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RANZCOG WRITTEN EXAM > Short SAQ questions > Flashcards

Short SAQ questions Flashcards

1
Q

What is the carrier frequency of cystic fibrosis?

A

1 in 35 in Australia

1 in 25 in New Zealand

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2
Q

What is the carrier frequency of spinal muscular dystrophy?

A

1 in 50

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3
Q

What is the carrier frequency of fragile X syndrome?

A

1 in 332

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4
Q

What are the risk factors for placenta accreta spectrum?

A
  • Previous accreta *
  • Previous CS *
  • Placenta praevia
  • Placenta praevia and previous CS *
  • Previous uterine surgery *
  • ART
  • Short inter-pregnancy interval
  • CUA
  • Increasing maternal age
  • Major risks
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5
Q

What are the risk factors for vasa praevia?

A
  • low-lying placenta/ placenta praevia
  • bilobed/succenturiate lobe
  • velamentous cord insertion
  • ART
  • Multiple pregnancy (not independent risk factor)
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6
Q

What are the risk factors for placenta praevia?

A
  • Prev CS (increasing risk with increasing # of CSs)
  • ART
  • Smoking
  • Prev praevia
  • AMA
  • Prev uterine surgery
  • Multiple pregnancy
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7
Q

How is BMI calculated?

A

kg/m2

weigh in kilograms divided by the square of height in metres

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8
Q

What are the risk factors for ovarian torsion?

A
  • Ovarian mass
  • Prev torsion
  • Ovulation induction
  • Pregnancy, particularly 1st trimester
  • Long ovarian suspensory ligament
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9
Q

What are possible complications of Dermoid cysts?

A
  • Torsion
  • Rupture
  • Hyperthyroidism if presence of active thyroid tissue
  • Infection
  • Malignancy
  • Chemical peritonitis
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10
Q

What features increase the risk of a failed operative delivery?

A
  • Suspected fetal macrosomia (>4kg)
  • Maternal obesity (BMI >30)
  • 1/5th head palpable abdominally
  • Malposition >45degrees from occipito-anterior position
  • Midcavity, station 0 to +2
  • Inadequate analgesia in delivery room
  • No descent of vertex with pushing
  • Poor maternal effort/pushing
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11
Q

What are the risk factors for shoulder dystocia?

A

Pre-labour:

  • Prev shoulder dystocia
  • Fetal macrosomia
  • Maternal diabetes mellitus
  • Maternal obesity

Intra-partum:

  • labour dystocia
  • prolonged 2nd stage
  • assisted vaginal delivery
  • epidural
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12
Q

What are the 5 principles of managing a PPH?

A
  1. Recognition
  2. Communication
  3. Resuscitation
  4. Monitoring and investigations
  5. Management of PPH
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13
Q

What is the definition of sepsis?

A

Life threatening organ dysfunction caused by a dysregulated host response to infection

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14
Q

What is the rate of reduction of early onset neonatal GBS with use of prophylaxis?

A

80%

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15
Q

What are the benefits of antenatal corticosteroids in women at risk of preterm birth?

A

Reduced risk of:

  • perinatal death
  • neonatal death
  • respiratory distress syndrome
  • probably reduces the risk of intraventricular haemorrhage
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16
Q

What are the causes of post-menopausal bleeding in order from most common to least common?

A
  1. Atrophy
  2. Exogenous estrogen
  3. Endometrial/cervical polyp
  4. Endometrial hyperplasia
  5. Endometrial cancer
  6. Cervical cancer
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17
Q

What are the risk factors for endometrial cancer?

A
  • Hyperplasia
  • Obesity
  • T2DM
  • Unopposed oestrogen therapy
  • PCOS
  • Early menarche/later menopause
  • Nulliparity
  • Age
  • Oestrogen secreting tumour (eg. Granulosa cell tumour)
  • Tamxifen therapy
  • Genetic syndromes eg. Lynch, Cowden
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18
Q

What prognostic factors for endometrial hyperplasia/cancer are associated with a poor outcome?

A
  • Increasing age (over 65)
  • Stage (>1b)
  • Increasing myoinvasion
  • Vascular invasion
  • Tumour extending beyond the fundus
  • Grade 3
  • Histological subtypes - clear cell, serous, adenosquamous
  • Tumour >2cm
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19
Q

Hyperplasia without atypia.

  • What is the risk of co-existent invasive endometrial carcinoma?
  • What is the risk of progression to invasive carcinoma?
A
  • What is the risk of co-existent invasive endometrial carcinoma? <1%
  • What is the risk of progression to invasive carcinoma? <5% over 20 years
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20
Q

Atypical hyperplasia

  • What is the risk of co-existent invasive endometrial carcinoma?
  • What is the risk of progression to invasive carcinoma?
A
  • What is the risk of co-existent invasive endometrial carcinoma? 25-59%
  • What is the risk of progression to invasive carcinoma? RR 14-45
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21
Q

What is endometrial hyperplasia?

A

Irregular proliferation of the endometrial glands with an increase in the gland to stroma ratio when compared with proliferative endometrium

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22
Q

What is the lifetime risk of uterine cancer?

A

1 in 45

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23
Q

What is the genetic bases of cystic fibrosis?

A

Autosomal recessive inheritance of a mutation in the cystic fibrosis transmembrane conductance regulator gene.

Over 1000 mutations have been identified. Phenotype depends of what combination of mutations they have inherited.

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24
Q

What is the anatomical pathology which defines placenta accreta?

A

Chorionic villi attach to the myometrium. Invasion through nitabuch layer (80% of placenta accreta spectrum)

Nitabuch layer is a fibrous junction of the decidua and cytotrophoblast, prevents excessive penetration of the decidua.

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25
Q

What is the anatomical pathology which defines placenta increta?

A

Chorionic villi invade the myometrium (15% of placenta accreta spectrum)

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26
Q

What is the anatomical pathology which defines placenta percreta?

A

Chorionic villi invade the myometrium and serosa, may invade adjacent organs (eg. bladder) (<5% of placenta accreta spectrum)

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27
Q

What USS features are suggestive of placenta accreta spectrum?

A
  • Loss of defined interface between decidual layer of placenta and myometrium
  • Presence of numerous placental lacunae
  • Myometrial thinning
  • Placental bulge
  • Hypervascularity
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28
Q

What are the USS features of vasa praevia?

A
  • Visualising aberrant linear or tubular echolucent structures with 2D imaging.
  • Aberrant vessels locations over or within 2cm of the internal os attached to the inner perimeter of the fetal membranes.
  • Demonstrating blood flow in these structures using colour or power Doppler.
  • Demonstrating umbilical artery/venous Doppler waveforms using pulse wave Doppler.
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29
Q

What are the prognostic features for whether a placenta will remain low lying following anatomy scan?

A
  • Posterior placenta less likely to migrate
  • Less likely to migrate if anterior placenta and previous CS
  • Less likely to migrate if placenta is covering the internal os by >2.5cm

90% of low-lying placentas resolve by term.

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30
Q

What is the Rotterdam criteria to diagnose PCOS?

A

2 out of 3 of:
- Oligomenorrhoea or anovulation
- Clinical and/or biochemical signs of hyperandrogenism
- Polycystic ovaries on USS (either 20 or more peripheral antral follicles or increased ovarian
volume)

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31
Q

What is the criteria to diagnose metabolic syndrome?

A

3 or more of:

  • High blood sugar
  • Reduced HDL
  • High triglycerides
  • High BP
  • Abdominal obesity
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32
Q

What are the different pathological causes of anaemia that may occur in pregnant women?

A
  1. Haemolytic anaemia eg. HELLP syndrome
  2. Haemorrhage eg. Placenta praevia
  3. Consumptive eg. DIC
  4. Hereditary eg. Thalasaemia
  5. Anaemia of chronic disease eg. Chronic kidney disease
  6. Nutritional deficiency eg. Iron
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33
Q

What are the potential adverse outcomes related to prolonged pregnancy for the mother?

A

Risks due to macrosomia:

  • PPH
  • Labour dystocia
  • Obstructed labour
  • Operative vaginal delivery
  • Perineal injury

Hypertension or PET risk increases as pregnancy progresses

Caesarean section

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34
Q

What are the potential adverse outcomes related to prolonged pregnancy for the fetus?

A
  • Stillbirth and neonatal death
  • Caesarean birth
  • Admission to NICU
  • Meconium aspiration
  • Oligohydramnios causing intrapartum cord compression and fetal distress

Macrosomia increasing the risk of:

  • Shoulder dystocia and related peripheral nerve damage and fracture
  • Hypogylcaemia
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35
Q

What are the evidence based strategies that reduce pregnancy duration beyond 42 weeks?

A
  • Membrane sweeping after 39/40
  • Induction of labour from 41/40
  • Accurate dating of pregnancy
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36
Q

Outline the FIGO PALM-COIEN classification system for AUB

A 
Structural abnormalities that can be imaged
o	P – endometrial polyps
o	A – adenomyosis
o	L – Leiomyomata
o	M – Malignancy
Non-structural abnormalities
o	C – coagulopathy
o	O – Ovulatory
o	I – Iatrogenic
o	E – Endometrial
o	N – Not otherwise specified
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37
Q

What are the short term risks of endometrial ablation?

A
  • Equipment failure 9%
  • Haemorrhage 1.2%
  • Uterine perforation 0.3%
  • Infection 1-2%
  • Uterine cramping 38%
  • Thermal injury to adjacent tissues 1:10,000
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38
Q

What are the long term complications of second generation endometrial ablation?

A
  • Treatment failure and need for hysterectomy (Balloon ablation 9% at 5 years, 21% at 7-10 years. Bipolar ablation <5% at 5 years).
  • If pregnancy occurs there is high morbidity, with case reports of uterine rupture and disordered placentation such as placenta accrete.
  • Intrauterine adhesions causing haematometra 1%.
  • Post ablation tubal sterilisation syndrome 6-8%.
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39
Q

What are the effects of overt hypothyroidism on maternal obstetric outcome?

A

Increased risk of:

  • Pre-eclampsia
  • Placental abruption
  • Post-partum haemorrhage
  • Anaemia
  • Postnatal depression
  • Miscarriage
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40
Q

What are the effects of overt hypothyroidism on fetal development?

A
  • Risk of prematurity
  • Perinatal mortality
  • FGR
  • Developmental delay/ Cretinism
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41
Q

How do you optimise the quality of a semen sample for analysis for infertility?

A
  • 2-3 days of abstinence prior to sample
  • Taken by masturbation
  • Avoid lubricant or saliva.
  • Deposited directly into a sterile container
  • If taken at home, keep it at body temperature during transport and take to lab within 1 hour
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42
Q

What are the major components of a semen analysis and the normal parameters?

A
  • Volume (≥1.5mL)
  • Sperm count (≥39 million)
  • Sperm concentration (≥15 million/mL)
  • Total motility (≥40%)
  • Progressive motility (≥32%)
  • Morphology (≥4% normal forms)
  • pH (≥7.2)
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43
Q

What are the modifiable risk factors that can impact male infertility?

A
  • Alcohol
  • Smoking
  • Obesity
  • Scrotal temperature
  • Certain drugs eg. cannabis
  • Occupational exposure eg. heat
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44
Q

How long do you wait to repeat a semen analysis?

A

3 months, which is how long spermatogenesis takes

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45
Q

What is the definition of premature ovarian insufficiency?

A

Loss of normal ovarian function before the age of 40

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46
Q

What are the causes of premature ovarian insufficiency?

A
  • Idiopathic (no cause found)
  • Genetic (eg. Complete gonadal dysgenesis XY, Turner’s Syndrome XO, Fragile X syndrome)
  • Autoimmune oophoritis (eg. Addison’s disease)
  • Environmental or toxic (Eg. chemotherapy, radiation, infection)
  • Surgery (eg. oophorectomy)
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47
Q

How do you diagnoses premature ovarian insufficiency?

A
  • Oligo/amenorrhoea for at least 4 months
  • Elevated FSH level in association with low oestradiol level, repeat measurements after at least 4 weeks to confirm diagnosis
  • Age less than 40
  • Rule out other causes
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48
Q

What are the risk factors for AFE?

A

No risk factors, rare and unpredictable

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49
Q

What are the potential causes of peripartum collapse?

A

Obstetric:

  • Haemorrhage
  • Eclampsia
  • Uterine rupture
  • Peripartum cardiomyopathy
  • Uterine inversion
  • AFE

Non-obstetric:

  • Thromboembolism (PE)
  • Sepsis/septic shock
  • Anaphylaxis
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50
Q

What is the pathophysiology of AFE?

A
  • has been compared to anaphylaxis or severe sepsis.
  • may be due to complement activation.
  • activation of the extrinsic coagulation cascade resulting in consumption of platelets and thrombocytopenia/DIC
  • Coagulopathy causing haemorrhage
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51
Q

What are the immunological and physiological changes that occur in pregnancy making pregnant women more likely to become unwell with respiratory infections?

A
  • Shift away from cell mediated immunity to humoral immunity
  • Reduced lung capacity
  • Increased oxygen consumption
  • Less buffering capacity
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52
Q

What are the differential diagnoses of vulval ulcers?

A 
Infectious causes of vulval ulcers:
-	Sexually transmitted infections:
o	Genital herpes (HSV)
o	Primary syphilis
-	Non-sexually transmitted infections:
o	Epstein barr virus (EBV)
o	Cytomegalovirus (CMV)
o	Chickenpox or herpes zoster (shingles) caused by varicella zoster virus (VZV)
o	Group A streptococcal
o	Vulvovaginal candidiasis

Non-infectious causes of vulval ulcers:

  • Vulval aphthosis
  • Autoimmune and autoinflammatory diseases eg. Lichen sclerosus
  • Malignancy
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53
Q

List 4 physiological factors that interact to regulate fetal heart rate variability

A
  • Change in blood pressure measured by baroreceptors.
  • Reduction in oxygenation measured by chemoreceptors.
  • Catecholamines and the sympathetic nervous system.
  • Acetylcholine and the parasympathetic nervous system.
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54
Q

What are 4 situations that account for absent variability on CTG?

A 
Decreased variability = 4 S’s
•	Sleep (20-40mins)
•	Sedation (drugs such as opiates, MgSO4, Anti-hypertensives)
•	Small (premature)
•	Sick (hypoxic)
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55
Q

What is the cause of a complete molar pregnancy?

A

Tumour of placental tissue arising due to fertilisation of an empty ovum (egg) by either 2 sperm or 1 sperm that duplicates.
Diploid.

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56
Q

What are the characteristic histopathological features of a complete molar pregnancy?

A
  • P57 negative
  • Absence of fetal tissue.
  • Extensive hydropic change to villi.
  • Excess trophoblastic proliferation.
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57
Q

What is the long term risk associated with molar pregnancy?

A

Persistent gestational trophoblastic disease requiring chemotherapy

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58
Q

What is the risk of a molar pregnancy with history of previous molar pregnancy?

A

1:70

59
Q

What are the mechanisms of PET?

A
  • Abnormal placentation (high resistance vessels)
  • Endothelial dysfunction (placental release of anti-angiogenic factors such as sFlt-1 causing vascular permeability)
  • Systemic vasoconstriction (increased throboxane A2 which is a vasconstrictor)
  • Inflammation (Increased pro-inflammatory cytokines)
60
Q

How do you reduce the risk of needing an assisted vaginal birth when there is an epidural in situ?

A
  • Passive descent, delay pushing for up to 2 hours or until strong urge to push.
  • Use of oxytocin infusion in 2nd stage.
  • Lower concentration of local anaesthetic
  • Use of patient controlled epidural analgesia
  • Minimise use of epidural in second stage
60
Q

What are the adverse outcomes that are associated with epidural in labour?

A
  • Hypotension
  • Fever
  • Urinary retention
  • Longer first and second stage
  • Oxytocin augmentation
61
Q

What are the risk factors for SGA?

A

Major risk factors as per RCOG guideline:

  • Maternal age >40 years
  • Smoker >/11 cigarettes a day
  • Cocaine use
  • Daily vigorous exercise
  • Previous SGA baby
  • Previous stillbirth
  • Maternal SGA
  • Chronic hypertension
  • Diabetes with vascular disease
  • Renal impairment
  • Antiphospholipid syndrome
  • Paternal SGA
  • Heavy vaginal bleeding with threatened miscarriage
  • Echogenic bowel
  • Pre-eclampsia
  • Unexplained APH
  • Low maternal weight gain
  • PAPP-A <0.4 MoM
62
Q

What are the macroscopic features of lichen sclerosus?

A
  • Vulva thin and crinkly with pearly white appearance
  • Often bilateral and symmetrical
  • May encircle the vulva and anus (figure of eight)
  • Does NOT extend into vagina or anus
  • Erosion
  • Shrinkage of introitus with loss or fusion of labia minora
  • In 1/5th of patient it also affects the limbs and trunk
63
Q

What are some strategies that prevent perforation during cervical dilatation?

A
  • Pre-treatment with misoprostol
  • Only insert dilators just beyond the internal os and in a controlled fashion, avoid excessive force
  • USS guidance during cervical dilatation
  • Perform hysteroscopy under direct vision (without prior mechanical dilatation)
  • Use instrument on cervix to straighten canal
64
Q

How do progestogen containing contraceptives cause unscheduled bleeding?

A
  • Initially thought to be due to a relatively thick endometrium transitioning to a relatively thing endometrium
  • With continued use, the endometrium develops a dense network of small, thin, fragile vessels with are prone to focal bleeding
65
Q

What is the FIGO definition of HMB?

A

Excessive menstrual blood loss which interferes with a women’s physical, social, emotional and/or material quality of life

66
Q

What is the FIGO definition of AUB?

A

Any uterine bleeding that is of abnormal frequency, duration, volume, regularity or is unscheduled

67
Q

List obstetric complications that are associated with fibroids in late pregnancy

A
  • Malpresentation
  • PPH
  • Obstructed labour
  • Labour dystocia
  • PTL/PPROM
  • Pain due to degeneration
  • Increased complication of CS
68
Q

What’s the mechanism by which the Mirena controls HMB?

A

Levonorgestrel downregulates estrogen and progesterone receptors in the endometrium which causes glandular atrophy and decidualisation of the endometrium resulting in less functional endometrium to shed during menses

69
Q

A patient has had an elective CS. She has no personal or family history of VTE or thrombophilia. What risk factors would make you consider using clexane?

A
  • Age > 35
  • BMI > 30
  • PPH > 1 L
  • Pre-eclampsia
  • Smoker
  • Systemic infection
  • Immobility
  • Gross varicose veins
  • Medical comorbidity
70
Q

Based on the 2015 Cochrane review on route of hysterectomy, what are the benefits of a vaginal hysterectomy over laparoscopic or abdominal (open)?

A
  • Faster return to normal activies
  • Shorter operating time
  • Less urinary tract injuries
  • Fewer febrile episode post-operatively
71
Q

What are the steps of vaginal hysterectomy? (brief)

A
  • Consent/GA/Abx prophylaxis/lithotomy/IDC
  • LA to cervix
  • Incise cervix
  • ant and post incisions into peritoneum
  • uterosacral ligaments (level 1 support)
  • Cardinal ligaments (uterine vessels) (level 1 support)
  • broad ligaments
  • utero-ovarian pedicle
  • remove uterus through vagina
  • suture vault, incorporate uterosacrals
72
Q

What are two tests that will enable you to distinguish between CAIS and MRKH?

A
  • Karyotype: 46XY for CAIS, 46XX for MRKH

- Testosterone: male levels in CAIS, female levels in MRKH

73
Q

Explain the adaptive immune system

A
  • Takes a few weeks to develop
  • Specific and has memory to a particular pathogen
  • Includes antibody production (Humoral)
  • Cellular immunitiy includes T cells, B cells and antigen presenting cells.
  • Augments and evolves over time
74
Q

Explain the innate immune system

A
  • 1st line
  • non-specific, no memory
  • Anatomical barries (eg cilia)
  • Soluble mediators (cytokines, complement)
  • Cellular mediators (neutrophils, mast cells etc)
75
Q

What does gardasil 4 and 9 protect against?

A

Gardasil 4 protects against the most common HPV strains that cause cervical cancer (type 16 and 18, 70% of cancers) and genital warts (6, 11).

Gardasil 9 includes 5 additional strains that are implicated in cervical cancer. 31, 33, 45, 52, 58 which cause an additional 20% of cervical cancers.

76
Q

What findings on colposcopy would indicate high grade change and warrant a biopsy?

A 
\+ Dense acetowhite
\+ rapid appearance of acetowhite
\+ Crypt glands
\+ Coarse mosaicism
\+ Coarse punctation
\+ Sharp border
77
Q

How does Adenomyosis cause pain and bleeding?

A

+ Endometrial tissue responds to hormonal changes and proliferates, unable to shed = large uterus and pain
+ Abnormal uterine contractility = pain and heavy bleeding
+ More vascularity due to endo in the myometrium = heavy bleeding

78
Q

What are the ultrasound findings of adenomyosis?

A
  • ‘Venetian blind’ effect from heterogenous myometrium
  • Asymmetrical wall thickening (posterior thicker)
  • Myometrial cysts due to entraped endometrial cells.
  • Disrupted myometrial/endometrial junction
  • Subendometrial lines or thickening
  • Focal hyperechoic lesions
  • Increased vascularity on Doppler
79
Q

When would you do urodynamics?

A

Before surgery for stress urinary incontinence in women who have any of the following:
• urge-predominant mixed urinary incontinence or urinary incontinence in which the type is unclear
• symptoms suggestive of voiding dysfunction
• anterior or apical prolapse
• a history of previous surgery for stress urinary incontinence.

80
Q

Contraindications to vaginal breech delivery include:

A
  • Cord presentation
  • Fetal growth restriction (estimated fetal weight< 10 th %) or macrosomia (estimated fetal weight >3.8kg)
  • Any presentation other than frank (extended) or complete (flexed) breech
  • Hyperextension of fetal neck on ultrasound
  • Evidence of antenatal fetal compromise (e.g. abnormal CTG)
  • Fetal anomaly incompatible with vaginal delivery.
81
Q

List the absolute and relative contraindications for performing ECV

A

Absolute Contraindicaitions:

  • Caesarean section delivery needed for other reasons eg. Placenta praevia
  • Abnormal CTG
  • APH within the last 7 days
  • ruptured membranes
  • where there is rhesus isoimmunisation
  • multiple pregnancy (except delivery of second twin)

Relative contraindications:

  • SGA with abnormal Dopplers
  • Oligohydramnios
  • Uterine anomaly (as less likely to be successful)
  • pre-eclampsia
  • major fetal anomalies
82
Q

What are the benefits of planned birth for PROM compared to expectant management?

A
  • less maternal chorioamnionitis
  • less early onset neonatal sepsis
  • less antibiotic administration to neonate
  • Less admissions to NICU or SCBU
83
Q

What are the criteria for expectant management of PROM?

A

Ideally, these women would be/have:
• Fully informed of increased risks of this decision
• Fixed cephalic presentation.
• Negative Group B streptococcus (GBS) status and no prior history of a baby with EOGBS infection.
• No signs of infection (maternal tachycardia, fever, uterine tenderness).
• Normal CTG and fetal movements.
• Clear amniotic fluid
• Adequate resource/staffing to provide support as an outpatient or inpatient.
• Commitment to regular assessment of maternal temperature, vaginal loss and fetal movements. (4- hourly temperature check during waking hours is recommended).
• Access to reliable transport.
• Clearly documented plan for review

84
Q

What are causes of thrombocytopenia in pregnancy?

A
  • Gestational thrombocytopaenia (75% of all thrombocytopenia in pregnancy)
  • Primary Immune thrombocytopenia (ITP) also called idiopathic thrombocytopenia purpura
  • Pre-eclampsia
  • HELLP syndrome
  • Artefactual thrombocytopenia
  • Medication/drugs
  • Type 2B von Willebrand disease
  • Inherited thrombocytopenia
  • Acute fatty liver of pregnancy
  • Thrombotic thrombocytopenia purpura (TTP)
  • Autoimmune disease eg. SLE, APS
  • Infection (esp viral)
  • Nutritional deficiency (eg. Vitamin B12/folate)
85
Q

What is the anatomical course of the ureter?

A
  • arises from renal pelvis
  • retroperitoneal
  • descends along anteriorly to psoas muscles
  • crosses the pelvic brim at the bifurcation of the common iliac vessels, at the level of the sacral promontory
  • extends along the pelvic side wall medial to the obturator internus muscle
  • At the level of the ischial spine, it turns medially within the parametrium to pass beneath the uterine artery, 1.5cm lateral to cervix
  • Tunnels within the cardinal ligament to enter the bladder obliquely at the trigone
86
Q

What is early onset Group B Streptococcus?

A

Neonatal infection with group B strep within first 7 days of life

87
Q

How do you take a swab for Group B Strep?

A

Low vaginal and anorectal swab either a single swab (vagina then anorectum) or 2 different swabs. At 35-37 weeks or 3-5 weeks prior to expected delivery.
Performed on selective enriched media with request to lab to identify GBS in pregnancy.
Comment if penicillin allergy so alternative sensitivities can be provided.

88
Q

What antibiotics do you use for Group B Strep prophylaxis with a penicillin anaphylaxis?

A

Vancomycin 1g IV every 12 hours

or as per sensitivities eg. erythromycin

89
Q

What is the success of PGE2 vs Balloon for achieving vaginal birth within 24 hours?

A

There may be little to no difference between PGE2 and balloon in vaginal deliveries not achieved within 24 hours.

90
Q

What is the mechanism of PGE2 for induction of labour?

A

Prostaglandins ripen the cervix and induce uterine contractions.

91
Q

What is the indication for using PGE2 for induction of labour?

A

IOL where cervix is unfavourable (Bishop’s score <6) and no contraindication to PGE2

92
Q

What are the contraindications for PGE2 for induction of labour?

A

Previous CS or other major uterine surgery (due to risk of uterine rupture)
Pre-existing regular painful uterine activity

93
Q

What are the side effects of PGE2 for induction of labour?

A 
Hyperstimulation
Vaginal mucosal irritation
Tachysystole
Fevers
Diarrhoea
94
Q

What is the mechanism of a balloon for induction of labour?

A

Direct physical pressure on the internal os ripens the cervix through dilatation of the canal and/or by increasing prostaglandin or oxytocin secretion from decidua, membranes and cervix.

95
Q

What is the indication for using a balloon for induction of labour?

A

IOL where cervix not favourable (Bishop’s score <6) and previous CS or uterine surgery or higher risk from uterine hyperstimulation.

96
Q

What are the contraindications to using a balloon for induction of labour?

A

Rupture of membranes

Low lying placenta

97
Q

What are the side effects of a balloon for induction of labour?

A

Discomfort during insertion.

Cervical bleeding.

98
Q

Describe McRoberts manoeuvre to resolve shoulder dystocia

A
  • Flexion and abduction of maternal hips, positioning thighs onto abdomen.
  • Relieves bony obstruction by straightening the maternal lumbosacral angle, rotating the maternal pelvis towards the mothers head and increases the relative AP diameter of the pelvis.
  • Success in 90% of cases, least invasive manoeuvre, so should be performed first
99
Q

Describe suprapubic pressure for resolving shoulder dystocia

A
  • Applied by assistance from the side of the fetal back in a downwards and lateral direction, just above the maternal pubic symphysis.
  • Reduces the fetal bisacromial diameter and rotates the anterior shoulder into the wider oblique pelvic diameter.
  • Shoulder is free to slip under the symphysis pubis.
  • Firstline in combination with McRoberts as effective and least invasive.
100
Q

What is the role of an episiotomy during a shoulder dystocia?

A
  • Shoulder dystocia is a bony pelvis obstruction and therefore an episiotomy is not going to relieve this.
  • Consider cutting an episiotomy in this situation in order to allow the passage of accoucheurs hand to perform internal manoeuvres.
101
Q

What actions increase the risk of a brachial plexus injury during shoulder dystocia?

A
  • Downward traction of fetal head

- Maternal propulsive force

102
Q

What are the most common complications during pregnancy with maternal mitral stenosis?

A

Pulmonary oedema

Arrythmia

103
Q

What is the risk of miscarriage after 3 first trimester miscarriages

A

40%

104
Q

Why should you screen for antiphospholipid syndrome with recurrent miscarriage?

A
  • Most important, treatable cause of recurrent miscarriage

- Antiphospholipid antibodies present in 15% of people with recurrent miscarriage.

105
Q

Why should you screen for karyotype abnormalities with recurrent miscarriages?

A
  • 2-5% of couples with recurrent miscarriage, one partner carries a structural chromosomal anomaly.
  • Mostly balanced reciprocal or Robertsonian translocation.
  • Usually phenotypically normal but their pregnancies at risk of miscarriage or congenital malformation.
  • If found can be referred to genetic counsellor.
106
Q

How would the diagnosis of antiphospholipid syndrome change pregnancy management?

A
  • Low dose aspirin
  • Consider antenatal LMWH
  • LMWH for 6 weeks postpartum
  • Risk of fetal growth restriction and pre-eclampsia. Monitor growth and BP/urine protein.
107
Q

What tests would you do to diagnosis antiphospholipid syndrome?

A

Lupus anticoagulant
anticardiolipin antibodies
anti-B 2 glycoprotein-I antibodies

108
Q

What are the recommendations for someone following evacuation of a complete molar pregnancy?

A
  • Risk of future molar pregnancy 1 in 70
  • Avoid pregnancy until follow-up complete
  • Contraception (barrier or oral)
  • No change to future fertility
  • Follow-up with weekly tHCG until negative and then monthly for 6 months
109
Q

What is the WHO recommended pregnancy interval spacing?

And why?

A

At least 24 months but no more than 5 years

Lower risk of subsequent:

  • infant, neonatal and perinatal mortality
  • small for gestational age
  • pre-term delivery
110
Q

What is Ca125 and why is it not a good screening test for ovarian cancer?

A

Ca125 is a large transmembrane glycoprotein derived from both coelamic (pericardium, pleura and peritoneum) and mullarian (fallopian tube, endometrium, endocervical) epithelia.

Not a good screening test as:

  • Not elevated in all forms of ovarian cancer (only elevated in 50% of stage 1 ovarian cancers)
  • Low specificity as it can be elevated in other conditions (eg. Endometriosis, diverticulitis, recent surgery)
111
Q

What percentage of Stage 3 Ovarian High Grade Serous Carcinomas are sensitive to chemotherapy?

A

80%

112
Q

Name two standard chemotherapy agents used in the treatment of ovarian cancer and give one side effect that occurs with both agents and one side effect that is specific to each agent (excluding hair loss and nausea/vomiting).

A

Common side effect:
- Bone marrow suppression

Platinum based eg.Cisplatin, carboplatin
- Ototoxicity resulting in tinnitus and hearing loss

Taxanes eg. Paclitaxel
- Peripheral neuropathy

113
Q

What investigations would you do for azoospermia?

A
  • FSH and testosterone (central vs obstructive cause)
  • Karyotype (Klinefelter, Y chromosome microdeletions, CFTR gene mutations)
  • Prolactin (hyperprolactinaemia can be a cause)
  • Anti-sperm antibodies
  • Testicular USS
114
Q

What are the effects on the fetus of maternal Anti-Kell (Anti-K) antibodies?

A

Anti-K antibodies can cross the placenta and destroy fetal red cells which have the K Antigen.
Results in erythroid suppression and immune destruction of early erythroid progenitor cells.
This causes anaemia which can lead to hydrops, PTB or perinatal death.

115
Q

Does planned CS reduce the rates of urinary incontinence?

A
  • Urinary incontinence is reduced if elective CS is performed before the onset of labour but this protective benefit is reduced with age and subsequent pregnancies regardless of mode of delivery
  • Postpartum urinary incontinence may have a multifactorial origin.
116
Q

Why do you plan an elective CS at 39 weeks gestation?

A
  • Timing of elective CS is a compromise between risk of neonatal respiratory morbidity following elective CS and risk of labour prior to CS
  • Delivery at 39/40 compared to earlier reduces the rate of NICU admission and incidence of respiratory distress.
  • 10% of women will go into labour prior to 39/40
  • Elective CS in women without additional risks should be carried out at approx. 39 weeks gestation.
117
Q

What is the definition or perinatal mortality?

A

Fetal and early neonatal death from 20/40 (or >400g if gestation unknown) until midnight on the 6th day of life

118
Q

What is the perinatal mortality rate?

A

Number of perinatal deaths per 1000 life births/stillbirths

119
Q

What is the definition of maternal mortality?

A

Death while pregnant or within 42 days of termination of pregnancy (eg. birth) irrespective of duration or site of pregnancy, from any cause related to or aggravated by pregnancy or it’s management (eg. not accidental)

120
Q

What is the maternity mortality ratio?

A

WHO - number of maternal deaths per 100,000 live births over a specified time period

NZ - number of deaths per 100,000 maternities over a specified time period

121
Q

What are the most common causes of maternal death in NZ?

A

(2006-2018)

  • Suicide 23.8%
  • AFE 11.1%
  • Cardiac 10.3%
  • Neurological 10.3%
  • Infection 4.8%
  • VTE 4.8%
122
Q

What is NZs maternal mortality rate?

A

15.5 per 100,000

2006-2016

123
Q

What is NZs perinatal mortality rate?

A

9.55 per 1000

2018

124
Q

What are some interventions that can reduce maternal mortality rate (MMR) in low income countries?

A
  • All births attended by skilled health professional
  • Reduce severe PPH by injecting uterotonic immediately after birth
  • Good hygiene and early antibiotics
  • Monitoring for HTN/PET and appropropriate management eg. MgSO4
  • Prevent unwanted pregnancies with access to contraception and safe abortion services
  • Routine screening for mental health during pregnancy and postpartum
125
Q

What is the evidence for Urso in obstetric cholestasis?

A
  • Probable reduction in pruritus however size of the effect is small (COCHRANE 2020)
  • No effect on prevalence of stillbirth (Ovadia et al)
126
Q

What is the difference between bipolar and monopolar?

A

Bipolar – 2 electrodes places at site of treatment, one acts as the active electrode, the other the receiver. Only tissue grasped is in the circuit

Monopolar – active electrode placed at site of treatment. Current passes through the body to the return electrode at a distant site.

127
Q

What are some techniques to reduce risk with electrosurgical technology?

A
  • Inspect insulation
  • Use lowest power setting
  • Use lowest waveform (cut)
  • Use intermittent activation
  • Don’t activate close to another instrument
  • Use bipolar where appropriate
  • Never have 2 active instruments in the patient
  • Always place instruments in the quiver
  • Use alternative eg. Harmonic
128
Q

What types of injuries can you get with electrosurgery?

A

Bipolar:

  • Direct thermal spread: direct spread to adjacent site (eg. prolonged application or high power setting)
  • Direct thermal injury: accidental activation of electrode (eg. on bowel)

Monopolar:

  • Direct thermal spread
  • Direct thermal injury
  • Direct coupling injury: 2nd metal instrument in contact with other tissue can act as alternate route for the current if contact is made between the electrode and the instrument
  • Alternate site burn: When current finds an alternate way out of the body (ie. not via the pad). Shouldn’t happen these days with better technology. Can cause burns.
  • Pad Site burn: If contact of pad to body is poor and the surface area of the pad is small enough, a pad site burn will occur. Choose a well vascularied muscle mass to place pad. Avoid bony prominences and irregular contours.
  • Capacitative coupling
  • Insulation failure
129
Q

What are the proven clinical benefits of HRT in post-menopausal women?

A
  • Reduced vasomotor symptoms (by 87%)
  • Reduced urogential symptoms
  • Reduced osteoporosis related fractures
  • Reduced colorectal cancer (combined HRT only)
  • Reduced coronary heart disease and mortality if started <10 years after menopause
130
Q

What is the change in risk profile for someone on HRT who is now over 60 years old?

A
  • Increased risk of stroke amongst women on HRT >age 60 (or >10 years post menopause)
  • May be a small absolute increase in breast cancer detection with prolonged use (increases with duration of use)
  • Increased risk of VTE with increasing age (however highest risk of VTE is within 1st year of HRT use)
131
Q

What are the USS features of an intersitial ectopic pregnancy?

A
  • Empty uterine cavity
  • GS location laterally in the interstital part of the tube
  • Surrounded by <5mm myometrium in all imaging planes
  • Presence of the ‘intersitial line’ (an echogenic line from the mass to the endometrial echo complex)
132
Q

Differentiate between caput succedaneum, subgaleal haemorrhage and cephalohaematoma

A

Caput:

  • caused by pressure on the head due to labour and birth (prominent artificial caput due to ventouse can occur but reduces within an hour of birth)
  • Serosanguinous, extra-aponeurotic collection, may extend across the midline or and over suture lines

Subgaleal:

  • bleeding into the space between the epicranial aponeurpsis and the periosteum caused by rupture of emissary veins.
  • Large volume blood loss can occur.
  • Vague, generalised scalp swelling, crosses suture lines, gravity dependent

Cephalohaematoma:

  • Friction forces generated during birth result in bleeding between the periosteum and the underlying skull.
  • Soft, fluctuant, localised swelling with a well defined outline
  • Swelling does not cross suture lines
133
Q

What is type 3 FGM?

A
  • Narrowing of the vaginal orifice with creation of a covering seal with appositon of the labia minora +/- labia majora
    +/- excision of the clitoris
134
Q

How would you counsel someone on Deinfibulation?

A

Counselling:

  • sensitively
  • minor surgical procedure
  • under local or sedation
  • incision made anteriorly to allow visualisation of the external urethral meatus
  • purpose is to restore vaginal introitus that is adequate for sexual function, normal voiding, menstruation, facilitate vaginal examinations, perform cervical smear and intrapartum care.
135
Q

What are 4 intra-partum interventions that reduce the risk of OASIS and their level of evidence?

A
  • Application of warm compress to perineum continuously during and between contractions in 2nd stage of labour (level 1++ evidence)
  • Episiotomy when performing an instrumental delivery (level 2 evidence)
  • If requiring episiotomy use mediolateral technique and ensure angle is 60degrees away from midline when the perineum is distended
  • Perineal protection at crowning and delivery (level 2+ evidence)
136
Q

What muscles are involved in a mediolateral episiotomy?

A

Transverse perineal muscle

Bulbocavernosus muscle

137
Q

How can you clinically differentiate between internal and external anal sphincter?

A

EAS:

  • more superficial
  • dark red fleshy colour
  • circumferential fibres

IAS:

  • deeper
  • pale white colour
  • longitudinal fibres
138
Q

A patient has an OASIS injury.

What is her risk of a future OASIS injury?

A

5-7%

139
Q

What are the signs of Magnesium toxicity?

A
  • Respiratory depression RR <12
  • Hypotension
  • Loss of deep tendon reflexes
  • Oliguria
  • Magnesium level >3.5
140
Q

What is the antidote for magnesium toxicity?

A

Calcium gluconate, IV, 1g, slow push

141
Q

Why is it recommended that Iodine is supplemented in pregnancy?

A

Increased Iodine requirements due to:

  • increased renal blood flow and glomerular filtration rate leads to increased iodine clearance
  • fetus reliant on transplacental transfer of maternal thyroid hormone until the fetal thyroid becomes functional at 12/40/
  • fetus dependent on maternal iodine for thyroid hormone synthesis

In general iodine deficiency increasing, may be in part to a reduction in iodised salt intake and reduction of iodine in milk.

142
Q

What are the maternal and fetal risks of overt hypothyroidism?

A
  • miscarriage
  • PET
  • placental abruption
  • anaemia
  • PPH
  • prematurity
  • perinatal mortality
  • developmental delay in childhood

RANZCOG WRITTEN EXAM (5 decks)

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