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Specialty Blocks > 6. Obs and Gyn > Flashcards

6. Obs and Gyn Flashcards

1
Q

What is the most common, and second most common, type of cervical cancer, accounting for 70-80% and 10% of cases respectively?

A

Squamous cell carcinoma

Adenocarcinoma

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2
Q

In women infected with HPV, what factors increase the risk of it progressing to cervical cancer? (5)

A

FHx in first degree relative

Oral contraceptive pill use for >5yrs

Smoking

Co-infection with other STIs

High parity and young age at first birth

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3
Q

When is the HPV vaccination given in the uk?

A

All children 12/13 years old (year 8)

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4
Q

Describe the HPV screening in the UK.

A

Women age 25-49 are invited for smear test every 3 years.

Women aged 50-64 are invited every 5 years.

Scotland = 25-64 every 5 years

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5
Q

When is the best time to perform cervical screening?

A

Mid cycle, day 10-20

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6
Q

Risk factors for ovarian cancer:

A

BRCA1 or BRCA2 mutations
Nulliparity
Late menopause
Early menarche
(All causes of many ovulations)

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7
Q

Which tumour marker is first investigated when ovarian cancer is suspected?

A

CA125

Should not be used in asymptomatic women

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8
Q

Give 4 conditions that could result in a raised CA125.

A

Ovarian cancer
Endometriosis
Menstruation
Benign ovarian cysts

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9
Q

What is the definition of pre-eclampsia?

A

Hypertension developing after 20 weeks gestation with one or more of proteinuria, maternal organ dysfunction or FGR.

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10
Q

State the 5 high-risk factors for pre-eclampsia.

A

Hypertension in previous pregnancy

Autoimmune condition e.g. SLE, APLS

CKD

T1DM, T2DM

Chronic hypertension

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11
Q

State 6 moderate-risk factors for pre-eclampsia.

A

First pregnancy

Age >40

Pregnancy interval of >10 years

BMI >35 at first visit

FHx of pre-eclampsia

Multiple pregnancy

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12
Q

To reduce the risk of hypertensive disorders in pregnancy (e.g. pre-eclampsia), two groups of women should take preventative medication. Which groups are these, and what medication should they take?

A

1 or more high risk factors
2 or more high risk factors

75mg-150mg aspirin daily from 12 weeks until birth

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13
Q

What is the definition of pre-eclampsia?

A

New onset hypertension >140/90 after 20 weeks gestation and 1 or more of a) proteinuria b) other organ involvement e.g. renal insufficiency, liver, neurological haematological, uteroplacental dysfunction

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14
Q

What is eclampsia?

A

The development of seizures in association with pre-eclampsia.

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15
Q

Describe the management of eclampsia.

A

Decision to deliver made.

IV bolus magnesium sulfate of 4g over 5-10 mins, followed by infusion.
Treatment should continue for 24 hours after last seizure or delivery.

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16
Q

What is tocolysis + give drug examples.

A

Tocolysis is the use of drugs to delay or stop preterm labour.

Terbutaline (beta-adrenergic receptor agonist)

Nifedipine (CCB)

Magnesium sulfate (inhibits entry of calcium into uterine smooth muscle)

Indomethacin (non-selective COX inhibitor, prostaglandin production reduced)

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17
Q

The initiation of labour is still very much a physiological mystery, but appears to be a coordinated inhibition of pro-pregnancy factors and activation of pro-labour factors. Give 4 pro-pregnancy factors and 5 pro-labour factors.

A

Pro-pregnancy;
Progesterone
Nitric oxide
Catecholamines
Relaxin

Pro-labour;
Oestrogens
Oxytocin
Prostaglandins and prostaglandin dehydrogenase
Corticotrophin releasing hormone (CRH)
Inflammatory mediators

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18
Q

Describe the pro-pregnancy effects of progesterone, including where it is derived from.

A

Derived from the corpus luteum for first 8 weeks, then the placenta.

Decreases uterine oxytocin receptor sensitivity, promoting uterine smooth muscle relaxation.

Anti-inflammatory role, decreasing cytokine production and influx of immune cells into the myometrium and cervix.

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19
Q

What is the pro-pregnancy role of catecholamines?

A

Act indirectly on the myometrial cell membrane to alter contractility.

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20
Q

Where is oxytocin produced?

A

Posterior pituitary gland

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21
Q

What is oxytocin a potent stimulator of?

A

Uterine contractility.
Unlikely to be a trigger of labour, but increases the frequency and force of contractions.

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22
Q

Describe what happens to oxytocin and oxytocin receptor levels as term approaches.

A

Receptor levels increase but circulating levels stay the same.

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23
Q

Describe the pro-labour effects of prostaglandins.

A

Promote cervical ripening and stimulate uterine contractility directly, and by upregulation of oxytocin receptors.

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24
Q

How are prostaglandins synthesised?

A

Synthesised from arachidonic acid via COX enzymes.

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25
Q

Inflammatory cells are recruited to fetal membranes, uterus and cervix at the onset of labour. Which cytokines are produced and what effects do they have on the pro-labour state?

A

IL-8, TNF-a, IL-6, IL1B

They contribute to cervical ripening and membrane rupture via increase in collagenase activity.

May also contribute to uterine activity by inhibiting progesterone and activating contractile genes (COX-2, oxytocin r)

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26
Q

The cervix is composed of a network of collagen fibres in ground substance of ECM. How do prostaglandins increase cervical ripening?

A

Inhibiting collagen syntehsis and stimulating collagenase activity to break down the collagen.

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27
Q

What score is used to assess cervical ripening?

A

Bishop Score

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28
Q

Describe the 3 stages of labour.

A

1st stage; onset of labour until full dilatation (of external os)

2nd stage; full dilatation until delivery of baby

3rd stage; delivery of baby until delivery of placenta

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29
Q

Cervical dilatation up to how many cm occurs in Stage 1 of labour?

A

4cm

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30
Q

What is PPROM?

A

Preterm pre-labour rupture of membranes

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31
Q

Complications of PPROM (fetal and maternal).

A

Fetal; prematurity, GBS neonatal infection, pulmonary hypoplasia

Maternal; chorioamnionitis

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32
Q

What should be seen on a speculum exam that confirms PROM?

A

Pool of liquor in posterior vaginal fornix

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33
Q

Delays in labour can be managed. What is offered when the 1st stage of labour is delayed?

A

Amniotomy /ARM (artificial rupture of membranes).

Reassess 2 hours later; would expect at least >1cm further dilatation.

Consider oxytocin augmentation.

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34
Q

What options are there for a delay in the 2nd stage of labour?

A

Must consider cause first; uterine activity, fetal position, maternal and fetal monitoring.

Assisted birth with instrument (forceps, ventouse)
C-section
Oxytocin considered if uterine activity suboptimal
Episiotomy if rigid perineum thought to be cause

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35
Q

Risk factors for ectopic pregnancy (6).

A

Damage to tubes e.g. PID, surgery
Previous ectopic pregnancy
Smoking
Maternal age over 35
IUD
IVF

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36
Q

Give a typical triad of clinical features of a stable woman presenting with an ectopic pregnancy.

A

Lower abdominal pain
Vaginal bleeding
Amenorrhoea 6-8 weeks / positive pregnancy test

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37
Q

Give 3 potential examination findings in an ectopic pregnancy.

A

Abdominal tenderness / distension
Cervical motion tenderness / cervical excitation
Adnexal mass (NICE recommends not palpating for due to risk of rupture)

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38
Q

What is a molar pregnancy?

A

Slow-growing cystic tumour which develops from trophoblastic cells after fertilisation.

Has abnormal chromosomes; either 2Y from male implants into an ‘empty’ egg, or 3 chr. Abnormal from the start and cannot progress into a normal pregnancy.

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39
Q

Give some differentials of an ectopic pregnancy.

A

Miscarriage
UTI
PID
Ruptured ovarian corpus luteal cyst
Pregnancy-related degeneration of a fibroid

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40
Q

What is the gold standard investigation for diagnosis of an ectopic pregnancy?

A

Transvaginal US

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41
Q

Methotrexate is offered to certain patients experiencing an ectopic pregnancy. Describe it’s MOA with regards to treatment of the ectopic.

A

It is an antifolate which inhibits the division of cells.
Inhibiting the division of cells causes the ectopic pregnancy tissue to regress.

42
Q

Who is surgical intervention of an ectopic pregnancy offered to?

A

Unable to return for a follow up after MTX treatment.

Significant pain
Adnexal mass >/= 35mm
Serum hCG 5000 IU/L or greater
Visible fetal heartbeat on US scan

43
Q

When is conservative management appropriate in an ectopic pregnancy?

A

Minimal symptoms / aSx
Size <35mm
Haemodynamic stability
Serum b-hCG levels are falling spontaneously / <1000 IU/L
No fetal heartbeat

44
Q

Which clinical features would a woman with an ectopic pregnancy typically have as a candidate for methotrexate therapy?

A

Little / no pain
Size <35mm
Haemodynamically stable
Can return for follow up appt
Serum hCG levels less than 1500 IU/L#
No fetal heartbeat

45
Q

Where do most ectopic pregnancies occur?

A

Fallopian tubes (~95%), most in ampulla

46
Q

Which two surgical options are available for surgical management of an ectopic pregnancy?

A

Salpingectomy; first line in women who have no other risk factors for infertility.

Salpingotomy; considered for women who have risk factors for infertility e.g. contralateral tube damage to try and preserve fertility.

47
Q

What does placenta praevia describe, and give 3 associated factors.

A

Placenta that is lying wholly or partly in the lower uterine segment.

Multiparity

Multiple pregnancy

Previous c-section; embryos are more likely to implant on a lower segment scar from previous c-section

48
Q

Outline the classical grading of placenta praevia.

A

I; placenta reaches lower segment but not the internal os
II; placenta reaches internal os but does not cover it
III; placenta covers internal os before dilation but not when dilated
IV; complete coverage of internal os

49
Q

What does RCOG recommend for placenta praevia diagnosis and why?

A

TVU (transvaginal US) as it improves accuracy of placental localisation and is considered safe, as opposed to digital vaginal examination which may provoke severe haemorrhage.

50
Q

What does placenta accreta describe, + 2 risk factors?

A

Abnormal invasion of placental trophoblasts into the uterine myometrium resulting in attachment of the placenta to the myometrium, due to a defective decidua basalis. Makes delivery of the placenta at time of birth very difficult.

Previous c-section; likely due to the loss of decidua in the c-section scar
?Placenta praevia

51
Q

What are the 3 types of placenta accreta?

A

Placenta accreta; chorionic villi attach to myometrium, rather than being confined within the decidua basalis
Placenta increta; chorionic villi invade into the myometrium
Placenta percreta; chorionic villi invade through the perimetrium

52
Q

Pre-eclampsia is pregnancy-induced hypertension + …

A

Proteinuria and / or oedema

53
Q

The mechanism of pregnancy-induced hypertension is poorly understood still but it is thought to be maybe due to poor placental perfusion due to abnormal placentation. Describe normal placentation.

A

Trophoblasts invade the myometrium and the spiral arteries in the uterus which destroys the tunica muscularis media.
The spiral arteries are therefore left dilated and unable to constrict, resulting in high flow and low resistance to the circulation.

54
Q

The mechanism of pregnancy-induced hypertension is poorly understood still but it is thought to be maybe due to poor placental perfusion due to abnormal placentation. Describe the abnormal placentation that is thought to occur in pre-eclampsia.

A

Incomplete spiral artery remodelling causes high resistance and low flow between the uterus and placenta, because the walls of the spiral arteries are still muscular so they constrict.
Blood pressure rises as a result to try and perfuse the placenta properly.
Hypoxia occurs leading to oxidative stress due to underperfusion.
Systemic inflammatory response occurs leading to endothelial dysfunction and ‘leaky’ blood vessels.

55
Q

Give some maternal complications of gestational hypertension and pre-eclampsia.

A

HELLP syndrome (10-20%)
Eclampsia
AKI
DIC
ARDS & pulmonary oedema
Future risk of hypertension increased
Cerebrovascular haemorrhage
Death, typically from cerebral oedema or airway compromise during eclampsia

56
Q

What is HELLP syndrome?

A

Complication of gestational hypertension / pre-eclampsia.

Haemolysis, Elevated Liver enzymes, Low Platelets

57
Q

Give some fetal complications of gestational hypertension and pre-eclampsia

A

Prematurity, both iatrogenic and idiopathic
IUGR
Placental abruption
Perinatal death
HIE

58
Q

Give the 3 types of urinary incontinence.

A

Stress urinary incontinence; stress
Overactive Bladder Syndrome; urge
Mixed urinary incontinence

59
Q

Give 2 classical symptoms of OAB.

A

Frequency
Nocturia

60
Q

Red flag symptoms in incontinence:

A

Voiding problems
Pain
Haematuria
Prolapse symptoms
UTI

61
Q

What are 3 options for conservative management for urinary incontinence?

A

Continence advice and lifestyle changes
Physiotherapy
Bladder retraining; best treatment for overactive bladder, min 6 weeks.

Must identify which type of incontinence you’re treating but often a lot of overlap for conservative management.

62
Q

Outline 2 medical management options for OAB.

A

Anticholinergic 1st line oxybutynin, tolterodine, solfenacin (oral and patch, patch may reduce side effects). O for Oxybutynin and Overactive bladder

X oxybutynin in over 65s as can cause confusion

B3 adrenoreceptor agonist 2nd line
Mirabegron. Adrenergic control, on sympathetic pathway.

63
Q

Side effects of anticholinergic drugs and Mirabegron

A

Dry mouth, dry eyes, constipation

Hypertension

64
Q

What are the medical management options for SUI?

A

Vaginal oestrogen

Duloxetine; SNRI, stimulates pudendal motor neurones, increased contraction of urethral striated muscle, increasing urethral closure pressure.
Poor results in clinical practice.

65
Q

Surgical management of OAB:

A

Botox; lasts 3-12 months, risk of voiding problems and requiring catheter use (3%). 70-80% success rate.

Sacroneuromodulation; pacing wire into base of spine, releases signals that alter nerve transmission to bladder. 70-80% success rate.

Reconstructive surgery; augmentation cystoplasty (make it bigger by adding a bit of bowel), urinary diversion (stoma)

66
Q

Surgical management of SUI:

A

Mesh tape (UK wide suspension); retropubic and transobturator

First line:
Colposuspension; stitch through vaginal wall up round the back of the pubic bone; provides support to the bladder, lifting everything up.

Biological / fascial sling (rectus fascia);

Second line:
Intramural bulking agents, not as effective

67
Q

What is the latest point you can prescribe PEP for eligible people?

A

72 hours (but much better if started within 24 hours)

68
Q

What is the course of PEP that is prescribed?

A

28 day course of Truvada and Raltegravir
Final HIV testing at 8 weeks (+/- HBV/HCV)

69
Q

Which medications are used in PrEP?

A

Tenofovir
Emtricitabine
Daily or event based dosing
86% effective in MSM
Was available on NHS in Scotland since 2017

70
Q

Management of genital warts?

A

Podophyllotoxin [caution in pregnancy]
Aldara [Imiquimod]
Cryotherapy

Would usually self resolve in 6-12 months

71
Q

What is the most common cause of abnormal discharge?

A

Bacterial vaginosis

Due to reduction in ‘healthy’ lactobacilli and overgrowth of Garnerella vaginalis, anearobes, mycoplasma

Can be recurrent, up to 50%

72
Q

A pregnant woman has bacterial vaginosis. What are two outcomes she is at increased risk of?

A

Pre-term labour
Low birth weight

73
Q

What are 3 risks of SGA/FGR?

A

HIE
Stillbirth

74
Q

Causes of oligohydramnios?

A

Prolonged pregnancy
Ruptured membranes
FGR
Fetal renal congenital abnormalities

75
Q

Implications of oligohydramnios:

A

May cause hypoxia due to cord compression

FGR/SGA

Pulmonary hypoplasia

76
Q

Pre-eclampsia can include maternal organ dysfunction. Give 4 organ system it can affect and how.

A

Renal insufficiency (creatinine >90micromol)
*Remember urea and creatinine level parameters are reduced in pregnancy.

Liver involvement; transaminase elevation + RUQ/epigastric pain.

Neurological Cx inc eclampsia. hyperreflexia, headache.

Thrombocytopenia, DIC, haemolysis.

77
Q

Name 3 drugs commonly used for hypertension in pregnancy.

A

Labetalol 1st line
Nifedipine e.g. if asthmatic
Hydralazine (widely used in hypertensive crisis)

78
Q

How does aspirin work?

A

Inhibits prostaglandin synthesis via COX enzyme inhibition.

79
Q

Describe normal glucose physiological changes in pregnancy.

A

Pregnancy is a state of increasing insulin resistance.
Fasting glucose goes down.
Post prandial glucose increases.
Glycosuria is common.
Ketosis is also more common.

80
Q

Which two hormones are produced by the placenta and drive hyperglycaemia + state their actions.

A

Human placental lactogen; increases insulin resistance

Human chorionic somatomammotrophin; increases insulin production

81
Q

High glucose levels at the time of organogenesis causes fetal congenital abnormalities. What are the top 3?

A

Cardiac defects
NTD
Renal abnormalities

Good glycaemic control pre-conception reduces this risk.

82
Q

Describe the mechanism of how increased maternal glucose causes macrosomia, potentially death and delivery complications.

A

Glucose crosses the placenta, insulin does not.
The fetus starts to produce insulin at 10 weeks, and this is needed for growth.
Increased maternal glucose increases fetal glucose and therefore fetal insulin, which results in macrosomia.

Hyperinsulinaemia leads to chronic hypoxia and acidaemia; macrosomic baby may be more at risk due to increased oxygen demands.

Labour complicated by shoulder dystocia, as macrosomic babies are larger and also carry more bulk up around the shoulders and head.

83
Q

Give risks of diabetes in pregnancy, split into pre-existing and gestational and ones common to both.

A

Pre-existing: miscarriage, congenital malformation, stillbirth, neonatal death.

Gestational: neonatal hypoglycaemia, perinatal death

Both: macrosomia, birth trauma, obesity / diabetes developing later in life, transient neonatal morbidity, IOL and CS

84
Q

Antenatal care will differ in patients with diabetes. Outline standard care and appts for those with diabetes.

A

5mg folic acid preconception to 12 weeks.
Early booking appt.
Obstetric review 4 weekly until 28 weeks, then 2 weekly until 36 weeks, then weekly.
Offer serum screening and detailed anomaly scan and cardiac scan.
Retinal and renal screening at booking and 28 weeks.

85
Q

Gestational diabetes accounts for 87.5% of women with diabetes in pregnancy. Outline the risk factors that would warrant testing for GDM at 24-28 weeks with a 2 hour 75g OGTT (5).

A

BMI >30
Previous macrosomic baby >4.5kg
Previous GDM
FHx of diabetes (first degree relatives only)
Minority ethnic family origin with high prevalence of diabetes

86
Q

When is a digital vaginal examination contraindicated and why?

A

APH until placenta praevia is excluded. If a previous scan from at least 20 weeks gestation proves that it is not low lying, this is evidence enough to proceed. Otherwise, there is risk of more bleeding.

87
Q

Give the primary and secondary definitions of a PPH.

A

Primary; bleeding from vaginal tract in excess of 500ml anytime from the second stage of labour until 24hrs post delivery.

Secondary; bleeding from the vaginal tract (excessive) after 24 hours until 6 weeks after delivery.

88
Q

What are the expected time frames for the stages of labour, for nulliparous vs parous women?

A

First labour average 8 hours, unlikely to last >18 hours.

Subsequent labour average 5 hours, unlikely to last >12 hours.

89
Q

If delay in the established first stage of labour, assess all aspects of progress in labour when diagnosing delay. Give 4 factors you must consider when assessing rate of labour.

A

Cervical dilatation <2cm in 4 hours for first labours.

Cervical dilatation <2cm OR a slowing in progress of labour for subsequent labours.

Descent and rotation of baby’s head.

Changes in the strength, duration and frequency of uterine contractions.

90
Q

What is the chromosomal configuration of a) partial hydatiform mole b) complete hydatiform mole

A

Partial = triploid. 23 mother, 46 father. May be an embryo present. 0.5% risk of malignancy.

Complete; diploid, 46 father, empty ovum. 1-2% risk of malignancy.

91
Q

What are the 3 types of malignant gestational trophoblastic diseases?

A

Invasive mole
Choriocarinoma
Placental site trophoblastic tumour (PSTT)

92
Q

Risk factors for GTD (4).

A

<20y = x3 risk
>40y = x10 risk
Previous molar pregnancy
Ethnicity; higher in Korea, Philippines, China.

93
Q

Clinical features of GTD:

A

PV bleeding
Enlarged uterus
Extreme hyperemesis gravidarium
Hyperthyroidism
Early-onset pre-eclampsia

US = ‘snowstorm’

94
Q

Nausea and vomiting is common in pregnancy, affecting more than 50% of women in the first trimester. 90% settle by 16 weeks. What is the cause thought to be associated with, and give 2 conditions that are associated with severe n&v?

A

Associated to high serum hCG levels; a similar subunit to TSH.

Multiple pregnancy and molar pregnancy are associated with severe cases of n&v, and these have high levels of hCG.

95
Q

What is the definition of hyperemesis gravidarium?

A

Persistent vomiting in pregnancy causing weight loss >5% body mass, dehydration and electrolyte imbalance.

Affects 1% of pregnant women.

96
Q

Give 3 complications of hyperemesis gravidarium, and 2 effects on the infant.

A

Wernicke’s encephalopathy from thiamine deficiency.

Central pontine myelinosis if rapid correction of hyponatraemia.

Maternal death (rare).

Fetus:
Higher incidence of IUGR
Significantly smaller at birth

97
Q

C-sections increase the risk of certain conditions in future pregnancies. Give some examples.

A

Future CS
Still birth
Ectopic pregnancy
Placenta praevia and accreta

98
Q

What do ‘small for gestational age’ and ‘fetal growth restriction’ refer to centile wise?

A

<10th centile = SGA
<3rd centile = FGR

99
Q

SGA and FGR are usually due to placental dysfunction. Give 4 mechanisms of monitoring used to assess fetal wellbeing when FGR is suspected / confirmed.

A

Acidosis and stillbirth risk increased in FGR.

Monitoring fetal wellbeing:
Liquor volumes
Growth pattern on charts
CTG
Dopplers

100
Q

Give 4 complications of FGR.

A

Stillbirth
HIE
Preterm birth
Pre-eclampsia

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