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
Define 'direct' maternal deaths.
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
26
Define 'indirect' maternal deaths.
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
27
Define late maternal death.
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.
28
Between 2012 and 2014, were direct or indirect causes of maternal death more common?
Direct (51% vs 46%)
29
How does age affect maternal mortality?
More dangerous at extremes of age.
30
How does parity affect maternal mortality?
3 or more is bad.
31
in 2012-2014, name the top 4 causes of maternal death.
1. Non-obstetric haemmorhage 2. Cardiovascular 3. VTE 4. Obstetric haemmorhage
32
Define the three levels of preterm birth.
- Extremely preterm (less than 28 weeks) - Very preterm (28 to 32 weeks) - Moderate to late preterm (32 to 37 weeks).
33
Define neonatal mortality.
A neonatal death is defined as a death during the first 28 days of life (0-27 days).
34
Define perinatal mortality.
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.
35
Define infant mortality.
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.
36
Define low birthweight.
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
37
Define standard deviation.
a quantity expressing by how much the members of a group differ from the mean value for the group.
38
Define standard error.
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.
39
Define confidence interval.
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%.
40
How is sample size calculated?
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.
41
Define prevalence.
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).
42
Define incidence.
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.
43
Define cumulative incidence.
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.
44
Define relative risk.
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.
45
Define odds ratio.
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.
46
Define attributable risk.
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.
47
Define number needed to treat.
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.
48
Define an RCT.
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.
49
Define a cohort study.
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.
50
Define a case-control study.
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.
51
Define a cross-sectional study.
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.
52
What is Level 1 evidence?
Level I | Evidence obtained from a systematic review of all relevant randomised controlled trials.
53
What is Level 2 evidence?
Level II | Evidence obtained from at least one properly designed randomised controlled trial.
54
What is Level 3 evidence?
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.
55
What is Level 4 evidence?
Level IV | Evidence obtained from case series, either post-test or pre-test and post-test.
56
Define selection bias.
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.
57
Define measurement bias.
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.
58
Define confounding.
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.
59
Define heard immunity.
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.
60
Following post-hysterectomy prolapse, what three outcomes is ASC better than SSF?
1. Dyspareunia 2. Post-op SUI 3. Recurrent vault prolapse
61
What are the 5 reasons for surgical management in endometrial hyperplasia without atypia?
(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.
62
How should endometrial hyperplasia be managed in women wishing to conceive?
Disease regression should be achieved on at least one endometrial sample before women attempt to conceive.
63
What are risk factors for ectopic pregnancy?
Risk factors for ectopic pregnancy include tubal damage following surgery or infection, smoking and in vitrofertilisation
64
What is the intradecidual sign?
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'
65
What is the double decidual sign?
The double decidual sign is described as anintrauterine fluid collection surrounded by 'two concentric echogenic rings'
66
What ultrasound findings are characteristic of cervical ectopic?
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.
67
What are the criteria for a Caesarean Scar ectopic?
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.
68
What are the ultrasound features of an interstitial pregnancy?
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.
69
What is the dose of Methotrexate for ectopic pregnancy?
50mg/m2
70
Name four predictors of success with Methotrexate treatment for ectopic pregnancy?
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
71
What should women avoid during treatment for ectopic pregnancy?
During treatment with methotrexate women should be advised to avoid alcohol and folate-co ntaining vitamins.
72
Name 6 characteristics that would make a woman a good candidate for Methotrexate treatment"
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.
73
What are the four elements that NICE recommend as first line Methotrexate treatment for ectopic
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).
74
What are the selection criteria for expectant management of ectopic pregnancy?
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.
75
What is the treatment of cervical ectopic?
Interestingly, surgical is not first line given risk of bleeding.
76
How long after methotrexate should women wait before getting pregnant?
3 months
77
Describe the time course of Parvovirus infection?
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.
78
What is the vertical transmission rate of Parvovirus infection?
The risk of vertical transmission is 50 per cent. Infection between eight and 20 weeks poses the greatest risk to the fetus.
79
What is the model of ultrasound monitoring of Parvovirus?
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.
80
At what MSV do you worry about fetal anemia?
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).
81
What is the pathophysiology of fetal anaemia with Parvovirus?
Parvovirus is cytotoxic to fetal haemoglobin precursors.
82
When is the cFTS carried out?
This is carried out between 11+0 and 13+6
83
When is CVS done?
This can be carried out between 11 and 14 weeks of gestation by chorionic villous sampling (CVS) of placental tissue.
84
What is the false positive rate of the cFTS?
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%.
85
What is normal vaginal pH?
They maintain the normal vaginal pH between 3.8 and 4.4.
86
What is the treatment for bacterial vaginosis?
Metronidazole
87
Name four non-infective causes of vaginal discharge?
Physiological Cervical ectopy Foreign bodies, such as retained tampon Vulval dermatitis
88
NAme two non-sexually transmitted infections that can cause vaginal discharge.
Bacterial vaginosis | Candida infection
89
What are the vaginal pHs of Candida and BV?
Bacterial vaginosis (pH ≥4.5) and vulvovaginal candidiasis (pH <4.5)
90
What are the antibiotics for chlamydia
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)
91
What are the antibiotics for gonorrhea
Cefixime 400 mg as a single oral dose or ceftriaxone 250 mg intramuscularly as a single dose
92
What is the treatment for trichomonas?
Metronidazole 2 g orally in a single dose or metronidazole 400-500 mg twice daily for five to seven days
93
What is the Amsel criteria for BV?
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
94
For what group is HRT recommended?
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).
95
What are the risks of HRT?
* 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
96
What effect does HRT have on VTE?
Combined oral estrogen plus progestin has been shown to increase the relative risk of VTE twofold.
97
What effect does HRT have on breast cancer?
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%.
98
What is the difference between cyclical and continuous HRT?
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).
99
What is the follow-up plan for someone on HRT?
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.
100
Which HRT risks are related to length of treatment?
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.
101
What is an alternative to HRT?
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.
102
What is the average age of menopause?
The menopause transition commonly starts around 47 years and the average age of natural menopause is 51 years.
103
What are the first line measures for perimenopausal symptoms?
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
104
What can you do to protect bone in women who have contraindications to HRT?
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.
105
What organisms are usually isolated from a TOA?
Common organisms include Escherichia coli, aerobic streptococci, Bacteroides fragilis, Prevotella, and other anaerobes, such as Peptostreptococcus. Not Chlamydia/Gonorrhoea!
106
What are the organisms identified from BV?
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.
107
When do you start MCVs for a non-Kell Ab?
24 weeks
108
When do you start MCVs for Kell ABs?
18 weeks
109
What are the critical levels for antibody titires?
>8 for Kell, >16 for non-Kell
110
What is the prevalence of red cell antibodies/
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%
111
When can you clear a woman with epilepsy?
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
112
What are the congenital abnormalities caused by AEDs?
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.
113
What is the risk of a woman with epilepsy relapsing during pregnancy?
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.
114
What do you need to ask an epileptic woman antenatally?
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
115
What do you give to babies of epileptic mums?
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.
116
Postnatal care of an epileptic mum?
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
117
How does APS cause procoagulation?
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.
118
pre-pregnancy planning forAPS?
https://obgyn.onlinelibrary.wiley.com/doi/pdf/10.1576/toag.13.1.15.27636
119
what is the prevalence of mesh erosion?
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.
120
What are contraindications to VBAC? Risk factors?
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.
121
What happens with synto on a VBAC?
2-3x risk of UR | 1.5x risk of CS
122
What other autoimmune conditions are associated with lichen sclerosis?
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%
123
Why do you check Ferritin in vulval conditions?
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.
124
What is second line medication for lichen sclerosis?
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.
125
What are the side effects of Imiquimod?
Adverse effects include pain, erythema and swelling and can result in non-compliance
126
Which HPV is vin associated with?
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)
127
Describe the use of clobetasol for lichen?
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
128
What is the next step for a woman positive for HPB 16/18?
Colposcopy
129
What has the entry age for cervical screening increased?
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.
130
What should you do with a woman who has non 16/18 oncogenic type and low grade?
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.
131
Referral of women with a positive oncogenic HPV (not 16/18) test result and LBC prediction of pHSIL, HSIL or any glandular abnormality
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.
132
Management after repeat HPV test at 12 months, following initial positive oncogenic HPV (not 16/18) test result
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
133
What do you do with a 'Women with a positive oncogenic HPV (not 16/18) test result (self-collected sample)'
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.
134
What do you do with a 'Women aged 75 years or older who request screening'
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.
135
Repeat LBC usually not necessary at time of colposcopy, unless:
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.
136
What happens when: For women who have had a colposcopy with significant discordance between the histopathology and the referral cytology?
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
137
When should you send for tertiary referral
Adenocarcinoma in situ Abnormalities in pregnancy Immune-deficient women Women with multifocal lower genital tract disease.
138
For cervical disease, Ablative therapy should be reserved for :
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.
139
Do not treat at first visit with a LBC report of a low-grade lesion. Is this true?
Women who have a LBC prediction of pLSIL/LSIL should not be treated at the first visit.
140
Repeat excision not necessarily required for incomplete excision of high-grade lesions. Is this true? Why?
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.
141
Describe the pathway of: Normal colposcopy following LBC prediction of negative or pLSIL/LSIL?
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.
142
Normal colposcopy following LBC prediction of HSIL: diagnostic excision of TZ
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.
143
What should you do in the case of: Type 3 TZ colposcopy and referral LBC negative or pLSIL/LSIL
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.
144
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?
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.
145
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
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
146
Is there an option for observation following cytological prediction of pHSIL?
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
147
HSIL (CIN2) and observation
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).
148
How do you Test of Cure after treatment for HSIL (CIN2/3)?
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
149
What is the cervical screening for ladies who had Total hysterectomy for benign disease
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.
150
What is the cervical screening for ladies who had Total hysterectomy after adenocarcinoma in situ (AIS)?
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.
151
The implantation of any foreign body generates a host response that is characterised by seven stages:
Injury, protein absorption, acute inflammation, chronic inflammation, foreign body reaction, granulation tissue formation and tissue encapsulation.
152
How many cells in the morula?
32
153
How many days after fertilisation is implantation?
5-8 days
154
What three hormones affect fetal growht?
Glucocorticords, insulin, thyroid
155
What are the two most important fetal growth factors?
IGF-I, IGF-III
156
What are the radiological definitions of oligo and poly?
Poly - AFI 25 or above, or DVP >8. | Oligo - AFI <5, DVP <2
157
When CVS done?
9-12 weeks
158
When Amnio done?
16-18 weeks
159
What are the attachments of the sacrospinous ligament?
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
Where are the greater and lesser foramen of the pelvis
The greater and lesser sciatic foramina are above and below the sacrospinous ligament.
161
Which two muscles is the levator ani made up of?
The levator ani is composed of 2 major muscles from medial to lateral: the pubococcygeus and iliococcygeus muscles.
162
What is the arcus tendineus
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
What is the levator plate?
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
Which nerve supplies the levator ani?
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
What muscles make up the urogenital diaphragm?
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
What is the perineal body?
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
What are the anterior pelvic supports?
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
What are the middle pelvic floor supports?
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
What are the attachments of the uterosacral ligaments?
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
Explain urethral control
Urethral support is provided by a coordinated action of fascia and muscles acting as an integrated unit under neural control
171
What is level 1 pelvic floor support?
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
What is level 2 pelvic floor support?
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
What is level 3 pelvic floor support?
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
Describe the directions that the anterior abdominal walls run?
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
What are the insertions and plane of the external oblique?
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
Describe the anatomy of the rectus sheath?
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
What is the arcuate line?
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
Describe the blood supply of the anterior abdominal wall?
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
What is the nerve supply of the anterior abdominal wall?
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
Describe breast changes in the first half of pregnancy?
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
What is the linea nigra produced by?
MSH from the placenta
182
Where does relaxin come from in pregnancy
Placenta
183
Name three hormones produced by the placenta, and their function:
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
Describe the change in thyroid over the course of pregnancy?
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
What is the change in systematic vascular resistance with pregnancy and why?
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
What happens to renal function in pregnancy and why?
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
What happens to cortisol during pregnancy?
Total cortisol increases to three times of non-pregnant levels by the third trimester.
188
Where is oestrogen produced during menopause?
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
What is the pathophysiology of hot flashes?
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
What is the effect of menopause on the CNS?
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
What is the definition of premature ovarian insufficiency?
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
How does chemotherapy cause premature ovarian failure?
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
Name 5 features of Down Syndrome
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
Name 3 soft markers of aneuploidy on US
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1681991/
195
How common is Trisomy 18?
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
What are the phenotypic features of Trisomy 18?
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
What is the rate of survival with Trisomy 18?
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
What are the features of Trisomy 13?
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
What is the prognosis of Trisomy 13?
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
What is Turner Syndrome caused by?
It is caused by loss of part or all of an X chromosome.
201
How common is Turner Syndrome?
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
What are the typical features of Turner Syndrome?
``` 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
What is the interaction between Turner Syndrome and pregnancy?
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
Are people with Turner Syndrome intellectually impaired?
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
What is the hormonal treatment of Turner Syndrome?
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
Which conditions are examined in newborn screening?
https://www.schn.health.nsw.gov.au/find-a-service/laboratory-services/nsw-newborn-screening/disorders
207
What is Li-Fraumeni syndrome?
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
What is Lynch syndrome?
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
What is a Category A drug?
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
What is a Category B1 drug?
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
What is a Category B2 drug?
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
What is a Category B3 drug?
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
What is a Category C drug?
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
What is a Category D drug?
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
What is a Category X drug?
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
What are some drugs contraindicated with breastfeeding?
Drugs contraindicated during breastfeeding include anticancer drugs, lithium, oral retinoids, amiodarone and gold salts.
217
What are the three types of drug transfer across the placenta?
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
There are four main mechanisms of drug transfer across the placenta. What are they?
1. Simple diffusion 2. Facilitated diffusion 3. Pinocytosis 4. Active transport
219
How does Progesterone cause contraception?
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
How does oestrogen cause contraception?
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
What is the mechanism of Clomiphene?
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
What class of drug is Clomiphene?
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
What is the mechanism of Mifepristone?
Mifepristone is an antiprogestogen and works by blocking the effects of progesterone and causing contractions of the uterus.
224
If the MSD and CRL don't meet criteria to diagnose miscarriage, when do you need to repeat the scan?
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
What are the ultrasound features of a corpus luteum?
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
What three features should be seen when measuring abdominal circumference?
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
Describe the role of the three different doppler ultrasound measures?
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
Describe uterine histopath during the menstrual cycle?
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
In the evaluation of chronic pelvic pain, what is the APQRST mnemonic?
associated, provocative/palliative, quality, radiation, setting, temporal aspects
230
How common is a history of abuse in the chronic pelvic pain population?
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
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?
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
Hwo good is MRI for evaluating DIE?
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
When do you go to diagnostic laparoscopy for investigation of endometriosis in a pelvic pain patient?
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
What is the treatment of choice for PID chronic pelvic pain?
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
What is the treatment of choice for adhesion-related pelvic pain?
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
How many women who undergo hysterectomy for adenomyosis related pelvic pain, still have pain, mate?
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
What are the four 'variant' PMDs?
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
What is the definition of pre-menstrual disorder?
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
What is the prevalence of PMS?
Four in ten women (40%) experience symptoms of PMS and of these 5 - 8% suffer from severe PMS.
240
What are the theories of PMS aetiologuy?
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
How do GNRH analogues diagnose PMS?
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
What are the simple options to treat PMS?
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
Name 4 people in the MDT for PMS
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
Does evening primrose oil work for PMS?
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
Name 5 effective complementary methods of treating PMS:
Exercise, Gingko, EPO, Reflexology, Vitamin D and calcium, Vitex agnus castus, Saffron, acupuncture,
246
Is CBT OK for PMS?
When treating women with severe PMS, CBT should be considered routinely as a treatment option.
247
Which COCPs are best for the treatment of PMS?
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
How do you monitor BMD in women taking GNRH analogues?
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
Can you use progesterone for management of PMS?
There is good evidence to suggest that treating PMS with progesterone or progestogens is not appropriate.
250
Which diuretic can be used to treat PMS?
Spironolactone can be used in women with PMS to treat physical symptoms.
251
What is the maximum amount of fluid that should be given, whilst awaiting blood transfusion in PPH?
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
When should you use FFP in PPH?
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
What do we use for fibrinogen replacement?
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
When do we give platelets?
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
What investigations should be undertaken for a secondary PPH?
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
What does RCOG consider a low Papp-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
Describe the role of uterine artery doppler as per the RCOG SGA guideline? When should you not repeat?
https://www.rcog.org.uk/globalassets/documents/guidelines/gtg_31.pdf - page 9
258
Why don't you do uterine artery dopplers on a lady with a major SGA risk factor?
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
What further tests should you do for an SGA?
Karyotyping? CMV, toxo
260
Should you do uterine dopplers in the third trimester?
No
261
When should you start Aspirin for prevention of SGA?
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
Up to how many weeks should an SGA receive steroids?
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
At what gestation should you give Mag Sulphate?
Australian guidelines recommend the administration of magnesium sulphate when delivery is before 30 weeks of gestation
264
What is the definition of primary versus secondary amenorrhea?
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
What is the definition of oligomenorrhea?
Oligomenorrhea (fewer than nine menstrual cycles per year or cycle length greater than 35 days)
266
Describe the structure for evaluating secondary amenorrhea. Which is the most common cause?
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
What is the most common cause of secondary amenorrhea?
Pregnancy
268
How does systemic illness or starvation cause secondary amenorrhea?
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
What are the characteristic hormonal changes in functional hypothalamic amenorrhea?
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
How does hyperprolactinemia cause amenorrhea?
Prolactin appears to cause amenorrhea by suppressing hypothalamic GnRH secretion, leading to low gonadotropin and estradiol concentrations
271
What is step 1 of evaluation of secondary amenorrhea?
Pregnancy test
272
What is the progestin withdrawal test?
Medroxyprogesterone 10 mg for 10 days
273
What are the first three blood tests for secondary amenorrhea?
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
When investigating for secondary amenorrhea, what does a high FSH mean?
A high serum follicle-stimulating hormone (FSH) concentration indicates POI, formerly referred to as premature ovarian failure.
275
Why is there a high Prolactin in hypothyroidism?
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
How do you manage Asherman's Syndrome?
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
What are the goals of management of PCOS?
●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
What is the first choice for COCP in PCOS?
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
Name 4 ways incontinence impacts quality of life
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
What is the prevalence of urinary incontinence in non-pregnant women?
Overall prevalence of urinary incontinence among non-pregnant women age 20 years and above has been reported at 10 to 17 percent.
281
What is the pathophysiology of thalassemia?
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
What are the steps to pre-conception counselling in a woman with thalassemia?
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
What are the risks of maternal anaemia and fetal growth restriction?
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
Why do you give Aspirin or Clexane in thalassemia?
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
What are risk factors for cord prolapse?
Inherent - anything that means there's lots of intrauterine space. Us - any intervention that is a bit rogue
286
What is the rate of cancer transformation in lichen planus?
Development of squamous cell carcinoma. In one study the incidence was as high as 3%.
287
What are the two types of VIN?
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
What is the PALM-COIN acronym stand for in AUB?
PALM: polyp, adenomyosis, leiomyoma, and malignancy and hyperplasia), four that are unrelated to structural anomalies (COEI: coagulopathy, ovulatory dysfunction, endometrial, iatrogenic
289
How can non-gynaecological medications cause AUB?
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
How old and premenopausal should you be to get a pipelle for AUB?
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
Name six risk factors for endometrial cancer?
https://www.uptodate.com.acs.hcn.com.au/contents/image?imageKey=OBGYN%2F62089&topicKey=OBGYN%2F3263&source=see_link
292
Yo, how good is this graph?
https://www.uptodate.com.acs.hcn.com.au/contents/image?imageKey=OBGYN%2F90595&topicKey=OBGYN%2F3263&source=see_link
293
What is the ET cut-off for symptomatic, postmenopausal bleeding?
Endometrial cancer can reasonably be excluded by ultrasound in postmenopausal women with a thin (≤4 mm), homogeneous endometrium.
294
What is the incidence of vasa praevia?
1 in 2500
295
What are the four diagnostic criteria on US of vasa praevia?
- 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
What is the gold standard of managment for Vasa praevia?
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
What are the greyscale US criteria for placenta accreta? (5)
● 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
What are the colour doppler US criteria for placenta accreta? (4)
● 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
What are the 3D doppler US criteria for placenta accreta? (4)
● 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
What are the MRI criteria for placenta accreta? (4)
● uterine bulging ● heterogeneous signal intensity within the placenta ● dark intraplacental bands on T2-weighted imaging
301
What are the RCOG cut-offs for GDM?
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
What is the global rate of IUCD use?
~15% - mostly Asia ??
303
What is the prevalence of contraception use in Australia?
~80%
304
What is the type of hormone in a Mirena? What is the dose
levonorgestrel, 25mcg/day, 52mg total
305
What is the hormone and dose in an Implanon?
68 mg of the active substance etonogestrel
306
Describe three risks associated with IUCDs?
1. Ectopic pregnancy 2. Pelvic infection 3. Change in bleeding patterns
307
Name some risks of the Implanon?
Ectopics, ovarian cysts,breast cancer and VTE
308
What is the complication of SLE in pregnancy you always forget?
VTE, and congenital cardiac conditions, Congenital heart block with Anti-Ro antibodies,
309
When should SLE mums NOT get pregnant?
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
What is the criteria for perinatal mortality?
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
What are the core tests for FDIU?
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
How do the features on a CTG relate to fetal physiology?
Baseline Heart Rate - Cardiac & CNS Function Baseline Variability - Autonomic Nervous System (CNS) Decelerations - Mechanical or hypoxic insult Accelerations - Somatic Nervous System
313
When should women with haemoglobinopathies be given Fe?
Women with known haemoglobinopathy should have serum ferritin checked and offered oral supplements if their ferritin level is <30 μg/l
314
When do you commence Metformin in GDM?
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
At what BSL should it be considered?
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
What are the BSL targets during GDM monitoring?
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
Does Metformin help fertility in PCOS?
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
Name the 4 most common causes of PMB?
In the early menopausal years, endometrial hyperplasia, polyps, and submucosal fibroids are also common etiologies
319
What is the ET cut-off for PMB?
Endometrial cancer can reasonably be excluded by ultrasound in postmenopausal women with a thin (≤4 mm), homogeneous endometrium.
320
What is the most common symptom of premenopausal bleeding with polyps?
Intermenstrual bleeding is the most frequent symptom in premenopausal women with endometrial polyps
321
What do you always forget to do with consent, baby?
DOCUMENTATION
322
Where is the ureter most commonly injured/
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
What are the 4 P's of Lichen PLanus?
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
What are the histological findings of Lichen Planus?
●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
What is Level 1 support structures?
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
What is Level 2 support structures?
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
Describe the nerve supply of the pelvic floor
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
What is point Aa on POPQ?
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
What is point Ba on POPQ
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
What is point C on POPQ?
Point C is the most distal (ie, most dependent) edge of the cervix or the leading edge of the vaginal cuff (posthysterectomy).
331
What is point D on POPQ?
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
What is point Ap on POPQ?
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
What is point Bp on POPQ?
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
Describe the different staging of POPQ
●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
What are the five key features on colposcopy?
1. Surface contour 2. Vascular pattern 3. Acetic acid changes 4. Topography 5. Iodine uptake
336
What are the embryological events going on with twin pregnancy timing?
https://en.wikipedia.org/wiki/Monoamniotic_twins
337
What is the dose of Doxylamine for HE
12.5 / 12.5 / 25
338
What is the dose of Pyridoxine for HE
25mg TDS PO
339
What are the two pain pathways in labour?
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
What are the six moderate risk factors for PET?
``` 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
Name 8 major risk factors for SGA
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
What do you find on US with adenomyosis?
Tender, enlarged uterus Hetero myometr - venetian blinds myometrial cyst asymmtety of uterine walls
343
What do you find on MRI with adenomyosis?
- Junctional zone thickened asymmetry of the walls | myometial cysts
344
What is the CAUSTIC acronym?
``` chromosomal anaemia unexplained structural twins infection cardiac ```
345
What are 5 prognostic factors for ECV?
* 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
Define gestational diabetes mellitus
• Glucose intolerance of variable severity with onset or first recognition during pregnancy (ADIPS)
347
What are the four primary outcomes of HAPO?
* Birth weight > 90th% * Primary caesarean section delivery * Neonatal hypoglycaemia * Cord C-peptide > 90th % (as index of fetal beta cell function; fetal hyperinsulinaemia)
348
What are the categories of PTB? What are their prevalence?
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
List six factors that predispose to genuine stress urinary incontinence.
* 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
Name the three poor obstetric outcomes as part of the APLS definition?
● 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
What tests do you order for inherited thrombophilias?
Women with second-trimester miscarriage should be screened for inherited thrombophilias including factor V Leiden, factor II (prothrombin) gene mutation and protein S.
352
What are the guidelines for DVT prohylaxis after emergency CS?
Following emergency CS thromboprophylaxis with LMWH or UFH is recommended, for at least 5 days or longer until recovery of full mobility
353
Name six ANZJOG major risk factors for VTE?
1. ELCS 2. Immobility 3. PET 4. BMI 30 5. Infection 6. Medical comorbidity
354
Name six ANZJOG minor risk factors for VTE?
1. Age 35 2. >24hr labour 3. Smoker 4. PPH >1000mL 5. Perineal trauma 6. Gross varicose veins
355
Compare vacuum with forceps:
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
The four major factors leading to preterm labor are...
intrauterine infection, decidual hemorrhage, excessive uterine stretch, and maternal or fetal stress
357
One classification based upon BW includes the following categories.
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
Contraindications to vaginal breech delivery include:
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
At what heart rate do you start neonatal chest compressions?
60
360
What should you not forget with Gynae-Onc management?
Staging, MDT, Psych, suvivorship, clincal trials
361
What are the additional benefits of antenatal corticosteroids?
●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
Name 8 MEC4 contraindications to COCP?
``` 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
Name 4 features of PND?
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
What are the perinatal risks of SSRIs?
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
So there's this heaps weird question in 2011 that asked about the 'organising principles in PPH' - this seems to be what they wanteD?
* 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
What the risk factors included in risk-based screening for GBS?
``` 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
What are the measures for a pregnancy after molar pregnancy?
- Early ultrasound when pregnant - Placental for histopathology - Check Hcg 6 weeks postpartum
368
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)
• 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
What is the hormone test for CAH
17-hydroxyprogesterone?
370
What are the 5 benign IOTA signs?
``` Unilocular cyst Smooth unilocular tumour <10cm Solid component <7 mm in diameter Presence of acoustic shadows No detectable Doppler signal ```
371
What are the 5 malignant IOTA signs?
``` Irregular solid tumour Irregular multilocular mass >10 cm in diameter ≥4 papillary structures ascites High Doppler signal ```
372
What is the course of the pudendal nerve?
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
Align ovarian tumour markers with their corresponding cancer type:
●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
What are the four categories of MEC for contraception?
..
375
Describe the difference in menstrual changes between hyper and hypo thyroidism
..
376
Name 10 risk factors for PPH
``` 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
Describe the physical examination for chronic pelvic pain, systematically?
..
378
What are the 5 elements of the Biophysical profile?
..
379
What is Hasse's Rule?
..
380
Under the new cervical cancer screening guidelines, when do women enter and exit the program?
..
381
Benefits of VBAC?
``` Shorter recovery, less pain Shorter hospital stay Earlier lactation More likely to have vaginal birth in the future Less adhesions ```
382
Benefit vs risk of tvt and tot
..
383
Management of epileptic seizures in labour?
..
384
What are 3 complementary methods for management of hyperemesis that are proven by Cochrane?
Ginger | Acupressure
385
Describe two theories of pathophysiology of hyperemsis
..
386
How does PCOS cause anovulation?
..
387
What are is the Rotterdam criteria for PCOS?
Hyperandorgenism (clincally or biochemically) Anovulatory cycles Polycystic appearance on USS
388
Describe the pattern of Progesterone during the menstrual cycle
..
389
Describe the pattern of Oestrogen during the menstrual cycle
..
390
Describe the pattern of LH during the menstrual cycle
..
391
Describe the pattern of FSH during the menstrual cycle
..
392
What is the role of theca cells?
..
393
What is the role of granulosa cells?
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