needed
- if pill missed in week 3, current pack should be finishedand new pack started immediately

497
Q

pros and cons of COCP

A

pros:
improves painful/heavy bleeding, endometriosis symptoms and PMS
reversible effects upon stopping
reduced risk of ovarian, endometrial and colorectal Ca

cons:
taken around same time every day
interactions with other medicines
increased risk of cervical and breast Ca
increased risk of VTE, stroke, IHD (risk factors)
hormonal side effects
irregular bleeding

498
Q

relative contraindications to COCP

disadvantages outweigh the advantages (UKMEC 3)

A
>35 yo and smoking <15 cigarettes/day
BMI >35
FHx of VTE in family member <45 
controlled HTN
immobility 
cancer mutations eg BRCA 
gallbladder or liver disese 
complicated DM
499
Q

absolute contraindications for COCP

should be avoided (UKMEC 4)

A

> 35 and smoking >15 cigarettes/day
migraine with aura
PMHx of VTE, thrombogenic mutation, stroke, IHD
uncontrolled HTN
current breast cancer
major surgery with prolonged immobilisation

500
Q

how to use transdermal contractpive patch

A

wear for 7 days
change on the 8th
wear for 3 weeks then a patch-free week
if patch removed for >48 hours additional contraception for 7 days

501
Q

how to use combined vaginal ring

A

have in vagina for 3 weeks, remove for 1 week, new ring

if out of vagina >3 hours in weeks 1/2 additional protection for 7 days

new ring no later than 7 days after last one removed

502
Q

how is the contraception injection given

A

every 13 weeks
depoprovera IM
sayana press SC (self-administered)

503
Q

pros and cons of contraceptive injection

A
pros:
long-acting and less user dependent 
no oestrogen 
can lead to amenorrhoea 
useful in HMB, dysmenorrhoea, endometriosis

cons:
non-reversible once injected
delayed retrun to fertility (up to 12 months)
irregular bleeding common in first 3 months
potential for weight gain
long term use associated with osteoporosis

504
Q

missed pill rules for POP

A

pill taken <12 hours later than usual time, take pill as normal
>12 hours, take missed pill ASAP and continue with rest of pack - use condoms until pill has been taken for 48 hours

older POPs have 3 hours window

505
Q

pros and cons of POPs

A

pros:
few contraindications
immediately reversible

cons:
irregular bleeding
D&V (assume missed pill)
liver enzyme inducers may reduce effectiveness
CI if PMHx of Br Ca or active liver disease

506
Q

pros and cons of implant

A
pros:
most effective form of contraception 
non-user decedent 
can be used if not suitable for oestrogen 
safe in breastfeeding and postpartum 
reduce painful/heavy bleeding 

cons:
irregular bleeding common in first 6/12
headache, ausea, breast pain, skin changes
efficacy reduced by enzyme inducing drugs (AEDs, rifampicin)
CI in current Br Ca and active liver disease

507
Q

risks of IUS

A

uterine perforation in 2/1000
increased risk of ectopic pregnancy compared to other contracptive but not compared to no contraception
small risk of PID in first 20 days
1/20 risk expulsion in first 3 months

508
Q

different types of IUS

A

Mirena: 52 mg LNG, 5 years, HMB etc, HRT

kyleena: 19.5 mg LNG, 5 years, smaller so less side effects, not for HMB or HRT
jaydess: 13.5 mg LNG, 3 years, more irregular bleeding

509
Q

when should dose of LNG EC be doubled

A

BMI >26
over 70 kg
taking enzyme inducing drugs

510
Q

how does LNG EC work

A

delays/prevent ovulation and reduced successful implantation

must be taken within 72 hours

511
Q

how does Uliprsital EC work

A

delays/inhibts ovulation

taken within 120 hours of UPSI

512
Q

when is breastfeeding a suitable contraceptive

A

exlcusive breastfeeding
up to 6 months
no periods

513
Q

which types of contraception are safe in postnatal periods

A

implant and POP can be used anytime after birth

depo safe anytime if not breastfededing

IUS/IUD can be inserted with 48 hours of SVD or wait at least 4 weeks

delay CHC for at least 3 weeks due to risk of VTE

514
Q

when is abortion permitted after 24 weeks

A

woman’s life is in danger
severe foetal abnormality
woman at grave risk of physical or mental injury

515
Q

how is medical abortion carried out

A

mifepristone (antoprogesterone)

48 hours laters

misoprostol (prostaglandin)

<10 weeks: at home
10+1 - 23+6 wks: admission to hospital or clinic advised, multiple doses of misoprostol may be required (5 doses in 24 hours)

516
Q

risks of medical abortion

A

heavy and prolonged bleeding, may need transfusion
incomplete ro failed procedure
pain
infection

risks increase with increased age

517
Q

how does surgical abortion take place

A

misoprostol to soften and dilate cervix

vacuum aspiration up to 14 weeks; dilation and evacuation >14 weeks (not in Scotland)

local/regional/general anaesthetic or conscious sedation

518
Q

post abortion management

A

if uncomplicated can go home same day, accompanied if under anaesthesia
contraception discussed (can be given same day)
anti-D if >9+6 weeks and Rh -ve

519
Q

function of sertoli cells

A

blood-testes barrier: protect sperm from antibodies, maintain fluid composition of testes

provide nutrient

destroy defective sperm

secrete seminiferous tubule fluid, androgen binding globulin, Inhibin hormone and activin hormone

520
Q

what is the function of the substance secreted by the Sertoli cells

A

seminiferous tubule fluid: essential for carrying spermatozoa to epididymis

androgen binding globulin: binds testosterone, for sperm production

Inhibin/activin: regulation of FSH secretion and control of spermatogenesis

521
Q

where does spermatogenesis take place

where does it go after

A

seminiferous tubules
rete testes
epididymis (storage and maturation)

522
Q

briefly describe the HPG axis in males

A

GnRH released in bursts from hypothalamus every 2-3 hours
anterior pituitary releases LH and FSH

LH stimulates testosterone secretion from leydig cells

testosterone and FSH surges stimulate spermatogensis in seminiferous tubules

inhibin from Sertoli cells decreases FSH secretion and testosterone decreases GnRH secretion

523
Q

what is capacitation

A

biochemical and electrical events that allow the sperm to penetrate the cell layer surrounding the oocyte

sperms’s tail movement increases in speed and strength to propel it forwards

524
Q

common causes of obstructive male infertility

endocrinological features

A
cystic fibrosis (obstructed or absent vas)
vasectomy 

normal LH, FSH and testosterone

525
Q

common non-obstructive causes of male infertility

A
cryptorchidism 
klinefelter's syndrome (47 XXY)
microdeletions of Y chromosome 
robertsonian translocation 
infection (mumps, STI) 
endocrine (pituitary tumours, hypothalamus disorders, thyroid, DM, DAH)
testicular tumours
526
Q

what is globozoospermia

A

rounded head, no acrosome

can’t fuse with zone pellucida

527
Q

hypothalamic causes of anovulatory infertility

A

anoerixa, bulimia, excessive exercise

Low FSH, LH and estradiol

528
Q

pituitary causes of anovulatroy infertility

A

hyperprolactinaemia
Sheehan’s syndrome
pituitary adenomas

529
Q

ovarian causes of anovulatory infertility

A

PCOS

premature ovarian failure

530
Q

causes of ovulatroy infertility

A

infection (PID, transperitoneal spread etc)
endometriosis
salpingitis isthmicya nodosa: nodular scarring of Fallopian tube
uterine polyps/fibroids

531
Q

important parts of infertility history

A

duration of infertility
primary or seconda
frequency of sexual activity
history of sexual function
libido
females: previous pregnancies, full obestetric Hx, menstrual history
both: general health, medical/surgical Hx, medications

532
Q

normal testicular volume

A

12-25 mls

533
Q

how to ensure good quality semen anaylsis

A
assessed quickly after production (<1 hour ideally)
kept at body temperature
patient in good health
avoid ejaculation for 72 hours prior 
avoid caffeine/alcohol
534
Q

investgiation oftubal patency

A

laparoscopy

hysterosalpingogram

535
Q

endocrine tests for males and females with infertility

A

male: LH and FSH, prolactin, TSH
female: LH and FSH, oestradiol, mid-luteal progesterone, free androgen index, testosterone and SHBG, prolactin, TSH

536
Q

what is IUI

what are the indications

A

intrauterine insemination
directly putting sperm inside the uterus
healthy sperm, ovulation is occuring and no tubal disease

sexual dysfunction, female same-sex with donor sperm, male same-sex with surrogate

537
Q

what IVF

what are the indication

A

In-vitro fertilisation
fertilising egg outside of body

unexplained infertility, pelvic disease, anovulatory infertility

538
Q

what is ICSI

what are the indictions

A

intra-cystoplasmic sperm injection
sperm injected directly in cytoplasm of oocyte

severe male factor infertility, previous failed IVF, pre-implantation genetic diagnosis

539
Q

how to harvest eggos

A

down regulation: synthetic GnRH used to shut down menstrual cycle, allows cycles to be scheduled

ovarian stimulation: gonadotrophin hormone injection to to stimulate relase of eggs

oocytes collection: under USS guidance, needle is inserted transvaginally and ovarian follicle aspirate

540
Q

at what stage are embryos transferred for IVF/ICSI

A

day five normally (blastocyst stage