Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Finals > Obstetrics & Gynaecology > Flashcards

Obstetrics & Gynaecology Flashcards

1
Q

Define gravidity and parity

A

Gravidity - no. of pregnancies at any stage, incl the current one

Parity - no. of pregnancies that resulted in a delivery beyond 24wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When would you expect to first feel the uterus in pregnancy?

A

From 12wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where would you palpate the uterus at 16wks gestation?

A

1/2 way between symphysis pubis and umbilicus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where would you be able to palpate the uterus at 20-24wks?

A

Level of the umbilicus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where would you be able to palpate the uterus at 36wks?

A

Under the ribs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of a discrepancy between fundal height and dates?

A 
Inaccurate menstrual Hx
Multiple gestation
Fibroids
Polyhydraminos
Adnexal mass
Maternal size
Hydatidiform mole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the ‘inspection’ part of the abdo exam in a pregnant woman

A

Size, asymmetry, fetal movement
Line of pigmentation between pubic hair to umbilicus - linea nigra
Striae gravidarum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the ‘palpation’ part of the abdo exam in a pregnant woman

A 
Measure SFH after 20wks
Estimate no. of fetuses
Assess fetal lie - longitudinal, oblique, transverse
Presentation - cephalic, breech
Engagement - measured in fifths palpable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the ‘auscultation’ part of the abdo exam in a pregnant woman

A

Fetal heart may be heard by Doppler US from ~12wks, and with a Pinard from ~24wks
Listen over the anterior shoulder of the fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Outline the hormonal changes that occur during pregnancy

A

Progesterone - synthesised by CL then placenta. Dec SM excitability and inc body temp

Oestrogens - inc breast + nipple growth, water retention, protein synthesis

Thyroid - maternal thyroid enlarges

Prolactin - pituitary secretion inc throughout pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Outline the genital changes that occur during pregnancy

A

Uterine muscle hypertrophy up to 20wks, stretching after that
Cervix may develop an ectopion
Vaginal discharge inc due to cervical ectopy, cell desquamation and inc mucus production from a vasocongested vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Outline the haemodynamic changes that occur during pregnancy

A

Blood - inc volume, inc RBC volume -> dilutional anaemia

CVS - inc CO (inc SV and HR), dec peripheral resistance, dec BP in 2nd tri, varicose veins

Aorto-caval compression - from 20wks the uterus compresses the IVC in supine women, reducting venous return and CO by 0%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Key points in pre-conception counselling

A 
Ensure rubella immune
Stop smoking
Weight loss
Exercise
Folic acid
Vitamin D
Lower alcohol
Avoid recreational drugs
Optimise medical disorders
Review meds
Genetic counselling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Briefly describe the development of the placenta

A

When the blastocyst implants and forms trophoblastic cells, forming sinuses (lacunae).
The placenta grows in circumference and thickness until 16wks, after this circumferentially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the uteroplacental circulation

A

Maternal blood
Set up to favour transfer of O2 and nutrients to the fetus
Spiral arteries are dilated and low-pressure to inc high-flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the fetoplacental circulation

A

Two umbilical arteries that carry deoxy blood from the fetus to the placenta where it’s oxygenated and returns to the fetus via the umbilical vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Outline the functions of the placenta

A

Attaches the fetus
Organ of gaseous exchange
Endocrine - hCG, growth factors, oestrogens, progestogens)
Barrier from infection and drugs
Transfers nutrients to and from the fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Outline the aims of antenatal care

A

Detect any disease in mother
Monitor and promote fetal well-being
Prepare mother for birth
Monitor trends to prevent/detect any complications
Are thromboprophylaxis or aspirin needed?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Outline what occurs in the 1st antenatal visit

A 
Full obs Hx
FHx HTN, DM, fetal abnormalities, inheritable disease
Concurrent illnesses?
Risk assess for VTE
Hx of mental illness?

Examine - heart, lungs, BP, weight, abdo

Tests:

  • bloods -> Hb, blood group, antibody screen, syphilis + rubella screen., HBsAg, HIV, vitamin D
  • MSU

Advise on smoking, alcohol, diet etc. Offer antenatal classes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When is the nuchal translucency scan carried out? What’s checked at this scan?

A

11+0 to 13+6 weeks
Determines viability, dates pregnancy, diagnoses multiple pregnancy and chorionicity
Can diagnose major structural abnormalities (anencephaly)
Screen for chromosomal abnormalities with nuchal fold measurement + blood test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can an increased nuchal translucency suggest?

A

May be seen in:

  • heart failure
  • series anomalies of the heart and great arteries
  • chromosomal abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When is the anomaly scan carried out? What is the purpose of it, and what anomalies are looked for?

A

18-22 wks
Detects structural malformations

Anomalies:

  • Skull shape + int structures (incl cerebellum, ventricular size, nuchal fold)
  • Spine
  • Abdo (shape + content)
  • Arms and legs
  • Heart
  • Face and lips
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the lethal fetal anomalies?

A

Anencephaly
Bilateral renal agenesis
Some major cardiac abnormalities
Trisomies 13 and 18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are soft markers on antenatal USS? Give some examples

A

Findings on anomaly scan that are in themselves of little significance, but are slightly more common in chromosomal abnormalities

Choroid plexus cells -> weak association with trisomy 18
Echogenic bowel -> inc risk chromosomal abnormalities, congenital infection, CF and bowel obs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What measurements are taken in a fetal growth scan? Who are offered growth scans?

A

Head and abdo circumference (and sometimes femur length), with liquor volume is used to determine pattern of growth.

Offered to those with inc risk of growth abnormality - prev growth restriction, pre-eclampsia, measuring SGA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Outline the screening for Trisomy 21

A

Combined test
Uses NT + free hCG + pregnancy-associated plasma protein + woman’s age
Used between 11 and 13+6 wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe chorionic villus biopsy

A

Carried out at 10-13wks (allows early termination)
Placenta is sampled transabdominally under US control.
Risks are miscarriage, inc transmission of BBVs, contamination by maternal cells, false +ve or -ves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe amniocentesis

A

Carried out from 16wks
Involves aspiration of fluid containing fetal cells shed from skin and gut
Small needle is passed transabdominally under US
Advantages are: can diagnose fetal infections such as CMV + lower miscarriage rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Signs and symptoms of pregnancy in the first 12wks

A

Amenorrhoea, nausea, vomiting, bladder irritability
Breasts engorge, nipples enlarge, Montgomery’s tubercles become prominent
Vulval vascularity inc and the cervix softens and looks bluish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Causes of heartburn in pregnancy

A

Progesterone-mediated pyloric sphincter relaxation allows irritant bile to reflux into the stomach.
This is worsened by the growing fetus pressing on the upper GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Define hyperemesis gravidarum

A

Persisting vomiting in pregnancy which causes weight loss (>5% of pre-pregnancy weight) and ketosis.
Risk is inc in multiple pregnancies, molar pregnancies, and those with prev HG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does hyperemesis gravidarum present?

A

Inability to keep food or fluids down
Weight loss ± nutritional deficiency, dehydration, hypovolaemia, tachycardia, postural hypotension, electrolyte disturbance
Haematemesis from Mallory-Weiss tears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Investigations for hyperemesis graidarum

A

Bedside - urine dip for ketones and UTI
Bloods - FBC, U+E, LFTs
Imaging - US to diagnose multiples and excl a mole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Management of hyperemesis gravidarum

A

Admit for rehydration if unable to keep anything down despite oral anti-emetics.
Aggressively fluid replace with either 0.9% saline + K, or Hartmann’s (not gluc)
Regular anti-emetics (promethazine, cyclizine, metoclopramide)
If treatment fails, consider course of corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Management of maternal depression during pregnancy

A

Try to wait until 2nd Tri, but don’t delay if severe

1st line = SSRIs (sertraline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe lithium in pregnancy

A

Linked with teratogenicity, neonatal thyroid abnormalities, floppy baby syndrome.
Should only be prescribed when alt are ineffective.
Offer fetal echo and monitor levels closely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Give the lab definition of anaemia in pregnancy

A

Hb <105g/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Maternal complications of diabetes in pregnacny

A

Hypoglycaemia unawareness
Inc risk pre-eclampsia and infection
Inc risk C-section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Fetal complications of diabetes in pregnancy

A 
Miscarriage
Inc malformation rates
Macrosomia (therefore should dystocia) or GR
Polyhydraminos
Preterm labour
Stillbirth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Define gestational diabetes

A

OGTT gluc >7.8mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

When would you screen for gestational DM?

A

If 1st degree relative, prev baby >4.5kg, BMI >30, ethnicity Asian/Caribbean/Middle East, or prev GDM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Causes of jaundice in pregnancy

A 
Obstetric cholestasis
Acute fatty liver of pregnancy
Viral hep
Jaundice of severe pre-eclampsia
HELLP syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe obstetric cholestasis

A

Pruritis (esp palm + soles), without rash
Liver transaminases, bili and bile acids inc
Risk of PTL, stillbirth etc
Ursodeoxycholic acid dec pruiritis and abnormal LFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What tests are included in the combined test for Downs?

A

Nuchal translucency
Serum B-HCG
Pregnancy associated plasma protein A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Common long term complications of vaginal hysterectomy with AP-repair

A

Enterocoele and vaginal vault prolapse

Urinary retention may occur acutely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Management of lactation mastitis

A

If systemically well - analgesia and encourage effective milk removal

If not improved after 12-24h, give oral flucloxacillin (500mg QDS 14d) or erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Pregnant woman with abdo pain, N+V, jaundice, hypoglycaemia, raised ALT and steatosis.
Diagnosis?

A

Acute fatty liver of pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Pregnant woman with pruritis (no rash) and raised bilirubin.

Diagnosis?

A

Intrahepatic cholestasis of pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Key risk factors for shoulder dystocia

A

Fetal macrosomia
High maternal BMI
DM
Prolonged labour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Management if infertility in PCOS

A

1) Weight reduction
2) Clomifene (anti-oestrogen)
3) Metformin (esp. if they’re obese
4) Ovarian diathermy and gonadotropin induction
5) IVF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Normal findings on cardiac examination, CXR and ECG during pregnancy

A

Ejection systolic murk in >90% of pregnant women
CXR: slight cardiomegaly, inc pulmonary vascular markings
ECG: ectopics, Q-wave and inverted T-wave in III, T-wave inversion in lateral leads. QRS shows left shift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Causes of anaemia in pregnancy

A

Physiological dilution occurs, but to cause a HB <105:
- iron deficiency (inadequate stores preconception)
- folate deficiency
Also consider coeliac, CKD, AI disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the transmission of HIV in pregnancy and labour

A

Without intervention ~15% of babies acquire HIV from +ve mother
2/3 of vertical transmission occurs during vaginal delivery
Breastfeeding doubles risk
Membrane rupture >4h doubles risk
Transmission inc with viral load >400, seroconversion during pregnancy, advanced disease, preterm labour, hep C

Can achieve =<1% risk with maternal anti-retroviral use, elective CS, and bottle feeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

NICE guidelines for delivery in women with diabetes

A

Elective delivery at 38wk (by 40wk if GDM)
Corticosteroids to promote fetal lung maturity if preterm labour

Continuous fetal monitoring is required
Avoid hyperglycaemia
Aim for glucose lever 4-7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe the normal changes to thyroid hormones during pregnancy

A

NB: normal pregnancy mimics hyperthyroidism

  • thyroid-binding globulin and T4 output inc to maintain free T4 levels
  • high levels of hCG mimic TSH
  • dec availability of iodine
  • TSH may fall below normal level in 1st trimester (suppressed by hCG)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Most common cause of hyperthyroidism in pregnancy. What are the risks? How would you manage it?

A

Graves’ disease
Risk - prematurity, fetal loss, malformations
Management - carbimazole, PTU are commonly used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Risks of hypothyroidism in pregnancy. How would you manage it?

A

If untreated, associated with inc miscarriage rates, stillbirth, anaemia, pre-eclampsia, IUGR, with dec IQ and neurodevelopmental delay in offspring

Manage with levothyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is postpartum thyroiditis? How would you manage it?

A

Thyroid destruction postpartum leading to transient hyperthyroidism followed by hypothyroid

Hyperthyroid phase can be managed with B-blockers
Monitor hypothyroid phase for 6m, treat if symptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe acute fatty liver of pregnancy. How would you manage it?

A

Rare but extremely serious
Mother develops abdo pain, jaundice, headache, vomiting, thrombocytopenia and pancreatitis from 30wks
Associated pre-eclampsia in 30-60%
There is hepatic steatosis with jaundice, uraemia, severe hypoglycaemia, clotting disorder (can progress to coma and death)

Manage in HDU or ITU
Monitor BP
Supportive treatment for liver and renal failure and treat hypos vigorously
Expedite delivery
Maternal mortality is 18%, fetal mortality is 23%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What U+Es would make you investigate further the renal function of a pregnant woman?

A

Creatinine >75

Urea >4.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Describe asymptomatic bacteriuria in pregnancy, and the rationale for screening

A

Up to 7% of pregnant women are affected (esp diabetics)
With dilation of calyces and ureters in pregnancy, 30% with develop pyelonephritis (causing FGR, fetal death, premature labour), therefore screened at booking.
If present on MSU give Cefalexin
Check MSU on regular basis to ensure eradication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Management of pyelonephritis in pregnancy

A

Cefuroxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Obstetric causes of AKI

A

Most commonly occurs postnatally and is rare. Anuria is uncommon.

  • sepsis
  • haemoptysis (HELLP, acute fatty liver, sickle cell crisis, malaria)
  • hypovolaemia
  • volume contraction (pre-eclampsia)
  • drugs (esp NSAIDs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Causes of seizures during pregnancy

A 
Epilepsy
Eclampsia
Cerebral vein thrombosis
IC mass
Stroke
Hypoglycaemia
Hyponatraemia
Drugs and withdrawal
Infection
Pseudoseizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Management of asthma in pregnancy

A

Most drugs are safe in pregnancy, but don’t start leukotriene receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Management of RA in pregnancy

A

RA is usually temporarily alleviated by pregnancy
Methotrexate is C/I, sulfasalazine may be used (but give extra folate). Azathioprine may cause IUGR.
NSAIDs can be used in 1st and 2nd trimester, but avoid in 3rd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Management of SLE in pregnancy

A

Advise planned pregnancy after 6m of stable disease without cytotoxic suppression
Disease suppression can be maintained with azathioprine and hydroxychloroquine
Aspirin 75mg daily should be commenced pre-conception and continued throughout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Management of antiphosholipid syndrome in pregnancy

A

Treat from conception with aspirin 75mg daily and heparin from when fetal heart is identified

Postpartum give either heparin or warfarin as risk of thrombosis is high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

BP aims during pregnancy

A

<150/90 (140/90 if end-organ damage), but with diastolic >= 80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Management of chronic HTN during pregnacny

A

Give aspirin 75mg daily from conception to birth
Admit if >160/110
Fetal US every 4wks from 28wks to assess fetal growth, amniotic fluid vol, umbilical artery Doppler

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Management of chronic HTN during labour

A

Monitor BP hourly if <159/109, or continuously if >160/100
If severe HTN doesn’t respond to treatment, advise operative delivery
Give oxytocin alone at 3rd stage (ergometrine causessevere HTN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Describe pregnancy-induced HTN. How would you manage it?

A

HTN in the 2nd half of pregnancy in the absence of proteinuria or other features of pre-eclampsia

Monitor BP and urine weekly
Start labetalol if >150/100 and check BP and urine twice weekly
If BP >160/110, admit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Risk factors for VTE in pregnancy

A
  • age >35
  • BMI >30
  • Parity >3
  • Smoker
  • Gross varicose veins
  • current pre-eclampsia
  • immobility
  • family Hx unprovoked VTE
  • thrombophilia
  • multiple pregnancy
  • IVF pregnancy

If 4 or more = immediate LMWH until 6wk PP
If 3 = LMWH from 28wks until 6wk PP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Management of maternal varicella zoster infection during pregnancy

A

If mother develops chickenpox near delivery, aim for delivery after 7d, give baby immunoglobulin at birth and monitor for 28d, give aciclovir if neonate develops chickenpox

If contact with someone with VZV earlier in pregnancy and mother has no Hx of having chickenpox before, check blood for varicella antibodies -> if none, give VZIG
If rash develops -> aciclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the indications for IV ABx for GBS in labour?

A

+ve GBS high vaginal swab at any time in pregnancy
Any baby previously infected with GBS
Any documented GBS bacteriuria in this pregnancy
Gestation <37wks
Any intrapartum fever
If culture result unknown and membranes are ruptured at term for >18h - give prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Which ABx is used for GBS?

A

Benzylpenicillin

Or Clindamycin if pen allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Triad of symptoms in uterine abruption

A

Abdo pain
Uterine rigidity
Vaginal bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Management of placental abruption

A

If live viable foetus -> rapid delivery as demise can be sudden
Prepare for DIC and beware PPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Describe uterine torsion

A

Uterus normally rotates 30-40’ to the right, rarely it rotates >90’ causing acute tine torsion in mid-late pregnancy

Presents with abdo pain, shock, tense uterus, urinary retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Maternal and fetal risks of obesity in pregnancy

A 
Pregnancy-induced HTN and pre-eclampsia is twice as likely 
Gestational diabetes 3x as likely
VTE is doubled
Miscarriage
Stillbirth
Maternal cardiac disease
IOL
Failed induction
CS
Instrumental delivery
Macrosomia
Shoulder dystocia
3rd and 4th degree perineal tears
Wound infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Risk factors for sepsis in pregnancy/labour

A 
Obesity
Impaired glucose tolerance/diabetes
Impaired immunity
Immunosuppressants
Anaemia
Vaginal discharge
Pelvic infection
Hx of GBS
Invasive procedures - amniocentesis, cervical cerclage, prolonged ROM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Most common causative organisms of sepsis in pregnancy

A

Streptococcus

E. Coil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe the ideal pelvis for pregnancy and labour

A

Rounded brim
Shallow cavity
Non-prominent ischial spines
Curved sacrum with large sciatic notches
Sacrospinous ligaments >3.5cm
AP diameter is at least 12cm, transverse is at least 13.5cm
Subpubic arch should be rounded and the intertuberous distance at least 10cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Describe the normal movement of the fetus during labour

A
  1. Descent with inc flexion as head enters cavity
  2. Int rotation at ischial spine level and head flexion inc
  3. Disengagement by extension as head comes out of vulva
  4. Restitution as shoulders are rotated by levators, head externally rotates
  5. Delivery of anterior shoulder
  6. Delivery of posterior shoulder
  7. Delivery of buttocks and legs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the two main types of fetal monitoring used during labour? When would you use each?

A 
Intermittent auscultation (IA)
Continuous cardiotocograph (CTG)

IA is used in low-risk women using a Doppler US for a full min after a contraction (every 15min in 1st stage, every 5min throughout 2nd)
CTG is used in high-risk woman

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Indications for CTG monitoring in labour

A 
IOL
Post-maturity
Previous LSCS
Maternal cardiac problems
Pre-eclampsia or HTN
Prolonged ROM
Prematurity <37wks
Diabetes
Antepartum or intrapartum haemorrhage
SFGA
Oligohydraminos
Abnormal umbilical artery Dopplers
Multiple pregnancy
Meconium-stained liquor
Abnormal lie
Oxytocin augmentation
Epidural anaesthesia
Pyrexia
Abnormality heard on IA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What mnemonic is used to describe CTGs? What does it stand for?

A

DR C BRAVADO

DR - determine risk (why are they having CTG?)
C - contractions (how many in 10min?)
BRA - baseline rate
V - variability
A - accelerations
D - decelerations
O - overall (normal, non-reassuring, abnormal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Define the baseline rate on CTG

A

Average level of fetal HR when any accelerations or decelerations have been excluded.
Appears as a straight line between other features of the trace.
Normal is 100-160bpm (Brady <100, tachy >160)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Define variability on CTG

A

‘Bandwidth’ of the baseline
Look at one small square on the CTG, each should contain a variation in FHR >5bpm

Reduced variability is <5bpm (but can be normal if baby is sleeping)
Other causes incl fetal hypoxia, malformation, magnesium, prematurity (<28wk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Define accelerations on CTG

A

Upward spike of >15bpm for >15seconds
Reassuring feature
Commonly occur when foetus is moving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Define decelerations on CTG

A

Downward spikes of >15bpm for >15seconds
May be normal feature of labour, and how concerning they are depends on the shape of them, and when they appear relative to a contraction.

Early - mimic shape and timing of contraction, caused by head compression (therefore seen in breech and 2nd stage)
Late - reach their worst point after the peak of a contraction has passed, sign of acidosis

Shallow - together with reduced variability represent an abnormal trace

Typical variable decels- V-shaped with shoulders on either side, associated with cord compression and not usually hypoxia
Atypical - loss of shouldering, last >60s, >60 beats from baseline, may be slow to recover, be a ‘W’ shape, lose variability within the decelerations, may be sign of fetal hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Outline a reassuring CTG

A

Baseline - 100-160
Variability - >5
Accelerations - present
Decelerations - none or early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Outline a non-reassuring CTG

A

Baseline - 161-180
Variability - <5 for 30-90mins
Decelerations - variable decels for >50% contractions for >90mins, taking <60s to recover, or drop from BR >60beats, or taking >60s to recover for <30min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Describe an abnormal CTG

A

Baseline - <100 or >180
Variability - <5 for >90min
Decelerations - late decels for >50% of contractions for >30mins, or a single prolonged deceleration for >3min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

How might you improve the CTG initially?

A

Left lateral position to shift weight off maternal vessels and correct cord compression
IV fluids if hypotension/dehydrated
Reduce or stop oxytocin infusion if contracting >5 in 10 or bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

When is fetal blood sampling indicated? What actions would you take depending on the results?

A

When CTG trace is abnormal (unless immediate delivery required)

Normal pH: >7.25, repeat in 1h if CTG still abnormal
Borderline pH: 7.21-7.24, repeat in 30min if CTG remains abnormal
Abnormal pH: <7.20, immediate delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Outline the aetiology of preeclampsia

A

Failure of trophoblastic invasion of spiral arteries leaving them vasoactive (if properly invaded they can’t clamp down in response to vasoconstrictors, this protects placental flow)
Inc BP partially compensates for this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Risk factors for pre-eclampsia

A

High risk:

  • prev severe or early-onset pre-eclampsia (<20wk)
  • chronic HTN or HTN in prev pregnancy
  • CKD
  • DM
  • AI disease

Moderate risk:

  • 1st pregnancy
  • > 40yo
  • pregnancy interval >10yr
  • FH pre-eclampsia
  • multiple pregnancy
  • low PAPP-A
  • uterine artery notching on Doppler US
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

When would you commence aspirin for pre-eclampsia prophylaxis?

A

If 1 high-risk, or 2 moderate-risk factors from 12th week of pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Outline the effect of pre-eclampsia

A 
Dec plasma volume
Inc peripheral resistance
Placental ischaemia
If BP >180/140, microaneurysms develop in arteries
DIC may develop
Oedema
Liver and HELLP syndrome

Severe complications are eclampsia, HELLP, cerebral haemorrhage, IUGR, renal failure, placental abruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Symptoms and signs of pre-eclampsia

A

Symptoms:
May be absent (esp if mild)
Ask about headache, flashing lights, epigastric or RUQ pain, N+V, swelling of face, fingers, and lower limbs

Signs:
Pregnancy-induced HTN
Proteinuria
Epigastric or RUQ tenderness
Brisk reflexes
>2 beats of clonus
Confusion
Fits
Placental abruption
IUGR
Stillbirth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Investigation results in pre-eclampsia

A 
Protein-creatinine ratio >30
Serum uric acid inc
Thrombocytopaenia 
Prolonged PT + APTT
Inc creatinine
Anaemia if haemoptysis (inc LDH)
Abnormal LFTs
Fetal growth restriction
Oligohydraminos
Abnormal uterine and umbilical arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Define HELLP syndrome

A 
Severe variant of pre-eclampsia and consists of:
H aemolysis
E levated 
L iver enzymes
L ow
P latelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Symptoms and management of HELLP syndrome

A

Symptoms - epigastric/RUQ pain, N+V, dark urine (due to haemolysis)

Management - as for eclampsia, indication for delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Define a premature birth. Give some causes

A

Before 37wks gestation

Causes include - multiple pregnancy, APH, cervical incompetence, chorioamnionitis, uterine abnormalities, DM, polyhydraminos, pyelonephritis, other infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Risk factors for a premature birth

A 
Previous preterm birth 
Multiple pregnancy
Cervical surgery (eg LLETZ)
Uterine anomalies
Pre-existing medical conditions
Pre-eclampsia
IUGR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Management of premature rupture of membranes

A

Admit for 48h
Rule out chorioamnionitis and sepsis -> if evidence, expedite delivery regardless of gestation
Give corticosteroids for fetal lung maturity and erythromycin for 10d
If labour doesn’t occur spontaneously, d/c after 48h and manage as outpatient -> advice to avoid intercourse and swimming
IOL after 34wk if cephalic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are the fetal risks of premature rupture of membranes?

A

Prematurity
Infection
Pulmonary hypolpasia
Limb contracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Management of preterm labour

A

In 50% the contractions cease spontaneously
Treat the cause
Give steroids
Tocolytics (eg nifedipine) may be beneficial but the evidence is limited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Outline the absolute and relative CIs to the use of tocolytics

A

Absolute - chorioamnionitis, fetal death or lethal abnormality, condition needing immediate delivery

Relative - FGR or distress, pre-eclampsia, placenta praevia, abruption, cervix >4cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Give some examples of tocolytics

A

Atosiban has fewer maternal effects but hasn’t been shown to benefit foetus
Nifedipine is as effective and associated with less newborn resp distress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Steroid used for fetal lung maturity

A

Betamethasone 12mg IM with a 2nd dose 12-24h later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

When would you give steroids for fetal lung maturity?

A

All woman at risk of iatrogenic or spontaneous preterm birth between 24+0 and 34+6 weeks
Before all elective CS up to 38+6 weeks
Consider at 35-36 weeks if delivery expedited for pre-eclampsia

Benefit occurs within 24hrs, repeat doses aren’t beneficial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Outline some placental and fetal factors causing SGA

A

Placental - abnormal trophoblast invasion (pre-ec), infarction, abruption
-> tend to cause asymmetrical growth restriction with head sparing and dec abdo circumference

Fetal - genetic abnormalities (tri 13, 18, 21, Turners), congenital abnormalities and infection (CMV, rubella), multiple pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Management of a SGA fetus

A

If umbilical artery dopplers are normal, growth scans every 2-3wks. If dopplers remain normal, IOL at 37weeks

If abnormal dopplers and preterm, delivery depends on other factors.

If there’s absent or reversed end-diastolic flow in umbilical artery Doppler, consider delivery via LSCS
Offer steroids up to 35+6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are the effects of IUGR in adult life?

A

Higher risks of HTN, coronary artery disease, T2DM, and AI thyroid disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Define postmaturity in pregnancy

A

Exceeding 42 completed weeks of pregnacny

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What are the problems associated with postmaturity in pregnancy?

A

4x intrapartum deaths
3x early neonatal deaths
Inc IOL and operative delivery
Possible placental insufficiency
Macrosomia, shoulder dystocia, and fetal injury
Fetal skull more ossified so less mouldable
Inc meconium passage in labour
Inc fetal distress in labour
In CS rates for labours after 41 completed weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Management of postmaturity in pregnancy

A

Confirm EDD. At 38 visit discuss recommendations if labour doesn’t occur by 41 weeks (incl sweep and IOL). Arrange 41-week visit if not delivered.

If woman declines IOL then arrange twice-weekly CTG, and US estimation of amniotic fluid depth to detect fetal hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Describe a membrane sweep

A

On vaginal exam as much membrane is swept from the lower segment as possible via a finger inserted through the cervix.
Thought to induce natural prostaglandins
May cause discomfort and a little bleeding
Offer at 40 and 41 weeks in nullips, 41 weeks in multips

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

NICE guidelines on IOL in postmaturity

A

IOL after 41 weeks reduces fetal death rate, so should be offered between 41+0 and 42+0 weeks
Induce via vaginal prostaglandin followed by oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Signs of postmaturity in a baby

A

Dry, cracked, peeling, loose skin
Dec SC tissue
Scaphoid (hollow) abdomen
Meconium staining of nails and cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Obstetric causes of maternal collapse

A 
Massive obstetric haemorrhage (ante- or postpartum)
Eclampsia
IC haemorrhage
Amniotic fluid embolism
Uterine inversion causing neurogenic shock
Post-surgical haemorrhage
Severe sepsis
Peripartum cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Non-obstetric causes of maternal collapse

A 
Massive PE
Pre-existing cardiac disease (MI or aortic dissection)
Anaphylaxis
Stroke
Meningitis
OD
DKA, hypo
Malari
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Define antepartum haemorrhage

A

Genital tract bleeding from 24+0 weeks gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

List the dangerous causes of antepartum haemorrhage

A

Abruption
Placenta praevia
Vasa praevia (baby may bleed to death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

List some benign causes of antepartum haemorrhage

A 
Circumvallate placenta
Placental sinuses
Cervical polyps, erosions etc
Cervicitis
Vaginitis
Vulval varicosities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is placental abruption? What is it associated with?

A

When part of the placenta becomes detached from the uterus

Associated with pre-eclampsia, smoking, IUGR, PROM, multiple pregnancy, polyhydraminos, inc maternal age, thrombophilia, abdo trauma, assisted reproduction, cocaine use, infection, non-vertex presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Potential consequences of placental abruption

A

Placental insufficiency may cause fetal anoxia or death
Compression of uterine muscles by blood causes tenderness, and may prevent good contraction at all stages of labour
May be uterine hypercontractility (>5/10min)
Thrombopastin release may cause DIC
Concealed bleeding may cause maternal shock - renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What features would suggest abruption over placenta praevia?

A 
Mat shock is out of keeping with visible loss
Constant pain
Tender, tense uterus
Normal lie and presentation
Fetal heart = absent/distressed
Coag problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What features would suggest placenta praevia over abruption

A 
Shock in proportion to visible loss
No pain
Uterus not tender
Both lie and presentation may be abnormal
Fetal heart is usually normal 
Coag problems are rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Outline the management of antepartum haemorrhage

A

Milder bleeds - IVI, Hb, X-match, coagulation, U+Es. Establish diagnosis (if placenta praevia keep in until delivery)
If pain and bleeding from a small abruption settles and the fetus isn’t compromised the woman may go home, but treat as high-risk
IOL if antepartum haemorrhage at term

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Define prelabour rupture of membranes at term

A

Rupture of the membranes prior to the onset of labour in women at or over 37 completed weeks’ gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Causes of prelabour rupture of membranes at term

A 
Mostly unknown
Infection of lower genital tract or amnion
Polyhydraminos
Multiple pregnancy
Malpresentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Management of prelabour rupture of membranes at term

A

Conservative up to 24hr (if liquor is clear, mother and fetus are well). Advice to take temp regularly and report to labour ward if any change in fetal movements, colour or smell of liquor, and avoid sex

IOL if labour hasn’t commenced in 24hr via vaginal prostaglandin then oxytocin.
Those giving birth after 24hr of ruptured membranes should deliver where there’s neonatal facilities.

If IOL is declined, monitor fetal heart at 1st contact and every 24hr after membrane rupture whilst they’re not in labour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Indications for immediate IOL in prelabour rupture of membranes at term

A 
Group B strep carriers
HIV carriers aiming for vaginal delivery
Signs of chorioamnionitis
Concerns regarding fetal movements
Meconium-stained liquor
Herpes simplex genital infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Describe the components of the first stage of labour

A

Latent phase = painful and often irregular contractions, cervix initially effaces (shortens and softens) then dilates to 4cm

Established phase = regular contractions with dilation from 4cm, dilating at a rate of 0.5cm/hr. This phase can take 8-18h in a primip, and 5-12h in a multip.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What monitoring is required during the established phase of labour?

A

Maternal BP and temp 4-hourly
Pulse hourly
Assess contractions every 30mins (strength and frequency)
Frequency of bladder emptying
Offer vaginal exam every 4hrs - dilation, position and station of head
Auscultate FH every 15min (if not cont monitored)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Outline the components of the second stage of labour

A

Passive stage = complete cervical dilatation but no pushing

Active = maternal pushing uses abdo muscles and Valsalva manoeuvre until baby is born. Expect birth within 3h in primips, or 2h for multips
Discourage supine maternal position, and encourage them to find a comfortable position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Monitoring required during second stage

A

Check BP and pulse hourly
Temp 4-hourly
Assess contraction every 30min - if they wane, oxytocin may be needed
Auscultate for 1min after a contraction every 5min
Offer vaginal exam hourly
Record urination during 2nd stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Define the 3rd stage of labour

A

Delivery of the placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Signs of placental separation in the 3rd stage of labour. How long should it take?

A

Cord lengthening -> rush of blood per vaginam -> uterus rises -> uterus contracts in the abdo

Should take <1h (if no drugs given)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What drugs may be given during the 3rd stage of labour?

A

Syntometrine (ergometrine + oxytocin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Contraindications to IOL

A 
Malpresentations (incl breech)
Fetal distress
Placenta praevia
Cord presentation
Vasa praevia
Pelvic tumour
145
Q

Options for IOL

A

If Bishops score >5, induction with artificial rupture of membranes should be possible, followed by 2-4hr of maternal mobilisation. Otherwise, prostaglandin pesseries/gel are used.

If spontaneous contractions have’t started within 4hr of amniotomy, begin oxytocin IV in 0.9% saline using pump.

146
Q

Problems associated with IOL

A 
Failed induction
Uterine hyperstimulation
Iatrogenic prematurity
Infection
Bleeding (vasa praevia)
Cord prolapse
C section and instrumental delivery rates are higher
Uterine rupture (rare)
147
Q

Common causes of delay in labour

A

Problems with power, passenger, and/or pelvis:

  • poor uterine contractions
  • malpresentation or malposition, or a large fetus
  • inadequate pelvis
  • combination
148
Q

Assessment and management of delay in 1st stage of labour

A

Assess them - review notes and obstetric Hx

  • palpate for lie, head palpable and contractions
  • check FH, colour of liquor
  • vaginal assessment of dilation, effacement, caput, moulding, station of head, position
  • does she need analgesia + rehydration?

Management = offer amniotomy and reassessment in 2hr

  • if membranes already ruptured, oxytocin infusion + reassess in 4hrs
  • if prev LSCS, get senior advice
149
Q

Non-pharmacological methods of pain-relief in labour

A

Education reduces anxieties
Supportive birth partner
Acupuncture, homeopathy, and hypnosis (not offered by NHS)
TENS machines
Water birth - temp <37.5, not possible for women on cont monitoring

150
Q

Pharmacological methods of pain relief in labour

A

Nitrous oxide - 50% in O2 can be inhaled throughout labour
Narcotic agents - pethidine, diamorphine
Pudendal nerve block (S2,3,4) - injected 1cm beyond a point just below and medial to ischial spine on each side. Given for instrumental delivery
Local anaesthetic into the perineum is used before episiotomy at time of delivery
Epidural (T10-S5)

151
Q

Predisposing factors to multiple pregnancy

A 
Previous twins
FH of twins (dizygotic only)
Inc maternal age
Induced ovulation and IVF
Race origin
152
Q

Features of a multiple pregnancy

A

Early - uterus large for dates, hyperemesis
Later - may be polyhydraminos

Signs - >2 poles felt, multiplicity of fetal parts felt, 2 FH rates
US confirms diagnosis

153
Q

Complications associated with multiple pregnancy

A 
Polyhydraminos
Pre-eclampsia
Anaemia is more common
APH incidence inc
Gestational diabetes
Operative delivery
154
Q

Fetal complications of twin pregnancy

A 
Inc perinatal mortality
Prematurity
Growth restriction
Inc malformation rates
In monochorionic pregnancies, risk of twin-twin transfusion syndrome
155
Q

Complications of labour in multiple pregnancy

A 
PPH
Malpresentation
Vasa praevia rupture
Cord prolapse
Placental abruption and cord entanglement
156
Q

Management of multiple pregnancy

A

US at 11+0 - 13+6, then monthly from 20wks (2-weekly if monochorionic)
High-risk - for consultant-led care

Offer elective birth at:

  • 37weeks if uncomplicated dichorionic
  • 36weeks if uncomplicated monochorionic
  • 35weeks if uncomplicated triplets
157
Q

Define monochorionic twins. What’s the main risk?

A

Twins that share a placenta - risk of fetofetal transfusion

158
Q

Define monoamniotic twins. What’s the risk?

A

Twins that share an amniotic sac - risks entanglement

159
Q

Rates of breech lie during pregancny

A

40% breech at 20wks
20% at 28wks
3% at term

160
Q

Causes/associations of breech presentation

A 
Idiopathic
Uterine abnormalities
Prematurity
Placenta praevia
Oligohydraminos
Fetal abnormalities
161
Q

What are the different types of breech presentation?

A 
Extended breech (70%) - flexed at hip, extended at knee
Flexed breech (15%) - hips and knees both flexed
Footling breech (15%) - greatest risk of cord prolapse
162
Q

Describe an external cephalic version. Give some contraindications

A

Turning the breech via a forward somersault (only turn if vaginal delivery is planned, after 36-37wks)

CIs - placenta praevia, multiple pregnancy (except delivery of 2nd twin), APH in last 7d, ruptured membranes, GR baby, abnormal CTG, uterine scars, fetal abnormality, pre-eclampsia or HTN

163
Q

Contraindications to vaginal breech delivery

A 
Inexperienced clinician
Footling or kneeling breech
Estimated fetal weight <3800g or >2000g
Prev LSCS
Hyperextended fetal neck
164
Q

Describe an OP presentation

A

‘Back-to-back’
Labour tends to be prolonged because of the degree of rotation needed -> adequate fluids and analgesia are important

65% rotate so the head is OA at time of birth
73% will have normal vaginal delivery
22% require forceps
5% CS

165
Q

Define cord prolapse and how is may present

A

Descent of the cord through the cervix, below the presenting part, after rupture of membranes.

Cord may be at the introitus, or only sign may be fetal bradycardia or variable FH decelerations

166
Q

Define shoulder dystocia. What are the risks?

A

Delivery requiring additional obstetric manoeuvres to release the shoulders after gentle downward traction has failed (1:200 births)

Risks - fetal mortality and morbidity, PPH, 4th degree perineal tear, brachial plexus injuries

167
Q

Management of shoulder dystocia

A

Episiotomy
McRoberts position - legs hyperflexed
Suprapubic pressure

168
Q

Describe meconium-stained liquor

A

In late pregnancy it’s normal for babies to pass meconium - stains fluid a dull green -> not significant

During labour, fresh meconium (dark green and sticky) may be passed - may be response to stress of normal labour, or a sign of distress so transfer to cons-led unit

169
Q

Criteria that must be met for an instrumental delivery

A

Consent!
1/5th or less head palpable per abdo
Ruptured membranes
Adequate analgesia (epidural or pudendal block)
Adequate contractions
Bladder empty and catheter balloon deflated
Fully dilated cervix with head at ischial spines of below
Cephalic presentation
Neonatal doctor in attendance

170
Q

Indications for operative vaginal delivery

A

Maternal - prolonged 2nd stage, exhaustion, medical avoidance of pushing, pushing not possible

Fetal - suspected fetal distress, for the after-coming head in a breech delivery

171
Q

Specific indications for forceps > ventouse

A 
Breech to deliver head
Delivery of preterm infant <34wks
Delivery of head at CS
Face presentation
Suspected coagulopathy or thrombocytopenia in fetus
Where maternal pushing is CI
Cord prolapse in 2nd stage
Instrumental under GA
172
Q

Describe forceps used in labour

A

Allow traction to be applied to fetal head
Require much less maternal effort than ventouse
Safer for baby, but can cause significant maternal genital tract trauma

173
Q

Describe a ventouse used in delivery

A

Uses a suction device to suck fetal scalp tissues into a cup (artificial caput created takes 24-48hrs to resolve -> warn mother!)
Baby must be >34wks with no maternal coagulopathy

174
Q

Complications of operative vaginal delivery

A

Maternal genital tract trauma (esp forceps)
Spiral vaginal tears with rotational forceps
Fetus injuries with forceps (rare) - facial n palsy, skull #, orbital injury, IC haemorrhage
Fetal injuries with ventouse - cephalhaematoma, retinal haemorrhage, scalp lacerations

175
Q

When would you abandon an operative delivery for CS?

A

No descent with each subsequent pull

Delivery not imminent after 3 pulls

176
Q

Give some indications for CS

A

Repeat CS
Fetal compromise - brady, pH <7.2, cord prolapse
Failure to progress, or failed IOL
Malpresentation
Severe pre-eclampsia
IUGR with absent/reversed end-diastolic flow
Twin pregnancy with non-cephalic presenting twin
Placenta praevia

177
Q

Outline the 4 categories of CS

A

1 (crash) - immediate threat to woman or fetus (abruption, Brady) -> deliver within 30min
2 - maternal or fetal compromise, not immediately life-threatening -> deliver within 30-60min
3 - semi-elective (pre-eclampsia, failed IOL)
4 - elective (term singleton breech)

178
Q

Complications of CS

A

Intraoperative - blood loss, uterine lacerations, blood transfusion, bladder laceration, bowel injury, ureteral injury, hysterectomy

Postoperative - wound infections, endometritis, UTI, VTE

179
Q

Long-term effects of CS

A

In subsequent pregnancies, there’s a higher incidence of placenta praevia and accreta.
Risk of uterine rupture is also inc with spontaneous labour.
Risk of antepartum stillbirth in the next pregnancy doubles (unclear cause).

180
Q

Risk factors for uterine rupture

A 
Prev CS (LSCS < classical scars)
Obstructed labour in multips (esp if oxytocin used)
Prev cervical or uterine surgery
High forceps delivery
Internal version
Breech extraction
181
Q

Describe VBACs

A

Vaginal birth after prev CS
Successful in 7/10
1/200 will experience scar rupture

182
Q

Symptoms and signs of uterine rupture

A

Symptoms - pain is variable, some have slight pain and tenderness, others have severe pain. Vaginal bleeding is variable

Signs - maternal tachycardia, sudden maternal shock, cessation of contractions, disappearance of the presenting part from the pelvis, fetal distress

183
Q

Postpartum indicators that a uterine rupture has occurred

A

Continuous PPH with a well-contracted uterus
Bleeding continues postpartum after vaginal repair
Whenever shock is present

184
Q

Management of uterine rupture

A 
If suspected in labour, cat 1 CS
15L/min O2
IV fluids
X-match 6U of blood
Post-op ABx -> cefuroxime and metronidazole
185
Q

Define stillbirth

A

Babies born dead after (but were alive at) 24weeks completed gestation.
Can occur at any stage of pregnancy or labour.
Within hours of fetal death in utero the skin begins to peel -> macerated stillbirths (as opposed to fresh)

186
Q

Causes of stillbirth

A 
No cause found (28%)
Placental cause (12%)
A- or PPH (11%)
Major congenital abnormality (9%)
Infection (5%)
HTN in pregnancy (6%)
Maternal disease (5%)
IUGR (7%)
Mechanical e.g. cord prolapse (8%)

Inc incidence is seen in - social deprivation, inc mat age, smoking, prev CS, IVF, and obesity

187
Q

How is a diagnosis of stillbirth made?

A

Mother usually reports absent fetal movements
No FH sounds (unreliable)
Diagnosis by absent FH beat on US

188
Q

Management of fetal death in utero

A

If mother Rh-ve give anti-D
Kleihauer stain on all women - amount fetal Hb in mat blood (fetomaternal haemorrhage)
Advise delivery if pre-eclampsia, abruption, sepsis, coagulopathy, or membrane rupture.
If safe, mother can go home to reflect and collect things
IOL with mifepristone PO, adding prostaglandin vaginally (oxytocin aug may be needed later)
Ensure good analgesia and don’t leave them unattended

189
Q

Investigations to establish cause of stillbirth

A

Maternal:

  • bloods -> Kleihauer, FBC, CRP, LFT, TFT, HbA1c, glucose, blood culture, viral screen (TORCH), thrombophilia, antibodies
  • other -> MSU, cervical swabs

Fetal:

  • thorough exam +/- post-mortem
  • blood -> cord sample
  • tissue sample -> metabolic studies
  • placental histology
190
Q

Define primary PPH

A

Loss of >500ml in the first 24h after delivery (major if >1L)

191
Q

Causes of PPH

A

4 Ts:

  • Tone -> uterine atony (90%)
  • Tissue -> retained products of conception
  • Trauma -> genital tract trauma (7%)
  • Thrombin -> clotting disorders (3%)
192
Q

Define massive obstetric haemorrhage

A

Loss of >1500mls

Should prompt a 2222 call

193
Q

Management of PPH

A

Help! - life-threatening emergency (senior midwife, obs reg and SHO, anaesthetic reg)

As normal A-E
Deliver placenta, empty uterus of clots or retained tissue
Massage uterus to generate contraction/perform bimanual compression
Drugs to contract uterus:
- IM ergometrine (or slow IVI), or
- IM Syntometrine (ergometrine + oxytocin), or
- consider carboprost
- if above fail, give misoprostol

If ongoing bleeding after 2 doses of carboprost - take to theatre for balloon compression

194
Q

Define secondary PPH

A

Excessive blood loss from the genital tract after 24h from delivery.
Usually occurs between 5 and 12d and is usually due to retained placental tissue or clot, often with infection.

195
Q

List some risk factors for PPH

A

Antenatal - prev PPH, BMI>35, mat Hb <85, APH, multips >4, age >35, uterine malformation/fibroids, large placental site (twins), low placenta, overdistended abdo, abruption

In labour - prolonged, induction or oxytocin use, precipitate labour, operative birth or CS

196
Q

Define a delayed 3rd stage of labour

A

If not complete within 30min of active management, or by 60min of physiological 3rd stage

197
Q

Associations with retained placenta

A 
Previous retained placenta or uterine surgery
Preterm delivery
Mat age >35
Placental weight <600g
Parity >5
Induced labour
Pethidine used in labour
198
Q

Management of retained placenta

A

Check placenta isn’t in vagina
Palpate abdo and put baby to breast (stimulates oxytocin)
Give 20IU oxytocin into umbilical vein
Empty bladder

If still not delivered in 30mins, examine and consider manual removal in theatre

199
Q

Define vasa praevia

A

Fetal vessels from velamentous insertion (umbilical vessels go within membranes before placental insertion) risk damage a membrane rupture, causing fetal haemorrhage.
CS is needed

200
Q

Define placenta accreta

A

Abnormal adherence of all or part of the placenta to the uterus.
Predisposed to PPH

201
Q

Define placenta praevia. What are the risks?

A

Placenta lies in lower uterine segment

Risks - significant haemorrhage by mother and fetus

202
Q

Associations of placenta praevia

A 
CS
Multip
Multiple pregnancy
Mother >40
Assisted conception
D+C
Fibroids
Endometritis
203
Q

Management of placenta praevia

A

Major (when placenta covers the internal OS) requires CS
Minor (in lower segment, but doesn’t cross int OS) can attempt vaginal delivery unless placenta encroaches within 2cm of OS

204
Q

Describe DIC in pregnancy. What are the known trigger?

A

Always 2’ to stimulation of coagulation by pro-coagulant substance release in the maternal circulation.

Triggers - retention of dead fetus, pre-eclampsia, placental abruption, endotoxic shock, amniotic fluid embolism, placenta accreta, prolonged shock from any cause, acute fatty liver of pregnancy

205
Q

Outline the pathogenesis of DIC in pregnancy

A

Thromboplastins are released into the circulation, fibrin and platelets are consumed as intravascular clotting occurs.

206
Q

Investigations for DIC in pregnancy

A

Dec factors II, V, VII
Dec fibrinogen
Inc fibrin degradation products

If DIC is possibility, also send for X-match, platelets, PTT, PT

207
Q

Management of DIC in pregnancy

A

Manage any heavy bleeding/shock
If prolonged bleeding and low platelets -> give platelets
Calcium gluconate may be needed (to counteract citrate in stored blood)
Get haematology help!

208
Q

Define AI thrombocytopenic purpura

A

IgG antibodies cause thrombocytopenia in the mother and in 10% can cause thrombocytopenia in fetus (can cross placenta)

209
Q

Management of AI thrombocytopenic pupura

A

If mat platelets fall below 50 near delivery, give steroids.
Splenectomy is rarely necessary during pregnancy
Aim for non-traumatic delivery (no FBS, FSE, ventouse, rotational forceps)
Treatment isn’t needed unless surgery is contemplated

210
Q

Causes of thrombocytopenia in pregancy

A 
Spurious
Gestation - usually mild and self-limiting
Idiopathic thrombocytopenic purpura
Pre-eclampsia 
DIC and haemolytic uraemic syndrome
Folate deficiency
Congenital
Bone marrow disease, hypersplenism
HELLP syndrome
211
Q

Risk factors for amniotic fluid embolism

A 
Multiple pregnancy
Mat age >35
CS
Instrumental delivery
Eclampsia
Polyhydraminos
Placental abruption
Uterine rupture
IOL
212
Q

What is moulding in a newborn?

A

Natural phenomenon where the skull bones override each other to dec diameter of head

213
Q

What is cephalhaematoma

A

Subperiosteal swelling of fetal head (usually over parietal bones)
Spontaneous absorption occurs but may take weeks

214
Q

Risk factors for maternal anal sphincter injury

A 
Baby >4K
Persistent OP position
Induced labour
Epidural
2nd stage >1hr
Midline episiotomy
Instrumental delivery
215
Q

Define 1st degree perineal tears

A

Superficial and don’t damage muscle

Should be sutured unless the skin edges are well apposed

216
Q

Define 2nd degree perineal tears

A

Involve perineal muscle

Repair is similar to an episiotomy

217
Q

Define 3rd degree perineal tears

A

Involves anal sphincter muscle

218
Q

Define 4th degree perineal tears

A

Anal/rectal mucosa involved

219
Q

Which tissues are incised in an episiotomy?

A

Vaginal epithelium
Perineal skin
Bulbocavernous muscle
Superficial and deep transverse perineal muscles

220
Q

Describe the repair of an episiotomy

A

Use resorbable suture
Start with vaginal mucosa, then muscles, then close skin
Perform rectal exam to check sutures haven’t penetrated the rectal muscles a

221
Q

Define the puerperium

A

6wks after delivery

222
Q

Outline the contraceptive options after birth

A

Lactational amenorrhoea - breastfeeding delays return of ovulation (98% if fully breastfeeding day and night, amenorrhoeic, and <6m PP)
PoP - can be started any time PP, but if after day 21 barrier contraception is needed for 2d
COCP - start at 3wks if not breastfeeding. Can affect early milk production so not recommended if breastfeeding until 6m
Depot injections/implant - not recommended until 6wks in those breastfeeding
IUD - should be inserted within 48hrs PP or delayed until 4wks

223
Q

Outline the normal sequence of puberty in girls

A

Breast buds -> growth of pubic hair -> axillary hair -> menarche

224
Q

Describe the hormonal changes during the menstrual cycle

A

1) Pulsatile production of GnRH by hypothal stimulates pit to produce FSH + LH
2) FSH + LH stimulate ovary to produce oestrogen + progesterone
3) Oes + Prog modulate production of FSH + LH via feedback
4) In 1st 4d FSH are high -> stimulating 1’ follicle to develop
5) Follicle produces oestrogen -> stimulates proliferative endometrium
6) 14d before menstruation oestrogen levels are high enough to produce LH surge -> stimulates ovulation
7) Follicle forms corpus luteum and produces prog -> endometrium prepares for implantation (secretory phase)
8) If egg isn’t fertilised, the corpus luteum breaks down and hormone levels fall -> causes spiral arteries in uterine endothelial lining to constrict and lining sloughs

225
Q

Define 1’ amenorrhoea

A

Failure to start menstruating

Needs investigating in a 16yo, or in a 14yo without breast development

226
Q

Define 2’ amenorrhoea. Give some causes

A

When periods stop for >6m, other than due to pregnancy.

Causes:

  • HPO causes are common as it’s easily disturbed (eg by stress, exercise, weight loss)
  • hyperprolactinaemia
  • ovarian causes -> PCOS, tumours, ovarian insufficiency/failure
  • uterine causes -> pregnancy-related, uterine adhesions after D+C
227
Q

Define oligomenorrhoea

A

Infrequent periods

Common in the extremes of reproductive life when regular ovulation often doesn’t occur

228
Q

Define 1’ dysmenorrhoea. How would you manage it?

A

Painful periods without organ pathology
Excess prostaglandins cause painful uterine contractions -> ischaemic pain

Manage with NSAIDs eg mefenamic acid or paracetamol

229
Q

Define 2’ dysmenorrhoea

A

Painful periods with associated pathology: adenomyosis, endometriosis, PID, fibroids
More constant throughout the period and may be associated with deep dyspareunia

230
Q

Causes of intermenstrual bleeding

A

May follow a mid cycle fall in oestrogen production
Others - cervical polyps, ectropion, carcinoma, cervicitis/vaginitis, hormonal contraception, IUD, chlamydia, pregnancy-related

231
Q

Causes of postcoital bleeding

A

Cervical trauma
Polyps
Cervical, endometrial and vaginal carcinoma
Cervicitis and vaginitis of any cause

232
Q

Define postmenopausal bleeding and give some causes

A

Bleeding occuring >1yr after last period
Endometrial carcinoma until proven otherwise
Other causes - vaginitis, foreign bodies, carcinoma of cervix or vulva, endometrial or cervical polyps, oestrogen withdrawal

233
Q

Investigations for amenorrhoea

A

Bedside - urine B-hCG
Bloods: free androgen index (inc in PCOS), FSH/LH (dec in HPO cause but may be normal), prolactin, TFTs, testosterone level

234
Q

What are the clinical features of PCOS

A

Hyperandrogenism
Oligomenorrhoea
PCO on US (in the absence of other causes of PCO - adrenal hyperplasia + Cushing’s)

235
Q

How is a diagnosis of PCOS made?

A

Rotterdam criteria (2/3 must be present)

  • PCO (12 or more follicles or ovarian volume >10cm3 on US)
  • oligo-ovulation or anovulation
  • clinical and/or biochemical signs of hyperandrogenism

Other causes of irregular cycles should be excluded before the diagnosis is made (thyroid, hyperprolactinaemia, adrenal hyperplasia, androgen secreting tumours, Cushing’s)

236
Q

Management of PCOS

A

Weight loss and exercise - inc insulin sensitivity
Metformin improves insulin sensitivity in short term and may improve menstrual disturbance and ovulatory function
Clomifene induces ovulation - only by specialist
Ovarian drilling
COCP - control bleeding

237
Q

Long-term consequences of PCOS

A 
Gestational DM
T2DM
CV disease
Endometrial cancer
-> no inc risk of ovarian or breast Ca
238
Q

Briefly outline the causes and investigations for menorrhagia

A

Causes:

  • mostly DUB -> absence of pelvic pathology
  • with inc age -> IUD, fibroids, endometriosis, adenomyosis, pelvic infection, polyps, hypothyroid, coag disorders
  • > 45yo -> consider endometrial Ca

Investigations:

  • exclude pregnancy
  • FBC, haematinics, TSH
  • smear + STI screen
  • if >45yo -> TVUS +/- biopsy
239
Q

Management of menorrhagia

A

1) Mirena IUS
2) Antifrinolytics -> tranexamic acid
3) NSAIDs -> mefanamic acid
4) COCP
5) IM progestogens

240
Q

Symptoms of the menopause

A

Menstrual irregularity as cycles become anovulatory, before stopping
Vasomotor disturbance - sweating, palpitations, flushes
Atrophy of oestrogen-dependent tissues (genitalia, breasts) and skin
Osteoporosis

241
Q

Management of menopausal symptoms

A

HRT:

  • oestrogen-only -> only in women without a uterus!
  • combined oestrogen/progestrogen (cyclical or continuous)
242
Q

CI to HRT

A 
Oestrogen-dependent Ca
Past PE
Undiagnosed PV bleeding
Raised LFTs
Pregnancy
Breastfeeding
Phlebitis
243
Q

SEs of HRT

A 
Fluid retention
Bloating
Breast tenderness
Nausea
Headaches
Leg cramps
Dyspepsia
Mood swings
Depression
Acne
Backache
244
Q

Alternatives to HRT

A

SSRIs can help with vasomotor symptoms
Osteoporosis treated with calcium + vit D + bisphosphonates
Local vaginal oestrogen or lubricants

245
Q

Benefits of HRT

A

Dec vasomotor symptoms
Improved urogenital symptoms and sexual function
Osteoporotic fractures are reduced
Dec risk of colorectal Ca

246
Q

Risks of HRT

A

Breast Ca risk inc
Unopposed oestrogens inc endometrial Ca risk
Doubles risk of VTE
Inc gallbladder disease

247
Q

Outline the 5 scenarios that an abortion is legal under the Abortion Act

A

1) Risk to mother’s life if pregnancy continues
2) Necessary to prevent permanent grave injury to physical/mental health of the woman
3) Continuance risks injury to the physical/mental health of the woman greater than if terminated (and fetus not >24wks)
4) Continuance risks injury to physical/mental health of existing children of the woman greater than if terminated (and fetus not >24wks)
5) Substantial risk that if the child were born he/she would be seriously handicapped

248
Q

What should be done before a TOP takes place?

A

Counselling and support - verbal + written info
US to confirm gestation and non-viable/ectopics
Screen for chlamydia +/- other STIs
ABx prophylaxis - metronidazole + azithryomycin
Discuss contraception
If RhD-ve she needs anti-D

249
Q

Outline what medications may be used in a medical TOP

A 
An antiprogestagen (mifepristone) to prime cervix
Prostaglandin (misoprostol)
250
Q

Complications of TOP

A 
Failed TOP (<1%)
Infection (2%)
Haemorrhage
Uterine perforation
Uterine rupture
Cervical trauma (1%)
Retained products of conception (1%)
251
Q

Define threatened miscarriage

A

Mild early pregnancy bleeding with a closed cervical os

75% will settle

252
Q

Define inevitable miscarriage

A

Severe early pregnancy bleeding and open cervical os

253
Q

Define incomplete miscarriage

A

Most products of conception have already been passed

254
Q

Define missed miscarriage. How is it confirmed?

A

Fetus dies but remains in utero

May have been bleeding and/or pain or no symptoms
Cervix is closed
US shows pole >7mm with no FH

255
Q

Management of miscarriage

A

Expectant - appropriate if not bleeding heavily, effective for incomplete, but less so for missed miscarriage. Rescan in 2wk

Medical - mifepristone and misoprostol

Surgical - if heavy/persistent bleeding >2wk, or pt choice. Surgical evacuation under GA

256
Q

Causes of mid-trimester miscarriage

A

Mechanical - cervical weakness, uterine abnormalities, chronic mat disease, infection

257
Q

Define recurrent miscarriage

A

Loss of 3 or more consecutive pregnancies before 24wks with the same biological father.
Prognosis for future successful pregnancy is affected by prev number of miscarriages, and mat age

258
Q

Causes of recurrent miscarriage

A

Endocrine - uncontrolled disease
Infection - BV
Parental chromosome abnormality - balanced reciprocal or Robertsonian translocation
Uterine abnormality
Antiphospholipid syndrome
Thrombophilia - factor V Leiden, protein C and S deficiency
Alloimmune causes - woman share HLA alleles with partner so don’t mount satisfactory protective response to the fetus

259
Q

Antibodies seen in antiphospholipid syndrome. How would you manage it?

A

Lupus anticoagulant, phospholipid, and anticardiolipin antibodies

Give aspirin from day of +ve test, and LMWH as soon as FH seen until delivery

260
Q

Predisposing factors for ectopic pregnancy

A 
Damage to tubes - PID, prev surgery, prev ectopic, 
Endometriosis
IUD
PoP
Subfertility and IVF
Smoking
261
Q

Common sites of ectopic pregnancy

A

97% are tubal, mosttly in ampulla, 25% in narrow isthmus

3% implant on ovary, cervix, or peritoneum

262
Q

Symptoms and signs of ectopic pregnacny

A

Consider in any sexually active woman with abdo pain, fainting, or D+V

  • often no symptoms or signs
  • amenorrhoea 6-8wks
  • pain -> may be nonspecific, usually unilateral
  • vaginal bleeding
  • diarrhoea +/- vomiting
  • dizziness
  • shoulder tip pain from diaphragmatic irritation from haemoperitoneum
  • collapse
  • normal sized uterus
  • cervical excitation +/- adnexal tenderness
  • rarely adnexal mass
  • peritonism
263
Q

Investigations for ectopic pregnancy

A

Bedside - urine B-hCG
Bloods - FBC, group and save, serum progesterone (identify failing pregnancy), serum hCG
Imaging - TVUS

264
Q

Management of ectopic pregnancy

A

If woman is stable, they should be offered the options of expectant and medical management so long as:

  • asymptomatic or mild symptoms
  • hCG <3000
  • ectopic pregnancy <3cm on scan with no FH
  • no haemoperitoneum on TVS
  • woman understands risks

Otherwise, surgical management is needed

265
Q

Outline expectant and medical management of ectopic pregnancy

A

Expectant - take hCG every 4h until fall, then weekly until <15

Medical - methotrexate single dose, then hCG level on days 4 and 7
-> advise to use reliable contraception for 3m afterwards

266
Q

Outline the surgical management of ectopic pregnancy

A

Laparoscopy is preferred treatment, but if haemodynamically unstable then laparotomy may be indicated.

If contralateral tube is healthy, a salpingectomy (removal of tube) is preferred over a salpingotomy (removal of ectopic though tubal incision).

267
Q

Describe hCG levels in early pregnancy

A

hCG should risk >66% every 48hr
No correlation between level and gestation
Unreliable in multiple pregnancies and after assisted conception with hCG support

268
Q

Define hydatidiform moles

A

Tumours consist of proliferating chorionic villi which have swollen and degenerated.
Derived from chorion
Produces lots of hCG -> exaggerated pregnancy symptoms and strongly +ve tests

269
Q

Management of hydatidiform moles

A

Removed by gentle suction
Give anti-D if rhesus -ve
Avoid pregnancy until hCG normal for 6m

270
Q

Causes of pruritus vulvae. How might you manage it?

A

Local - infection (candida), allergy, infestation (scabies, lice), vulval dystrophy (lichen sclerosis, carcinoma)
Systemic - general pruritis or skin disease (psoriasis, lichen plans)

Treat underlying cause. Betamethasone may help

271
Q

What is lichen sclerosis? How is it managed?

A

AI disorder where elastic tissue turns to collagen
Vulva gradually becomes white, flat, and shiny, and is intensely itchy
May be pre-malignant

Treat with clobetasol cream daily for 28d, then alt days for 4wks

272
Q

What is VIN? What are the known causes?

A

Vulval intra-epithelial neoplasia

Cause is most often HPV (esp 16), may not be visible warts.

273
Q

Management of VIN

A

If VIN found on biopsy, examine cervix and anal canal (if <1.5cm)
Surveillance is key, with biopsy of suspicious lesions
Painful or irritating lesions can be removed, but not recommended otherwise due to high recurrence rates and poor functional outcome.

Medical - imiquimod cream

274
Q

Causes of vulval lumps

A 
Local varicose veins
Boils
Sebaceous cysts
Viral warts
Bartholin’s cyst or abscess
Uterine prolapse or polyp
Inguinal hernia
Carcinoma
275
Q

Describe viral warts (virus strains, incubation etc) and their treatment

A

HPV 6 and 11
Incubation may be weeks, and partner may not have obvious warts
Warts can be florid in the pregnant and immunosuppressed

Treat with cryotherapy, trichloroacetic acid, or electrocautery in clinic, or with podophyllotoxin at home

276
Q

Describe Bartholin’s cysts and abscesses

A

Bartholin’s glands and ducts lie under the labia minora and secrete thin lubricating mucus during sexual excitation.
If the duct blocks, a painless cyst forms
If the cyst becomes infected the resulting abscess is extremely painful and a hugely swollen, hot red labium is seen

Treat with incision and drainage

277
Q

Causes of vulval ulcers

A

Consider syphilis
Herpes simplex is common in young
Others - carcinoma, chancroid, lymphogranuloma, TB, Behcet’s, aphthous ulcers, Crohn’s

278
Q

Describe herpes simplex infection of the genitals

A

Type II is the strain that classically causes genital infection, but either type can be the cause.
3rd most common STI in UK

1’ infection is usually most severe - prodrome of itching/tingling and flu-like symptoms, progressing to vulvitis, pain and small vesicles on the vulva.
Recurrent attacks are usually less severe and may be triggered by illness, stress, sexual intercourse ad menstruation

279
Q

Treatment of HSV infection of the vulva

A

Strong analgesia, lidocaine gel, salt baths
Exclude coexistence infections
Aciclovir shortens symptoms (oral, not topical)

280
Q

Describe the transmission of HSV

A

Can be transmitted during asymptomatic phases of viral shedding, and from areas of the genitals not protected by condoms

281
Q

Describe carcinoma of the vulva and its management.

A

90% are squamous
Others - melanoma, BCC, or carcinoma of Bartholin’s glands

Present as lump or ulcer (may not be notices unless it causes pain or bleeding)

Management - excision of tumour +/- lymph node excision

282
Q

Describe the epithelium of the cervix. Describe the transitional zone

A

Endocervical canal = mucous columnar epithelium
Vaginal cervix = squamous epithelium

The transitional zone between them (squamo-columnar junction) is the area most at risk of malignant change

283
Q

Define cervical ectropion/erosion. When would you expect to see it?

A

There is a red ring around the os because the endocervical epithelium has extended its territory over the paler epithelium of the ectocervix.
Ectropion is prone to bleeding, excess mucus production, and to infection

Seen temporarily under hormonal influence during puberty, the COCP, and during pregnancy

284
Q

What’s looked for on cervical smears?

A

Cervical cells are collected for microscopy for dyskaryosis

  • Borderline or mild changes are tested for HPV, if +ve -> colposcopy
  • moderate or severe changes require colposcopy regardless of HPV status
285
Q

Risk factors for CIN

A 
Persistent high-risk HPV infection
Exposure to HPV is inc by multiple partners
Smoking 
Immunocompromise
OCP
286
Q

Outline the English cervical screening criteria

A

Sexually active women aged 25-64

3-yearly for women 25-50, and 5-yearly until 64 (if normal)

287
Q

Describe what happens in colposcopy

A

Examination of cervix with colposcope (microscope) and speculum
Transformation zone is painted with acetic acid which is taken up preferentially by neoplastic cells
Punch biopsy of any white areas (taken up acetic acid) for histological diagnosis
Colposcopy cannot diagnoses adenocarcinoma

288
Q

Complications for LLETZ

A 
Haemorrhage
Infection
Vasomotor-vagal symptoms and signs
Anxiety
Cervical stenosis
Small risk of cervical incompetence and premature delivery
289
Q

Symptoms and signs of cervical Ca

A

Post-coital and/or post-menopausal bleeding or watery vaginal discharge
Features of advanced disease - heavy vaginal bleeding, ureteric obstrucion, W/L, bowel disturbance, vesicovaginal fistula, pain

290
Q

Causes and presentation of endometritis

A

Uncommon unless cervical mucus and acid vaginal pH is damaged - miscarriage, TOP, childbirth, IUD insertion, surgery

Presentation - lower abdo pain, fever, uterine tenderness, offensive vaginal discharge

291
Q

Tests and treatment of endometritis

A

High vaginal swabs
Blood cultures if septic
Remove IUD if not responding to ABx
Give cefalexin with metronidazole

292
Q

Outline the normal thickness of the endometrium during a cycle

A

<5mm early cycle
11mm in proliferative phase
7-16mm in late cycle

293
Q

What measurements of endometrial thickness would warrant a hysterosopy?

A

> 20mm, or >4mm if postmenopausal

294
Q

Describe fibroids

A

Benign SM tumours of the uterus (leimyomas)
Often multiple and vary in size
They’re oestrogen dependent - enlarge in pregnancy and on COCP and atrophy after the menopause

295
Q

Presentation of fibroids

A

Menorrhagia - heavy and prolonged
Fertility problems - may interfere with implantation
Pain - due to torsion of a pedunculated fibroids
Mass - may be felt abdominally, press on bladder, or on veins

296
Q

Management of fibroids

A

If symptoms are minimal, no treatment is needed.

  • GnRH analogues prior to surgery can shrink them, but isn’t long-term option
  • myomectomy
  • uterine artery embolisation
  • hysterectomy
297
Q

Describe endometrial cancer and its risk factors

A

Most are adenocarcinomas
Risk factors - obesity, T2DM, HTN, nulliparity, anovulatory cycles (PCOS), early/late menopause, generic predisposition (HNPCC), breast Ca, oestrogen-only HRT

Protective factor are parity and the COCP

298
Q

How is diagnosis of endometrial Ca made?

A

Suspect if PMB - early sign
TVS shows thickness >4mm
Hysteroscopy + biopsy
CT/MRI for staging

299
Q

Presentation of ovarian cysts

A

Asymptomatic
Chronic pain with dull ache, dyspareunia, cyclical pain, pressure effects
Acute pain due to bleeding into cyst, ovarian torsion, or rupture
Irregular vaginal bleeding
Hormonal effects
Abdo swelling or mass

300
Q

Management of ovarian cyst

A

If acute and unstable -> laparoscopy

Premen:

  • If stable, no features of malignancy, asymptomatic and <5cm -> no surgical intervention
  • If >5cm, symptomatic or features of a dermoid/endometriosis -> ovarian cystectomy

Postmen:
Calculate risk of malignancy index
- low risk and <5cm -> TVS and CA125 every 4m for 1y
- moderate risk -> bilateral oophorectomy
- high risk -> refer to cancer centre

301
Q

Define functional cysts

A

Enlarged or persistent follicular or corpus luteum cysts
Can be considered normal if <5cm
Can cause pain by rupture, failing to rupture at ovulation, or bleeding
If <5cm, usually resolve over 2-3 cycles

302
Q

Define endometriomas

A

Ovarian cysts filled with old blood (aka chocolate cysts)

303
Q

Risk and protective factors for ovarian cancer

A

Nulliparity
Early menarche and/or late menopause
BRCA 1 and 2 mutations
HNPCC

Protective factors - pregnancy, breastfeeding, COCP, tubal ligation

304
Q

Presentation of ovarian Ca

A 
Often vague symptoms - misinterpreted at IBS, diverticula disease
Bloating
Unexplained W/L, loss of appetite, early satiety
Fatigue
Urinary symptoms
Change in bowel habit
Abdo or pelvic pain
Vaginal bleeding
Pelvic mass
305
Q

Investigations for ovarian cancer

A

Bloods - CA125, (AFP, LDH, hCG if <45)
Imaging - TVS, CXR, CT abdo/pelvis, MRI
Other - any ascites should be sampled and sent for cytology

306
Q

Describe the presentation, investigations, and treatment of thrush

A

Presentation - red, fissures and sore vulva, non-offensive discharge

Diagnosis - clinical, or via microscopy and culture

Treat - topical clotrimazole (pessary + cream), or fluconazole PO

307
Q

Describe the presentation, investigations, and treatment of trichomoniasis

A

STI producing vaginitis and a bubbly, thin, fish-smelling discharge

Diagnosis - exclude gonorrhoea, motile flagellates are seen on wet films

Treat - metronidazole

308
Q

Describe the presentation, investigations, and treatment of bacterial vaginosis

A

Mostly asymptomatic. Discharge has fishy odour, and vagina is not inflamed or itchy

Diagnosis - culture

Treat - metronidazole

309
Q

Describe the presentation, complications, investigations, and treatment of chlamydia

A

70% are asymptomatic
May have dysuria, vaginal discharge, and/or IMB or PCB

Complications - PID, perihepatitis
Diagnosis - vulvovaginal or endocervical swab

Treat - azithromycin or doxycycline (erythro in pregnancy)

310
Q

Describe the presentation, complications, investigations, and treatment of gonorrhoea

A

Often no symptoms, may have lower abdo pain, vaginal discharge, IM or PCB

Complications - PID, disseminated gonorrhoea
Diagnosis - vulvovaginal or endocervical swab

Treat - ceftriaxone IM + azithromycin PO

311
Q

Causes and presentation of PID

A

Causes - STIs, uterine instrumentation, postpartum

Presentation - lower abdo pain, deep dyspareunia, vaginal discharge, IM or PCB, dysmenorrhoea, and/or fever
O/E there’s cervical excitation +/- adnexal tenderness

312
Q

Investigations for PID

A

Bedside - vulvovaginal/endocervical swabs for STI
If acutely unwell:
- bloods -> FBC, CRP, blood cultures

If turbo-ovarian abscess suspected -> TVS

313
Q

Complications of PID

A 
Turbo-ovarian abscess
Fits-Hugh-Curtis syndrome
Recurrent PID
Ectopic pregnancy
Subfertility from tubal blockage
314
Q

Management of PID

A

Ceftriaxone IM stat + doxycycline PO 14d + metronidazole PO 14d

315
Q

Define endometriosis. What’s adenomyosis?

A

Endometriosis = presence of endometriotic tissue outside the uterus (hormonally driven - oestrogen)

Adenomyosis = pence of endometrial tissue within myometrium

316
Q

Causes of endometriosis

A

Unknown! Three theories:

1) Retrorade menstruation -> adherence, invasion, and growth of tissue
2) Metaplasia of mesothelial cells
3) Impaired immunity -> cells from retrograde menstruation aren’t destroyed by immune response

317
Q

Presentation of endometriosis

A 
Pain:
- cyclical due to endometrial tissue responding to menstrual cycle
- constant due to adhesions
- severe dysmenorrhoea
- deep dyspareunia
- dysuria
Subfertility
No symptoms
318
Q

Investigations for endometriosis

A

TVS for ovarian endometriotic cysts
MRI for suspected bowel involvement

Laparoscopy is gold-standard

319
Q

Management of endometriosis

A

Medical - COCP, progestagens, GnRH analogues (short-term)

Surgical (if medical therapy has failed) - laparoscopy with ablation or excision of endometriosis

320
Q

Describe prolapses. What are the different types?

A

Occurs when weakness of supporting structures allows pelvic organs to protrude within vagina.

Cystocele
Rectocele
Enterocele
Uterine prolapse

321
Q

Outline the grading of prolapse

A

1st-degree - lowest part of prolapse descends 1/2way down vaginal axis
2nd - lowest part of prolapse extends to level of introitus, and through on straining
3rd - lowest part of prolapse extends through introitus and outside the vagina

322
Q

Symptoms of prolapse

A 
May be asymptomatic
Dragging sensation
Discomfort
Dyspareunia
Backache

With cystocele - urgency, frequency, incomplete emptying, retention
With rectocele - constipation, difficulty with defectation

323
Q

Management of prolapse

A

Mild - reduction in intra-abdo pressure (w/l, stop smoking, stop straining), improved muscle tone

Pessaries are useful if surgery not wanted/CI, but affect sexual function

Surgery if symptoms are severe, they’re specially active, and pessaries have failed. Type of repair depends on type of prolapse

324
Q

When would you offer investigation for subfertility?

A

After 1yr of trying, or earlier if:

  • maternal age >35
  • amenorrhoea
  • oligomenorrhoea
  • past PID
  • undescended testes
  • prev Ca treatment
325
Q

Causes of subfertility

A 
Unexplained (28%)
Male factor (25%)
Anovulation (21%) - premature ovarian failure, Turner’s, surgery, chemo, PCOS
Tubal factor (15-20%)
Endometriosis (6-8%)
326
Q

Primary care investigations for subfertility

A

Chlamydia screening
Baseline hormonal profile (day 2-5 FSH and LH)
TSH, prolactin, testosterone, rubella status
Mid-lateral progesterone level to confirm ovulation (7d before period)
Semen analysis

327
Q

Secondary care investigations for subfertility

A

TVS - rule out adnexal masses, fibroids, or polyps

Hysterosalpingogram - X-RAY + contrast injected through cervix to see anatomy and tubal potency

328
Q

Outline the methods of ovulation induction

A 
Weight loss or gain
Clomifene - anti-oestrogen that inc FSH via neg feedback
Laparoscopic ovarian drilling - in PCOS
Gonadotrophins
Metformin - controversial, used in PCOS
329
Q

Indications for IVF

A 
Tubal disease
Male factor
Endometriosis
Anovulation 
Subfertility due to mat age
Unexplained subfertility >2yrs
330
Q

Outline the NHS funding of IVF

A

Inclusion criteria ranges, but generally limited to:

  • couples with no children
  • non-smokers
  • BMI <30
  • <42yrs of age (35 in some counties)
  • no requirement of gamete donation
331
Q

Outline the process of spermatogenesis

A

Takes place in the seminiferous tubules
Undifferentiated diploid germ cells (spermatogonia) multiply and are transformed into haploid spermatozoa (takes 74d)
FSH and LH are both important for initiation of spermatogenesis at puberty - LH simulates Leydig cells to produce testosterone, test+FSH stimulate Sertoli cells to produce substances for metabolic support of spermatogenesis

332
Q

Outline some of the male factors leading to subfertility

A

Semen abnormality
Azoospermia
Immunological
Coital dysfunction

333
Q

Problems with IUD

A

May be expelled (esp if nulliparous or distorted uterus
Associated with PID
May cause dysmenorrhoea and menorrhagia
Risk of ectopic pregnancy is 1:20 if she becomes pregnant

334
Q

CI to IUD

A 
Pregnancy
Current pelvic infection/STF
Allergy to copper
Wilson’s disease
Heavy/painful periods
Trophoblastic disease or gynae malignancy
Undiagnosed abnormal uterine bleeding
Distorted cavity
335
Q

What are the options for emergency contraception?

A

IUD - more effective than meds, can be inserted within 5d
Ullipristal acetate (EllaOne) - initiate with 5d of UPSI, inbihits/delays ovulation. Avoid if taken/taking enzyme inducer
Levonorgestrel - initiate within 3d of UPSI (preferably within 12h)

Warn that effective contraception should be used until the next period (unless immediately starting OCP, then additional precaution for 7d COCP, or 2d PoP)

336
Q

Reasons to avoid COCP

A

Venous disease - current/past VTE, if >1 of: >35, smoker, BMI >30, FHx VTE, immobility
Arterial disease - valvular or congenital HD with complications, Hx stroke, TIA, IHD, PVD, HTN retinopathy, Hx migraine with aura, BP<140
Liver disease
Cancer
Prev pregnancy complications - pruritis, obstetric cholestasis, chorea
Hepatic enzyme-inducing drugs - rifampicin etc

337
Q

Absolute CI to COC use

A

Migraine with aura
Migraine without aura in women with >1 risk factor for stroke
Severe migraine or migraine lasting >72h
Migraine treated with ergot derivatives

338
Q

Short term SEs of COC use

A

Oestrogenic - breast tenderness, nausea, cyclical weight gain, bloating, vaginal discharge
Progestogeic - mood swings, PMT, vaginal dryness, sustained weight gain, dec libido, acne
Headache
Breakthrough bleeding

339
Q

When is the best time to start CHCs or PoPs?

A

Day 1 of cycle (if started on day 1-5, cover is immediate, otherwise, use condoms for 7d)
Day of TOP
>21d postpartum (>6wk if CHC and breastfeeding)
>2wks after fully mobile post major surgery

340
Q

Reasons to avoid PoC

A

Current breast Ca
Trophoblastic disease
Liver disease
New symptoms or diagnosis of migraine with aura, IHD, stroke/TIA when taking PoC
Avoid if SLE with antiphospholipid antibodies
Any undiagnosed vaginal bleeding should be investigated first

341
Q

SEs of PoP

A 
Higher failure rate than COCP
Menstrual irregularities
Inc risk ectopics
Breast tenderness
Depression
Acne
Dec libido
Weight change
342
Q

Describe the maintenance of continence in women

A

Maintained in the urethra by the external sphincter and pelvic floor muscles maintaining a urethral pressure higher than bladder pressure.

343
Q

Investigations for incontinence

A

Bedside - urine dip and MC+S/MSU
Bloods - OGTT if DM suspected
Imaging - not routinely used but US to exclude incomplete bladder emptying
Others - urodynamics, cystoscopy

344
Q

Management of stress incontinence

A

Conservative - optimise medical problems, pelvic floor exercises
Medical - duloxetine (rarely used)
Surgical - peri-urethral injections of bulking ages to, tension-free vaginal tape, transobturator tape

345
Q

Management of overactive bladder syndrome

A

Avoid excessive fluid intake
Dec caffeinated and carbonated drinks + alcohol
Bladder retraining to suppress urge and extend intervals between voiding
Anticholinergic relax deter us or (oxybutynin)
IV oestrogen cram
Botulinum toxin injection into detrusor

346
Q

Total vs subtotal hysterectomy

A 
Total = including cervix
Subtotal = leaving cervix behind (will need to have smears)
347
Q

Risks of a hysterectomy

A

Bleeding
Infection
Injury to bladder, bowel, vessels or ureters
Scarring
VTE
Earlier menopause even if ovaries retained (share blood supply with uterine arteries)

348
Q

What is pelvic congestion?

A

Controversial diagnosis!
Congested lax pelvic veins cause pain that’s worse on standing, walking, and premenstrually.
Typically variable in site and intensity
Deep palpating reveals max tenderness over ovaries
Vagina and cervix may look blue from congestion

349
Q

What is ovarian hyperstimulation syndrome? What are the characteristic features?

A

Complication of ovulation induction or superovulation
Systemic disease

Features - ovarian enlargement, fluid shift from IV to EV space

350
Q

Risk factors for ovarian hyperstimulation syndrome

A

Young age
Low BMI
Polycystic ovaries
Previous OHSS

351
Q

Presentation and management of ovarian hyperstimulation syndrome

A

Presentation - abdo discomfort, N+V, abdo distension +/- dyspnoea

Manage mild/mod OHSS with outpatient analgesia (avoid NSAIDs), avoid strenuous exercise and sex
Manage severe OHSS as inpatient - analgesia and antiemetics, daily bloods, strict fluid balance, thromboprophylaxis

352
Q

Features of severe pre-eclampsia

A 
HTN (>170)
Proteinuria
Headache
Visual disturbance
Papilloedema
RUQ/epigastric pain
Hyperreflexia
Plts <100
353
Q

Management of pre-eclampsia

A

Treat any BP >160
Oral labetalol 1st line (nifedipine and hydralazine 2nd line)
Delivery is only definitive management

354
Q

In what scenario should anti-D immunoglobulin be given?

A
  1. Delivery of Rh +ve infant
  2. Any TOP
  3. Miscarriage >12w
  4. Ectopic managed surgically
  5. Ext cephalic version
  6. APH
  7. Amniocentesis, CVS, FBS
355
Q

When is anti-D prophylaxis given?

A

28wks

356
Q

Treatment for baby born to Hep B carrier

A

Hep B vaccine + 0.5ml HBIG within 12hrs of birth

Further hep vaccine at 1-2m, and 6m

357
Q

Outline the recommendations for folic acid during pregnacny

A

All women should take folic acid 400mcg until 12wks
Women at higher risk should take 5mg until 12wks:
- either partner has NTD, prev pregnancy with NTD, FHx NTD
- woman is taking AED or has coeliac, DM, or thalassaemia
- woman is obese (BMI>30)

358
Q

Blood test to diagnose premature ovarian failure

A

FSH level

Finals (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions