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3a. O&G > Pregnancy & Labour > Flashcards

Pregnancy & Labour Flashcards

1
Q

Screening tests play a key role in antenatal care. Define sensitivity and specificity, in relation to these tests.

A 
Sensitivity = [true +] / [+ve + false -ve]. Identifies those with a disease
Specificity = [true -] / [-ve + false +ve]. Identifies those without a disease.
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2
Q

Describe the key investigations undertaken at the antenatal booking visit [5].

A
  • histories: O&G, medical, surgical, allergies, psychiatric, family and social health
  • physical health: height, weight, BP
  • blood tests: Hb, ABO, Rh status, infection screen (syphilis, HIV, HBV, HCV)
  • urinalysis (e.g., DM)
  • ultrasound: estimates gestational age, detects major structural anomalies
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3
Q

At what time is the antenatal booking visit normally undertaken?

A

8-12 weeks gestation

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4
Q

Describe how gestational age is estimated until ultrasound is performed at the booking visit.

A

Naegele’s rule: LMP (last menstrual period) + 9 months and 7 days (280 days)

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5
Q

What is placenta previa?

A

The placenta encroaches on the cervix at the anomaly scan; it does not move at the repeat scan 2 weeks later and requires Caeseran section

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6
Q

Name and describe the three screenable trisomies in pregnancy, and describe how screening for these changes as first presentation changes with gestational age.

A
  • trisomy 13 [Patau syndrome]; trisomy 18 [Edward syndrome]: both generally lethal, mosaics assc. with severe physical and mental disability
  • trisomy 21: varies widely from mild to profound disability (structural defects in heart, duodenum, thyroid; increased rates of cancer, learning disability)
  • all three may be screened for in the first trimester. only Down syndrome may be screened for in the second trimester
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7
Q

Describe the non-invasive methods for genetic screening.

A
  • nuchal thickness (on USS): increased thickness at the back of the foetal neck
  • NIPT (non-invasive prenatal testing): assesses placental (foetal) DNA in maternal serum; >90% accuracy, although results affected by maternal BMI
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8
Q

Describe the key differences in amniocentesis and chorionic villous sampling.

A
  • amniocentesis: >15 weeks, risk of miscarriage <1%

- CVS: >12 weeks, risk of miscarriage 2%

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9
Q

Describe how rhesus sensitisation works [4].

A
  • Rh +ve father and Rh -ve mother produces a Rh +ve foetus
  • Rh +ve foetus blood exchanged into maternal circulation
  • this causes production of maternal antibodies, which remain lifelong
  • second pregnancy with Rh +ve foetus will cause maternal antibodies to cross and attack foetus
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10
Q

What are the risks of rhesus sensitisation in mother and foetus of opposite status?

A

May cause foetal hydrops and death

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11
Q

Describe how rhesus problems are treated, both during pregnancy and in other O&G situations.

A
  • early delivery; blood or intrauterine transfusion
  • anti-D injections to prevent antigens forming in Rh -ve women given at 28w and after any sensitising event (TOP, APH, trauma etc.)
  • after birth, cord blood is tested and anti-D is given if the baby is Rh +ve
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12
Q

Define ‘small for gestational age’ and ‘foetal growth restriction’.

A
  • SGA: birth weight <10th centile.
    • abdominal circumference (AC) / estimated foetal weight (EFW) <3rd centile
    • AC / EFW <10th centile, plus evidence of placental dysfunction
  • FGR: failure to achieve genetic potential for growth, implying pathological restriction of genetic growth potential
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13
Q

Describe the main causes of a SGA foetus [3].

A
  • placental: infarct, abruption, hypertension
  • foetal: infection (particularly rubella, CMV), congenital (e.g., absent kidneys), chromosomal abnormalities
  • maternal: lifestyle, BMI, age, disease
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14
Q

Describe the increased risks to the foetus and mother with an SGA foetus [3].

A
  • stillbirth
  • morbidity, GDM, PET
  • mortality: hypoxia, hypoglycaemia, chronic asphyxia, hypothermia, polycythaemia, hyperbilirubinaemia, abnormal neurodevelopment
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15
Q

Describe how foetal size is screened during pregnancy [4].

A
  • SFH (symphysis-fundal height)
  • performed from 24 weeks and plotted on a graph
  • single SFH <10th centile / serial measurement crossing centile lines should be referred for USS
  • SFH inaccuracies (BMI > 35, large fibroids, hydramnios) require USS use.
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16
Q

Describe the risk factors for an SGA foetus [8].

A

[first quantifier indicates minor factor, second indicates major]

  • age (>35, >40)
  • nulliparity, IVF
  • pregnancy interval <6 or >60 months
  • BMI (<20/25-35, >35)
  • smoking (<10/day, >11/day)
  • previous SGA, parental SGA [major]
  • non-O&G conditions: chronic HTN, DM w/ vascular disease, renal impairment, APLS
  • O&G conditions: previous PET, heavy bleeds, large fibroids, uterine artery notching at 20wks
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17
Q

Describe the management of an SGA foetus [4].

A
  • aspirin 150mg for 12 weeks, steroids from 24-35+6wk, magnesium sulfate <32 wk
  • genetic tests, infection screen, serial scans for growth, measurement of liquour volume, umbilical artery Doppler
  • <3rd centile: delivery from 37 - 37+6 wk
  • 3rd-10th centile: delivery at 39w
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18
Q

Define LGA.

A

SFH >2cm for gestational age (e.g., 28cm at 24w is +4cm)

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19
Q

What are the main causes of LGA? [5]

A
  • foetal macrosomia
  • polyhydramnios
  • multiple pregnancy
  • pre-existing diabetes
  • GDM
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20
Q

Define foetal macrosomia, describe associated risks and management.

A
  • EFW >90th centile, AC >97th centile
  • risks: anxiety, shoulder and labour dystocia, PPH
  • Mx: exclude DM, reassure, offer options (conservative, IOL, C/S; latter is only option when weight >5kg)
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21
Q

Regarding polyhydramnios, describe the:

  • definition
  • causes
  • symptoms
  • investigations
A
  • excess amniotic fluid within the uterus; may be quantified as AFI >25cm or a deepest pool >8cm
  • maternal (DM), foetal (anomlies, monochorionic twin pregnancy, hydrops, viral infection)
  • abdominal discomfort, pre-labour rupture of membranes, preterm labour, cord-prolapse,, malpresentation, tense shiny abdomen
  • OGTT, viral serology (parvovirus B19, toxo, CMV), serial USS survey
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22
Q

Multiple pregnancy develops differently depending on at which stage the egg splits; describe the timeline [3].

A
  • morula: forms DC/DA. Lambda sign on USS
  • blastocyst: forms MC/DA. T sign on USS
  • implanted blastocyst: forms MC/MA
    [MC = monochorionic, DC = dichorionic, MA = monoamniotic, DA = diamniotic]
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23
Q

Two risks of multiple pregnancy are single foetal death and selective growth restriction. Describe how these are managed.

A
  • single foetal death: MRI on surviving foetal brain 4 weeks after IUD. perform MCA PSV for foetal anaemia
  • selective growth restriction: selective reduction (early onset + abnormal Doppler)
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24
Q

Describe TTTS (twin-to-twin transfusion syndrome) and its main complication, TAPS (twin anaemia polycythaemia sequence). [3]

A
  • TTTS: donor twin perfuses recipient via artery-vein anastomoses
  • treatment is via foetoscopic laser ablation
  • TAPS is a complication of laser ablation. MCA PSV is used to monitor for anaemia
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25
Q

Describe the symptoms and management of multiple pregnancy.

A
  • exaggerated symptoms (hyperemesis gravidarum), inc AFP, LGA uterus, increased foetal poles
  • Mx: Fe, aspirin, folic acid; USS scanning 2.4 weekly.
    • deliver DCDA 37-38wk
    • delivery MCDA 36wk
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26
Q

Describe the management of diabetics who become pregnant [4].

A
  • aim for HbA1C of 48 mmol/mol. avoid pregnancy if >86
  • stop embryopathic drugs (e.g., ACE, statins)
  • folic acid + aspirin
  • deliver by 38+6
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27
Q

Regarding GDM, describe the:

  • pathology
  • risk factors
  • investigations
  • timing of delivery
A
  • pregnancy is diabetogenic, and is a state of insulin resistance due to HPL and cortisol
  • risks: previous GDM / LGA, obesity, FH, ethnic variation, polyhydramnios, glycosuria
  • previous GDM: BP monitoring/OGTT. others: OGTT 24-28wk
  • timing of delivery: insulin 38-39wk, metformin 39-40wk, diet alone 40-41wk
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28
Q

Describe the effects of pregnancy on drug pharmacokinetics / pharmacodynamics.

A
  • kinetics (ADME):
    • absorption reduced by morning sickness
    • increased distribution with increased PV/fat stores
    • increased liver metabolism
    • increased elimination renally (due to increased GFR)
  • no significant changes to dynamics; may be more prone to hypotension with anti-HTN drugs
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29
Q

Name the main classes of teratogenic drugs and their main effects on pregnancy.

A
  • ACE/ARB: oligohydramnios, renal hypoplasia
  • androgens: female foetus virilisation
  • AEDs: cleft palate, facial abnormalities, neural tube defects
  • carbimazole: hypothyroidism, bone growth abnormalities
  • cytotoxics: multiple defects, abortion
  • lithium: Ebstein’s
  • MTX: skeletal defects
  • misoprostol: Moebius syndrome
  • retinoids: ear, heart, skeletal defects
  • thalidomide: phocomelia
  • warfarin: limb, facial defects; risk of haemorrhage during delivery
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30
Q

Beta-blockers should not be used for the treatment of HTN, as they may inhibit foetal growth. When may they be used instead? [4]

A
  • tachyarrhythmia
  • mitral stenosis, possible aortic dissection
  • migraine
  • hyperthyroidism
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31
Q

Describe which drugs can be safely used for common conditions in pregnancy [4].

A
  • N&V: cyclizine
  • UTI: nitrofuratoin, cefalexin (trimethoprim in 3rd trimester)
  • pain: paracetamol
  • heartburn: antacids
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32
Q

Which chemical class of drugs are more likely to accumulate in breastmilk and which babies are they more likely to affect?

A
  • small, lipophilic drugs more likely to accumulate in breastmilk
  • few enter in sufficient quantities to cause problems
  • foremilk (rich in protein) -> hindmilk (rich in fat and therefore fat-soluble drugs); those who suckle longer therefore more likely to be affected
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33
Q

Which drugs are particularly dangerous in breastfeeding? [5]

A
  • phenobarbitone (affects suckling)
  • amiodarone (hypothyroidism)
  • cytotoxics
  • BZDs (drowsiness)
  • bromocriptine (suppresses lactation)
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34
Q

Describe the risks and management of obesity in pregnancy [4 + 4]

A
  • risks split into following:
    • pre-pregnancy: menstrual disorder, subfertility, miscarriage, foetal anomaly
    • pregnancy: PET, GDM, VTE
    • labour: inc IOL, dysfunctional labour, operative delivery, haemorrhage, birth injury
    • post-labour: infection, red. breastfeeding, prolapse, incontinence
  • handling risk assessment, assess risk of venous access and anaesthesia
  • screen those with BMI >30 for GDM
  • folic acid, aspirin, vitamin D
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35
Q

Why is VTE more common in the left leg (9:1)?

A

The gravid uterus compresses the left common iliac vein. Groin pain is an important feature to consider in these.

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36
Q

Describe the investigations and management of VTE in pregnancy [4].

A
  • compression duplex USS, MRI venography
  • pulmonary: V/Q, CTPA; V/Q preferred as no irritation to breast (and subsequent inc. risk of malignancy)
  • use LMWH, as warfarin crosses the placenta and causes embryopathy
  • neither heparin nor warfarin are contraindications to breastfeeding
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37
Q

Describe the presentation, risks, and management associated with intrahepatic cholestasis of pregnancy.

A
  • pruritis (of soles, palms), dark urine, anorexia, steatorrhoea. inc. bile acids, GGTs, ALT, bili
  • USS, viral serology, autoantibodies normal. biopsy, if performed (not indicated) would show centrilobar cholestasis
  • risks: foetal distress, amniotic fluid meconium aspiration, IUD, preterm birth
  • ursodeoxycholic acid 1-2g/daily; alternatives = piriton, aqueous menthol cream
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38
Q

What are the three categories of hypertension that may affect a pregnant woman?

A
  • pre-existing (consider renal causes, Cushing’s, Conn’s, phaeochromocytoma)
  • pregnancy-induced (resolves within 6/52 of delivery; no features of proteinuria/PET)
  • pre-eclampsia and eclampsia
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39
Q

What are the main clinical features of pre-eclampsia (toxaemia - PET)? [4]

A
  • cardinal 3: hypertension (!), ✨rapidly progressive✨ oedema, and proteinuria (>0.3g/24h)
  • neuro: headache, blurring/flashing of vision, disorientation, hyperreflexia
  • GI: N&V, E/RUQ pain
  • O&G: SGA foetus, IUD
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40
Q

Describe the pathology of PET, and how timing of gestation may affect this [3].

A
  • abnormal placental perfusion, due to endothelial dysfunction (‘stiffness’) causes ischaemia and an anti-angiogenic state
  • early (<34wk), 12%: extensive villous/vascular lesions of the placenta, higher risks of complication
  • late (>34wk), 88%: minimal placental lesions
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41
Q

Describe the risk factors and investigations associated with PET.

A
  • risks: age >40, BMI >30, PMH, nulliparity, twins, previous PE, birth interval >10y, molar pregnancy
  • ‘standard’ investigations: FBC, U&Es, LFTs, UPCR, coagulation screen
  • maternal uterine artery Doppler: shows resistance of diastolic flow via ‘notching’
42
Q

Describe the medical management of PET [4].

A
  • first line Tx: labetalol (a + b antagonist) or nifidepine (CCB); consider methyldopa (C/I in PMH depression)
  • second line: hydralazine, doxazocin
  • the only cure is delivery. indications for this include term gestational age, inability to control BP, rapidly deteriorating biochem/haem or crises
  • at delivery, stabilise the mother and give her betamethasone for lung maturation of foetus
43
Q

What is HELLP syndrome? [3]

A
  • a crisis associated with PET
  • Haemolysis, Elevated Liver enzymes, Low Platelets
  • E/RUQ pain, N&V, jaundice, more common if multiparous
44
Q

Name the crises associated with PET [7].

A
  • eclampsia
  • HELLP syndrome
  • pulmonary oedema
  • placental abruption
  • cerebral haemorrhage, cortical blindness
  • DIC
  • AKI, hepatic rupture
45
Q

Describe the purpose, parameters, and results of the Bishop’s score.

A
  • enables prediction of the likely outcome of induction of labour.
  • five main parameters
    • dilatation (larger score with larger dilation)
    • effacement (larger score with larger %)
    • station (larger when positive)
    • colposcopy (larger score when soft)
    • cervix position (larger score when anterior)
  • score <5: cervical ripening required
  • score >5: strongly predictive of labour following induction
46
Q

Name the methods of inducing labour.

A
  • manual rupture of membranes (finger)
  • artificial rupture of membranes (ARM) via amniotomy
  • medical induction with syntocinon
  • cervical ripening by prostaglandin E2 or balloon catheter
47
Q

Describe the stages of labour.

A
  • stage 1: regular contractions until cervical dilatation (early latent <4cm, active 4-10cm)
  • stage 2: full dilatation to delivery of foetus
    • passive: full dilatation in absence of contractions
    • active: baby visible / persistent contractions
  • stage 3: delivery of foetus to delivery of placenta and membranes; average 10min
48
Q

Describe the active management of stage 3 labour.

A
  • oxytocin or syntometrine
  • bladder catheter
  • deferred cord clamping
  • controlled cord traction after signs of membrane seperation
  • indications: excessive bleeding, failure to deliver placenta <1, maternal desire
49
Q

Describe how the foetal head moves through the pelvis in labour [7].

A
  • engagement: head is engaged at 3/5 (2/5 still in abdomen)
  • descent: downward movement
  • flexion: passively in descent due to shape of pelvis and soft tissue
  • internal rotation: transverse to anterior, ROT –> ROA –> OA
  • extension: reaches introitus, base of occiput in contact with inferior pubic symphysis
  • external rotation: ROA –> ROT
  • expulsion
50
Q

Describe the options for analgesia in labout.

A
  • narcotic (inc. remifentanil)
  • inhalational (entonox)
  • TENS, acupuncture, massage etc.
  • epidural (complete relief in 95%)
  • pudendal nerve block
  • general anaesthetic
51
Q

Describe the benefits of delayed cord clamping.

A

increased RBC flow, decreased anaemia, increased breastfeeding, increased Hct/Hb, increased BP/PV, decreased need for blood transfusion or oxygen

52
Q

Define the following terms.

  • malpresentation
  • breech presentation
  • malposition
A
  • malpresentation: anything other than the vertex presents
  • breech: baby’s buttocks, feet, or both come out first during birth; often determined by USS at end of gestation
  • malposition: baby in OP/transverse position
53
Q

Define failure to progress, give the main causes and complications.

A
  • <2cm dilatation in 4hr
  • causes by 3Ps:
    • power: inadequate contraction
    • passenger: big baby, malposition, cephalopelvic disproportion
    • passage: trauma, shape, disproportion
  • maternal sepsis, PPH, fistula, asphyxia, neonatal sepsis, uterine rupture, AKI
54
Q

Describe how low risk mothers are assessed for progress during labour.

A

intermittent auscultation every 15m 1st stage, and 5m 2nd stage, with USS doppler or Pinard stethoscope

55
Q

Describe how a CTG should be interpreted.

A

DR C BRAVADO

  • define risk (why on CTG)
  • contractions (3-5 / 10min)
  • baseline rate (110-160bpm)
  • variability (>5bpm/10min)
  • accelerations (>15 beats for 15s)
  • deceleration
  • overall impression
56
Q

Describe the normal, non-reassuring, and abnormal findings on CTG.

A

normal / non-reassuring / abnormal

  • HR: 100-160 / 161-180 / <100 or >180
  • acceleration: >5 / <5 30-90m / <5 <90m
  • deceleration: variable / late <30m <50% contractions / late > 30m, bradycardia, single deceleration >3m
57
Q

Describe the management of non-reassuring and abnormal CTG.

A
  • non-reassuring: foetal blood sampling, treat dehydration, hyperstimulation, hypotension, place in L lateral position, stop oxytocin, consider tocolysis
  • abnormal: inform senior, category I C/S
58
Q

Describe the findings of foetal blood gas analysis.

A

normal / borderline / abnormal

  • lactate: <4.1 / 4.2-4.8 / >4.9
  • pH: >7.25 / 7.2-7.25 / <7.2
  • Mx: conservative / repeat CTG 30min / deliver C/S or forceps
59
Q

Name and describe the three types of forceps.

A
  • outlet (e.g. Wrigley’s): when scalp is visible w/o separating labia, foetal skull reached pelvic floor
  • low/mid-cavity (Neville-Barnes, Andersons, Simpsons): 1/5 palpable abdomen, station >+2 but not above spines
  • rotational (Kielland’s): in theatre with regional anaesthesia
60
Q

Name the requirements for forceps delivery.

A

FORCEPS

  • Fully dilated (>10cm)
  • OA position
  • Ruptured membranes
  • Cephalic presentation
  • Engaged presenting part
  • Pain relief
  • Sphincter (bladder) empty (by catheter)
61
Q

Describe the complications of forceps delivery.

A
  • mark on baby’s face, brachial plexus injury, perineal trauma, psychological trauma, bowel/urinary symptoms
  • rarer: neonatal trauma, ICH, facial nerve palsy
62
Q

Describe the risk factors, complications, and management of shoulder dystocia.

A
  • normally, the head is delivered in one contraction, followed by the shoulder in the next. Dystocia describes where the shoulder becomes stuck on the pubic symphysis
  • risks: previous dystocia, macrosomia, DM, obesity, slow labour, IOL, operative vaginal delivery
  • complications: hypoxia, brachial plexus injury, clavicle, humerus fracture, ICH, maternal PPH, genital tract trauma, pelvic injury
  • HELPERR: call for Help, Evaluate, Legs, external suprapubic Pressure, Enter (via rotational manoeuvres), Remove posterior arm, Roll patient onto hands and knees
63
Q

Define the difference types of postpartum haemorrhage (PPH) and give the four main causes.

A
  • primary <24h after delivery, secondary 24h-6wk
  • minor: SVD >500ml / OVD >750 / C/S >1000
  • major: >1000ml or signs of cardiovascular collapse or ongoing bleeding
  • 4Ts: tone (70%), trauma (20%), tissue (RPOC, 10%), thrombin (<1%, encephalopathy)
64
Q

Describe the management of maternal haemorrhage (APH/PPH)

A
  • ABCDE, O2 15l/min
  • bloods: G&S, FBC, coag, fibrinogen, U&Es, LFTs, x-match 6 units
  • warmed crystalloid (e.g. Hartmann’s) + 0.9% saline
  • uterine massage with bimanual compression
  • syntocinon (bolus / infusion)
  • ergometrine (+ antiemetic)
  • carboprost, misoprostol
  • balloon insertion, B-lynch sutures, embolisation, artery ligation, hysterectomy
65
Q

Describe the classification of perineal tears.

A
  • 1st: perineal skin only
  • 2nd: perineal skin and levator ani
  • 3a: <50% external anal sphincter
  • 3b >50% external anal sphincter
  • 3c: both external and internal sphincters
  • 4th: involves anal epithelium / mucosa
66
Q

What is an episiotomy?

A

Surgical cut with patient consent (unlike perineal tear), local anaesthetic given to pudendal nerve branches

67
Q

Describe the management of perineal tears.

A
  • repaired in theatre with regional anaesthesia, repair of mucosa, internal and external anal sphincters
  • antibiotics, laxatives
  • physiotherapy allowed pelvic-floor function
68
Q

Describe the key features of chickenpox and foetal varicella syndrome.

A
  • facial vesicular rash, spreading to the trunk and back
  • foetal varicella syndrome: scarring, limb hypoplasia, congenital cataract, microphthalmia, CNS abnormalities
  • blood test for IgG antibodies. if not immune, offer VZ Ig ASAP
  • treat with aciclovir, paracetamol, fluids, light cotton clothes, and use calamine lotion
69
Q

Describe the key features of rubella and congenital rubella syndrome.

A
  • initially maculopapular rash on face, spreading to the trunk and back
  • levels so low WHO declared eliminated in the UK due to MMR vaccine
  • congenital rubella syndrome: sensorineural hearing loss, PDA, glaucoma / cataract
  • check for rubella specific IgG/IgM <10 days exposure
  • if not immune: TOP. immune: supportive treatment
70
Q

Describe the key features of measles infection.

A
  • blotchy rash on the forehead, Koplik spots in the mouth, runny nose and cough
  • caused by paramyxovirus
  • IUGR, microcephaly, miscarriage, stillbirth, preterm birth
71
Q

Describe the key clinical features of CMV infection.

A
  • hearing loss, visual impairment, blindness, learning difficulties, epilepsy
  • most infected women have symptoms similar to mono (fever, malaise, myalgia, lymphadenopathy)
  • jaundice, hepatospleno megaly, SGA, microcephaly
72
Q

Describe the key features of slapped cheek syndrome.

A
  • slapped cheek appearance, followed by a lacy rash sparing the palms and soles
  • foetal infection: anaemia, heart failure, hydrops foetalis
  • specific IgM -> MCA doppler for foetal anaemia
73
Q

Describe the risks of foetal Zika, COVID-19, and influenza infection.

A
  • Zika: microcephaly, birth defects, hearing/vision/mobility, seizures, developmental delay
  • COVID: severe disease, ITU admission, death
  • influenza: miscarriage, preterm labour if virulent
74
Q

Describe the key features of listeriosis in pregnancy.

A
  • caused by listeria monocytogenes, 10x more likely in pregnancy
  • this is why pregnant women should avoid soft cheese (camembert, brie), unpasteurised milk, and deli food
  • headache, diarrhoea, abdominal aches, nausea
  • treated with ampicillin and gentamicin, or trimethoprim and sulfamethoxazole
75
Q

Describe the key features of group B streptococcus infection.

A
  • GBS is a common bacteria (20-40%). most have no problems, so no recommended screening programme
  • if detected: benzylpenicillin / clindamycin and deliver <37wks
76
Q

Describe the risk factors for maternal sepsis.

A

anaemia, PROM, long labour, assisted delivery, obesity, DM, cervical suture, RPOC, immunosuppression (esp. DMARDs, UC, cancer)

77
Q

Describe the key infectious sources of sepsis and which symptoms they may present with.

A
  • offensive PV loss - chorioamnionitis
  • sore throat, cough - GBS, flu, CAP, COVID
  • pain - endometritis, RPOC
  • urinary frequency, dysuria - UTI, esp. with bladder catheter
  • wound erythema - LSCS, episiotomy
  • breast tenderness - mastitis
78
Q

Describe the investigation and management of maternal sepsis.

A
  • survival is directly related to early recognition and management
  • swabs (HVS, throat, MSSU, wound, paired blood culture, sputum)
  • ABCDE + sepsis 6 (give 3: O2, IV abx, fluid challenge) and (take 3: blood culture, lactate, urine)
  • co-amoxiclav [+ gentamicin if severe] [+ clindamycin if sore throat]
79
Q

Describe the key features of chorioamnionitis.

A
  • 96% by ascending infection and polymicrobial (E coli, mycoplasma, anaerobes, GBS)
  • risks: amniocentesis, CVS, prolonged ROM / labour, repeated digital examination, nulliparity, meconium stained liquor
  • IOL / LSCS required if not in established labour
80
Q

Quantify the blood loss of antepartum and postpartum haemorrhage.

A
  • spotting (staining, streaking)
  • minor <50ml
  • major 50-1000ml, no signs of shock
  • massive: >1000ml or signs of shock
81
Q

Give the main features of placental abruption.

A
  • separation of the placenta, normally implanted, partially or fully
  • caused by vasospasm and arteriole rupture into the decidua, allowing blood to escape into the placenta
  • severe continuous pain, backache, bleeding (unless concealed), maternal collapse, tender ‘woody hard’ uterus, Couvelaire (blue) uterus)
  • risks: PET/HTN, trauma, drugs, thrombophilia, renal disease, polyhydramnios, PROM
82
Q

Give the key features of placenta previa.

A
  • placenta directly overlies cervical os (low-lying: <2cm from os)
  • bright red painless bleeding, unprovoked (or after coitus), abnormal foetal presentation
  • speculum exam may be helpful but vaginal exam should be avoided until previa excluded
  • risks: previous C/S, age >40, multiparity, assisted contraception, multiple pregnancy, smoking, uterine scar, fibroid
83
Q

Define the terms placenta accreta, increta, and percreta.

A
  • accreta: morbidly adherent placenta to uterine wall
  • increta: invades myometrium
  • perceta: invades bladder from uterus
84
Q

Give the key features of uterine rupture.

A
  • full thickness of uterine opening (including serosa) prolapse; if the serosa is intact = dehiscence
  • acute, constant pain, may be referred to shoulder tip, loss of contraction, acute abdomen, peritonism, IVD, acute foetal distress
  • risks: surgery for fibroids, C/S, perforation etc.
85
Q

Give the key features of vasa previa.

A
  • type 1: velamentous umbilical cord
  • type 2: multiple lobes (succentuate, accessory lobes)
  • vessels rupture during labour or amniotomy. not screened for as this is so common
  • symptoms: ARM, dark red bleeding, foetal bradycardia
86
Q

Name the 5 main causes of maternal collapse.

A

5H’s:

  • head: eclampsia, epilepsy, CVA, vasovagal response
  • heart: MI, arrhythmia, peripartum cardiomyopathy
  • hypoxia: asthma, PE, pulmonary oedema, anaphylaxis
  • haemorrhage: abruption, atony, trauma, rupture, inversion
  • wHole body/hazards: hypoglycaemia, amniotic fluid embolism, sepsis, trauma, anaesthetic complications
87
Q

Describe the pathology and key feature of amniotic fluid embolism.

A
  • sudden acute resp distress, cardiovascular collapse, acute hypotension, acute hypoxia
  • defect in membranes allows amniotic fluid to enter maternal circulation
88
Q

Give the management of maternal collapse.

A
  • anticipation with MEWS
  • ABCDE and early help (999/2222)
  • left tilt / manual displacement of uterus to avoid aortocaval compression, gravid uterus overlies IVC
  • C/S after 3 min unsuccessful CPR
89
Q

Define the postpartum period and describe the physiological changes that occur in this time.

A
  • from the end of the 3rd stage of labour to 6 weeks
  • the uterus involutes (returns to normal position) by day 10
  • lochia becomes rubra, sera, then alba
  • CO and PV returns to non-pregnant levels by the end of the first week
  • dilatation of ureters occurs with decrease of GFR to normal over 3 months
90
Q

Describe the risk factors conferring moderate and high risk for thromboembolism and the management.

A
  • moderate: hospital admission, single VTE related to major surgery, high risk thrombophilia, medical co-morbidities, any surgery, OHSS in first term
  • high risk: any previous VTE except a single event related to major surgery
  • moderate: 10 days, high: 6 weeks prophlyactic LMWH
91
Q

Describe the causes, history taking, and management of mastitis.

A
  • s aureus, coagulase positive staph, anaerobes (smokers)
  • duct ectasia, foreign objects (e.g. ring)
  • MAIDS Hx: milk stasis, abscess (tender lump), inflammation (warmth, pain, swelling, firmness, erythema), discharge (purulent), systemic (fever, malaise, myalgia)
  • flucloxacillin or augmentin; abscess: USS / aspiration
92
Q

Describe the risk factors for perinatal mental illness, substance misuse, or suicide.

A
  • young, single, lacks support, unplanned / unwanted, pre-existing Hx
  • white, deprivation, known domestic violence, social work input
93
Q

Describe the screening questions for perinatal psychiatry and the criteria for admission to a mother-baby psychiatric unit.

A
  • screening: feeling depressed/down/hopeless? lost interest in things? feel like you need/want help?
  • red flags/requires admission to mother-baby unit: rapidly changing mental state, suicidal ideation, significant feelings of estrangement or inadequacy as a mother, pervasive guilt, evidence of psychosis
94
Q

Describe the key features of baby blues.

A
  • affects 50-70%
  • brief period of emotional instability: tearfulness, irritability, anxiety, poor sleep, confusion
  • occurs 3-10days after birth; treated with support and reassurance
95
Q

Describe the key features of puerperal psychosis.

A
  • occurs <2wk delivery, in 0.1% of women
  • disproportional mortality rate: 5% suicide, 4% infanticide
  • sleep disturbance, confusion, irrational ideas, mania, delusion, hallucination, confusion
  • it is an emergency requiring admission to a mother-baby unit; Mx with antidepressants, antipsychotics, mood stabilisers, and/or ECT
96
Q

Describe the key features of postnatal depression.

A
  • 1/3 of mothers suffer from postnatal depression; two peaks at 2-4wk and 10-14wk
  • prevalence is 10% (same as non-pregnant); however, postnatal depression tends to be more severe
  • tearfulness, irritability, anxiety, anhedonia, poor sleep, weight loss
  • treated as non-pregnant depression
97
Q

Describe the key risks of alcohol dependence in pregnancy.

A
  • abstinence is best, but 2 units/week not shown to be detrimental
  • foetal alcohol syndrome (FAS): facial deformities, low IQ, neurodevelopmental delay, epilepsy, hearing, heart, and kidney defects
  • withdrawal
  • Wernicke’s encephalopathy
  • Korsakoff’s syndrome
98
Q

Describe the key risks of drug dependency (esp. cocaine, amphetamine, ecstasy) in pregnancy, along with its management.

A
  • can cause stroke and arrhythmia
  • teratogenic
  • PET, abruption, IUGR, preterm labour, miscarriage
  • methadone, child protection, social services, smear Hx, breastfeeding, early IV access, postnatal contraception
99
Q

Describe the use of SSRIs, TCAs, and antipsychotics in pregnancy.

A
  • SSRIs generally safest: sertraline has least placental exposure, fluoxetine thought to be safest, peroxetine increased cardiac malformations
  • rarer risks of SSRIs: PHN, low birth weight, increased early birth (by days), PPH
  • TCAs may cause cardiac defects or cleft palate
  • antipsychotics may cause GDM (esp. second gen.), decreased fertility due to reduced PRL release
100
Q

Describe the breast changes that occur during pregnancy.

A
  • 1st trimester: elongation and gland proliferation
  • 2nd trimester: secretory alveoli differentiate
  • 3rd trimester: maturation, development of extensive rER

3a. O&G (6 decks)

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