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NP- Phase 3a Medicine > Obstetrics > Flashcards

Obstetrics Flashcards

1
Q

pregnancy- when is the window of blastocyst formation and why?

A

cycle day 20-24- perfect balance of hormones

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2
Q

pregnancy- what happens after blastocyst formation?

A

blastocyst buries- interstitial implantation

this starts the primary decidual reaction

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3
Q

pregnancy- what basic placental structures form after interstitial implantation?

A

floating and anchoring villi

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4
Q

pregnancy- what do cytotrophoblast progenitor stem cells differentiate into?

A

1- terminal differentiation into syncytiotrophoblast

2- extra-villus trophoblasts

3- regenerate new cytotrophoblasts

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5
Q

pregnancy- what are the functions of the extra-villous trophoblasts?

A

spinal artery remodelling- endovascular invasion of the myometrium

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6
Q

during pregnancy, when does full placental blood flow occur?

A

week 10-12

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7
Q

during pregnancy, what can poor endovascular remodelling lead to?

A

reduced fetal O2 and nutrient supply, which results in:

  • pre-eclampsia
  • intrauterine growth restriction
  • preterm birth
  • recurrent miscarriage
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8
Q

pregnancy- what is human chorionic gonadotrophin (hCG)?

A
  • hormone secreted from day 6-7 trophoblast cells of the blastocyst
  • promotes maintenance fo corpus luteum
  • maintains production of oestrogen and progesterone
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9
Q

where is progesterone produced?

A

up to week 7/8- corpus luteum

after this it is made in the placenta

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10
Q

what are the functions of progesterone in pregnancy?

A
  • prepare uterus for implantation
  • makes cervical mucous thick and impenetrable to sperm after fertilisation
  • decrease immune response- allows pregnancy to occur
  • decreases contractility of uterine smooth muscle to prevent pre-term labour
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11
Q

what does progesterone inhibit during pregnancy?

A

lactation

after delivery, falling progesterone levels triggers milk production

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12
Q

what is the function of human placental lactogen (hPL)?

A
  • mobilises glucose from fat
  • insulin antagonist to facilitate energy supply to foetus
  • converts mammory glands into milk-secreting tissue
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13
Q

what is the function of prolactin?

A

milk production

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14
Q

what is the function of oxytocin?

A

milk ejection reflex

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15
Q

what happens to maternal glucose levels during the early stages of pregnancy?

A

low- due to fat deposition and glycogen synthesis

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16
Q

what happens to maternal glucose levels during the late stages of pregnancy?

A

high

alongside maternal insulin resistance- ensures glucose sparing for foetus

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17
Q

what happens to maternal insulin levels throughout pregnancy?

A

rise until week 32

hPL then induces insulin resistance

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18
Q

what immunity changes occur after fertilisation?

A

increases in GF’s, proteolytic enzymes and inflammatory mediators to facilitate implantation

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19
Q

why is blastocyst implantation not rejected?

A

change in self: non-pattern recognition molecules (HLA and MHC)

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20
Q

Why are syncytiotrophoblasts and extra-villus trophoblasts not rejected?

A
  • Syncytiotrophoblast has no self:non-self markers

- extra-villus trophoblast has modified self:non self markers

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21
Q

what happens to the T helper ratio during pregnancy?

A

pregnancy- more Th2 (in ‘normal’ physiology, Th1 and Th2 are balanced)

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22
Q

what are the functions of the following antibodies in pregnancy

IgA
IgD
IgE
IgG
IgM
A

IgA- secreted in breast milk

IgD- on B-cell membranes

IgE- mast cells (anaphylaxis)

IgG- only one that crosses placenta

IgM- early antibody

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23
Q

explain the pathophysiology of Rhesus disease

A
  • haemolytic disease of new born
  • Rh -ve mother (dd) and Rh +ve father (Dd or DD)
  • sensitisation in first pregnancy igM
  • rapid response by IgG of subsequent pregnancy
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24
Q

what is the definition of a normal pregnancy and birth?

A
  • term- 37-42 weeks
  • spontaneous onset
  • infant born spontaneously in vertex position

birth occurs without:

  • induction of labour
  • spinal/ epidural/ general analgesia
  • forceps/ ventrose delivery
  • caesarean section/ episiotomy
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25
Q

what occurs in each of the 3 stages of labour (generally)?

A

1st- contractions- has two phases- early labour (cervix gradually effaces and dilates) and active labour (cervix dilates rapidly and contractions are longer, stronger and closer together)

2nd- fully dilated, ends with birth of baby

3rd- right after birth, ends with delivery of placenta

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26
Q

what are the 3P’s of pregnancy?

A

Power- contractions need to be strong enough

Passage- pelvis- anterior-posterior diameter and transverse diameter

Passenger- baby needs to be in correct position

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27
Q

describe the landmarks of the baby’s head felt on vaginal examination to assess the baby’s position

A
  • attitude- how much neck is flexed (ideally is well flexed). can be deflexed- brow presentation (extended to 90’) or face presentation hyperextended to 120’)
  • position- OT (occipito-transverse), OA (occipito-anterior)
  • size of head- head compressed through pelvis (moulding), swelling causes during delivery (caput)
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28
Q

how long on average is the first stage of pregnancy?

A

5-12= multiparious

8-12- primiparous

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29
Q

describe the early/ latent phase of the first stage of labour

A
  • irregular, painful contractions
  • ‘show’- plug of cervical mucus and blood
  • cervix is effacing and thinning
  • dilates to 4cm
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30
Q

what is engagement?

A

how far above the pubic symphysis the babies head is

3/5 of the head within pelvic brim is classed as engaged

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31
Q

what is presentation?

A

anatomical part of the foetus which presents itself first through birth canal

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32
Q

what is ‘lie’ during labour?

A

relationship between long axis of fetus and long axis of the uterus

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33
Q

what is ‘station’ during labour?

A

relationship between the lowest point of presenting part and the ischial spines

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34
Q

describe the active phase of labour (2nd)

A
  • further dilation from 4cm (0.5cm each hour)
  • 3-4 regular contractions per hour
  • vaginal exam every 4 hours to assess degree of dilation
  • oxytocin- syntocinon relationship induces labour
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35
Q

how is pain (generally) managed in labour?

A
  • psychological- relaxation, hypnosis
  • sensory methods- hydrotherapy, posture
  • birth environment
  • complementary - message, aromatherapy
  • pain relief mediations
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36
Q

what 3 types of pain relief medications are commonly used in labour?

A
  • entonox
  • opiates- morphine. pethidine
  • epidural
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37
Q

what is entonox and what are side effects of it?

A
  • used in labour- ‘gas and air’

SE- nausea and vomiting

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38
Q

what opiates are used in labour and what are some maternal and fetal side effects?

A
  • pethidine/ morphine
  • maternal SE- euphoria/ dysphoria, nausea/ vomiting, increased length of 1st and 2nd stage of labour
  • fetal SE- respiratory depression, diminishes breath seeking/ breast feeding behaviours
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39
Q

what are some maternal and fetal side effects of epidurals?

A
  • maternal- increased length of 1st and 2nd stage, increased incidence of malposition, loss of mobility, loss of bladder control, hypotension, pyrexia
  • fetal- tachycardia, diminishes breast feeding behaviour
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40
Q

describe the initial transition stage of the second stage of labour

A
  • SROM- spontaneous rupture of membranes
  • irritable, anxious, distressed
  • start to feel pressure
  • contractions can slow/ stop
  • support/ reassurance required
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41
Q

describe the second stage of transition during labour

A
  • full dilatation- 10cm
  • externally- head visible
  • spent bearing down
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42
Q

in what timeframe would you:

  • suspect delay
  • diagnose delay
  • expect baby to be born

in primigravid women

A
  • suspect delay- 1 hour
  • diagnose delay- 2 hour
  • born- within 3 hours of pushing
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43
Q

in what timeframe would you:

  • suspect delay
  • diagnose delay
  • expect baby to be born

in multiparous women

A
  • suspect delay- 30 mins
  • diagnose delay- 1 hour
  • born within 2 hours of pushing
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44
Q

what happens in the 3rd stage of labour?

A
  • pushing out placenta
  • physiological management- blood less
  • active management- oxytocin
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45
Q

function of relaxin during labour

A
  • released from placement, membrane surrounding baby and uterine lining
  • softens ligaments and cartilages of pelvis so it can expand
  • helps cervix loosen and soften
  • makes baby’s body more flexible and allows head to mould
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46
Q

function of oxytocin during labour

A
  • stimulates uterine contractions during orgasm and childbirth
  • large amounts released when cervix is opened, trigging fetal ejection reflex
  • contracts uterus post-birth to deliver placenta and limit bleeding
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47
Q

functions of prostaglandins during labour

A
  • ripens cervix and causes it to begin process of thinning and opening
  • stimulates uterine contractions
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48
Q

what are the 5 types of malpresentation during pregnancy?

A
  • breech
  • occipitoposterior position
  • face presentation
  • brow presentation
  • transverse lie
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49
Q

causes of a breech presentation

A
  • idiopathic
  • uterine abnormalities
  • prematurity
  • placenta previa
  • oligohydramnios
  • foetal abnormalities- hydrocephalus
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50
Q

how can a breech presentation be reversed?

A

external cephalic version

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51
Q

what are the complications of an external cephalic version?

A
  • placenta previa
  • APH
  • ruptured membranes
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52
Q

how is a breech presentation diagnosed?

A

ultrasound

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53
Q

what are the 3 types of breech presentation?

A

frank breech

complete breech

footling breech

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54
Q

what is a frank breech?

A

where the hips are flexed and the legs are extended

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55
Q

what is a complete breech?

A

hips and knees are flexed and the feet are below the level of the foetal buttocks

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56
Q

what is a footling breech?

A

where one or both feet are presenting as the lowest part of the foetus

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57
Q

which breech presentation is associated with the highest risk of cord prolapse?

A

footling breech

there is nothing to act as a plug over the cervix if the membranes rupture

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58
Q

what mode of delivery is most appropriate for a breech presentation?

A
  • vaginal delivery has a risk of foetal hypoxia and birth trauma
  • planned C-section
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59
Q

how is an occipitoposterior position diagnosed?

A

antenatally via palpation

vaginal examination

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60
Q

why is labour prolonged in occipitoposterior position?

A

because of the degree of rotation needed, so adequate analgesia and hydration are required

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61
Q

describe a face presentation and the method of delivery

A
  • occurs by chance- head extends rather than flexes as it engages
  • early vaginal examination- nose and eyes may be felt
  • forceps delivery
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62
Q

describe a brow presentation and the management of it

A
  • head is between full flexion and full extension- can revert to either
  • vaginal delivery NOT possible !
  • delivery by LSCS
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63
Q

what is an LSCS delivery?

A

lower segment caesarean section

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64
Q

how is a transverse lie antenatally diagnosed?

A
  • ovoid uterus wider at the sides
  • lower pole is empty
  • head lies in one flank
  • foetal heart heard in variable positions
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65
Q

what are the most common reasons for inducing labour?

A
  • prolonged pregnancy
  • premature rupture of membranes
  • diabetic mother >38 weeks
  • rhesus incompatibility
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66
Q

what is the Bishop score?

A

used to assess if induction is required

  • score <5= unlikely to start without induction
  • score >9= likely to start spontaneously
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67
Q

what 5 factors are included within the bishop score?

A
  • cervical dilation (cm)
  • length of cervix (cm)
  • station of head (cm above ischial spines)
  • cervical consistency
  • position of cervix
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68
Q

in the bishop score, each factor has a score of 0,1 or 2.

for cervical dilation, state what each score implies

A

0= 0cm

1= 1-2cm

2= 3-4cm

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69
Q

in the bishop score, each factor has a score of 0,1 or 2.

for the length of the cervix, state what each score implies

A

0= >2cm

1= 1-2cm

2= <1cm

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70
Q

in the bishop score, each factor has a score of 0,1 or 2.

for ‘station of head’ , state what each score implies

A

0= 3cm above ischial spines

1= 2cm above ischial spines

2= 1cm above

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71
Q

in the bishop score, each factor has a score of 0,1 or 2.

for cervical consistency, state what each score implies

A

0= firm

1= medium

2= soft

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72
Q

in the bishop score, each factor has a score of 0,1 or 2.

for position of cervix, state what each score implies

A

0= posterior

1= middle

2= anterior

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73
Q

what must be checked prior to induction?

A
  • lie and position of foetus
  • volume of amniotic fluid
  • tone of uterus
  • ripeness of cervix
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74
Q

what are contra-indications for induction?

A
  • severe degree of placenta praevia
  • transverse fetal lie
  • severe cephalopelvic disproportion
  • cervix <4 on bishops score
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75
Q

what is the induction procedure?

A
  • membrane sweep
  • prostaglandin gel or pessary high in vagina (misoprostol)
  • amniotomy- ROM
  • Oxytocin/ syntocinon infusion (post ROM)
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76
Q

What is cardiotocography?

A

electronic fetal monitoring for risk factors

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77
Q

what is a normal CTG?

A
  • HR 110-160
  • variability of 5bpm
  • no decelerations
  • accelerations present- reassuring when baby is moving
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78
Q

on CTG, what would a heart rate over 160 indicate?

A

maternal pyrexia

chorioamnionitis

hypoxia

prematurity

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79
Q

on CTG, what would a heart rate under 100 indicate?

A

increased foetal vagal tone

maternal beta blocker use

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80
Q

on CTG, what would a loss of baseline variability inicate?

A

prematurity/ hypoxia

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81
Q

on CTG, what would late deceleration indicate?

A

foetal distress- asphyxia/ placental insufficiency

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82
Q

on CTG, what would variable decelerations indicate?

A

cord compression

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83
Q

what mnemonic is helpful for interpreting CTG’s?

A

DR C BRAVADO

DR- Define risk- why are they having it? (e.g pre-eclampsia)

C- Contractions (5 in 10 mins)

BRA- Baseline rate should be 110-160bpm

V- Baseline variability
Normal = 5-25 bpm
Reduced = <5bpm

A- Accelerations
Rise by 15 beats for more than 15 seconds. Should be 2 separate accelerations every 15 mins

D- Decelerations
Reduction of 15 beats for at least 15 seconds

Late decelerations = sign of slow recovery hypoxia

O- Overall Impression

Terminal Bradycardia = <100bpm for >10 mins

Terminal Deceleration = HR drops and does not recover for more than 3 minutes

These make up a ‘pre-terminal’ CTG and indicators of emergency C-section

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84
Q

what is hyperemesis gravidarum?

A

vomiting in early pregnancy, starts from 4-10 weeks and ends by week 20

associated with WL of more than 5% body mass and ketosis

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85
Q

clinical features of hyperemesis gravidarum

A
  • persistent vomiting
  • > 5% weight loss
  • dehydration

TRIAD OF:

  • > 5% weight loss
  • electrolyte imbalance
  • dehydration

(plus vomiting)

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86
Q

how is hyperemesis gravidarum managed?

A
  • mild-moderate- reassurance, avoid fatty foods, avoid large volume drinks
  • severe- admissions and antoemetics
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87
Q

what anti-emetics are used in the treatment of hyperemesis gravidarum?

A
  • dopamine antagonist- metoclopramide
  • phenothiazines- prochloperazine
  • ondansteron
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88
Q

complications of hyperemesis gravidarum

A
  • Wernicke’s
  • mallory-weiss tear
  • pre-term baby
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89
Q

what is puerperal pyrexia?

A

defined as a temperature of >38’c in the first 14 day following delivery

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90
Q

causes of puerperal pyrexia

A

endometritis

UTI

wound infection

mastitis

VTE

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91
Q

risk factors for VTE in pregnancy

A
  • age over 35
  • BMI >30
  • parity >3
  • immobility
  • FH
  • smoker
  • varicose veins
  • pre-eclampsia
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92
Q

what is the leading cause of morbidity and mortality in pregnancy in developed countries?

A

VTE

preventable- includes ,DVT, PE

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93
Q

when are VTE risk assessments done?

A
  • booking
  • antenatal admission
  • labour
  • postnatally
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94
Q

what are some indications for LMWH thromboprophylaxisis and compression stockings in pregnancy?

A
  • risk factors of VTE present

if required, LMWH must be given until 6 weeks postpartum

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95
Q

if a pregnant/ post partum lady collapses what is the immediate concern?

A

PE

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96
Q

investigations in a suspected VTE during pregnancy

A
  • FBC, U&E, LFT, clotting screen
  • if suspected PE- ABG, ECG, CXR

imaging:

  • DVT- duple US
  • PE- CXR, duplex us
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97
Q

what is anaemia in pregnancy defined as?

A

HB <105g/l

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98
Q

risk factors for anaemia during pregnancy

A
  • starting pregnancy anaemic
  • frequent pregnancies
  • twin pregnancy
  • poor diet
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99
Q

what antenatal screening is done for anaemia?

A
  • Hb estimation at booking and at 28 weeks

black patients- must check sickle cell

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100
Q

risk factors for group B strep infection?

A
  • prematurity
  • prolonged ROM
  • previous group B strep sibling
  • maternal pyrexia
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101
Q

group B strep- if a patient is isolated during labour what should be given?

A

IV benzyl penicillin to reduce neonatal transmission

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102
Q

clinical features of group b strep infection in pregnancy

A
  • UTI- frequency, urgency, dysuria
  • chorioamnionitis- fever, foul discharge, tachycardia
  • endometritis- fevers, lower abdo pain, intermenstrual bleeding, foul discharge
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103
Q

symptoms of measles in pregnancy

A

fever

generalised maculopapular, erythematous rash

Koplik’s spots

cough

coryza

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104
Q

how is rubella spread?

A

respiratory droplets

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105
Q

features of rubella

A

Cataracts 8-9 weeks

Deafness 5-7 weeks

Cardiac lesions 5-10 weeks

  • Cerebral Palsy
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106
Q

what congenital defects are associated with cytomegalovirus?

A 
IUGR
microcephaly
hepatoslenomegaly 
jaundice 
chorioetinitis

later- motor and cognitive impairment

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107
Q

what are the symptoms of toxoplasmosis?

A

similar to glandular fever- fever, rash and eosinophilia

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108
Q

cause and treatment of toxoplasmosis

A

cause- raw meat/ cat faeces

tx- pyrimethamine + sulphadiazine + spiramycin

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109
Q

how is parvovirus B19 spread?

A

DNA virus

respiratory droplets

4-20 day incubation period

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110
Q

what syndrome may occur in pregnancy with Parvovirus B19?

A

slapped cheek syndrome

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111
Q

what are the consequences to the foetus of Parvovirus B19 infection?

A
  • foetal suppression of erythropoiesis

- cardiac toxicity- leading to cardiac failure

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112
Q

what should you give to a mother with hepatitis B?

A
  • Screen all mothers

- give immunoglobulin and vaccinate babies of carriers and infected mothers at birth

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113
Q

what should be done if a pregnant mother develops chickenpox near delivery?

A
  • aim for delivery after 7 days
  • give baby varicella immune immunoglobulin at birth
  • monitor for 28 days
  • if baby develops chickenpox- treat with acyclovir
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114
Q

features of foetal varicella syndrome

A
  • skin scarring
  • eye defects
  • neurological abnormalities
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115
Q

what is gonococcal conjunctivitis and what are the features of it?

A
  • occurs within 4 days of birth

- purulent discharge and lid swelling

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116
Q

how should infants born with gonorrhoea be managed?

A

cefotaxime and chloramphenicol

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117
Q

what investigations must be done in an infant with jaundice?

A
  • LFT’s
  • urine dip- bile
  • serology
  • HBsAG- Hep B surface antigen
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118
Q

when is obstetric cholestasis (intrahepatic cholestasis of pregnancy) typically seen and what are some features of it?

A
  • 3rd trimester

- jaundice, pruritis of palms and soles, NO RASH, worse at night, raised bilirubin

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119
Q

how is obstetric cholestasis managed?

A
  • ursodeoxycholic acid

- symptoms resolve upon delivery

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120
Q

complications of obstetric cholestasis

A

stillbirth
preterm labour
meconium
foetal distress

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121
Q

when does acute fatty liver of pregnancy occur and what are some features?

A
  • rare- occurs in 3rd trimester
  • very serious !
  • jaundice, abdo pain, malaise etc, hypoglycaemia, pre-eclampsia
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122
Q

complications of acute fatty liver of pregnancy

A

hepatic steatosis

coma, death

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123
Q

investigations and management of acute fatty liver of pregnancy

A
  • high ALT

management- delivery is definitive management

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124
Q

where do the majority of ectopic pregnancies lie?

A

97%- fallopian tubes- typically the ampullary (most common) or isthmic portions

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125
Q

what is an ectopic pregnancy?

A

pregnancy that occurs anywhere outside the uterus

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126
Q

risk factors for an ectopic pregnancy?

A
  • IVF
  • age
  • PID
  • Previous ectopic
  • smoking
  • adhesions from infection and inflammation from endometriosis
  • previous tubal surgery
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127
Q

clinical presentation of an ectopic pregnancy

A
  • abdo/pelvic pain and tenderness
  • amenorrhoea- 6-8 weeks
  • vaginal bleeding
  • dizziness, fainting, syncope
  • rebound tenderness
  • shoulder tip pain- diaphragmatic irritation from blood if ruptures
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128
Q

differential diagnosis of an ectopic pregnancy

A

threatened miscarriage

appendicitis

bowel ischaemia

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129
Q

diagnostic tests and results in an ectopic pregnancy

A
  • pregnancy test- no rapid decline of bhCG
  • transvaginal USS
  • empty uterus and positive pregnancy test
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130
Q

treatment of an ectopic pregnancy

A
  • medical- if no complications- single dose methotrexate

- surgery- salpingectomy, salpingotomy

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131
Q

side effects of methotrexate treatment (in an ectopic pregnancy)?

A

conjuctivitis

stomatitis

diarrhoea

abdo pain

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132
Q

what must be given/ used alongside methotrexate?

A

contraception- methotrexate is teratogenic

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133
Q

what is a molar pregnancy?

A

gestational trophoblastic disease

  • molar pregnancy- non-viable fertilised egg= implants into uterus- will not come to term
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134
Q

aetiology of a complete molar pregnancy

A

all genetic material comes from father- so empty oocyte is fertilised

sperm+ empty egg

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135
Q

aetiology of a partial molar pregnancy

A
  • trophoblast cells have 3 sets of chromosomes (triploid)
  • 2 sperms fertilise ovum at same time
  • 2 sperms plus one egg
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136
Q

what follows a molar pregnancy in 2-3% of cases?

A

choriocarcinoma

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137
Q

risk factors for a molar pregnancy

A
  • age <16 or >45
  • multiple pregnancies
  • previous molar pregnancy
  • women with menarche over the age of 12
  • OCP
  • asian
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138
Q

what is an invasive mole?

A

when. complete mole invades the myometrium

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139
Q

how does a molar pregnancy present clinically?

A
  • first half of pregnancy- vaginal bleeding
  • uterine evacuation- 10 weeks of gestation
  • exaggerated Sx of pregnancy- hyperemesis gravidarum
  • pre-eclampsia
  • unexplained anaemia
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140
Q

how is a molar pregnancy diagnosed?

A
  • bhCG- very high levels in blood and urine
  • history
  • USS- ‘snowstorm appearance’ in 2nd trimester
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141
Q

treatment of a molar pregnancy

A
  • urgent referral
  • suction curettage and HCG monitoring
  • chemo- cisplatin
  • effective contraception- ensure female does not get pregnant until hCG levels have been normal for 6 months
  • ERPC- evacuation of retained products of contraception
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142
Q

what is the definition of a miscarriage?

A

defined as the loss of pregnancy before 24 weeks of gestation

  • does not include ectopic or molar
143
Q

what is a complete miscarriage?

A

TVUS shows crown rump length >7mm

gestational sack >25mm

no foetal heartbeat

144
Q

what is a threatened miscarriage?

A

mild symptoms of bleeding with little/ no pain, cervical os is closed

145
Q

what is an inevitable miscarriage?

A

heavy bleeding with clots and pain

cervical os is open

pregnancy will not continue- proceeds to incomplete/ complete

146
Q

what is an incomplete miscarriage?

A

products of conception are partially expelled

cervical os is open

pain and vaginal bleeding

147
Q

what is a missed miscarriage?

A

foetus is dead but retained

uterus is small for dates

pregnancy test remains +ve

closed cervical os

148
Q

how does a missed miscarriage present?

A

presents with a history of threatened miscarriage

persistent dirty brown discharge

149
Q

what is a habitual/ recurrent miscarriage?

A

3 or more consecutive miscarriages

150
Q

causes of a miscarriage?

A
  • abnormality- foetal development, cervix, uterus, placenta
  • PCOS
  • previous miscarriage
  • BV infection
151
Q

risk factors of miscarriage

A
  • age >30
  • incidence increase with parity
  • smoking >14 per day
  • excess alcohol
  • illicit drug use
  • uncontrolled DM
  • uterine surgery
152
Q

epidemiology of miscarriages

A

15-20% of recognised pregnancies

85% occur in 1st trimester

153
Q

clinical presentation of a miscarriage?

A
  • vaginal bleeding with/ without abdo pain
  • passing products of contraception
  • cervical os open enough to admit 1 finger
  • uterine size small for dates
154
Q

differentials of a miscarriage

A
  • ectopic pregnancy
  • neoplasia
  • hydatiform mole
  • chorionic cyst
155
Q

diagnosis of a miscarriage

A
  • transvaginal USS

- serum hCG- to exclude ectopic pregnancy

156
Q

medical, surgical and social treatment of a miscarriage

A

medical:
- <12 weeks- mifepristone (anti-progesterone), then give misoprostol 36-48 hours later

  • > 12 weeks- vaginal misoprostol

surgical:
- if <13 weeks, suction evacuation under GA

social:
- counselling

  • anti-D rhesus prophylaxis
157
Q

causes of recurrent miscarriages

A
  • antiphospholipid syndrome
  • endocrine- poorly controlled DM, thyroid, PCOS
  • Smoking
  • parental chromosomal abnormalities
  • uterine abnormality- uterine septum
158
Q

when must pregnancies be terminated before?

A

week 24 of gestation

159
Q

what exceptions can be made for terminating a pregnancy after week 24?

A
  • risk to mothers life
  • risk of grave, permanent injury to mothers physical/ mental health
  • substantial risk to child- physical/ mental abnormalities serious enough
160
Q

how are pregnancies terminated?

A

medical:

  • mifepristone to prime cervix
  • misoprostol

surgical:
- vaccum aspiration

161
Q

what is pre-eclampsia?

A

defined as pregnancy-induced hypertension in association with proteinuria (>0.3g in 24h) with or without oedema

162
Q

how is severe pre-eclampsia defined?

A

diastolic BP of at least 110mmHg or systolic BP of at least 160mmHg and/ or symptoms of biochemical and haematological impairment

163
Q

what may happen to the foetus in severe pre-eclampsia?

A

neurological damage due to hypoxia

164
Q

describe the 2 stages of pre-eclampsia

A

stage 1- incomplete trophoblastic invasion of spiral arterioles, decreased utreroplacental blood flow

stage 2- endothelial cell damage resulting in vaso-constriction, lotting dysfunction and increased vascular permeability

165
Q

what must be given and when for women with high/ moderate risk factors of pre-eclampsia?

A

aspirin at 12 weeks

166
Q

what are some high risk factors of pre-eclampsia?

A
  • pre-eclampsia/ HTN in previous pregnancy
  • CKD
  • autoimmune disease- SLE/ antiphospholipid syndrome
  • T1/2 DM
167
Q

what are some moderate risk factors of pre-eclampsia?

A
  • 10+ years since last pregnancy
  • first pregnancy
  • age >40
  • BMI > 25
  • FH (mother/sister) of pre-eclampsia
  • multiple pregnancies
168
Q

clinical presentation of pre-eclampsia

A
  • systolic BP >140mmHg or diastolic BP >90mmHg in second half of pregnancy
  • 1+ proteinuria
  • new HTN
  • severe HTN
169
Q

what are some signs of severe HTN seen in pre-eclampsia?

A
  • severe headache
  • visual disturbance
  • sudden swelling of face, hands and feet
  • RUQ pain
  • epigastric pain +/- vomiting
  • HELLP syndrome- haemolysis, elevated liver enzymes, low platelets
  • pappiloedmea
  • foetal distress/ reduced foetal movement
  • small for gestational age infant
170
Q

diagnosis + results for pre-eclampsia

A
  • urinalysis- dipstick for proteinuria
  • urine culture- exclude infection
  • clotting studies
  • USS of foetus- foetal growth, volume of amniotic fluid
171
Q

if a urine dipstick shows no proteinuria in a patient with suspected pre-eclampsia, what is the diagnosis?

A

gestational HTN

172
Q

what BP measurements indicate, mild, moderate and severe pre-eclampsia?

A

mild- 140-149 systolic, 90-99 diastolic

moderate- 150-159 systolic, 100-109 diastolic

severe- >160/110

173
Q

management of mild pre-eclampsia

A

monitor BP 4x daily

twice weekly blood tests

174
Q

management of moderate pre-eclampsia

A

monitor BP 4x daily

start labetalol (BB)

3 blood tests each week

175
Q

management of severe pre-eclampsia

A
  • monitor BP 4x daily
  • labetalol
  • blood tests 3x week
  • magnesium sulphate
  • deliver baby once woman is stable and baby is >34 weeks
176
Q

what medications must be avoided in pre-eclampsia?

A

ACE inhibitors and angiotensin- II receptor antagonists

177
Q

maternal complications of pre-eclampsia

A
  • eclampsia
  • cerebrovascular haemorrhage
  • HELLP
  • DIC
  • liver failure, rupture
  • renal failure
  • pulmonary oedema
178
Q

foetal complications of pre-eclampsia

A

IUGR

placental abruption

preterm birth

179
Q

what is eclampsia?

A

onset of convulsion in a pregnancy complicated by pre-eclampsia

180
Q

how is eclampsia treated and managed?

A

obstetric emergency !

  • control fits- magnesium sulphate
  • control BP- labetalol, nifedipine, epidural analgesia
  • infant delivery
181
Q

what is the function of magnesium sulphate in eclampsia?

A
  • helps control fits
  • suppresses convulsions and inhibits muscular activity
  • reduces DIC risk as it reduces platelet aggregation
182
Q

what is the risk of the use of magnesium sulphate in pre-eclampsia?

A

reduced reflexes and respiratory depression

183
Q

what is HELLP syndrome?

A

Haemolysis, Elevated Liver enzymes, Low Platelets

complication of pregnancy which usually presents in women who have pre-eclampsia/ eclampsia

184
Q

risk factors for developing HELLP syndrome

A
  • age >35
  • nulliparity
  • previous gestational HTN
  • multiple pregnancies
  • previous HELLP
  • caucasian
  • antiphospholipid syndrome
185
Q

when do cases of HELLP syndrome typically present

A

usually in last half of pregnancy- 70% between 27-37 weeks

30% present post-partum

186
Q

symptoms and signs of HELLP syndrome

A
  • non-specific- malaise, fatigue, RUQ pain etc
  • rapid onset
  • headache and isual disturbance
  • worse at night, better during day

SIGNS
- hepatomegaly

  • bruising/ purpura
  • oedema, HTN and proteinuria
  • jaundice
187
Q

differential diagnosis of HELLP syndrome

A
  • acute fatty liver of pregnancy
  • TTP/ ITP
  • exacerbation of SLE
  • viral hepatitis
188
Q

how is HELLP syndrome diagnosed?

A
  • haemolysis w/ fragmented red cells on blood film
  • raised LDH with a raised bilirubin
  • raised liver enzymes
  • low platelets
189
Q

how is HELLP syndrome treated?

A
  • deliver foetus
  • magnesium sulphate
  • blood transfusion and control BP
190
Q

what is intrauterine growth retardation (IUGR)?

A

When a baby’s growth slows or ceases when it is in the uterus

191
Q

give some maternal, placental, foetal and genetic factors that can contribute to IUGR?

A

maternal- >40, smoker, cocaine, previous SGA baby, diabetes, antiphospholipid syndrome

placental- pre-eclampsia

foetal- trisomy 13/18/21, turners, infection- CMV, rubella

genetic- FH

192
Q

what is the acronym for the high and rare high risk factors for IGUR?

A

SHITS CRAP

high:
Smoking 
HTN/ pre-eclampsia
IUGR previously
Twins
Stillbirth
rare high:
Cocaine
Renal disease
Antiphospholipid snydrome 
PAAP-A levels low
193
Q

what is PAPP-A?

A

Pregnancy Associated Plasma Protein-A (PAPP-A)

produced by placenta- low levels associated with low birth weights and early delivery

194
Q

what is symmetrical IUGR?

A
  • cause of IUGR earlier in pregnancy
  • antenatal scan shows small head, abdo and femur length
  • postnatal weight, length and head circumference all reduced
195
Q

what is asymmetrical IUGR?

A
  • cause of IUGR later in pregnancy
  • antenatal scan shows small abdo circumference (head and femur length normal)
  • postnatal- reduction in weight but length and head circumference normal
196
Q

long term complications of IUGR?

A
  • lower scores on cognitive testing
  • developmental delay
  • cerebral palsy
  • ADHD
  • more susceptible to adult onset diseases- diabetes, HTN, obesity, CHD
197
Q

how is IUGR diagnosed?

A
  • foetal abdo circumference or estimated foetal weight <10th centile
  • reduced amniotic fluid index (AFI)
198
Q

management of IUGR

A
  • LSCS

- corticosteroids to assist lung development

199
Q

what is the difference between sepsis, severe sepsis and septic shock?

A

sepsis- infection + systemic manifestations of infection

severe sepsis- sepsis w/ sepsis-induced organ dysfunction or evidence of tissue hypo-perfusion

septic shock- persistent tissue hypo-perfusion despite adequate fluid replacement

200
Q

what is the most common cause of sepsis?

A

group A strep (community acquired)

201
Q

causes of sepsis in pregnancy

A
  • pyelonephritis
  • chorioamnionitis
  • post-partum endometritis
  • wound infection
  • pneumonia
202
Q

risk factors of sepsis in pregnancy

A
  • usual stuff- obesity, diabetes etc
  • vaginal discharge
  • history of pelvic infection
  • invasive procedures- amniocentesis
  • cervical discharge
203
Q

signs and symptoms of sepsis

A
  • fever, rigors, diarrhoea, vomiting
  • rash
  • abdo/ pelvic pain
  • SIRS criteria
  • hypoxia, HTN
  • oliguria
  • impaired consciousness
204
Q

what is the SIRS criteria for sepsis?

A

3T’s white with sugar

Temperature >38 or <36
Tachycardia >90bpm
Tachypnoea- >20bpm 
WBC <4 or >12
Sugar (glucose) >7.7 in absence of dm
205
Q

What is the sepsis 6 and what else must be considered in a pregnant patient with sepsis?

A

blood cultures, urine output, fluid resuscitation, broad spec antibiotics IV, lactate, 02

  • consider delivery and VTE prophylaxis
206
Q

what is chorioamnionitis?

A

acute inflammation of foetal amnion and chorion membranes due to ascending bacterial infection in setting of membrane rupture

207
Q

clinical features of chorioamnionitis

A

uterine tenderness
ROM
foul odour of amniotic fluid
maternal signs of infection- tachycardia, pyrexia, leucocytosis

208
Q

how is chorioamnionitis managed?

A

delivery (C section if necessary) and IV Abx

209
Q

what is the definition of a premature labour?

A

presence of contractions of sufficient strength and frequency to effect progressive effacement and dilation of the cervix before week 37 of gestation

210
Q

risk factors for a premature labour

A
  • multiple pregnancy
  • cervical incompetence that requires surgery
  • previous preterm labour/ miscarriage
  • previous prelabour rupture of membranes
211
Q

clinical presentation of a premature labour

A
  • contractions
  • bleeding/ amniotic fluid loss
  • dilatation of cervix
212
Q

how is a premature labour managed?

A
  • not viable if <24 weeks
  • tocolysis
  • corticosteroids- betamethasone or dexamethasone
  • magnesium sulphate
213
Q

what is tocolysis and what medications are used in a premature labour?

A

tocolysis- obstetrical procedure carried out with the use of medications with the aim of delaying the delivery of a foetus in women presenting with preterm contractions

  • prostaglandin synthesis inhibitors- indomethacin
  • CCB- nifedipine
  • atosiban
214
Q

what is the definition of preterm premature rupture of membranes and give some RF for this?

A

rupture of the membranes <37 weeks

RF:

  • UTI
  • multiple pregnancy
  • polyhyromnias
  • malpresentation
215
Q

in a patient with suspected preterm premature rupture of membranes, what musnt be done on a speculum exam?

A

dont put fingers in !

216
Q

how is preterm premature rupture of membranes treated in mid-trimester, early and late?

A

mid-trimester (<24 weeks)- poor outcomes- pulmonary hypolasia

early (24-34 weeks)- dexamethasone+erythromycin

late (>34 weeks)- induce labour

217
Q

what is an antepartum haemorrhage?

A

bleeding from birth canal after 24th week of pregnancy

218
Q

aetiology of antepartum haemorrhage

A
  • placenta praevia
  • placenta abruption
  • vasa previa
  • cervical polyps/ erosions/ carcinoma
  • cervicitis/ vaginitis
219
Q

clinical presentation of an antepartum haemorrhage

A
  • bleeding
  • pain may be present
  • uterine contractions
  • malpresentation/ failure of foetal head to engage
  • foetal distress
  • hypovolaemic shock
220
Q

in a patient with an antepartum haemorrhage, what differential must be excluded and how is this done?

A

placenta praevia- USS

221
Q

treatment of an antepartum haemorrhage

A
  • ABC + IV access
  • left lateral position to avoid aortocaval compression
  • group+save/ cross match
  • replacement fluid/ blood
  • ANTI-D
222
Q

what is abruptio placenta?

A

premature separation of placenta from the uterus

significant cause of third-trimester bleeding associated with foetal and maternal morbidity and mortality

223
Q

aetiology of abruptio placenta

A
  • maternal HTN (most common)
  • maternal trauma
  • smoking, alcohol, drugs
  • short umbilical cord
  • sudden decompression of uterus
224
Q

risk factors for abruptio placenta

A
  • smoking
  • previous abruption
  • HTN/ pre-eclampsia
  • thrombophillia
  • cocaine
  • trauma
225
Q

how does a patient with abruptio placenta present clinically?

A
  • pain
  • vaginal bleeding- dark red blood
  • foetal distress
  • ‘woody, hard uterus’
226
Q

how is abruptio placenta treated?

A

same as antepartum haemorrhage:
- ABC + IV access

  • left lateral position to avoid aortocaval compression
  • group+save/ cross match
  • replacement fluid/ blood
  • ANTI-D
227
Q

what is placenta praevia?

A

when the placenta is inserted wholly or in part into the lower segment of the uterus

228
Q

RF for placenta praevia

A
  • previous
  • previous C section
  • increased maternal age + parity
  • smoking
  • cocaine use during pregnancy
229
Q

what is the difference between major and minor placenta praevia?

A

major- placenta covers the internal os of the cervix (grade 3/4)

minor/ partial- if the leading edge is in the lower segment but not covering the os (grade 1/2)

230
Q

clinical presentation of placenta praevia

A
  • painless bleeding after week 28 (acute onset)
  • bright red blood
  • pre-term delivery
  • high-presenting part/ abdominal lie
231
Q

how is placenta praevia treated?

A
  • minor- deliver vaginally
  • C-section at week 38
  • ANTI-D
  • steroids if <34 weeks
232
Q

give 3 complications of placenta praevia?

A
  • PPH (post-partum haemorrhage)
  • Placenta accreta
  • Placenta percreta
233
Q

what is placenta accrete?

A

abnormal adherence of all/part of the placenta to the uterus

234
Q

what is the difference between placenta increta and placenta percreta?

A
  • increta- myometrium is invaded

- percreta- reaches serosa

235
Q

how are placenta increta/ percreta diagnosed?

A

prenatally- colour doppler US MRI

236
Q

what is vasa praevia and how is it managed?

A
  • foetal vessels run/ cross the internal os, resulting in a risk of membrane rupture- leading to foetal haemorrhage

managed via Caesarean section

237
Q

what is a primary post-partum haemorrhage?

A

defined as bleeding from the genital tract in excess of 500ml’s in the first 24h after delivery of the baby

238
Q

what is a secondary post-partum haemorrhage?

A

abnormal vaginal bleeding any time in the puerperium up to 6 weeks

239
Q

how are post-partum haemorrhages classified into massive, major and minor?

A

massive= >1500ml

major= >1000ml

minor= 500-100ml

240
Q

aetiology of primary post-partum haemorrhage

A

4 T’s

TONE- atonic uterus
Tissue- retained placenta w/ prolonged 3rd stage
Trauma- tears and repairs
Thrombin- pre-eclampsia/ DIC

241
Q

what is the most common cause of a secondary post-partum haemorrhage?

A

secondary to infection

242
Q

risk factors for a post-partum haemorrhage

A
  • uterine over-distension (due to multiple pregnancies)
  • prolonged labour/ instrumental delivery
  • previous
  • multiple fibroids
  • thrombin- HELLP, sepsis, DIC
243
Q

what must be given as prophylaxis to prevent a post-partum haemorrhage with an anterior shoulder delivery?

A

oxytocin IM

244
Q

how is a post-partum haemorrhage treated and managed?

A
  • ABC- fluid resus
  • bi-manual uterine compression (massage and compress uterus to expel clots)
  • IV oxytocin +/- ergometrine
  • misoprostol

surgical- evacuation, balloon tamponade, hysterectomy

245
Q

the seven cardinal movements- what are they (definition)?

A

positional changes that assist the baby in the passage through the birth canal

engagement, descent, flexion, internal rotation, extension, external rotation, expulsion

246
Q

the seven cardinal movements- what happens during engagement?

A

entering of the biparietal diameter (measuring ear tip to ear tip across the top of the baby’s head) into the pelvic inlet

247
Q

the seven cardinal movements- what is descent?

A
  • lightening- baby’s head moves deep into pelvic cavity
  • head becomes moulded
  • biparietal diameter descends into pelvic inlet
248
Q

the seven cardinal movements- what is flexion?

A
  • occurs due to resistance between head and soft tissues of pelvis
  • resistance causes flexion of head so chin meets chest
  • smallest diameter of head presents into pelvis
249
Q

the seven cardinal movements- what is internal rotation?

A
  • head rotates as it reaches pelvic floor
  • baby moves from a sideways position to one where the sagittal suture is in the AP diameter of outlet (back of baby’s head is against front of pelvis)
250
Q

the seven cardinal movements- what is extension?

A
  • rest- neck is under pubic arch

- extension occurs as head, face and chin are born

251
Q

the seven cardinal movements- what is external rotation?

A
  • pause after head is born

- restitution- baby rotates to fit shoulders under pubic arch

252
Q

the seven cardinal movements- what is expulsion?

A
  • after external rotation- anterior shoulder moves out from under pubic bone
  • rest of baby is then born with an upward motion by care provider
253
Q

what is shoulder dystocia?

A

occurs when baby’s shoulders are halted at pelvic outlet due to inadequate space through which to pass

usually the anterior shoulder which impacts on the maternal symphysis

254
Q

aetiology of shoulder dystocia

A

3P’s= Power (uterus), Passenger (foetus), Pelvis

Power/ uterine factors= infrequent contractions, primigravid

Passenger/ foetal= position or lie, macrosomia

Pelvic passage= long, oval brim, cephalopelvic disproportion (due to scoliosis, kyphosis or rickets)

255
Q

risk factors of shoulder dystocia

A
  • maternal DM
  • foetal macrosomia
  • maternal obesity
  • induction + prolonged labour
  • use of oxytocin
  • assisted vaginal delivery
256
Q

how does shoulder dystocia present clinically (i.e. during birth)?

A
  • difficulty with delivery of face
  • head remaining tightly applied to vulvula or retracting (turtle-neck sign)
  • failure of head to restitute
  • failure of shoulders to descend
257
Q

how is shoulder dystocia managed?

A
  • stop mother pushing
  • McRobert’s manoeuvre- hyperflex mothers hips to abdomen
  • Woods screw manoeuvre
  • epiostomy
  • Zavvenelli’s- may require C section
258
Q

complications for foetus and mother of shoulder dystocia

A

foetal:

  • brachial plexus injury (Erb’s palsy)
  • perinatal morbidity and mortality from hypoxia
  • fractured humerus or clavicle
  • pneumothorax

maternal:

  • PPH
  • 3/4th degree tear
  • vaginal lacerations
  • cervical tear
  • bladder/ uterine rupture
259
Q

what is a cord prolapse?

A

when the umbilical cord descends below the presenting part and causes hypoxia in the baby

260
Q

risk factors for cord prolapse

A
  • pre-term labour
  • breech presentation
  • spontaneous early rupture of membranes
  • polyhydramnios
  • abnormal lie
  • twin pregnancy
261
Q

how can cord prolapse be prevented?

A

elevate presenting part manually or by filling urinary bladder to stop presenting part occluding cord

262
Q

how is a cord prolapse managed?

A
  • tocolytics to reduce compression
  • push presenting part of foetus back into uterus
  • patient on all 4’s
263
Q

what is an amniotic fluid embolism?

A

liquid enters maternal circulation- leading to anaphylaxis with sudden, dyspnoea, hypoxia and hypotension

264
Q

what severe consequences can amniotic fluid embolism cause?

A

DIC
pulmonary oedema
ARDS

265
Q

how is an amniotic fluid embolism managed?

A

resus and support- O2, fluids, bloods etc

266
Q

what are some clinical signs of uterine rupture?

A
  • foetal heart rate abnormalities
  • vaginal bleeding
  • cessation of contractions
  • maternal shock
  • foetal distress
267
Q

risk factors for uterine rupture

A
  • labour with scarred uterus- from C section, deep myomectomy or previous surgery
  • neglected obstructed labour
  • breech extraction
268
Q

management of uterine rupture

A
  • maternal resus

- emergency C section if suspected in labour

269
Q

what is Bishops score?

A
  • pre-labour scoring system used to assist in predicting whether induction of labour will be required
  • used to assess the odds of spontaneous preterm delivery
270
Q

what causes gestational diabetes?

A
  • increased resistance to insulin due to placental production of anti-insulin hormones (hPL, glucagon and cortisol)
  • plus increased appetite in pregnancy (particularly to fatty foods)
271
Q

risk factors for the development of gestational diabetes

A
  • previous large infant
  • previous GD
  • 1st deg. relative with diabetes
  • obesity
  • south asian, black Caribbean or middle eastern
  • macrosomia
  • glycosuria
272
Q

clinical features of gestational diabetes

A
  • can be asymptomatic
  • polydipsia
  • polyuria
  • dry mouth
  • tiredness
273
Q

how is gestational diabetes screened for?

A

screen at risk groups by 75g OGTT (oral glucose tolerance test) at 28 weeks

274
Q

what are the implications of gestational diabetes to each trimester of the pregnancy?

A

1st- none

2nd- pre-eclampsia and macrosomia

3rd- same as 2nd + recurrent infections, intrauterine death, polyhydramnios, congenital malformations

275
Q

what is the effect of gestational diabetes on:

  • labour
  • delivery
  • post-natal
  • long term (for both mother and baby)
A
  • labour- risk of still/ premature birth, induction required
  • delivery- C-section usually/ instrumental birth, shoulder dystocia
  • post-natal- neonatal hypoglycaemia, respiratory distress syndrome, jaundice
  • long term, T2DM (mother), obesity (baby)
276
Q

what acronym can be used to remember the risk from Gestational diabetes?

A

SMASH

Shoulder dystocia
Macrosomia
Amniotic fluid excess (polyhydromnias)
Stillbirth
HTN+neonatal hypoglycaemia
277
Q

why is polyhydromnias seen in gestational diabetes?

A

increased in foetal glucose results in polyuria, hence more amniotic fluid

278
Q

why does macrosomia occur in gestational diabetes?

A

increased foetal insulin- too much glucose is absorbed

279
Q

what is the ‘rule’ for the results of the OGTT in gestational diabetes?

A

5.6.7.8

fasting= >5.6

after 2 hours= >7.8

280
Q

how is gestational diabetes managed?

A
  • diet and exercise
  • metformin and glibenclamide
  • insulin
281
Q

what is Lochia?

A
  • normal discharge/ bleeding in the first 2 weeks after giving birth
282
Q

in a patient presenting with Lochia, what symptoms indicate the need for further investigation?

A

smell

increased volume of blood

bleeding hasn’t stopped

283
Q

why are infections common in pregnancy?

A

placental surface in the surface is vulnerable to infection- it is exposed to the vagina

284
Q

what peripartum events and lead to a chronic infection in pregnancy?

A
  • prolonged membrane rupture
  • chorioamnionitis
  • repeated vaginal examinations
  • poor personal hygiene
  • catheterisation
  • C section/ instrumental deliveries
  • perineal trauma
  • manual removal of placenta
285
Q

for Endometritis, state:

  • symptoms
  • aetiology
  • clinical features
A
  • symptoms- fever, lower abdo pain
  • secondary to PPH+foul-smelling vaginal discharge
  • aetiology- group A haemolytic strep, aerobic gram-negative rods
  • CF- tachycardic and tender
286
Q

predisposing factors to developing a UTI during pregnancy

A
  • previous UTI
  • polycystic kidneys
  • congenital abnormalities of renal tract
  • neuropathic bladder
287
Q

clinical features of a UTI

A
  • voiding difficulty- urgency and frequency
  • dysuria
  • fever
  • pain
288
Q

diagnosis of a UTI

A
  • nitrates

- urinalysis- protein and leucoytes

289
Q

what organisms commonly cause UTI’s?

A

E.coli, Kliebsiella, proteus

290
Q

features of lactation mastitis

A
  • breast pain
  • fever
  • erythema
  • arises after breast feeding
291
Q

what organism commonly causes lactation mastitis?

A

staph aureus

292
Q

how is lactation mastitis managed?

A
  • pain- analgesia, warm compresses and ensure Pt completes emptying of breast after feeding
  • if infected nipple fissure + bacteria culture +ve, give oral flucloxacillin
293
Q

what antibiotics cannot be given to mothers who are breastfeeding?

A
  • ciprofloxacin
  • tetracycline
  • chloramphenicol
  • sulphonamides
294
Q

what psychiatric drugs cannot be given to mothers who are breastfeeding?

A
  • lithium
  • benzo’s
  • fluoxetine
295
Q

other than antibiotics and psychiatric drugs, what other medications cannot be given to to breastfeeding mothers?

A
  • aspirin
  • carbimazole
  • methotrexate
  • sulphonlyureas
  • cytotoxic drugs
  • amiodarone
296
Q

what are some risk factors for developing psychiatric illness after birth?

A
  • hx of mental health problems
  • alcohol/ drug misuse
  • womans attitude towards pregnancy
  • mother-baby relationship
  • living conditions/ social isolation
  • FH
  • domestic violence and abuse
  • socioeconomic status
297
Q

clinical features of post-natal depression

A
  • low mood
  • low energy
  • exhausted
  • irritable
  • unable to cope
  • feeling guilty about not being able to cope/ not loving baby enough
  • anxiety about baby
  • tearful
  • difficulties in bonding with baby
  • difficulties in relationships with family
298
Q

features of the ‘baby blues’

A
  • common, transient
  • 3-7 days after primip birth- may last 2 weeks
  • tearful, anxious and irritable
  • reassurance and support
299
Q

when is post-natal depression commonly seen?

A
  • 10% of pregnancies

- starts within a month and peaks at 3 months

300
Q

how is post-natal depression treated?

A
  • reasurrance and support
  • CBT
  • SSRI’s (sertraline/ paroxetine)
  • tricyclics
301
Q

How does puerperal psychosis present and how is it managed?

A
  • rare- presents up to 2-3 weeks after birth
  • severe mood swings and disordered perception
  • treatment= mood stabilisers, antidepressants, ECT
  • to treat psychotic symptoms= antipsychotics/ long acting benzo’s
302
Q

causes of placental insufficiency

A
  • abnormal trophoblast invasion- pre-eclampsia, palcenta accreta
  • infarction
  • abruption
  • placenta praevia
  • tumours- chorioangioma
303
Q

how is a retained placenta diagnosed?

A

when the placenta does not spontaneously delivery within an hour after birth

304
Q

risk factors for a retained placenta

A
  • high parity
  • prolonged use of oxytocin
  • history of uterine surgery
  • IVF conception
305
Q

why is a retained placenta such a serious complication?

A

delivery of the placenta allows the uterus to contract; without this it will continue to bleed leading to haemorrhage

306
Q

how is a retained placenta managed?

A
  • by hand- but risk of infection

- physiological processes can also help- e.g. urinating and breastfeeding

307
Q

what is Sheehan’s syndrome?

A

excessive blood loss during pregnancy/ after delivery leading to dysfunction of the pituitary gland. This results in hypopituitarism

essentially postpartum hypopituitarism caused by necrosis of the pituitary gland

308
Q

how does sheehan’s syndrome present clinically?

A

lactation failure post-partum

can take a long time to diagnosis

  • axillary/ pubic hair loss
  • weakness
  • premature ageing
  • hyperpigmentation
  • amenorrhoea
  • hypothyroidism
309
Q

explain the pathology of rhesus disease

A
  • fetal cells cross into maternal circulation (normal)
  • fetus carries gene for antigen which the mother does not have- fetus nay be D/d (rhesus D +ve) whereas mother is d/d (-ve)
  • if this is the first occurence/ first pregnancy, IgM is produced which cannot cross placenta so pregnancy is not at risk
  • re-exposure in a subsequent pregnancy causes B cells to produce IgG which crosses into foetal circulation and destroys erythrocytes, resulting in haemolytic anaemia (fatal to foetus)
310
Q

when are pregnant women screened for rhesus?

A

booking, 28 and 34 weeks

311
Q

how can foetal RBC lysis be prevented in rhesus negative mothers?

A

Anti-D prophylaxis is given- destroys Rh+IgG- hence no RBC’s are destroyed

312
Q

when may sensitisation to Rhesus disease occur during pregnancy?

A
  • miscarriage
  • abortion
  • amniocentesis
  • placental abruption
  • delivery
313
Q

what must be given to a rhesus negative mother whilst having amniocentesis?

A

Anti D- risk of sensitisation

314
Q

give some clinical signs for polyhydramnios

A
  • increased abdo size (out of proportion)
  • AFI (amniotic fluid index) >20 on USS
  • maternal dyspnoea
  • faint foetal heart sounds
315
Q

aetiology of polyhydramnios

A
  • maternal diabetes
  • foetal- dudonal atresia
  • multiple gestation
316
Q

what are some consequences of polyhydramnios?

A
  • cord prolapse
  • PPH
  • IGUR
  • preterm labour
317
Q

what is oligohydramnios?

A

low amniotic fluid level- defined as <8cm AFI

318
Q

Aetiology of oligohydramnios

A
  • leakage of amniotic fluid
  • reduced fetal urine production- IUGR, fetal renal failure
  • obstruction to foetal urine output- posterior urethral valves
319
Q

what are some complications of oligohydramnios?

A
  • preterm rupture of membranes
  • IUGR
  • reduced volume- lung hypoplasia
320
Q

how is oligohydramnios managed?

A
  • 34-36 weeks- induce labour

- if before 34-36 weeks- give oral erythromycin, monitor for infection, monitor until induction at 34-36 weeks

321
Q

what trisomies are tested for during pregnancy?

A

13- Patau’s

18- Edward’s

21- Down’s

322
Q

what does the Combined test assess for and how is this done?

A
  • Down syndrome- done in 1st trimester

- Nuchal transulcency scan + serum levels of PAPP-A and free beta HCG

323
Q

What is the quadrouple test?

A
  • test for Down’s in 2nd trimester
324
Q

if screening for Down’s has a positive result, what is done next?

A
  • app at foetal medicine unit within 3 days

- diagnostic test- Chorionic Villous Biopsy and Amniocentesis

325
Q

when are screening ultrasounds done and what do they aim to identify?

A
  • 8-10- viability of pregnancy
  • 11-13- dating and gestational age
  • 20- anomaly scan- identify major abnormalities (spina bifida, cleft lip, trisomy 13,18 etc)
326
Q

what are haemoglobinopathies?

A

recessively inherited disorders of haemoglobin

327
Q

what are the Quantitate haemoglobinopathies?

A
  • Alpha thalassaemia- if major= incompatible with extra-uterine life
  • Beta thalassaemia- life threatening anaemia
328
Q

what Qualitative haemoglobinopathy is screened for?

A

sickle cell anaemia

329
Q

how are haemoglobinopathies screened for?

A
  • identification of carriers
  • 8-10 weeks
  • haematological test rather than genetic
330
Q

what is the New-born blood spot (NBBS)?

A
  • early diagnosis and treatment of conditions to prevent irreversible damage
  • heel prick in days 5-8
331
Q

how many conditions does the NBBS screen for (and what are the main 3 !)?

A
  • 9 in total

main 3:

  • Cystic fibrosis
  • congenital hypothyroidism
  • sickle cell anaemia
332
Q

how is the newborn’s hearing screened?

A
  • within 4 weeks of birth

- automated otoacoustic emission identifies response in cochlea to soft sounds from earpiece

333
Q

what are the 2 categories of disorders that can lead to female infertility/ subfertility?

A
  • disorders of ovulation

- disorders of anatomy (tubes, uterus, cervix)

334
Q

examples of ‘disorders of ovulation’ leading to female infertility

A
  • PCOS
  • pituitary tumour
  • ovarian failure
  • Sheehans
335
Q

examples of ‘disorders of anatomy’ leading to female infertility

A
  • PID
  • endometriosis
  • Ashermans
  • STI
336
Q

what should a patient be instructed to do if they have missed 1 COCP?

A
  • take the missed one (even if thats 2 in 1 day)

- still ‘covered’ for protection as long as missed dose is taken within 12 hours

337
Q

what should a patient be instructed to do if they have missed 2 COCP?

A
  • take last missed pill (not both)

- must use condoms until back on track with pill regime for 7 days

338
Q

give some contraindications for the use of the COCP

A
  • migraine with aura
  • breast feeding <6 weeks post-partum
  • current breast cancer
  • > 35 BMI
  • carrier of breast cancer gene
339
Q

when does the progesterone only pill offer protection?

A
  • up to day 5 of cycle

- additional contraception needed for 2 days

340
Q

what should be done >3 and <3 hours after missing a dose?

A

<3 hours- continue as normal

> 3 hours- take missed pill and use barrier methods for next 48 hours

341
Q

what is the Depo Provera method of contraception?

A

contains medroxyprogesterone acetate 150mg

given via IM injection every 12 weeks

342
Q

what is the function of the IUD and what are some consequences of this?

A
  • prevents fertilisation by decreasing sperm motility and survival
  • is effective immediately
  • makes periods heavier, longer and more painful
  • risk of PID after insertion
343
Q

what is levonorgestrel?

A
  • progesterone- given as emergency contraception

- delays ovulation, must be taken within 72 hours

344
Q

Give some causes of infertility

A
  • ovulatory
  • tubal
  • uterine
  • male factors
345
Q

what investigations would a GP do in a couple presenting with infertility?

A
  • hormones- D2, FSH, D21 progesterone

TFT

Rubella

Smear

semen analysis

346
Q

how is ovulation assessed in a patient presenting with infertility?

A

measure mid-luteal progesterone

347
Q

what sperm count level warrants further investigation?

A

<5m/ml

  • endocrine tests
  • karyotyping
348
Q

what 2 hormones are assessed to determine the patients ovarian reserve?

349
Q

how is tubal patency investigated in a patient presenting with infertility?

A
  • HSG (hysterosalpingogram) imaging

- laparoscopy

350
Q

if a mild, moderate, severe abnormality is present in a patient concerned with infertility, what can be done?

A

mild- intrauterine insemination

moderate- IVF

severe- intra-cytoplasmic sperm injection

351
Q

describe the process of IVF

A

Ovarian stimulation -> egg collection -> insemination -> fertilisation check -> embryo culture -> embryo transfer -> luteal support

352
Q

give 4 risk factors associated with IVF

A
  • multiple pregnancy
  • miscarriage
  • ectopic pregnancy
  • foetal abnormality
353
Q

what is the APGAR scoring system?

A

assesses how well the baby is doing after birth (1-10, above 7 is good)

Appearance (Skin colour)
Pulse
Grimace (reflex irritability)
Activity
Respiration

NP- Phase 3a Medicine (22 decks)

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