Qs and content to learn Flashcards

1
Q

What are the two types of vasa praevia

A

In Type 1, there is a velamentous insertion with vessels running over the cervix. In Type 2, unprotected vessels run between lobes of a bilobed or succenturiate lobed placenta.

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2
Q

What are the ADIPS cut-offs for GDM?

A

Fasting glucose ≥ 5.1mmol/L
1‐hr glucose ≥ 10.0mmol/L
2‐hr glucose ≥ 8.5mmol/L

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3
Q

What is the Rubella serology cut-off for postnatal MMR?

A

<30

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4
Q

What is a normal ET for a pre-menopausal woman?

A
  • during menstruation: 2-4 mm 1,4
  • early proliferative phase (day 6-14): 5-7 mm
  • late proliferative / preovulatory phase: up to 11 mm
  • secretory phase: 7-16 mm
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5
Q

What is a normal ET for a post-menopausal woman?

A
vaginal bleeding (and not on tamoxifen): suggested upper limit of normal is <5 mm
no history of vaginal bleeding:
the acceptable range of endometrial thickness is less well established in this group, cut-off values of 8-11 mm have been suggested
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6
Q

What is Type 1 FGM?

A

Type I — Partial or total removal of the clitoris and/or the prepuce.
Type Ia, removal of the clitoral hood or prepuce only;
Type Ib, removal of the clitoris with the prepuce.

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7
Q

What is Type 2 FGM?

A

Partial or total removal of the clitoris and the labia minora, with or without excision of the labia majora (excision).
Type IIa, removal of the labia minora only;
Type IIb, partial or total removal of the clitoris and the labia minora;
Type IIc, partial or total removal of the clitoris, the labia minora and the labia majora.

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8
Q

What is Type 3 FGM?

A

Narrowing of the vaginal orifice with creation of a covering seal by cutting and appositioning the labia minora and/or the labia majora, with or without excision of the clitoris (infibulation).
Type IIIa, removal and apposition of the labia minora;
Type IIIb, removal and apposition of the labia majora.

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9
Q

What is Type 4 FGM?

A

All other harmful procedures to the female genitalia for non-medical purposes, for example: pricking, piercing, incising, scraping and cauterization.

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10
Q

What is the risk of NTD recurrence?

A

~5%

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11
Q

What is the preferred form of contraception in Epilepsy and why?

A

LARC, Depot - Some anti-epileptics induce liver enzymes that increase OCP metabolism.

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12
Q

Leveteracitem, Lamotrigine are examples of what?

A

Non-enzyme inducing anti-epileptics. However, OCPs decrease Lamotrigine concentrations. They also have lower teratogenicity.

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13
Q

Name 8 risk factors for SGA.

A
  1. Low BMI
  2. Nullip
  3. Prev SGA
  4. Ethnicity
  5. Smoking
  6. Drugs
  7. Maternal age
  8. Maternal medical disease
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14
Q

In an SGA baby with abnormal dopplers and AEDF, when do you repeat the dopplers?

A

Daily.

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15
Q

In an SGAbaby with abnormal dopplers but present EDF, when do you repeat dopplers?

A

Twice weekly.

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16
Q

What is the physiological cause of abnormal DV doppler?

A

The Ductus venosus (DV) Doppler flow velocity pattern reflects atrial pressure-volume changes during the cardiac cycle. As FGR worsens velocity reduces in the DV a-wave owing to increased afterload and preload, as well as increased end-diastolic pressure, resulting from the directs effects of hypoxia/acidaemia and increased adrenergic drive.

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17
Q

What is the physiological cause of abnormal MCA doppler?

A

Cerebral vasodilatation is a manifestation of the increase in diastolic flow, a sign of the ‘brain-sparing effect’ of chronic hypoxia, and results in decreases in Doppler indices of the middle cerebral artery (MCA) such as the PI. Reduced MCA PI or MCA PI/umbilical artery PI (cerebroplacental ratio) is therefore an early sign of fetal hypoxia in SGA fetuses.

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18
Q

Name 8 risk factors for placental abruption

A
  1. Prev PA
  2. Low BMI
  3. HTN
  4. PET
  5. AMA
  6. Multiparity
  7. Smoking and drugs
  8. Abdominal trauma
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19
Q

What are the three tests for APLS?

A
  1. Lupus anti-coagulant
  2. Anti-cardiolipin antibodies, IgG/IgM
  3. Anti-beta-2 glycoprotein 1
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20
Q

What is the global maternal mortality rate?

A

Global estimates from the World Health Organization (WHO) show that the maternal mortality ratio (MMR) fell from 385 per 100,000 women giving birth in 1990 to 216 per
100,000 women giving birth in 201

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21
Q

What is the Australian maternal mortality rate?

A

This led to a maternal mortality ratio of 6.8 deaths per 100,000 women giving birth. The remaining 10 deaths were classified as incidental to the pregnancy.

In 2015 the MMR for developed
countries, which includes Australia, New Zealand, the United Kingdom and the United States
of America, was 12 per 100,000 women giving birth, which is lower than in regions such as
Oceania (MMR estimate 187 per 100,000 women giving birth), South-East Asia (110 per
100,000 women giving birth) and Sub-Saharan Africa (546 per 100,000 women giving birth).

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22
Q

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

A

The most common causes of the Australian maternal deaths from 2012-2014 were non-obstetric haemorrhage, cardiovascular conditions and thromboembolism. Maternal
suicide was less prominent in this period than in the 2006-2010 and 2008-2012 reports
(AIHW: Johnson et al. 2014b; AIHW: Humphrey et al. 2015)

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23
Q

How much higher in the maternal mortality rate for indigenous Australians?

A

3x

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24
Q

How many of the maternal deaths are thought to have been avoidable?

A

Exploration of contributory factors to these deaths suggests that up to one-third may be avoidable.

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25
Q

Define ‘direct’ maternal deaths.

A

Those resulting from obstetric complications of the pregnant state (pregnancy, labour and puerperium) from interventions, omissions, incorrect treatment or from
a chain of events resulting from any of the above

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26
Q

Define ‘indirect’ maternal deaths.

A

Those resulting from previous existing diseases or diseases that developed during pregnancy, and which were not due to a direct obstetric cause, but were
aggravated by the physiologic effects of pregnancy

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27
Q

Define late maternal death.

A

Late maternal deaths are deaths that occur between 43 and 365 days after pregnancy ends and and
result from obstetric complications of the pregnancy or previous existing diseases or
diseases that developed during pregnancy.

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28
Q

Between 2012 and 2014, were direct or indirect causes of maternal death more common?

A

Direct (51% vs 46%)

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29
Q

How does age affect maternal mortality?

A

More dangerous at extremes of age.

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30
Q

How does parity affect maternal mortality?

A

3 or more is bad.

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31
Q

in 2012-2014, name the top 4 causes of maternal death.

A
  1. Non-obstetric haemmorhage
  2. Cardiovascular
  3. VTE
  4. Obstetric haemmorhage
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32
Q

Define the three levels of preterm birth.

A
  • Extremely preterm (less than 28 weeks)
  • Very preterm (28 to 32 weeks)
  • Moderate to late preterm (32 to 37 weeks).
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33
Q

Define neonatal mortality.

A

A neonatal death is defined as a death during the first 28 days of life (0-27 days).

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34
Q

Define perinatal mortality.

A

The World Health Organization defines perinatal mortality as the “number of stillbirths and deaths in the first week of life per 1,000 total births, the perinatal period commences at 22 completed weeks (154 days) of gestation, and ends seven completed days after birth.

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35
Q

Define infant mortality.

A

It is measured by the infant mortality rate (IMR), which is the number of deaths of children under one year of age per 1000 live births. The under-five mortality rate is also an important statistic, considering the infant mortality rate focuses only on children under one year of age.

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36
Q

Define low birthweight.

A

Low birth weight (LBW) is defined by the World Health Organization as a birth weight of a infant of 2,499 g or less, regardless of gestational age. … Normal weight at term delivery is 2500-4200 g

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37
Q

Define standard deviation.

A

a quantity expressing by how much the members of a group differ from the mean value for the group.

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38
Q

Define standard error.

A

a measure of the statistical accuracy of an estimate, equal to the standard deviation of the theoretical distribution of a large population of such estimates.

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39
Q

Define confidence interval.

A

A confidence interval is an interval that will contain a population parameter a specified proportion of the time. The confidence interval can take any number of probabilities, with the most common being 95% or 99%.

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40
Q

How is sample size calculated?

A

The sample size is an important feature of any empirical study in which the goal is to make inferences about a population from a sample. In practice, the sample size used in a study is determined based on the expense of data collection, and the need to have sufficient statistical power.

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41
Q

Define prevalence.

A

Prevalence in epidemiology is the proportion of a particular population found to be affected by a medical condition (typically a disease or a risk factor such as smoking or seat-belt use).

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42
Q

Define incidence.

A

Incidence in epidemiology is a measure of the probability of occurrence of a given medical condition in a population within a specified period of time. Although sometimes loosely expressed simply as the number of new cases during some time period, it is better expressed as a proportion or a rate[1] with a denominator.

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43
Q

Define cumulative incidence.

A

Cumulative incidence is defined as the probability that a particular event, such as occurrence of a particular disease, has occurred before a given time.[2] It is equivalent to the incidence, calculated using a period of time during which all of the individuals in the population are considered to be at risk for the outcome. It is sometimes also referred to as the incidence proportion.

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44
Q

Define relative risk.

A

In statistics and epidemiology, relative risk or risk ratio (RR) is the ratio of the probability of an event occurring (for example, developing a disease, being injured) in an exposed group to the probability of the event occurring in a comparison, non-exposed group.

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45
Q

Define odds ratio.

A

An odds ratio (OR) is a measure of association between an exposure and an outcome. The OR represents the odds that an outcome will occur given a particular exposure, compared to the odds of the outcome occurring in the absence of that exposure.

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46
Q

Define attributable risk.

A

In epidemiology, attributable risk or excess risk is the difference in rate of a condition between an exposed population and an unexposed population. Attributable risk is mostly calculated in cohort studies, where individuals are assembled on exposure status and followed over a period of time.

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47
Q

Define number needed to treat.

A

The NNT is the average number of patients who need to be treated to prevent one additional bad outcome (e.g. the number of patients that need to be treated for one of them to benefit compared with a control in a clinical trial). It is defined as the inverse of the absolute risk reduction.

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48
Q

Define an RCT.

A

Randomized controlled trial: (RCT) A study in which people are allocated at random (by chance alone) to receive one of several clinical interventions. One of these interventions is the standard of comparison or control.

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49
Q

Define a cohort study.

A

A study design where one or more samples (called cohorts) are followed prospectively and subsequent status evaluations with respect to a disease or outcome are conducted to determine which initial participants exposure characteristics (risk factors) are associated with it.

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50
Q

Define a case-control study.

A

A study that compares patients who have a disease or outcome of interest (cases) with patients who do not have the disease or outcome (controls), and looks back retrospectively to compare how frequently the exposure to a risk factor is present in each group to determine the relationship between the risk factor.

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51
Q

Define a cross-sectional study.

A

In medical research and social science, a cross-sectional study (also known as a cross-sectional analysis, transverse study, prevalence study) is a type of observational study that analyzes data from a population, or a representative subset, at a specific point in time—that is, cross-sectional data.

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52
Q

What is Level 1 evidence?

A

Level I

Evidence obtained from a systematic review of all relevant randomised controlled trials.

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53
Q

What is Level 2 evidence?

A

Level II

Evidence obtained from at least one properly designed randomised controlled trial.

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54
Q

What is Level 3 evidence?

A

Level III-1

Evidence obtained from well-designed pseudo-randomised controlled trials (alternate allocation or some other method).

Level III-2

Evidence obtained from comparative studies with concurrent controls and allocation not randomised (cohort studies), case control studies, or interrupted time series with a control group.

Level III-3

Evidence obtained from comparative studies with historical control, two or more single-arm studies, or interrupted time series without a parallel control group.

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55
Q

What is Level 4 evidence?

A

Level IV

Evidence obtained from case series, either post-test or pre-test and post-test.

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56
Q

Define selection bias.

A

Selection bias is the bias introduced by the selection of individuals, groups or data for analysis in such a way that proper randomization is not achieved, thereby ensuring that the sample obtained is not representative of the population intended to be analyzed.

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57
Q

Define measurement bias.

A

Measurement bias results from poorly measuring the outcome you are measuring. For example: The survey interviewers asking about deaths were poorly trained and included deaths which occurred before the time period of interest.

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58
Q

Define confounding.

A

In statistics, a confounder (also confounding variable, confounding factor or lurking variable) is a variable that influences both the dependent variable and independent variable causing a spurious association.

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59
Q

Define heard immunity.

A

the resistance to the spread of a contagious disease within a population that results if a sufficiently high proportion of individuals are immune to the disease, especially through vaccination.

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60
Q

Following post-hysterectomy prolapse, what three outcomes is ASC better than SSF?

A
  1. Dyspareunia
  2. Post-op SUI
  3. Recurrent vault prolapse
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61
Q

What are the 5 reasons for surgical management in endometrial hyperplasia without atypia?

A

(i) progression to atypical hyperplasia occurs during follow-up, or (ii) there is no histological regression of hyperplasia
despite 12 months of treatment, or (iii) there is relapse of endometrial hyperplasia after completing
progestogen treatment, or (iv) there is persistence of bleeding symptoms, or (v) the woman declines
to undergo endometrial surveillance or comply with medical treatment.

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62
Q

How should endometrial hyperplasia be managed in women wishing to conceive?

A

Disease regression should be achieved on at least one endometrial sample before women attempt to conceive.

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63
Q

What are risk factors for ectopic pregnancy?

A

Risk factors for ectopic pregnancy include tubal damage following surgery or infection, smoking and in vitrofertilisation

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64
Q

What is the intradecidual sign?

A

Theintradecidual sign is described as a fluid collection with an echogenic rim located ‘within a markedly thickened decidua on one side of the uterine cavity’

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65
Q

What is the double decidual sign?

A

The double decidual sign is described as anintrauterine fluid collection surrounded by ‘two concentric echogenic rings’

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66
Q

What ultrasound findings are characteristic of cervical ectopic?

A

an empty uterus, a barrel-shaped cervix, a gestational sac present below the level of theinternal cervical os, the absence of the ‘sliding sign’ and blood flow around the gestational sacusing colour Doppler.

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67
Q

What are the criteria for a Caesarean Scar ectopic?

A
  1. Empty uterine cavity. Gestational sac or solid mass of trophoblast located anteriorly at the level of the internal os embedded at the site of the previous lower uterine segment caesarean section scar. Thin or absent layer of myometrium between the gestational sac and the bladder. Evidence of prominent trophoblastic/placental circulation on Doppler examination. Empty endocervical canal.
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68
Q

What are the ultrasound features of an interstitial pregnancy?

A
  1. Empty uterine cavity.2. Products of conception/gestational sac located later ally in the interstitial (intramural) part of the tube and surrounded by less than 5 mm of myometrium in all imaging planes.3. The ‘interstitial line sign’, which is a thin echogenic line extending from the central uterine cavity echo to the periphery of the interstitial sac. The ‘interstitial line sign’ has been shown to have a sensitivity of 80% and a specificity of 98% for the diagnosis of interstitial ectopic pregnancy.
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69
Q

What is the dose of Methotrexate for ectopic pregnancy?

A

50mg/m2

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70
Q

Name four predictors of success with Methotrexate treatment for ectopic pregnancy?

A
  1. Initial HCG of ~1000
  2. Ultrasound appearance of the ectopic pregnancy
  3. Pretreatment changes in serum b -hCG levels - The smaller the increase in b-hCG level prior to administration of methotrexate, the higher the chance of successful medical management.
  4. Decrease in b-hCG levels from day 1 to day 4 after methotrexate
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71
Q

What should women avoid during treatment for ectopic pregnancy?

A

During treatment with methotrexate women should be advised to avoid alcohol and folate-co ntaining vitamins.

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72
Q

Name 6 characteristics that would make a woman a good candidate for Methotrexate treatment”

A

haemodynamic stability
low serum b-hCG, ideally less than 1500 iu/l but can be up to 5000 iu/l
no fetal cardiac activity seen on ultrasound scan
certainty that there is no intrauterine pregnancy
willingness to attend for follow-up
no known sensitivity to methotrexate.

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73
Q

What are the four elements that NICE recommend as first line Methotrexate treatment for ectopic

A

no significant pain
an unruptured ectopic pregnancy with a mass smaller than 35 mm with no visible heartbeat
a serum b-hCG between 1500 and 5000 iu/l
no intrauterine pregnancy (as confirmed on ultrasound scan).

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74
Q

What are the selection criteria for expectant management of ectopic pregnancy?

A

Selection criteria for expectant management were clinical stabi lity with noabdominal pain, no evidence of significant haem operitoneum on ultrasound scan, an ectopic pregnancymeasuring less than 30 mm in mean diameter with no evidence of embryonic cardiac activity, a serumb-hCG level of less than 1500 iu/l and the woman’s consent.

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75
Q

What is the treatment of cervical ectopic?

A

Interestingly, surgical is not first line given risk of bleeding.

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76
Q

How long after methotrexate should women wait before getting pregnant?

A

3 months

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77
Q

Describe the time course of Parvovirus infection?

A

Viraemia is typically present six days after exposure and lasts for around a week. As people are contagious before they are symptomatic, containing the spread of disease is not easily done. The development of rash marks the end of the infectious period, usually one-to-two weeks after infection.

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78
Q

What is the vertical transmission rate of Parvovirus infection?

A

The risk of vertical transmission is 50 per cent. Infection between eight and 20 weeks poses the greatest risk to the fetus.

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79
Q

What is the model of ultrasound monitoring of Parvovirus?

A

This monitoring should start four weeks post conversion/infection and continue for up to 12 weeks, as this is the window of greatest risk to the fetus.

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80
Q

At what MSV do you worry about fetal anemia?

A

Diagnosis of fetal anaemia should be suspected when assessment of the middle cerebral artery Doppler peak systolic velocity (MCA PSV) is greater than 1.5MoM (multiples of the mean).

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81
Q

What is the pathophysiology of fetal anaemia with Parvovirus?

A

Parvovirus is cytotoxic to fetal haemoglobin precursors.

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82
Q

When is the cFTS carried out?

A

This is carried out between 11+0 and 13+6

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83
Q

When is CVS done?

A

This can be carried out between 11 and 14 weeks of gestation by chorionic villous sampling (CVS) of placental tissue.

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84
Q

What is the false positive rate of the cFTS?

A

Using the cFTS, a detection rate of approximately 85-90% can be achieved for trisomy 21, 18 and 13, at a false positive rate of 4-5%.

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85
Q

What is normal vaginal pH?

A

They maintain the normal vaginal pH between 3.8 and 4.4.

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86
Q

What is the treatment for bacterial vaginosis?

A

Metronidazole

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87
Q

Name four non-infective causes of vaginal discharge?

A

Physiological
Cervical ectopy
Foreign bodies, such as retained tampon
Vulval dermatitis

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88
Q

NAme two non-sexually transmitted infections that can cause vaginal discharge.

A

Bacterial vaginosis

Candida infection

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89
Q

What are the vaginal pHs of Candida and BV?

A

Bacterial vaginosis (pH ≥4.5) and vulvovaginal candidiasis (pH <4.5)

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90
Q

What are the antibiotics for chlamydia

A

Doxycycline 100 mg twice daily for seven days (contraindicated in pregnancy), azithromycin 1 g orally in a single dose (WHO recommends azithromycin in pregnancy but the British National Formulary advises against its use unless no alternatives are available)

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91
Q

What are the antibiotics for gonorrhea

A

Cefixime 400 mg as a single oral dose or ceftriaxone 250 mg intramuscularly as a single dose

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92
Q

What is the treatment for trichomonas?

A

Metronidazole 2 g orally in a single dose or metronidazole 400-500 mg twice daily for five to seven days

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93
Q

What is the Amsel criteria for BV?

A

Amsel criteria for diagnosis of BV (at least three criteria must be present):
Vaginal pH >4.5.
●Homogeneous, thin, grayish-white discharge that smoothly coats the vaginal walls.
●Vaginal pH >4.5.
●Positive whiff-amine test, defined as the presence of a fishy odor when a drop of 10 percent potassium hydroxide (KOH) is added to a sample of vaginal discharge.
●Clue cells on saline wet mount. Clue cells are vaginal epithelial cells studded with adherent coccobacilli that are best appreciated at the edge of the cell. For a positive result, at least 20 percent of the epithelial cells on wet mount should be clue cells. The presence of clue cells diagnosed by an experienced microscopist is the single most reliable predictor of BV

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94
Q

For what group is HRT recommended?

A

This continued decline occurred in spite of reassuring data that the benefits of MHT outweigh the risks for most young menopausal women (within 10 years of menopause or under age 60 years).

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95
Q

What are the risks of HRT?

A
  • Coronary heart disease (CHD) - 2.5 additional cases
  • Invasive breast cancer - 3 additional cases
  • Stroke - 2.5 additional cases
  • Pulmonary embolism - 3 additional cases
  • Colorectal cancer - 0.5 fewer cases
  • Endometrial cancer - no difference
  • Hip fracture - 1.5 fewer cases
  • All-cause mortality - 5 fewer events
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96
Q

What effect does HRT have on VTE?

A

Combined oral estrogen plus progestin has been shown to increase the relative risk of VTE twofold.

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97
Q

What effect does HRT have on breast cancer?

A

The attributable risk is small and decreases when treatment is stopped. Cumulative long term follow up of the
Women’s Health Initiative RCT11 found no increase in risk for women receiving estrogen only therapy but an
increased risk for those receiving combined therapy amounting to approximately 0.1%.

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98
Q

What is the difference between cyclical and continuous HRT?

A

For women with an intact uterus MHT may be prescribed as estrogen plus a progestogen for 14 days per month (cyclical therapy) or every day (continuous combined therapy).

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99
Q

What is the follow-up plan for someone on HRT?

A

All women using MHT should be reviewed after 6 months therapy. This should include a general health check, a breast check and a mammogram every two years, Bone densitometry should be performed where
indicated18 and any unexpected vaginal bleeding after 6 months therapy requires appropriate investigation.
The need for ongoing MHT should be reviewed regularly.

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100
Q

Which HRT risks are related to length of treatment?

A

Consider the potential impact of recurrent symptoms on quality of life. The risks of HRT may be related to duration of HRT use - for example, the risk of venous thromboembolism is greatest in
the first year of use, but the risk of breast cancer increases with duration of use.

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101
Q

What is an alternative to HRT?

A

Several serotonin-norepinephrine reuptake inhibitors (venlafaxine and desvenlafaxine) and selective serotonin reuptake inhibitors (paroxetine, citalopram, and escitalopram) have been shown in short-term trials
to alleviate VMS but to a lesser degree than MHT.

Gabapentin is the only non-hormonal product shown to be equally effective as low dose estrogen for
vasomotor symptoms.

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102
Q

What is the average age of menopause?

A

The menopause transition commonly starts around 47 years and the average age of natural menopause is 51 years.

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103
Q

What are the first line measures for perimenopausal symptoms?

A

Women seeking relief from menopausal symptoms should first be offered advice on life style
changes including stress reduction, regular exercise, optimal weight management, appropriate diet and
avoidance of smoking and excessive alcohol and caffeine intake should also be addressed.

Recent high
quality evidence suggests that mindfulness training and cognitive behaviour therapy may reduce both
the impact and severity of vasomotor symptoms

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104
Q

What can you do to protect bone in women who have contraindications to HRT?

A

Evidence-based non-hormonal options should first be considered (e.g. bisphosphonates or SERMs for osteoporosis, cholesterol lowering agents and aspirin for cardiovascular disease). Some
individual menopausal symptoms may be ameliorated with individual selected therapies eg
venlafaxine, desvenlafaxine, escitalopram, citalopram and paroxetine, clonidine and gabapentin for
vasomotor symptoms, vaginal lubricants for superficial dyspareunia, and anticholinergics for urinary
urgency. Please note that paroxetine and tamoxifen should not be prescribed together.

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105
Q

What organisms are usually isolated from a TOA?

A

Common organisms include Escherichia coli, aerobic streptococci, Bacteroides fragilis, Prevotella, and other anaerobes, such as Peptostreptococcus.
Not Chlamydia/Gonorrhoea!

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106
Q

What are the organisms identified from BV?

A

The major bacteria detected in women with BV are Gardnerella vaginalis, Prevotella species, Porphyromonas species, Bacteroides species, Peptostreptococcus species, Mycoplasma hominis, and Ureaplasma urealyticum, as well as Mobiluncus, Megasphaera, Sneathia, and Clostridiales species. Fusobacterium species and Atopobium vaginae are also common.

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107
Q

When do you start MCVs for a non-Kell Ab?

A

24 weeks

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108
Q

When do you start MCVs for Kell ABs?

A

18 weeks

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109
Q

What are the critical levels for antibody titires?

A

> 8 for Kell, >16 for non-Kell

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110
Q

What is the prevalence of red cell antibodies/

A

A Netherlands found that red cell antibodies were detected in 1.2% of pregnancies,
while the prevalence of clinically significant antibodies was placed at 0.4%

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111
Q

When can you clear a woman with epilepsy?

A

Women who have remained seizure-free for at least 10 years (with the last 5 years off AEDs) and those with a childhood epilepsy syndrome who have reached adulthood seizure- and
treatment-free are considered no longer to have epilepsy

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112
Q

What are the congenital abnormalities caused by AEDs?

A

The most common major congenital malformations associated with AEDs are neural tube defects, congenital heart disorders, urinary tract and skeletal abnormalities and cleft
palate.
Sodium valproate is associated with neural tube defects, facial cleft and
hypospadias; phenobarbital and phenytoin with cardiac malformations; and phenytoin and
carbamazepine with cleft palate in the fetus.

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113
Q

What is the risk of a woman with epilepsy relapsing during pregnancy?

A

The majority of women (67%) do not experience a seizure in pregnancy. The seizure-free
duration is the most important factor in assessing the risk of seizure deterioration.
In women who were seizure free for at least 9 months to 1 year prior to pregnancy, 74-92%
continued to be seizure free in pregnancy.

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114
Q

What do you need to ask an epileptic woman antenatally?

A

In the antenatal period, WWE should be regularly assessed for the following: risk factors for seizures, such as sleep deprivation and stress; adherence to AEDs; and seizure type and frequency

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115
Q

What do you give to babies of epileptic mums?

A

All babies born to WWE taking enzyme-inducing AEDs should be offered 1 mg of intramuscular vitamin K to prevent haemorrhagic disease of the newborn.

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116
Q

Postnatal care of an epileptic mum?

A

Women should ensure that they take their AEDs as prescribed in the postnatal period. Nausea and
vomiting should be treated and if there is no oral intake, consideration should be given to parenteral
administration of AEDs. Sleep deprivation-related seizures could be reduced by arranging help for the
mother, especially for night-time feeds.If the mother breastfeeds, storage of breast milk and pumped during
the day might be beneficial. Reviewing the daily activities of the mother and identifying high-risk
situations can reduce the risks to the mother and baby due to seizures.

If the AED dose was increased in pregnancy, it should be reviewed within 10 days of delivery to avoid
postpartum toxicity.

WWE should be screened for depressive disorder in the puerperium. Mothers should be informed about
the symptoms and provided with contact details for any assistance

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117
Q

How does APS cause procoagulation?

A

2GPI antibodies disrupt normal coagulation mechanisms in several ways: direct cellular effects
caused by bound 2GPI-antibody complexes,
activating platelets, endothelial cells and
monocytes, hence inducing tissue factor
expression; interference with haemostatic factors;
resistance to activated protein C; and reduction in
fibrinolysis.

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118
Q

pre-pregnancy planning forAPS?

A

https://obgyn.onlinelibrary.wiley.com/doi/pdf/10.1576/toag.13.1.15.27636

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119
Q

what is the prevalence of mesh erosion?

A

Erosion occurs as a complication of between 1-2% of operations where a midurethral sling is placed, and up to 10-12% of operations where transvaginal mesh is used for prolapse.

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120
Q

What are contraindications to VBAC? Risk factors?

A

Classical, prev rupture. Factors that potentially increase the risk of uterine rupture include short inter-delivery interval
(less than 12 months since last delivery), post-date pregnancy, maternal age of 40 years or
more, obesity, lower prelabour Bishop score, macrosomia and decreased ultrasonographic
lower segment myometrial thickness.

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121
Q

What happens with synto on a VBAC?

A

2-3x risk of UR

1.5x risk of CS

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122
Q

What other autoimmune conditions are associated with lichen sclerosis?

A

The most common autoimmune conditions in women with lichen sclerosus are thyroid disorders,alopecia areata,pernicious anaemia,type 1 diabetes and vitiligo.
The reported prevalence of autoimmune conditions in first-degree relatives is around 30%

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123
Q

Why do you check Ferritin in vulval conditions?

A

Correction of iron-deficiency anaemia or low serum ferritin can relieve vulval symptoms.In a case series of 38 women with vulval dermatitis, 20% were found to have iron-deficiency anaemia.

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124
Q

What is second line medication for lichen sclerosis?

A

Approximately 4-10% of women with anogenital lichen sclerosus will have symptoms that do not improve with topical ultrapotent steroids (steroid-resistant disease). The recommended second-line treatment
is topical tacrolimus under the supervision of a specialist clinic.

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125
Q

What are the side effects of Imiquimod?

A

Adverse effects include pain, erythema and swelling and can result in non-compliance

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126
Q

Which HPV is vin associated with?

A

Nearly all VIN is of usual type: warty, basaloid and mixed (warty and basaloid). Usual type VIN is more common in women aged 35-55.It is associated with HPV (especially HPV-16)

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127
Q

Describe the use of clobetasol for lichen?

A

Once daily for 1 month then on alternate days for 1 month
then twice a week for 1 month
then once a week for 1 month
then gradually reduce this until you can use it occasionally or not at all

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128
Q

What is the next step for a woman positive for HPB 16/18?

A

Colposcopy

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129
Q

What has the entry age for cervical screening increased?

A

Research shows that beginning cervical screening at age 25 years is safe.
Cervical cancer in people under the age of 25 is rare.
After more than 20 years of screening women under 25 years of age, the incidence of cervical cancer in this age group has not reduced.
Most women and men under 25 years of age have been vaccinated for HPV and people under the age of 25 have robust immune systems that will usually clear the infection quickly and without treatment.
Commencing screening at age 25 will reduce the investigation and treatment of common cervical abnormalities that would usually resolve by themselves in women under the age of 25. This is because it usually takes 10 to 15 years for a persistent HPV infection to develop into cervical cancer.

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130
Q

What should you do with a woman who has non 16/18 oncogenic type and low grade?

A

Women with a positive oncogenic HPV (not 16/18) test result, with a LBC report of negative or prediction of pLSIL/LSIL, should have a repeat HPV test in 12 months.

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131
Q

Referral of women with a positive oncogenic HPV (not 16/18) test result and LBC prediction of pHSIL, HSIL or any glandular abnormality

A

Women with a positive oncogenic HPV (not 16/18) test result, with a LBC prediction of pHSIL/HSIL or any glandular abnormality, should be referred for colposcopic assessment at the earliest opportunity, ideally within 8 weeks.

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132
Q

Management after repeat HPV test at 12 months, following initial positive oncogenic HPV (not 16/18) test result

A

At repeat HPV testing 12 months after a positive oncogenic HPV (not 16/18) test result with reflex LBC negative or pLSIL/LSIL: if a woman has a positive oncogenic HPV (any type) test result, reflex LBC will be performed and she should be referred for colposcopic assessment
if oncogenic HPV is not detected, the woman should be advised to return to routine 5-yearly screening

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133
Q

What do you do with a ‘Women with a positive oncogenic HPV (not 16/18) test result (self-collected sample)’

A

Women who have undergone HPV testing on a self-collected sample and who have a positive oncogenic HPV (not 16/18) test result should be advised to visit their GP or healthcare professional to obtain a cervical sample for LBC:
If the LBC test result is negative or pLSIL/LSIL, HPV testing should be repeated in 12 months, preferably by a healthcare professional.
If the LBC test result is pHSIL/HSIL or any glandular abnormality the woman should be referred for colposcopy at the earliest opportunity, ideally within 8 weeks.

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134
Q

What do you do with a ‘Women aged 75 years or older who request screening’

A

Women who are 75 years or older who have never had a cervical screening test, or have not had one in the previous five years, may request a test and can be screened.

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135
Q

Repeat LBC usually not necessary at time of colposcopy, unless:

A

Delay in attending for colposcopy > 3 months after referral LBC is unsatisfactory
referral LBC is negative but lacks an endocervical component
prior LBC is not available because the HPV test was performed on a self-collected sample
the woman has developed symptoms suggestive of cervical cancer since undergoing her screening test.

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136
Q

What happens when: For women who have had a colposcopy with significant discordance between the histopathology and the referral cytology?

A

Both specimens should be reviewed by a pathologist from at least one of the reporting laboratories who should then convey the results of the review to the colposcopist in order to inform the management plan

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137
Q

When should you send for tertiary referral

A

Adenocarcinoma in situ
Abnormalities in pregnancy
Immune-deficient women
Women with multifocal lower genital tract disease.

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138
Q

For cervical disease, Ablative therapy should be reserved for :

A

Women intending to have children, and when the following conditions have all been met:
TZ is completely visible (Type 1 or Type 2).
There is no evidence of invasive or glandular disease.
A biopsy has been performed prior to treatment.
HSIL (CIN2/3) has been histologically confirmed.
There is no significant discordance between the histopathology and referral cytology results.

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139
Q

Do not treat at first visit with a LBC report of a low-grade lesion. Is this true?

A

Women who have a LBC prediction of pLSIL/LSIL should not be treated at the first visit.

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140
Q

Repeat excision not necessarily required for incomplete excision of high-grade lesions. Is this true? Why?

A

Women who have incomplete excision of HSIL (CIN2/3) with positive endocervical or stromal margins do not necessarily require immediate repeat excision and could be offered test of cure (HPV and LBC) surveillance, with the exception of:
women aged 50 years or over
women who may not be compliant with recommended follow-up
women in whom subsequent adequate colposcopy and follow-up cytology cannot be guaranteed.

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141
Q

Describe the pathway of: Normal colposcopy following LBC prediction of negative or pLSIL/LSIL?

A

For women with a positive oncogenic HPV (any type) test result, a LBC report of negative or pLSIL/LSIL, and normal colposcopy, the HPV test should be repeated in 12 months:
If HPV is not detected at 12 months, the woman should return to routine 5-yearly HPV screening.
If the woman has a positive oncogenic HPV (not 16/18) test result at 12 months and a LBC report of negative or pLSIL/LSIL, the HPV test should be repeated in another 12 months.
If the woman has a positive oncogenic HPV ( any type) test at the 24 month HPV test, she should be referred directly for colposcopic assessment, which will be informed by the result of the reflex LBC.
If the woman has a positive oncogenic HPV (not 16/18) test result at 12 months and a LBC prediction of pHSIL/HSIL or any glandular abnormality, she should be referred for colposcopic assessment at the earliest opportunity, ideally within 8 weeks.
If the woman has a positive oncogenic HPV (16/18) test result at 12 months, she should be referred directly for colposcopic assessment at the earliest opportunity, ideally within 8 weeks, and the reflex LBC result will inform the colposcopy.

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142
Q

Normal colposcopy following LBC prediction of HSIL: diagnostic excision of TZ

A

For women who have a positive oncogenic HPV (any type) test result, normal colposcopy, and a LBC prediction of HSIL on cytopathology review, diagnostic excision of the TZ should be performed.

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143
Q

What should you do in the case of: Type 3 TZ colposcopy and referral LBC negative or pLSIL/LSIL

A

For women who have a positive oncogenic HPV (any type) test result with a LBC report of negative or pLSIL/LSIL, and colposcopy is reported as Type 3 TZ,† the HPV test should be repeated in 12 months:
If oncogenic HPV is not detected at 12 months, the HPV test should be repeated 12 months later.
If oncogenic HPV is not detected again at the second repeat HPV test, the woman should be advised to return to routine 5-yearly screening.
If the woman has a positive oncogenic HPV (any type) test result at 12 months, she should be referred directly for colposcopic assessment, with the LBC report available to inform the assessment.

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144
Q

Diagnostic excision of the TZ should not be performed if there is no cytological or histological evidence of a high-grade lesion after Type 3 TZ colposcopy. Why?

A

For asymptomatic women who have a positive oncogenic HPV (any type) test result, Type 3 TZ† colposcopy, and no cytological, colposcopic or histological evidence of a high-grade lesion, further diagnostic procedures (such as diagnostic excision of the transformation zone) should not routinely be performed.

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145
Q

Women who have a positive oncogenic HPV (any type) test result with a LBC report of either negative or pLSIL/LSIL, and histologically confirmed ≤ CIN1 on biopsy

A

should have a repeat HPV test 12 months later:
If oncogenic HPV is not detected at the repeat HPV test, the woman should return to routine 5 yearly screening.
If the repeat test is positive for oncogenic HPV (not 16/18) and the LBC report is negative or pLSIL/LSIL, the woman should have a further repeat HPV test in 12 months.
If the second follow-up HPV test is negative the woman should return to routine 5-yearly screening.
If the second follow-up test is HPV positive, the woman should be referred for colposcopic assessment informed by reflex LBC.
If the repeat test is positive for oncogenic HPV (not 16/18) and the LBC report is pHSIL/HSIL, the woman should be referred for colposcopic assessment.
If the repeat test is positive for oncogenic HPV (16/18), the woman should be referred for colposcopic assessment informed by the reflex LBC

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146
Q

Is there an option for observation following cytological prediction of pHSIL?

A

REC9.4: Option for observation following cytological prediction of pHSIL.
Women who have a positive oncogenic HPV (any type) test result with a LBC prediction of pHSIL (confirmed after cytopathology review), and who have undergone colposcopy and have a histologically confirmed LSIL (≤ CIN1), could be offered diagnostic excision of the TZ.
If the colposcopist considers a period of observation is preferable to treatment, or the woman with these findings wishes to defer diagnostic excision, she can be offered observation with a HPV test and colposcopy at 6-12 months.
Women should not be offered observation unless the colposcopic assessment meets all the following conditions:
Colposcopy is adequate.
TZ is completely visualised (Type 1 or 2 TZ^).
LSIL (≤ CIN1) has been confirmed on histopathological review

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147
Q

HSIL (CIN2) and observation

A

In some circumstances, it may be acceptable to offer a period of observation (generally 6-12 months) to women who have a histological diagnosis of HSIL (CIN2), and this would usually be supervised by an experienced colposcopist or at a tertiary centre. Observation may be considered for:
women who have not completed childbearing
women with discordant histology and LBC prediction of pLSIL/LSIL
women with focal minor changes on colposcopy and HSIL (CIN2) on histology
women recently treated for HSIL (CIN2).

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148
Q

How do you Test of Cure after treatment for HSIL (CIN2/3)?

A

A woman who has been treated for HSIL (CIN2/3) should have a co-test† performed at 12 months after treatment, and annually thereafter, until she receives a negative co-test on two consecutive occasions, when she can return to routine 5 yearly screening.
Any abnormal finding goes to colp

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149
Q

What is the cervical screening for ladies who had Total hysterectomy for benign disease

A

Women with a normal cervical screening history, who have undergone hysterectomy for benign disease (e.g. menorrhagia, uterine fibroids or utero-vaginal prolapse), and have no cervical pathology at the time of hysterectomy, do not require further screening or follow up.

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150
Q

What is the cervical screening for ladies who had Total hysterectomy after adenocarcinoma in situ (AIS)?

A

Women who have had a total hysterectomy, have been treated for AIS, and are under surveillance, should have a co-test on a specimen from the vaginal vault at 12 months and annually thereafter, indefinitely.

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151
Q

The implantation of any foreign body generates a host response that is characterised by seven stages:

A

Injury, protein absorption, acute inflammation, chronic inflammation, foreign body reaction, granulation tissue formation and tissue encapsulation.

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152
Q

How many cells in the morula?

A

32

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153
Q

How many days after fertilisation is implantation?

A

5-8 days

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154
Q

What three hormones affect fetal growht?

A

Glucocorticords, insulin, thyroid

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155
Q

What are the two most important fetal growth factors?

A

IGF-I, IGF-III

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156
Q

What are the radiological definitions of oligo and poly?

A

Poly - AFI 25 or above, or DVP >8.

Oligo - AFI <5, DVP <2

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157
Q

When CVS done?

A

9-12 weeks

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158
Q

When Amnio done?

A

16-18 weeks

159
Q

What are the attachments of the sacrospinous ligament?

A

Extends from the ischial spines to the lateral margins of the sacrum and coccyx anteriorly to the sacrotuberous ligament. Its anterior surface is muscular and constitutes the coccygeus; the ligament is often regarded as the degenerate part of the muscle.

160
Q

Where are the greater and lesser foramen of the pelvis

A

The greater and lesser sciatic foramina are above and below the sacrospinous ligament.

161
Q

Which two muscles is the levator ani made up of?

A

The levator ani is composed of 2 major muscles from medial to lateral: the pubococcygeus and iliococcygeus muscles.

162
Q

What is the arcus tendineus

A

The arcus tendineus of the levator ani is a dense connective tissue structure that runs from the pubic ramus to the ischial spine and courses along the surface of the obturator internus muscle.

163
Q

What is the levator plate?

A

The fibers from both sides also fuse to form a raphe and contribute to the anococcygeal ligament. This median raphe between the anus and the coccyx is called the levator plate and is the shelf on which the pelvic organs rest.

164
Q

Which nerve supplies the levator ani?

A

Direct innervation of the levator ani muscle on its cranial surface is primarily from the third and fourth sacral nerve roots via the pudendal nerve.

165
Q

What muscles make up the urogenital diaphragm?

A

The muscles of the male and female urogenital diaphragm include the following: (1) superficial transversus perinei, a small bundle of muscle fibers that pass along the back border of the urogenital diaphragm and assists other muscles in supporting the pelvic tissues; (2) the bulbospongiosus muscles, which are united and surround the base of the penis; (3) the ischiocavernosus muscle, a tendinous structure that extends down to the margin of the pubic arch and assists the function of the bulbospongiosus muscles; and (4) the sphincter urethrae are muscles that arch around the urethra and unite with those on the other side.

166
Q

What is the perineal body?

A

Attached to the perineal body are the rectum, vaginal slips from the pubococcygeus, perineal muscles, and the anal sphincter; it also contains smooth muscle, elastic fibers, and nerve endings.

167
Q

What are the anterior pelvic supports?

A

There is agreement among investigators that the connective tissue supports of the urethra, bladder, and vagina extend to the arcus tendineus of the pelvic fascia on the pelvic diaphragm.T here is also agreement that a “hammock” of anterior vaginal wall tissue, bridging the gap medially in the urogenital hiatus, supports the vesical neck and urethra. There is controversy, however, focusing on the connective tissue structures that are associated with this hammock.

168
Q

What are the middle pelvic floor supports?

A

The paracolpium and parametrium are the connective tissues surrounding the vagina and the uterus, respectively. In the midvagina, the paracolpium fuses with the pelvic wall and fascia laterally. The cardinal ligaments (also called the transverse cervical ligaments of Mackenrodt) extend from the lateral margins of the cervix and upper vagina to the lateral pelvic walls.

169
Q

What are the attachments of the uterosacral ligaments?

A

The uterosacral ligaments are attached to the cervix and upper vaginal fornices posterolaterally. Posteriorly, they attach to the pre-sacral fascia in front of the sacroiliac joint.
The connective tissue of the uterosacral ligaments is continuous with that of the cardinals around the cervix.

170
Q

Explain urethral control

A

Urethral support is provided by a coordinated action of fascia and muscles acting as an integrated unit under neural control

171
Q

What is level 1 pelvic floor support?

A

Suspension - The upper part of the vagina and the cervix are suspended from above. The suspending structure that is attached to the uterus is called the parametrium and
that attached to the vagina is the known as the paracolpium. The parametrium
is made up of what is clinically referred to as the cardinal and uterosacral
ligaments, and continues down the vagina as the paracolpium. The upper
portion of the paracolpium is responsible for suspending the apex of the vagina
after hysterectomy

172
Q

What is level 2 pelvic floor support?

A

Attachment - In the middle portion of the vagina, the paracolpium becomes shorter and is attached medially to the vaginal wall and laterally to the pelvic side walls.

173
Q

What is level 3 pelvic floor support?

A

This corresponds to the region of the vagina that extends 2-3 cm above the hymenal ring; the vagina is fused laterally to the levator muscle and posteriorly to the perineal
body while anteriorly it blends with the urethra.
Damage to the upper suspensory fibres of the parametrium and paracolpium causes a
different type of prolapse from damage to the midlevel support of the vagina

174
Q

Describe the directions that the anterior abdominal walls run?

A

The fibers of the rectus run vertically. In general, those of the external oblique muscle (cf. the external intercostal muscles) run inferior and anterior (as in inserting a hand in a pocket), those of the internal oblique muscle (cf. the internal intercostal muscles) go mostly superior and anterior, and those of the transversus pass transversely.

175
Q

What are the insertions and plane of the external oblique?

A

The aponeurosis of the external oblique muscle passes anterior to the rectus abdominis. Its inferior edge extends from the anterior superior iliac spine to the pubic tubercle and is known as the inguinal ligament.

176
Q

Describe the anatomy of the rectus sheath?

A

The rectus sheath is described as consisting of anterior and posterior layers (lamella) formed by the aponeuroses of the external and internal oblique and transversus abdominus muscles. These aponeuroses meet at the lateral edge of the rectus along a curved line termed the linea semilunaris, which extends from the 9th costal cartilage to the pubic tubercle and is often visible in thin, muscular people.

177
Q

What is the arcuate line?

A

Inferior to the plane that is located approximately halfway between the umbilicus and the symphysis pubis, all three aponeuroses pass anterior to the rectus muscle. This anterior displacement of the aponeuroses creates a crescentic line of demarcation in the posterior lamella of the rectus sheath called the arcuate line, below which only the transversalis fascia separates the rectus abdominis muscle from the parietal peritoneum.

178
Q

Describe the blood supply of the anterior abdominal wall?

A

The cutaneous veins and lymphatic vessels drain in two directions from approximately the level of the umbilicus: (1) upward to the thoraco-epigastric and lateral thoracic veins (thereby providing collateral circulation in caval obstruction) and to the axillary nodes, respectively, and (2) downward to the great saphenous vein and superficial inguinal nodes, respectively. Subcutaneous veins near the umbilicus anastomose with the portal vein by way of branches along the ligamentum teres of the liver.

179
Q

What is the nerve supply of the anterior abdominal wall?

A

The abdominal wall is supplied by intercostal nerves 7 to 11 (the thoraco-abdominal nerves) and by the subcostal, iliohypogastric, and ilio-inguinal nerves. A band of skin is supplied by the lateral and anterior cutaneous branches of each of these nerves (except the ilio-inguinal, which is a branch of the first lumbar nerve).

180
Q

Describe breast changes in the first half of pregnancy?

A

In the first half of pregnancy secretory differentiation (the differentiation of alveolar epithelial cells into milk-secreting cells), ductal branching and lobular formation of the breast (mammogenesis) occur.

181
Q

What is the linea nigra produced by?

A

MSH from the placenta

182
Q

Where does relaxin come from in pregnancy

A

Placenta

183
Q

Name three hormones produced by the placenta, and their function:

A

HCg - maintain corpus luteum
Human placental lactogen - increase glucose by acting on maternal insulin
Insulin-like growth factors -
Corticotropin releasing hormone - start labour
Estrogen
Progesteron
Glucocoritcoids

184
Q

Describe the change in thyroid over the course of pregnancy?

A

During the 1st trimester, human chorionic gonadotropin (hCG) induces a transient increase in free thyroxine (FT4) levels, which is mirrored by a lowering of thyroid-stimulating hormone (TSH) concentrations. Following this period, serum FT4 concentrations decrease of approximately 10 to 15%, and serum TSH values steadily return to normal. Also starting in early gestation, there is a marked increase in serum thyroxine-binding globulin (TBG) concentrations, which peak around midgestation and are maintained thereafter. This event, in turn, is responsible for a significant rise in total T4 and triiodothyronine (T3). Finally, significant modifications in the peripheral metabolism of maternal thyroid hormones occur, due to the expression and activity of placental types 2 and 3 iodothyronine deiodinases (D2 and D3, respectively).

185
Q

What is the change in systematic vascular resistance with pregnancy and why?

A

Total systematic vascular resistance decreases by 20% secondary to the vasodilatory effect of progesterone. Overall, the systolic and diastolic blood pressure drops 10-15 mm Hg in the first trimester and then returns to baseline in the second half of pregnancy.

186
Q

What happens to renal function in pregnancy and why?

A

Progesterone causes vasodilatation and increased blood flow to the kidneys, and as a result glomerular filtration rate (GFR) commonly increases by 50%, returning to normal around 20 weeks postpartum.

187
Q

What happens to cortisol during pregnancy?

A

Total cortisol increases to three times of non-pregnant levels by the third trimester.

188
Q

Where is oestrogen produced during menopause?

A

The body still makes small amounts of oestrogen by changing hormones called androgens into oestrogen. Androgens are produced by the adrenal glands, which are above the kidneys. A hormone called aromatase changes androgens into oestrogen. Aromatase is produced mainly by fatty tissue.

189
Q

What is the pathophysiology of hot flashes?

A

Despite extensive research, the pathophysiology of hot flashes is not entirely understood. The onset of hot flashes is hypothesized to be related to dysfunction of the thermoregulatory nucleus, which is essential in regulating the homeostatic range and the core body temperature.
Instead, it is the relative decline in estrogen levels that appears to mediate these central changes in norepinephrine and serotonin.

190
Q

What is the effect of menopause on the CNS?

A

Psychological disturbances such as depression, anxiety, irritability and mood fluctuation are related to estrogen-induced changes in the lymbic system. The hypothesis of specific neuroanatomical and neurophysiological effects of estrogen on the brain may also explain the correlation between estrogen deficiency and cognitive disturbances such as Alzheimer’s type dementia (AD).

191
Q

What is the definition of premature ovarian insufficiency?

A

Diagnosis of POI requires follicle-stimulating hormone (FSH) levels in the menopausal range on two occasions, at least four to six weeks apart in a woman aged <40 years, after more than four months of amenorrhoea or menstrual irregularity.

192
Q

How does chemotherapy cause premature ovarian failure?

A

Chemotherapy/ radiotherapy causes POI due to impaired follicular maturation and/or direct primordial follicle loss. The extent of damage depends on the age and pre-treatment ovarian reserve of the patient, type of drug, radiation field/ type and cumulative dose.

193
Q

Name 5 features of Down Syndrome

A

Developmental: delayed development, learning disability, short stature, or speech delay in a child.
Eyes: lazy eye or spots
Also common: difficulty thinking and understanding, brachycephaly, upslanting palpebral fissures, atlantoaxial instability, bent little finger, congenital heart disease, displacement of the tongue, excess skin on the back of the neck, flaccid muscles, hearing loss, immune deficiency, low-set ears, mouth breathing, obesity, obstructive sleep apnea, polycythemia, seborrheic dermatitis, single line on palm, thickening of the skin of the palms and soles, thyroid disease, or vision disorde

194
Q

Name 3 soft markers of aneuploidy on US

A

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1681991/

195
Q

How common is Trisomy 18?

A

Trisomy 18 is the second most common autosomal trisomy observed in live births (1 in 5500 live births) [23,35]. As with trisomy 21, there is a relationship between advanced maternal age and the occurrence of trisomy 18 in offspring due to meiotic nondisjunction. There is a 3:1 female to male ratio among affected infants.

196
Q

What are the phenotypic features of Trisomy 18?

A

The major phenotypic features include intrauterine growth restriction (IUGR), hypertonia, prominent occiput, small mouth, micrognathia, pointy ears, short sternum, horseshoe kidney, and flexed fingers, with the index finger overlapping the third finger and the fifth finger overlapping the fourth.

197
Q

What is the rate of survival with Trisomy 18?

A

In a series of 23 pregnancies with diagnosed fetal trisomy 18, 14 fetuses died in utero, and the remainder died within 48 hours of birth

198
Q

What are the features of Trisomy 13?

A

The classic triad is micro/anophthalmia, cleft lip and/or palate, and postaxial polydactyly, but the clinical presentation in patients with trisomy 13 can be quite variable

199
Q

What is the prognosis of Trisomy 13?

A

The majority of prenatally diagnosed cases of trisomy 13 die in utero. The median survival for liveborn children is seven days, and 91 percent die within the first year, with the majority (approximately 80 percent) dying within the first month of life.

200
Q

What is Turner Syndrome caused by?

A

It is caused by loss of part or all of an X chromosome.

201
Q

How common is Turner Syndrome?

A

Turner syndrome is one of the most common sex chromosome abnormalities in females and occurs in approximately 1 in 2000 to 1 in 2500 live female births, based on epidemiological and newborn genetic screening data from Europe, Japan, and the United States.

202
Q

What are the typical features of Turner Syndrome?

A
Primary hypogonadism (gonadal dysgenesis) is one of the most common features of Turner syndrome, and Turner syndrome is one of the most common causes of premature ovarian failure. Most affected women have no breast development and have primary amenorrhea.
The most consistent characteristic of girls and women with Turner syndrome is their short stature (table 2 and picture 1). Other anomalies include a "shield" chest with widely spaced nipples, a short and webbed neck, cubitus valgus, and Madelung deformity of the forearm and wrist (picture 2 and image 1). The shield chest and short stature sometimes gives a disproportionately broad or stocky appearance. Neonates may have congenital lymphedema of the hands and feet, webbed neck, nail dysplasia, narrow and high-arched palate, and short fourth metacarpals and/or metatarsals [39].

Hearing loss, hypothyroidism, and liver function abnormalities often occur as these girls get older. Liver enzymes are mildly elevated in approximately 35 to 45 percent of adult patients and improve with estrogen/progestin hormone therapy. Intelligence is usually within the normal range, but patients may have specific neurocognitive deficits, eg, problems with visuospatial organization or a nonverbal learning disorder. (See ‘Psychologic and educational issues’ below.)

Other manifestations include increased risk of autoimmune diseases (including autoimmune thyroiditis) and specific morphologic defects of facial development and cardiovascular, urologic, and bone structure, as detailed in the following sections.

Turner syndrome is associated with an increased risk of autoimmune disorders, most importantly, hypothyroidism (Hashimoto’s thyroiditis), celiac disease, and inflammatory bowel disease (IBD)

203
Q

What is the interaction between Turner Syndrome and pregnancy?

A

Pregnancy and cardiovascular risk — The risk for aortic dissection or rupture is particularly high during pregnancy, which is typically achieved through in vitro fertilization (IVF) with oocyte donation. The risk of death during pregnancy may be as high as 2 percent. The increased risk persists into the postpartum period, owing to pregnancy-related aortic changes. Therefore, before attempting to become pregnant, women with Turner syndrome should undergo a complete medical evaluation, with particular attention to cardiovascular and renal function, as recommended by the American Society of Reproductive Medicine

204
Q

Are people with Turner Syndrome intellectually impaired?

A

No. Intelligence is usually normal in patients with Turner syndrome. The exception is the rare patient with a tiny X-ring chromosome, who may have severe mental retardation, probably because such tiny X-ring chromosomes fail to undergo X-inactivation

205
Q

What is the hormonal treatment of Turner Syndrome?

A

Ultimately, almost all girls with Turner syndrome need exogenous estrogen. This includes the 15 to 30 percent of girls with Turner syndrome who experience spontaneous puberty, which may persist for some time [41]. Later, cyclic progestins are added to the regimen to induce cyclic uterine bleeding and prevent endometrial hyperplasia.

206
Q

Which conditions are examined in newborn screening?

A

https://www.schn.health.nsw.gov.au/find-a-service/laboratory-services/nsw-newborn-screening/disorders

207
Q

What is Li-Fraumeni syndrome?

A

Li-Fraumeni syndrome (LFS) is associated with germline mutations of the tumor suppressor tumor protein gene TP53, and carriers are at increased risk of developing multiple primary cancers in childhood or young adulthood. These include breast cancer, sarcomas, brain cancer, leukemias, and adrenocortical cancers. The lifetime risk of breast cancer development for female mutation carriers approaches 50 percent by age 60 years.

208
Q

What is Lynch syndrome?

A

Lynch syndrome, also called hereditary nonpolyposis colon cancer (HNPCC), is associated with mutations in mismatch repair (MMR) genes (MSH2, MLH1, MSH6, and PMS2) and a mutation in the epithelial cell adhesion molecule (EPCAM) gene.
The primary cancers associated with Lynch syndrome involve the colon, endometrium, ovaries, and stomach.

209
Q

What is a Category A drug?

A

Drugs which have been taken by a large number of pregnant women and women of childbearing age without any proven increase in the frequency of malformations or other direct or indirect harmful effects on the fetus having been observed.

210
Q

What is a Category B1 drug?

A

Drugs which have been taken by only a limited number of pregnant women and women of childbearing age, without an increase in the frequency of malformation or other direct or indirect harmful effects on the human fetus having been observed.
Studies in animals have not shown evidence of an increased occurrence of fetal damage.

211
Q

What is a Category B2 drug?

A

Drugs which have been taken by only a limited number of pregnant women and women of childbearing age, without an increase in the frequency of malformation or other direct or indirect harmful effects on the human fetus having been observed.
Studies in animals are inadequate or may be lacking, but available data show no evidence of an increased occurrence of fetal damage.

212
Q

What is a Category B3 drug?

A

Drugs which have been taken by only a limited number of pregnant women and women of childbearing age, without an increase in the frequency of malformation or other direct or indirect harmful effects on the human fetus having been observed.
Studies in animals have shown evidence of an increased occurrence of fetal damage, the significance of which is considered uncertain in humans.

213
Q

What is a Category C drug?

A

Drugs which, owing to their pharmacological effects, have caused or may be suspected of causing, harmful effects on the human fetus or neonate without causing malformations. These effects may be reversible. Accompanying texts should be consulted for further details.

214
Q

What is a Category D drug?

A

Drugs which have caused, are suspected to have caused or may be expected to cause, an increased incidence of human fetal malformations or irreversible damage. These drugs may also have adverse pharmacological effects. Accompanying texts should be consulted for further details.

215
Q

What is a Category X drug?

A

Drugs which have such a high risk of causing permanent damage to the fetus that they should not be used in pregnancy or when there is a possibility of pregnancy.

216
Q

What are some drugs contraindicated with breastfeeding?

A

Drugs contraindicated during breastfeeding include anticancer drugs, lithium, oral retinoids, amiodarone and gold salts.

217
Q

What are the three types of drug transfer across the placenta?

A
  1. Complete transfer (type 1 drugs): for example, thiopental
  2. Exceeding transfer (type 2 drugs): for example, ketamine
  3. Incomplete transfer (type 3 drugs): for example, succinylcholine
218
Q

There are four main mechanisms of drug transfer across the placenta. What are they?

A
  1. Simple diffusion
  2. Facilitated diffusion
  3. Pinocytosis
  4. Active transport
219
Q

How does Progesterone cause contraception?

A

Progestogen negative feedback decreases the pulse frequency of gonadotropin-releasing hormone (GnRH) release by the hypothalamus, which decreases the secretion of follicle-stimulating hormone (FSH) and greatly decreases the secretion of luteinizing hormone (LH) by the anterior pituitary. Decreased levels of FSH inhibit follicular development, preventing an increase in estradiol levels. Progestogen negative feedback and the lack of estrogen positive feedback on LH secretion prevent a mid-cycle LH surge. Inhibition of follicular development and the absence of an LH surge prevent ovulation.

220
Q

How does oestrogen cause contraception?

A

Estrogen was originally included in oral contraceptives for better cycle control (to stabilize the endometrium and thereby reduce the incidence of breakthrough bleeding), but was also found to inhibit follicular development and help prevent ovulation. Estrogen negative feedback on the anterior pituitary greatly decreases the secretion of FSH, which inhibits follicular development and helps prevent ovulation

221
Q

What is the mechanism of Clomiphene?

A

Clomiphene triggers the brain’s pituitary gland to secrete an increased amount of follicle stimulating hormone (FSH) and LH (luteinizing hormone). This action stimulates the growth of the ovarian follicle and thus initiates ovulation.

222
Q

What class of drug is Clomiphene?

A

Clomifene is in the selective estrogen receptor modulator (SERM) family of medication. It works by causing the release of GnRH by the hypothalamus, and subsequently gonadotropin from the anterior pituitary.

223
Q

What is the mechanism of Mifepristone?

A

Mifepristone is an antiprogestogen and works by blocking the effects of progesterone and causing contractions of the uterus.

224
Q

If the MSD and CRL don’t meet criteria to diagnose miscarriage, when do you need to repeat the scan?

A

No embryo with heartbeat ≥2 weeks after TVUS showed a gestational sac without a yolk sac.
No embryo with heartbeat ≥11 days after TVUS showed a gestational sac with a yolk sac.

225
Q

What are the ultrasound features of a corpus luteum?

A

The corpus luteum is a thick walled cyst with characteristic “ring of fire” peripheral vascularity. It usually has a crenulated inner margin and internal echoes.

226
Q

What three features should be seen when measuring abdominal circumference?

A

Transverse section through the upper abdomen, which should demonstrate the following fetal landmarks:
fetal stomach
umbilical vein
portal sinus

The kidneys and cord insertion should not be visible. The umbilical vein should not be seen up to the skin line.

227
Q

Describe the role of the three different doppler ultrasound measures?

A

Doppler ultrasound allows an assessment of placental resistance (umbilical artery; UmA), preferential organ blood flow (middle cerebral artery; MCA) and fetal cardiac function and myocardial haemodynamics (ductus venosus; DV).

228
Q

Describe uterine histopath during the menstrual cycle?

A

https: //embryology.med.unsw.edu.au/embryology/index.php/Menstrual_Cycle_-_Histology
http: //www.ganfyd.org/index.php?title=Endometrial_cycle_histology#Proliferative_Phase

229
Q

In the evaluation of chronic pelvic pain, what is the APQRST mnemonic?

A

associated, provocative/palliative, quality, radiation, setting, temporal aspects

230
Q

How common is a history of abuse in the chronic pelvic pain population?

A

In a questionnaire study of over 700 women referred to a CPP clinic, nearly one-half reported a history of physical or sexual abuse, and nearly one-third screened positive for post-traumatic stress disorder

231
Q

The “negative sliding sign” when assessed with dynamic ultrasound, has a sensitivity of 85 percent and specificity of 96 percent for the presence of DIE - what is it looking for?

A

In women with DIE, uterorectal adhesions can fix the posterior uterus to the anterior rectal wall and thus the sliding of rectum against posterior uterine wall is absent or impaired.

232
Q

Hwo good is MRI for evaluating DIE?

A

In a Cochrane review of six studies with 266 participants, MRI had excellent sensitivity (0.94, 95% CI 0.90-0.97) and specificity (0.77, 95% CI 0.44-1.00) for the diagnosis DIE, thus approaching the criteria for a replacement diagnostic test in lieu of surgical biopsy

233
Q

When do you go to diagnostic laparoscopy for investigation of endometriosis in a pelvic pain patient?

A

For women whose symptoms do not improve after three to four months of hormonal suppression, or in whom medical management is not appropriate, the authors perform laparoscopy for diagnosis and excision of endometriosis lesions, when identified.

234
Q

What is the treatment of choice for PID chronic pelvic pain?

A

Up to 30 percent of women with prior PID will develop CPP [87]. Women with CPP (particularly uterine pain), a history of PID, and no other identified causes of CPP, are offered neuromodulators, consistent with guidelines for chronic pain syndromes (strategy similar to treatment of general neuropathic pain outlined in algorithm, although opioid analgesia is generally avoided)

235
Q

What is the treatment of choice for adhesion-related pelvic pain?

A

In a randomized double-blind controlled trial of 100 patients with chronic abdominal pain and adhesions comparing laparoscopic lysis of adhesions versus diagnostic laparoscopy alone, no difference was identified between the groups after 12 years of follow-up (27 percent of patients in each group noted initial pain relief), but the data suggested that the group undergoing diagnostic laparoscopy alone overall did better

236
Q

How many women who undergo hysterectomy for adenomyosis related pelvic pain, still have pain, mate?

A

However, the presence of adenomyosis does not predict the success of hysterectomy in curing pelvic pain. Approximately 25 percent of women who undergo hysterectomy for the indication of adenomyosis and CPP have persistent pelvic pain that does not resolve postoperatively

237
Q

What are the four ‘variant’ PMDs?

A

Premenstrual exacerbation of an underlying diso rder’, such as diabetes, depression, epilepsy, asthmaand migraine. These patients will experience symp toms relevant to their disorder throughout the menstrualcycle.2. ‘Non-ovulatory PMDs’ occur in the presence of ovari an activity without ovulation. This is poorly understooddue to a lack of evidence, but it is thought that follicula r activity of the ovary can instigate symptoms.3. ‘Progestogen-induced PMDs’ are caused by exogenous progestogens present in hormone replacementtherapy (HRT) and the combined oral contraceptive (COC) pill. This reintroduces symptoms to women whomay be particularly sensitive to progestogens. Although progestogen-only contraceptives may introducesymptoms, as they are noncyclical they are not included within variant PMDs and are considered adverse effects(probably with similar mechanisms) of continuous progestogen therapy.
PMDs with absent menstruation’ include women who still have a functioning ovarian cycle, but for reasons such as hysterectomy, endometrial ablation or the levonorgestrel-releasing intrauterine system (LNG-IUS) they do not menstruate

238
Q

What is the definition of pre-menstrual disorder?

A

The symptoms of core PMDs are nonspecific and recur in ovulatorycycles. They must be present during the luteal phase and abate as menstruation begins, which is then followed by asymptom-free week. There is no limit on the type or number of symptoms experienced; however, some individuals will have predominantly psychological, predominantly somatic or a mixture of symptoms

239
Q

What is the prevalence of PMS?

A

Four in ten women (40%) experience symptoms of PMS and of these 5 - 8% suffer from severe PMS.

240
Q

What are the theories of PMS aetiologuy?

A

The first suggests that some women are ‘sensitive’ to progesterone and progestogens, since the serum concentrations of estrogen or progesterone are the same in those with or without PMS. The second theory implicates the neurotransmitters serotonin and c-aminobutyric acid (GABA). Serotonin receptors are responsive to estrogen and progesterone, and selective seroton in reuptake inhibitors (SS RIs) are proven to reduce PMS symptoms. GABA levels are modulated by the metabolite of progesterone, allopregnanolone, and in women with PMS the allopregnanolone levels appear to be reduced.

241
Q

How do GNRH analogues diagnose PMS?

A

GnRH analogues, which are widely used within gynaecology, can be useful in separating those with and those without PMS by inhibiting cyclical ovarian function.

242
Q

What are the simple options to treat PMS?

A

Referral to a gynaecologist should be considered when simple measures (e.g. COCs, vitamin B6, SSRIs) have been explored and failed and when the severity of the PMS justifies gynaecological intervention.

243
Q

Name 4 people in the MDT for PMS

A

Women with severe PMS may benefit from being managed by a multidisciplinary team comprising a general practitioner, a general gynaecologist or a gynaecologist with a special interest in PMS, a mental health professional (psychiatrist, clinical psychologist or counsellor) and a dietician.

244
Q

Does evening primrose oil work for PMS?

A

Yeah - Unsaturated fatty acids, as contained in evening primrose oil, have been shown in one prospective randomised trial to improve menstrual symptoms compared with placebo at both 1 g/day and 2 g/day dosages. There was no measurable change in cholesterol levels.

245
Q

Name 5 effective complementary methods of treating PMS:

A

Exercise, Gingko, EPO, Reflexology, Vitamin D and calcium, Vitex agnus castus, Saffron, acupuncture,

246
Q

Is CBT OK for PMS?

A

When treating women with severe PMS, CBT should be considered routinely as a treatment option.

247
Q

Which COCPs are best for the treatment of PMS?

A

Despite the combined pill’s ability to suppress ovulation, studies initially illustrated no benefit in the treatment of PMS
hen treating women with PMS, drospirenone-containing COCs may represent effective treatment for PMS and should be considered as a first-line pharmaceutical intervention

248
Q

How do you monitor BMD in women taking GNRH analogues?

A

Women on long-term treatment should have measurement of BMD (ideally by dual-energyX-ray absorptiometry [DEXA]) every year. Treatment should be stopped if bone density declines significantly.

249
Q

Can you use progesterone for management of PMS?

A

There is good evidence to suggest that treating PMS with progesterone or progestogens is not appropriate.

250
Q

Which diuretic can be used to treat PMS?

A

Spironolactone can be used in women with PMS to treat physical symptoms.

251
Q

What is the maximum amount of fluid that should be given, whilst awaiting blood transfusion in PPH?

A

Traditionally, a total volume of 3.5 l of clear fluids (up to 2 l of war med isotoniccrystalloid as rapidly as possible, followed by up to a further 1.5 l of warmed colloid if blood is still notavailable) comprises the maximum that should be infused while awaiting compatible packed red cells

252
Q

When should you use FFP in PPH?

A

If no haemostatic results are available and bleeding is continuing, then, after 4 units of RBCs,FFP should be infused at a dose of 12-15 ml/kg until haemostatic test results are known

253
Q

What do we use for fibrinogen replacement?

A

Cryoprecipitate should be used for fibrinogen replacement.
A pragmatic view based on available evidence is that, during continuing PPH, cryoprecipitate or fibrinogen concentrate should be used to maintain a fibrinogen level of at least 2 g/l, even if PT/APTT are normal.

254
Q

When do we give platelets?

A

There is general consensus that platelets should be transfused at a trigger of 75 9 109/l to maintain a levelgreater than 50 9 109/l during ongoing PPH.

255
Q

What investigations should be undertaken for a secondary PPH?

A

In women presenting with secondary PPH, an assessment of vaginal microbiology should be performed (high vaginal and endocervical swabs) and appropriate use of antimicrobial therapy should be initiated when endometritis is suspected.DA pelvic ultrasound may help to exclude the presence of retained products of conception (RPOC), although the diagnosis of retained products is unreliable. Surgical evacuation of retained placental tissue should be undertaken or supervised by an experienced clinician.

256
Q

What does RCOG consider a low Papp-A?

A

A low level (< 0.415 MoM) of the first trimester marker PAPP-A should be considered a major risk factor for delivery of a SGA neonate

257
Q

Describe the role of uterine artery doppler as per the RCOG SGA guideline? When should you not repeat?

A

https://www.rcog.org.uk/globalassets/documents/guidelines/gtg_31.pdf - page 9

258
Q

Why don’t you do uterine artery dopplers on a lady with a major SGA risk factor?

A

The developers’ interpretation of the evidence relating to uterine artery Doppler screening is that the LR- is
insufficient to negate the risk associated with a major risk factor for a SGA neonate. In these women we would
not recommend uterine artery Doppler, as it would not change care.

259
Q

What further tests should you do for an SGA?

A

Karyotyping? CMV, toxo

260
Q

Should you do uterine dopplers in the third trimester?

A

No

261
Q

When should you start Aspirin for prevention of SGA?

A

A recent systematic review and meta-analysis of five trials, with 414 women, has suggested that, with respect to women at risk of pre-eclampsia, the timing of commencement of aspirin is important. Where aspirin was
started at 16 weeks of gestation or less the RR of a SGA infant was 0.47 (95% CI 0.30-0.74) and the number
needed to treat was 9 (95% CI 5.0-17.0). No reduction in risk of a SGA infant was found when aspirin was
started after 16 weeks of gestation (RR 0.92, 95% CI 0.78-1.10).

262
Q

Up to how many weeks should an SGA receive steroids?

A

Women with a SGA fetus between 24+0 and 35+6 weeks of gestation, where delivery is being considered, should receive a single course of antenatal corticosteroids.

263
Q

At what gestation should you give Mag Sulphate?

A

Australian guidelines recommend the administration of magnesium sulphate when delivery is before 30 weeks of gestation

264
Q

What is the definition of primary versus secondary amenorrhea?

A

It is often classified as either primary (absence of menarche by age 15 years) or secondary (absence of menses for more than three months in girls or women who previously had regular menstrual cycles or six months in girls or women who had irregular menses)

265
Q

What is the definition of oligomenorrhea?

A

Oligomenorrhea (fewer than nine menstrual cycles per year or cycle length greater than 35 days)

266
Q

Describe the structure for evaluating secondary amenorrhea. Which is the most common cause?

A

Hypothalamus - 35 percent (almost all functional hypothalamic amenorrhea)

●Pituitary - 17 percent (13 percent hyperprolactinemia, 1.5 percent “empty sella,” 1.5 percent Sheehan syndrome, 1 percent Cushing’s syndrome)

●Ovary - 40 percent (30 percent polycystic ovary syndrome [PCOS], 10 percent primary ovarian insufficiency [POI, also known as premature ovarian failure])

●Uterus - 7 percent (all due to intrauterine adhesions)

●Other - 1 percent (congenital adrenal hyperplasia, ovarian and adrenal tumors, hypothyroidism)

267
Q

What is the most common cause of secondary amenorrhea?

A

Pregnancy

268
Q

How does systemic illness or starvation cause secondary amenorrhea?

A

Systemic illness may be associated with menstrual cycle disorders when it is severe enough to result in a decrease in hypothalamic GnRH secretion and/or when it is associated with nutritional deficiencies.

269
Q

What are the characteristic hormonal changes in functional hypothalamic amenorrhea?

A

The abnormal GnRH secretion characteristic of functional hypothalamic amenorrhea leads to decreased pulses of gonadotropins, absent midcycle surges in luteinizing hormone (LH) secretion, absence of normal follicular development, anovulation, and low serum estradiol concentrations

270
Q

How does hyperprolactinemia cause amenorrhea?

A

Prolactin appears to cause amenorrhea by suppressing hypothalamic GnRH secretion, leading to low gonadotropin and estradiol concentrations

271
Q

What is step 1 of evaluation of secondary amenorrhea?

A

Pregnancy test

272
Q

What is the progestin withdrawal test?

A

Medroxyprogesterone 10 mg for 10 days

273
Q

What are the first three blood tests for secondary amenorrhea?

A

The initial laboratory evaluation (after ruling out pregnancy) for women with secondary amenorrhea should include follicle-stimulating hormone (FSH), serum PRL, and thyroid-stimulating hormone (TSH) to test for POI, hyperprolactinemia, and thyroid disease, respectively.

274
Q

When investigating for secondary amenorrhea, what does a high FSH mean?

A

A high serum follicle-stimulating hormone (FSH) concentration indicates POI, formerly referred to as premature ovarian failure.

275
Q

Why is there a high Prolactin in hypothyroidism?

A

In some cases of profound hypothyroidism, there may be a slight increase in serum PRL (due to a presumed increase in hypothalamic thyrotropin-releasing hormone [TRH], which stimulates both TSH and PRL secretion)

276
Q

How do you manage Asherman’s Syndrome?

A

Therapy of Asherman syndrome (intrauterine adhesions) consists of hysteroscopic lysis of adhesions followed by a course of estrogen treatment to stimulate regrowth of endometrial tissue

277
Q

What are the goals of management of PCOS?

A

●Amelioration of hyperandrogenic symptoms (hirsutism, acne, scalp hair loss)
●Management of underlying metabolic abnormalities and reduction of risk factors for type 2 diabetes and cardiovascular disease
●Prevention of endometrial hyperplasia and carcinoma, which may occur as a result of chronic anovulation
●Contraception for those not pursuing pregnancy, as women with oligomenorrhea ovulate intermittently and unwanted pregnancy may occur

●Ovulation induction for those pursuing pregnancy

278
Q

What is the first choice for COCP in PCOS?

A

We typically start with an OC containing 20 mcg of ethinyl estradiol combined with a progestin with minimal androgenicity (such as norgestimate). Other progestins with minimal androgenicity or antiandrogenic properties include desogestrel and drospirenone, but both have been associated with a possible higher risk of venous thromboembolism (VTE)

279
Q

Name 4 ways incontinence impacts quality of life

A

Quality of life - Urinary incontinence is associated with depression and anxiety, work impairment, and social isolation. Urinary incontinence adversely impacts quality of life in nursing home residents as well as those who live independently .

●Sexual dysfunction - Incontinence during sexual activity (coital incontinence), which may affect up to one-third of all incontinent individuals, and fear of incontinence during sexual activity both contribute to incontinence-related sexual dysfunction [16-18]. Urgency incontinence had greater negative impact on sexual function compared with urgency or frequency without incontinence [19,20].

●Morbidity - Medical morbidities associated with urinary incontinence include perineal infections (eg, candida or cellulitis) from moisture and irritation as well as falls and fractures that in turn increase overall morbidity, mortality and health care costs [21,22]. In older women with urinary urgency or urge incontinence, falls are 1.5 to 2.3 times more common than among women without urinary symptoms [22].

●Increased caregiver burden - In addition to being a burden for caregivers, urinary incontinence is negatively associated with the ability to perform other activities of daily living, thus increasing the need for caregiver assistance [23,24]. Six to 10 percent of nursing home admissions in the United States are attributable to urinary incontinence

280
Q

What is the prevalence of urinary incontinence in non-pregnant women?

A

Overall prevalence of urinary incontinence among non-pregnant women age 20 years and above has been reported at 10 to 17 percent.

281
Q

What is the pathophysiology of thalassemia?

A

The basic defect in the thalassaemia syndromes is reduced globin chain synthesis with the resultant red cells having inadequate haemoglobin content.

The pathophysiology of thalassaemia
syndromes is characterised by extravascular haemolysis due to the release into the peripheral circulation of
damaged red blood cells and erythroid precursors because of a high degree of ineffective erythropoiesis

282
Q

What are the steps to pre-conception counselling in a woman with thalassemia?

A

At each visit with the thalassaemia team, there should be a discussion and documentation of intentions regarding pregnancy. This should include screening for end-organ damage and optimisation of
complications prior to embarking on any pregnancy.

Yeah, diabetes, cardiac, thyroid, liver, bone health, Hep Bs and Cs

283
Q

What are the risks of maternal anaemia and fetal growth restriction?

A

Severe maternal anaemia predisposes to FGR in women with thalassaemia. Chronic anaemia affects placental transfer of nutrients and can therefore adversely affect fetal growth.

284
Q

Why do you give Aspirin or Clexane in thalassemia?

A

Women with thalassaemia who have undergone splenectomy or have a platelet count greater than 600 x 109
/l should commence or continue taking low-dose aspirin (75 mg/day).
Women with thalassaemia who have undergone splenectomy and have a platelet count above
600 x 109
/l should be offered low-molecular-weight heparin thromboprophylaxis as well as low-dose
aspirin (75 mg/day).

285
Q

What are risk factors for cord prolapse?

A

Inherent - anything that means there’s lots of intrauterine space.
Us - any intervention that is a bit rogue

286
Q

What is the rate of cancer transformation in lichen planus?

A

Development of squamous cell carcinoma. In one study the incidence
was as high as 3%.

287
Q

What are the two types of VIN?

A

In Genitourinary Medicine clinics the commonest aetiological agent is Human papillomavirus (HPV) this is known as
usual type and is mainly associated with HPV 1629. A second type, generally not
HPV related occurs in conjunction with lichen sclerosus or lichen planus (known
as differentiated type)30

288
Q

What is the PALM-COIN acronym stand for in AUB?

A

PALM: polyp, adenomyosis, leiomyoma, and malignancy and hyperplasia), four that are unrelated to structural anomalies (COEI: coagulopathy, ovulatory dysfunction, endometrial, iatrogenic

289
Q

How can non-gynaecological medications cause AUB?

A

Medications can cause AUB in a variety of ways: (1) anticoagulants may result in heavy or prolonged uterine bleeding; (2) a variety of medications can cause hyperprolactinemia, resulting in oligomenorrhea or amenorrhea.

290
Q

How old and premenopausal should you be to get a pipelle for AUB?

A

Age 45 years to menopause - In women who are ovulatory, any AUB, including intermenstrual bleeding. In any woman, bleeding that is frequent (interval between the onset of bleeding episodes is <21 days), heavy, or prolonged (>5 days). Younger than 45 years - In reproductive-age women, the majority of cases of endometrial neoplasia occur in the setting of ovulatory dysfunction due to estrogenic proliferation with absent or inadequate progestational protection [37]. Endometrial sampling is indicated if AUB is persistent, occurs in the setting of a history of unopposed estrogen exposure (obesity, chronic ovulatory dysfunction) or failed medical management of the bleeding, or in women at high risk of endometrial cancer (eg, tamoxifen therapy, Lynch or Cowden syndrome).

291
Q

Name six risk factors for endometrial cancer?

A

https://www.uptodate.com.acs.hcn.com.au/contents/image?imageKey=OBGYN%2F62089&topicKey=OBGYN%2F3263&source=see_link

292
Q

Yo, how good is this graph?

A

https://www.uptodate.com.acs.hcn.com.au/contents/image?imageKey=OBGYN%2F90595&topicKey=OBGYN%2F3263&source=see_link

293
Q

What is the ET cut-off for symptomatic, postmenopausal bleeding?

A

Endometrial cancer can reasonably be excluded by ultrasound in postmenopausal women with a thin (≤4 mm), homogeneous endometrium.

294
Q

What is the incidence of vasa praevia?

A

1 in 2500

295
Q

What are the four diagnostic criteria on US of vasa praevia?

A
  • Visualising aberrant linear or tubular echolucent structures with 2D imaging. Demonstrating blood flow in these structures using colour or power Doppler.
    Demonstrating umbilical arterial/venous Doppler waveforms using pulse wave Doppler.
    Aberrant vessels located over or within 2cm of the internal os attached to the inner perimeter of the
    fetal membranes
296
Q

What is the gold standard of managment for Vasa praevia?

A

Admission to hospital from 30 weeks gestation until the time of delivery to expedite urgent emergency delivery in the event of membrane rupture, vaginal bleeding or preterm labour;
Administration of corticosteroids for fetal lung maturation in anticipation of preterm delivery;
Admission and delivery in a hospital with paediatric expertise and appropriate level of neonatal care;
Delivery by elective caesarean section prior to the onset of labour.

297
Q

What are the greyscale US criteria for placenta accreta? (5)

A

● loss of the retroplacental sonolucent zone
● irregular retroplacental sonolucent zone
● thinning or disruption of the hyperechoic serosa-bladder interface
● presence of focal exophytic masses invading the urinary bladder
● abnormal placental lacunae

298
Q

What are the colour doppler US criteria for placenta accreta? (4)

A

● diffuse or focal lacunar flow
● vascular lakes with turbulent flow (peak systolic velocity over 15 cm/s)
● hypervascularity of serosa-bladder interface
● markedly dilated vessels over peripheral subplacental zone.

299
Q

What are the 3D doppler US criteria for placenta accreta? (4)

A

● numerous coherent vessels involving the whole uterine serosa-bladder junction (basal view)
● hypervascularity (lateral view)
● inseparable cotyledonal and intervillous circulations, chaotic branching, detour vessels (lateral view).

300
Q

What are the MRI criteria for placenta accreta? (4)

A

● uterine bulging
● heterogeneous signal intensity within the placenta
● dark intraplacental bands on T2-weighted imaging

301
Q

What are the RCOG cut-offs for GDM?

A

a fasting plasma glucose level of 5.6 mmol/litre or above or a 2‑hour plasma glucose level of 7.8 mmol/litre or above.

302
Q

What is the global rate of IUCD use?

A

~15% - mostly Asia ??

303
Q

What is the prevalence of contraception use in Australia?

A

~80%

304
Q

What is the type of hormone in a Mirena? What is the dose

A

levonorgestrel, 25mcg/day, 52mg total

305
Q

What is the hormone and dose in an Implanon?

A

68 mg of the active substance etonogestrel

306
Q

Describe three risks associated with IUCDs?

A
  1. Ectopic pregnancy
  2. Pelvic infection
  3. Change in bleeding patterns
307
Q

Name some risks of the Implanon?

A

Ectopics, ovarian cysts,breast cancer and VTE

308
Q

What is the complication of SLE in pregnancy you always forget?

A

VTE, and congenital cardiac conditions, Congenital heart block with Anti-Ro antibodies,

309
Q

When should SLE mums NOT get pregnant?

A

Thus, recent stroke, cardiac involvement, pulmonary hypertension, severe interstitial lung disease, and advanced renal insufficiency can be dangerous to both mother and fetus. For at least 6 months of control.

310
Q

What is the criteria for perinatal mortality?

A

The NPMDC is a national collection of all stillbirths and neonatal deaths occurring in the state or territory of at least 20 weeks gestation or 400 grams birthweight.

311
Q

What are the core tests for FDIU?

A

Comprehensive maternal (medical, social, family) and pregnancy history
• Kleihauer-Betke test/Flow cytometry for fetal to maternal haemorrhage
• External examination of the baby performed by the attending clinician
• Clinical photographs of the baby
• Autopsy
• Detailed macroscopic examination of the placenta and cord
• Placental histopathology
• Cytogenetics (Chromosomal microarray (CMA) or karyotype if CMA is not
available).

312
Q

How do the features on a CTG relate to fetal physiology?

A

Baseline Heart Rate - Cardiac & CNS Function
Baseline Variability - Autonomic Nervous System (CNS)
Decelerations - Mechanical or hypoxic insult
Accelerations - Somatic Nervous System

313
Q

When should women with haemoglobinopathies be given Fe?

A

Women with known haemoglobinopathy should have serum ferritin checked and offered oral supplements if their ferritin level is <30 μg/l

314
Q

When do you commence Metformin in GDM?

A

Offer metformin[2] to women with gestational diabetes if blood glucose targets are not met using changes in diet and exercise within 1-2 weeks.

315
Q

At what BSL should it be considered?

A

Offer immediate treatment with insulin, with or without metformin, as well as changes in diet and exercise, to women with gestational diabetes who have a fasting plasma glucose level of 7.0 mmol/litre or above at diagnosis.
Consider immediate treatment with insulin, with or without metformin, as well as changes in diet and exercise, for women with gestational diabetes who have a fasting plasma glucose level of between 6.0 and 6.9 mmol/litre if there are complications such as macrosomia or hydramnios.

316
Q

What are the BSL targets during GDM monitoring?

A

Advise pregnant women with any form of diabetes to maintain their capillary plasma glucose below the following target levels, if these are achievable without causing problematic hypoglycaemia:
fasting: 5.3 mmol/litre

and

1 hour after meals: 7.8 mmol/litre or

2 hours after meals: 6.4 mmol/litre.

317
Q

Does Metformin help fertility in PCOS?

A

Correction of hyperinsulinemia with metformin has been shown to have a beneficial effect in anovulatory women with PCOS by increasing menstrual cyclicity and improving spontaneous ovulation. However, it does not appear to improve live-birth rates when given alone or in combination with clomiphene citrate.

318
Q

Name the 4 most common causes of PMB?

A

In the early menopausal years, endometrial hyperplasia, polyps, and submucosal fibroids are also common etiologies

319
Q

What is the ET cut-off for PMB?

A

Endometrial cancer can reasonably be excluded by ultrasound in postmenopausal women with a thin (≤4 mm), homogeneous endometrium.

320
Q

What is the most common symptom of premenopausal bleeding with polyps?

A

Intermenstrual bleeding is the most frequent symptom in premenopausal women with endometrial polyps

321
Q

What do you always forget to do with consent, baby?

A

DOCUMENTATION

322
Q

Where is the ureter most commonly injured/

A

Injury occurs most frequently in the lower third of the ureter (51%), followed by the upper third
(30%) and the middle third (19%). The most
common sites of injury are:
• lateral to the uterine vessels
• the area of the ureterovesical junction close
to the cardinal ligaments
• the base of the infundibulopelvic ligament
as the ureters cross the pelvic brim at the
ovarian fossa
• at the level of the uterosacral ligament.
Most studies show the most common site of
injury to be lateral to the uterine vessels,14 but
Daly et al.
6 report this to be at the ovarian fossa.
During laparoscopy the ureter is injured most
frequently adjacent to the uterosacral ligaments.

323
Q

What are the 4 P’s of Lichen PLanus?

A

The classic presentation of cutaneous lichen planus is a papulosquamous eruption characterized by the development of flat-topped, violaceous papules on the skin (picture 1A-D). Often, the clinical manifestations are described as the four “P’s:”
●Pruritic

●Purple (actually a slight violaceous hue)

●Polygonal

●Papules or plaques

324
Q

What are the histological findings of Lichen Planus?

A

●Hyperkeratosis without parakeratosis
●Vacuolization of the basal layer

●Civatte bodies (apoptotic keratinocytes) in the lower epidermis

●Wedge-shaped hypergranulosis, “saw-tooth” shaped rete ridges

●Small clefts at the dermal-epidermal junction (Max-Joseph spaces)

●Band-like lymphocytic infiltrate at the dermal-epidermal junction

●Eosinophilic colloid bodies (apoptotic keratinocytes) in the papillary dermis

●Pigment incontinence (most prominent in dark-skinned individuals)

325
Q

What is Level 1 support structures?

A

Level 1 - Uterosacral/cardinal ligament complex, which suspends the uterus and upper vagina to the sacrum and lateral pelvic side wall. Level 1 support represents vertical fibers of the paracolpium that are a continuation of the uterosacral/cardinal ligament complex which inserts variably into the cervix and vagina

326
Q

What is Level 2 support structures?

A

Paravaginal attachments along the length of the vagina to the superior fascia of the levator ani muscle and the arcus tendineus fascia pelvis (also referred to as the “white line”). Loss of level 2 support contributes to anterior vaginal wall prolapse (cystocele).

327
Q

Describe the nerve supply of the pelvic floor

A

The innervation of the pelvic region derives from the S2, S3, and S4 segments of the spinal cord, which fuse to form the pudendal nerve. The pudendal nerve innervates the external anal sphincter, whereas the levators, coccygeus muscles, and urogenital diaphragm appear to be innervated by a direct connection of S2, S3, and S4 nerve fibers

328
Q

What is point Aa on POPQ?

A

Point Aa is located in the midline of the anterior vaginal wall, 3 cm proximal to the external urethral meatus, corresponding approximately to the urethrovesical junction. The quantitative value of point Aa is anywhere from -3 to +3 cm from the hymenal plane, depending upon the extent of anterior wall prolapse.

329
Q

What is point Ba on POPQ

A

Point Ba is the most distal (ie, most dependent) position of any part of the anterior vaginal wall between point Aa and the vaginal cuff or anterior vaginal fornix. If there is no prolapse, point Ba is -3 cm by definition. In a woman with total posthysterectomy vault prolapse, Ba has a positive value equal to the distance between the vaginal apex and hymenal plane (so the quantitative value of point Ba can range from the most supported measurement [-3], to the most prolapse portion beyond the hymenal ring [this may exceed +3 cm]).

330
Q

What is point C on POPQ?

A

Point C is the most distal (ie, most dependent) edge of the cervix or the leading edge of the vaginal cuff (posthysterectomy).

331
Q

What is point D on POPQ?

A

Point D is measured only in women with a cervix. It is the deepest point of the posterior fornix, corresponding approximately to where the uterosacral ligaments attach to the posterior cervix. Measuring this point distinguishes between suspensory failure of the uterosacral-cardinal ligament complex and cervical elongation: if point C is significantly more positive than point D (>4 cm), the cervix is elongated.

332
Q

What is point Ap on POPQ?

A

Point Ap is located in the midline of the posterior vaginal wall, 3 cm proximal to the posterior hymen. The quantitative value of point Ap is anywhere from -3 to +3 cm from the hymenal plane, depending upon the extent of posterior wall prolapse.

333
Q

What is point Bp on POPQ?

A

Point Bp is the most distal (ie, most dependent) position of any part of the upper posterior vaginal wall between point Ap and the vaginal cuff or posterior vaginal fornix. If there is no prolapse, point Bp is -3 cm by definition. In a woman with total posthysterectomy vaginal prolapse, Bp has a positive value equal to the distance between the vaginal apex and hymenal plane (so the quantitative value of point Bp can range from the most supported measurement [-3], to the most prolapse portion beyond the hymenal ring [this may exceed +3 cm]).

334
Q

Describe the different staging of POPQ

A

●Stage 0 - No prolapse. Points Aa, Ap, Ba, and Bp are all -3 cm and point D (if uterus is present) or C (posthysterectomy) equals or nearly equals TVL (-TVL cm to -[TVL-2] cm).
●Stage II - The most distal portion of the prolapse is between ≤1 cm proximal to the hymenal plane and ≥1 cm distal to the hymenal plane (ie, quantitation value ≥ -1 cm to ≤ +1 cm).

●Stage III - The most distal portion of the prolapse is between >1 cm distal to the hymenal plane, but no further than 2 cm less than the total vaginal length in centimeters (quantitative value >+1 cm but

335
Q

What are the five key features on colposcopy?

A
  1. Surface contour
  2. Vascular pattern
  3. Acetic acid changes
  4. Topography
  5. Iodine uptake
336
Q

What are the embryological events going on with twin pregnancy timing?

A

https://en.wikipedia.org/wiki/Monoamniotic_twins

337
Q

What is the dose of Doxylamine for HE

A

12.5 / 12.5 / 25

338
Q

What is the dose of Pyridoxine for HE

A

25mg TDS PO

339
Q

What are the two pain pathways in labour?

A

The pain of labour in the first stage is mediated by T10 to L1 spinal segments, whereas that in the second stage is carried by T12 to L1, and S2 to S4 spinal segments.

340
Q

What are the six moderate risk factors for PET?

A
First pregnancy
age 40 years or older
Pregnancy interval of more than 10 years
Body mass index (BMI) of 35 kg/m2 or more at first visit
Family history of pre-eclampsia
Multiple pregnancy.
341
Q

Name 8 major risk factors for SGA

A

These major risk factors include previous small for gestational age infants, previous fetal death in-utero, current
pre-eclampsia, current significant unexplained antepartum haemorrhage, diabetes mellitus with
vascular disease, renal impairment, antiphospholipid antibody syndrome, systemic lupus
erythematosis, smoking ≥ 11 cigarettes a day, daily vigorous exercise and maternal age >40
Prenatal Screening for Adverse Pregnancy Outcomes
C-Obs 61
Page |8
years.

342
Q

What do you find on US with adenomyosis?

A

Tender, enlarged uterus
Hetero myometr - venetian blinds
myometrial cyst
asymmtety of uterine walls

343
Q

What do you find on MRI with adenomyosis?

A
  • Junctional zone thickened asymmetry of the walls

myometial cysts

344
Q

What is the CAUSTIC acronym?

A
chromosomal
anaemia
unexplained
structural
twins
infection
cardiac
345
Q

What are 5 prognostic factors for ECV?

A
  • Parity primiparity lower success compared to multiparity
  • Amniotic fluid volume oligohydramnios lower success compared to polyhydramnios (yet polyhydramnios more likely to re-vert to breech post successful version)
  • Maternal BMI increased BMI less likely to be successful
  • Presentation frank breech less likely to turn compared to complete breech
  • Placental position anterior placenta less successful
  • Engagement of breech engaged deep in pelvis less likely to be successful
  • Use of tocolysis increase rate of success
  • Estimated fetal weight macrosomia less likely to be successful
346
Q

Define gestational diabetes mellitus

A

• Glucose intolerance of variable severity with onset or first recognition during pregnancy (ADIPS)

347
Q

What are the four primary outcomes of HAPO?

A
  • Birth weight > 90th%
  • Primary caesarean section delivery
  • Neonatal hypoglycaemia
  • Cord C-peptide > 90th % (as index of fetal beta cell function; fetal hyperinsulinaemia)
348
Q

What are the categories of PTB? What are their prevalence?

A

Preterm birth category Prevalence < 37/40: Preterm 7.4%
32 - 37/40: Late preterm 5.9%
28 - 31+6/40: Very preterm 0.7%
< 27+6/40: Extreme preterm 0.8%

349
Q

List six factors that predispose to genuine stress urinary incontinence.

A
  • Multiparity - 2 or more normal vaginal births
  • Obesity
  • Frequent coughing - smokers, chronic pulmonary disease
  • Age
  • Post-menopausal status (hypo-oestrogenised tissues)
  • History of chronic heavy lifting (weight lifting)
  • Constipation
  • Neurogenic: diabetes, CVD
350
Q

Name the three poor obstetric outcomes as part of the APLS definition?

A

● three or more consecutive miscarriages before 10 weeks of gestation
● one or more morphologically normal fetal losses after the 10th week of gestation
● one or more preterm births before the 34th week of gestation owing to placental disease.

351
Q

What tests do you order for inherited thrombophilias?

A

Women with second-trimester miscarriage should be screened for inherited thrombophilias including factor V Leiden, factor II (prothrombin) gene mutation and
protein S.

352
Q

What are the guidelines for DVT prohylaxis after emergency CS?

A

Following emergency CS thromboprophylaxis with LMWH or UFH is recommended, for at least 5 days or longer until recovery of full mobility

353
Q

Name six ANZJOG major risk factors for VTE?

A
  1. ELCS
  2. Immobility
  3. PET
  4. BMI 30
  5. Infection
  6. Medical comorbidity
354
Q

Name six ANZJOG minor risk factors for VTE?

A
  1. Age 35
  2. > 24hr labour
  3. Smoker
  4. PPH >1000mL
  5. Perineal trauma
  6. Gross varicose veins
355
Q

Compare vacuum with forceps:

A

Vacuum extraction compared with forceps
● more likely to fail delivery with the selected instrument (OR 1.7; 95% CI 1.3-2.2)
● more likely to be associated with cephalhaematoma (OR 2.4; 95% CI 1.7-3.4)
● more likely to be associated with retinal haemorrhage (OR 2.0; 95% CI 1.3-3.0)
● more likely to be associated with maternal worries about baby (OR 2.2; 95% CI 1.2-3.9)
● less likely to be associated with significant maternal perineal and vaginal trauma (OR 0.4; 95% CI 0.3-0.5)
● no more likely to be associated with delivery by caesarean section (OR 0.6; 95% CI 0.3-1.0)
● no more likely to be associated with low 5-minute Apgar scores (OR 1.7; 95% CI 1.0-2.8)
● no more likely to be associated with the need for phototherapy (OR 1.1; 95% CI 0.7-1.8). is:

356
Q

The four major factors leading to preterm labor are…

A

intrauterine infection, decidual hemorrhage, excessive uterine stretch, and maternal or fetal stress

357
Q

One classification based upon BW includes the following categories.

A

Low birth weight (LBW) - BW less than 2500 g
Very low birth weight (VLBW) - BW less than 1500 g
Extremely low birth weight (ELBW) - BW less than 1000 g

358
Q

Contraindications to vaginal breech delivery include:

A

a) Cord presentation
b) Fetal growth restriction or macrosomia
c) Any presentation other than frank or complete breech
d) Extension of the fetal head
e) Clinically inadequate maternal pelvis
f) Fetal anomaly incompatible with vaginal delivery

359
Q

At what heart rate do you start neonatal chest compressions?

A

60

360
Q

What should you not forget with Gynae-Onc management?

A

Staging, MDT, Psych, suvivorship, clincal trials

361
Q

What are the additional benefits of antenatal corticosteroids?

A

●Intraventricular hemorrhage (IVH) (RR 0.55, 95% CI 0.40-0.76; 16 trials, 6083 infants)
●Necrotizing enterocolitis (NEC) (RR 0.50, 95% CI 0.32-0.78; 10 trials , 4602 infants)
●Neonatal mortality (NNM) (RR 0.69, 95% CI 0.59-0.81; 22 trials, 7188 infants)
●Systemic infection in the first 48 hours of life (RR 0.60, 95% CI 0.41-0.88; 8 trials, 1753 infants)

362
Q

Name 8 MEC4 contraindications to COCP?

A
o Current DVT/prev DVT
o Myocardial infarction
o Migraine with Aura
o Hypertension >160/95
o Systemic lupus erythematous
o Stroke
o Immobility (3)
o Obesity =>35 (3)
o Thrombogenic mutations
o Liver disease/cirrhosis/tumour

o Postpartum within 6 weeks and breast feeding
o Postpartum <=21 days if not breast feeding
o >=35 year old and smoking >=15 cigarettes per day

363
Q

Name 4 features of PND?

A

o Affect - low mood, anhedonia
o Behaviour - loss of energy, sleep disturbance, poor appetite
o Cognition - guilt, suicidal ideation and persistent low self esteem
o Examination - assess slow motor retardation, low affect

364
Q

What are the perinatal risks of SSRIs?

A

No treatment
Teratogenicity
Miscarriage
Reduction in birth weight and preterm birth
Poor neonatal adaptation or neonatal behavioral syndromes
Neurobehavioral effects
Maternal relapse (if medication is ineffective, or if dosing is suboptimal)

365
Q

So there’s this heaps weird question in 2011 that asked about the ‘organising principles in PPH’ - this seems to be what they wanteD?

A
  • Effective team management to assess, investigate and treat simultaneously
  • Recognition of PPH
  • Communication
  • Resuscitation
  • Monitoring and Investigation
  • Directed Treatment
  • Document/debrief and incident report
366
Q

What the risk factors included in risk-based screening for GBS?

A
o If previous baby affected by GBS
o GBS bacteruria
o Prolonged rupture of membranes >18hrs
o Prematurity<37/40
o Intrapartum pyrexia >38
o Evidence of chorioamnionitis
o Evidence of GBS on LVS in the current pregnancy
367
Q

What are the measures for a pregnancy after molar pregnancy?

A
  • Early ultrasound when pregnant
  • Placental for histopathology
  • Check Hcg 6 weeks postpartum
368
Q

Can you apply the findings of this study to a healthy 51 year old non-smoker female who is experiencing postmenopausal symptoms and why? (2 marks)

A

• No these results can not be directly applied to such a patient.
o Median age of trial participants - 63
o Most had HRT much later after menopause and were largely asymptomatic did not address quality of life or menopausal symptoms
o Had other medical comorbidities thus more predisposed to CHD
Hypertension, heart disease etc, BMI > 30 in 34%
50% were current or past smokers
o 42% of treatment group and 38% of placebo group stopped using their medication during study thus HRT effects may be underestimated
o Trial was stopped early and thus less chance of detecting change and only one therapy was tested

369
Q

What is the hormone test for CAH

A

17-hydroxyprogesterone?

370
Q

What are the 5 benign IOTA signs?

A
Unilocular cyst
Smooth unilocular tumour <10cm
Solid component <7 mm in diameter
Presence of acoustic shadows
No detectable Doppler signal
371
Q

What are the 5 malignant IOTA signs?

A
Irregular solid tumour
Irregular multilocular mass >10 cm in diameter
≥4 papillary structures
ascites
High Doppler signal
372
Q

What is the course of the pudendal nerve?

A

The pudendal nerve comes down from sacral nerve roots 2,3, and 4, runs underneath the piriformis muscle, goes between the (SS)sacrospinous and (ST)sacrotuberous ligaments at the ischial spine, travels through alcock’s canal between the obturator internus and levator ani muscles, and divides into 3 branches.

373
Q

Align ovarian tumour markers with their corresponding cancer type:

A

●hCG - Embryonal cell carcinomas and ovarian choriocarcinomas, mixed germ cell tumors, and some dysgerminomas.
●AFP - Yolk sac tumors, embryonal cell carcinomas and polyembryoma carcinomas, mixed germ cell tumors, and some immature teratomas [8,9]; most dysgerminomas are associated with a normal AFP.
●Lactate dehydrogenase (LDH) - Dysgerminomas.

374
Q

What are the four categories of MEC for contraception?

A

..

375
Q

Describe the difference in menstrual changes between hyper and hypo thyroidism

A

..

376
Q

Name 10 risk factors for PPH

A
Previous PPH
Long labour
Prolonged second stage
Assisted vaginal birth
Big baby
Elevated BMI
Low starting Hb
Grandmultiparity
Multiple pregnancy
Induced or augmented labour
Rapid labour
377
Q

Describe the physical examination for chronic pelvic pain, systematically?

A

..

378
Q

What are the 5 elements of the Biophysical profile?

A

..

379
Q

What is Hasse’s Rule?

A

..

380
Q

Under the new cervical cancer screening guidelines, when do women enter and exit the program?

A

..

381
Q

Benefits of VBAC?

A
Shorter recovery, less pain
Shorter hospital stay
Earlier lactation
More likely to have vaginal birth in the future
Less adhesions
382
Q

Benefit vs risk of tvt and tot

A

..

383
Q

Management of epileptic seizures in labour?

A

..

384
Q

What are 3 complementary methods for management of hyperemesis that are proven by Cochrane?

A

Ginger

Acupressure

385
Q

Describe two theories of pathophysiology of hyperemsis

A

..

386
Q

How does PCOS cause anovulation?

A

..

387
Q

What are is the Rotterdam criteria for PCOS?

A

Hyperandorgenism (clincally or biochemically)
Anovulatory cycles
Polycystic appearance on USS

388
Q

Describe the pattern of Progesterone during the menstrual cycle

A

..

389
Q

Describe the pattern of Oestrogen during the menstrual cycle

A

..

390
Q

Describe the pattern of LH during the menstrual cycle

A

..

391
Q

Describe the pattern of FSH during the menstrual cycle

A

..

392
Q

What is the role of theca cells?

A

..

393
Q

What is the role of granulosa cells?

A

..